Diabetes · 2019-09-10 · Diabetes Management Journal 4 DIABETES MANAGEMENT JOURNAL August 2019...

August 2018

DiabetesManagement Journal

August 2019

REALITY CHECKWhat I detest about glucose tolerance tests

FOOD STUFFHealthy at every size and non-hungry eating

HIS BRILLIANT CAREERMy father’s T1D couldn’t stop him

DEPRESSION AND ANXIETYHow they interact with diabetes

AIMING FOR INJECTION PERFECTIONTechnique matters for optimal diabetes management

LATE-ONSET T1D More common than you think

The official journal from

DIABETIC KIDNEY DISEASE

A PRACTICAL APPROACH

Pull-out guide: The new injectables for diabetes

www.diabetesaustralia.com.au

For T2DM patients on insulin: The concern of hypoglycaemia is never far away1-3

Please review Product Information before prescribing Toujeo®. Full Product Information is available at http://products.sanofi.com.au/aus_pi_toujeo.pdf or by calling 1800 818 806.

Minimum Product Information: Toujeo (insulin glargine 300 units/mL). Indications: Treatment of diabetes mellitus in adults. Contraindications: Hypersensitivity to insulin glargine or any of the excipients. Precautions: Not recommended for treatment of diabetic ketoacidosis; hypoglycaemia; switching between insulin glargine 100 U/mL and Toujeo; switching between other insulins and Toujeo; intercurrent illness; insulin antibodies; insulin label must always be checked before each injection to avoid medication errors between Toujeo and other insulins; pregnancy category B3; lactation; careful glucose monitoring and dose adjustments may be necessary in elderly patients; not studied in children; renal and hepatic impairment. Interactions: Oral antidiabetic medicinal products; cardiovascular, analgaesic, anti-inflammatory, neurological, antipsychotic agents (see full PI); antibiotics; corticosteroids, other hormonal therapies (see full PI); diuretics; protease inhibitors; sympathomimetic agents; lithium; alcohol; sympatholytics including β-blockers; others, see full PI. Adverse Effects: Hypoglycaemia; visual impairment; injection site reactions; others, see full PI. Dosage and Administration: Subcutaneous, once daily. Not for intravenous use. Dose adjustment may be required e.g. if patient’s weight or life-style changes or change in timing of insulin dose. The desired blood glucose levels as well as doses and timing of anti-diabetic medication must be determined and adjusted individually. Instruct patients to never re-use a needle. Toujeo must not be drawn from the cartridge of the pre-filled pen into a syringe. Insulin glargine 100 U/mL and Toujeo are not bioequivalent and are not directly interchangeable. Toujeo must not be diluted or mixed with any other insulin products. When switching from insulin glargine 100 U/mL or other basal insulin products to Toujeo, dose may need to be adjusted. Close metabolic monitoring is recommended during the switch and in the initial weeks thereafter. ≥18 years. Date reviewed: 1 July 2015 Reference Document: PI, 30 June 2015.References: 1. Edridge CL et al. PLoS ONE 2015;10(6):e0126427. 2. Shafiee G et al. Journal of Diabetes & Metabolic Disorders 2012;11:17. 3. Lingvay I. US Endocrinology 2011;7(2):95-102. 4. Ritzel R et al. Diabetes Obes Metab 2018; 20(3):541–8.

T2DM = type 2 diabetes mellitus

PBS information: Toujeo® SoloStar® is listed on the PBS as a long-acting insulin analogue for the treatment of adults with type 1 and type 2 diabetes.

DIB0038_DMJ_Ads_DoublePageSpread_275x420_PR_2.indd 1 9/5/19 3:29 pm

http://products.sanofi.com.au/aus_pi_toujeo.pdf

For T2DM patients on insulin: The concern of hypoglycaemia is never far away1-3

Please review Product Information before prescribing Toujeo®. Full Product Information is available at http://products.sanofi.com.au/aus_pi_toujeo.pdf or by calling 1800 818 806.

Minimum Product Information: Toujeo (insulin glargine 300 units/mL). Indications: Treatment of diabetes mellitus in adults. Contraindications: Hypersensitivity to insulin glargine or any of the excipients. Precautions: Not recommended for treatment of diabetic ketoacidosis; hypoglycaemia; switching between insulin glargine 100 U/mL and Toujeo; switching between other insulins and Toujeo; intercurrent illness; insulin antibodies; insulin label must always be checked before each injection to avoid medication errors between Toujeo and other insulins; pregnancy category B3; lactation; careful glucose monitoring and dose adjustments may be necessary in elderly patients; not studied in children; renal and hepatic impairment. Interactions: Oral antidiabetic medicinal products; cardiovascular, analgaesic, anti-inflammatory, neurological, antipsychotic agents (see full PI); antibiotics; corticosteroids, other hormonal therapies (see full PI); diuretics; protease inhibitors; sympathomimetic agents; lithium; alcohol; sympatholytics including β-blockers; others, see full PI. Adverse Effects: Hypoglycaemia; visual impairment; injection site reactions; others, see full PI. Dosage and Administration: Subcutaneous, once daily. Not for intravenous use. Dose adjustment may be required e.g. if patient’s weight or life-style changes or change in timing of insulin dose. The desired blood glucose levels as well as doses and timing of anti-diabetic medication must be determined and adjusted individually. Instruct patients to never re-use a needle. Toujeo must not be drawn from the cartridge of the pre-filled pen into a syringe. Insulin glargine 100 U/mL and Toujeo are not bioequivalent and are not directly interchangeable. Toujeo must not be diluted or mixed with any other insulin products. When switching from insulin glargine 100 U/mL or other basal insulin products to Toujeo, dose may need to be adjusted. Close metabolic monitoring is recommended during the switch and in the initial weeks thereafter. ≥18 years. Date reviewed: 1 July 2015 Reference Document: PI, 30 June 2015.References: 1. Edridge CL et al. PLoS ONE 2015;10(6):e0126427. 2. Shafiee G et al. Journal of Diabetes & Metabolic Disorders 2012;11:17. 3. Lingvay I. US Endocrinology 2011;7(2):95-102. 4. Ritzel R et al. Diabetes Obes Metab 2018; 20(3):541–8.

T2DM = type 2 diabetes mellitus

PBS information: Toujeo® SoloStar® is listed on the PBS as a long-acting insulin analogue for the treatment of adults with type 1 and type 2 diabetes.


Please review Product Information before prescribing Lantus®. Full Product Information is available at http://products.sanofi.com.au/aus_pi_lantus.pdf or by calling 1800 818 806.

Minimum Product Information: Lantus (insulin glargine 100 units/mL). Indications: Once-daily subcutaneous administration for type 1 diabetes mellitus patients (adults and children) and type 2 diabetes mellitus patients (adults) who require insulin for control of hyperglycaemia. Contraindications: Hypersensitivity to insulin glargine or any excipient. Precautions: Hypoglycaemia; hepatic, renal and visual impairment; lipodystrophy and other injection site reactions; antibody production; intercurrent conditions; not studied in children <2 years, pregnancy category B3, lactation; not intended for i.v. use; not recommended for treatment of diabetic ketoacidosis; LANTUS MUST NOT BE DILUTED OR MIXED WITH ANY OTHER INSULIN OR SOLUTION. Instruct patient to check insulin label before each injection to avoid accidental mix-ups between insulins. Interactions: Oral antidiabetic agents; cardiovascular, analgaesic, anti-inflammatory, neurological, antipsychotic agents (see full PI); antibiotics; corticosteroids, other hormonal therapies (see full PI); diuretics; protease inhibitors; sympathomimetic agents; lithium; alcohol; sympatholytics including ϐ-blockers; others, see full PI. Side effects: Hypoglycaemia; injection site reactions; visual disturbances; others, see full PI. Dosage and Administration: ≥6 years. Subcutaneous, once daily. Lantus is equipotent to human insulin. Initial dose determined depending on desired blood glucose levels and doses and timing of any antidiabetic medication. For changeover from once daily NPH or ultralente, initial dose usually not changed; for changeover from twice-daily NPH to once-daily Lantus, initial dose usually reduced by approximately 20% compared to total daily NPH dose; for initiation of type 2 patients, initial dose usually approximately 10 IU. For changeover from once daily insulin glargine 300 units/mL to once daily Lantus, recommended initial dose is approximately 80% of insulin glargine 300 units/mL that is being discontinued. Date reviewed: 04 December 2017. Reference Document: PI, 04 October 2017. ®Toujeo and Lantus are registered trademarks of sanofi-aventis australia pty ltd. Sanofi-aventis australia pty ltd trading as Sanofi, ABN 31 008 558 807, Talavera Corporate Centre, Building D, 12–24 Talavera Road, Macquarie Park, NSW 2113. SAANZ.TJO.19.05.0260a. Date of preparation: May 2019.

Learn more about Toujeo by visiting

www.mysanoficonnect.com.au

Toujeo: Lower risk of hypoglycaemia and the same

HbA1c control as insulin glargine 100 units/mL in adults with T2DM

4

PBS information: Lantus® SoloStar® and Lantus® cartridges are listed on the PBS as a long acting insulin analogue for the treatment of type 1 and type 2 diabetes.


http://products.sanofi.com.au/aus_pi_lantus.pdf

www.mysanoficonnect.com.au


4 D I A B E T E S M A N A G E M E N T J O U R N A L A u g u s t 2 0 1 9

CUSTOM PUBLISHED by The Tangello Group Pty Ltd on behalf of Diabetes Australia, Lvl 1, 101 Northbourne Ave, Turner ACT 2612

ABN 47 008 528 461 EDITOR Justin Coleman - [email protected] ART DIRECTOR Maree Lockhart

WRITERS Dr Justin Coleman, Dr Nasir Shah, Dr Brendan Smyth, Prof. Vlado Perkovic, Prof. Sergio Starkstein, Prof. David Bruce, Dr Kate Marsh,

Tim Perry, Assoc Prof. Spiros Fourlanos, Dr Meredith Hansen-Knarhoi, Rebecca Harcourt, Zoe Nicholson

ADVERTISING Darren Dawkins - [email protected] PUBLISHER Lucinda Mitchell - [email protected] SUBMIT ARTICLES TO [email protected]

TO REQUEST COPIES or for permission to reprint contact Caroline Wells - [email protected]. © Diabetes Management Journal 2018. All rights reserved. ISSN 2209-931X

EDITORIAL ADVISORY BOARD

Prof Peter Colman, AMEndocrinologist, Diabetes and EndocrinologyRoyal Melbourne Hospital

Diabetes Management Journal is an Editorial Advisory Board reviewed publication. All views expressed by authors in Diabetes Management Journal are their own.

CONTENTS

DIABETES AUSTRALIA PUBLICATION MANAGER

Caroline WellsCEO, Diabetes Tasmania

25LATE-

ONSET T1D

The official journal from

Dr Kate MarshAdvanced Accredited Practising Dietitian & Credentialled Diabetes Educator

Dr Tang WongEndocrinologist, Bankstown-Lidcombe & Prince of Wales Hospitals, Sydney Endocrinology and Diabetes

Dr Aajuli ShuklaGeneral PractitionerThe Practice Blacktown

Dr Spiros FourlanosDirector, Department of Diabetes & Endocrinology, Royal Melbourne Hospital

5 NEWS & VIEWS The latest diabetes news.

8 DIABETIC KIDNEY DISEASEA practical approach

14 DEPRESSION AND ANXIETYHow they interact wtih diabetes

18 PULL OUT GUIDEThe new injectables for managing diabetes

20 INJECTION PERFECTIONTechnique matters

28 REALITY CHECK A GP struggles with mandatory GTTs in pregnancy

30 PATIENT POINT OF VIEW T1D couldn’t stop my dad at any age

33 FOOD STUFFHealth at every size and non-hungry eating

Cover image: ©krishnacreations / Adobe Stock

More common than you think

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www.diabetesaustralia.com.au

www.tangello.com.au

NEWS & VIEWSby Justin Coleman

5D I A B E T E S M A N A G E M E N T J O U R N A L A u g u s t 2 0 1 9

From the Ed’s desk

Diagnosing diabetes in Australian general practice

In a journal so full of useful information for practising clinicians, it is the editor’s prerogative to start with

something useless-but-interesting. And yes, it involves Facebook.

It turns out that the language we use in our Facebook posts is significantly better than demographic data (age, sex, race) for predicting the presence of diabetes. What’s more, the tell-tale words are not things like sugar or needle but, in the US at least, words with a religious theme.

In a clever study (PLOS One, June 2019)1 involving more computing power than the moon landing, a thousand attendees at a US health centre gave permission for their entire historic Facebook posts to be data-mined and have hundreds of word categories compared to the individual’s known medical conditions. In a concession this editor would never have condoned, even misspelled words were allowed.

Even after controlling for age and gender, when individuals were ranked according to the frequency of mentioning words from within the specific cluster [god, pray, family] the top 25% were 15 times more likely to have diabetes than the bottom 25%.

Strangely, this was among the most statistically significant of all the thousands of potential associations between any word cluster and a list of 21 medical conditions. What it all means is anyone’s guess.

Besides diabetes, the other standout medical conditions associated with particular word use were mental health conditions and substance abuse. Alcohol abuse was marked by the use of [drink, drunk, bottle], while drug abuse and psychosis were associated with various profanities—no doubt frequently misspelled. Word clusters strongly associated with depression ranged from the predictable [pain, crying, tears] to the more curious, such as allusions to physical symptoms [stomach, head, hurt].

Dr Justin ColemanEditor

1. Merchant R, et al. Evaluating the predictability of medical conditions from social media posts. PLOS One, published online 17 June 2019. Avail at https://doi.org/10.1371/journal.pone.0215476

It’s always exciting to see a rural Australian GP try his hand at research, and come up with useful information from his own practice that should spark interest more broadly.

A case series2 by Toowoomba GP Dr Ashraf Saleh looked at the concordance between HbA1c and fasting plasma glucose (FPG): the two most widely used diagnostic tests for type 2 diabetes (T2D).

Over a 12-month period he identified via his practice software all patients who met the criteria for a new diagnosis of T2D based on either FPG or HbA1c, but not both. By excluding those who met both diagnostic criteria, Dr Saleh concentrated on early, borderline diabetes – a realm familiar to those who work in primary care.

Twenty-five individuals met the definition of diabetes by FPG criteria (>7 mM in two consecutive laboratory readings) but not HbA1c (<6.5%, averaged over two laboratory samples). None of the 25 had any clinical feature that would render their HbA1c reading inaccurate.

Five individuals met the HbA1c definition of diabetes (>6.5%) but not FPG (<7 mM) over two samples.

Therefore, using HbA1c as the sole diagnostic test for T2D would have missed 25 of 30 (83%) people in this ‘early stage of diabetes’ group, whereas using FPG as the sole test would only have missed 17%.

The FPG-diagnosed group (i.e. those whose diagnosis would have been missed with just HbA1c) had an average AUSDRISK score of 21. This score reflects their very-high-risk status, despite a ‘typical’ member of that group in this study being a 66-year-old non-smoker with no family history of T2DM, who eats two serves of fruit every day and exercises with moderate intensity for more than 30 minutes per day.

Although the use of HbA1c is attractive in primary care as a non-fasting test, FPG would seem to be better at detecting early T2D.

Of course, a pragmatist might argue that the HbA1c is probably just lagging behind the FPG, and that as long as lifestyle advice and follow-up was offered in any case, little harm would be done by slightly delaying formal diagnosis at this mild end of the T2D spectrum.2. Saleh A. Diagnosis of type 2 diabetes using serial fasting plasma glucose versus HbA1c in the primary care setting. AJGP vol 48, no 5, May 2019.

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https://doi.org/10.1371/journal.pone.0215476

NEWS & VIEWSby Justin Coleman

D I A B E T E S M A N A G E M E N T J O U R N A L A u g u s t 2 0 1 9

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Proteinuria or retinopathy? Worry about amputation.

6

Lower limb amputation is self-evidently strongly associated with arterial disease, but new research supports the growing recognition of amputation’s independent association with microvascular disease.

A cohort study published in Circulation (July 2019)4 followed 125,000 US veterans for almost a decade, capturing 1185 amputations. Microvascular disease (microVD) was defined as peripheral neuropathy, retinopathy or nephropathy (proteinuria).

The presence of microVD alone—without peripheral arterial disease (PAD)—conferred a 3.7-fold risk of amputation. PAD alone conferred a 13.9-fold risk, and the presence of both a 22.7-fold risk.

Although PAD is clearly the bigger risk factor of the two, because the number of veterans with microVD is almost 50% higher than the number with PAD, up to one in every six below-knee amputations may be attributable to microVD.

MicroVD was more strongly associated with below-ankle amputations than it was with higher amputations. People with diabetes comprised 41% of the group who had amputations and microVD alone (without PAD).

Whereas individuals with PAD have long been firmly on the radar for amputation prevention strategies, the same cannot be said of microVD. For example, the 2018 NEJM review ‘Chronic limb-threatening ischemia’3 made no

mention at all of microVD. This veterans study suggests a new amputation ‘red flag’ for clinicians to consider.

The findings also add weight to the theory that microVD is a systemic phenomenon. It questions the understandable tendency of clinicians to focus on the specific microvascular bed affected (the retina, kidney or periphery) and encourages us to broaden our gaze once we have discovered clinical evidence anywhere of a microVD ‘phenotype’.

3. Beckman J, et al. Microvascular disease, peripheral artery disease, and amputation. Circulation. 2019;140:449–458 4. Farber A. Chronic limb-threatening ischemia. N Engl J Med. 2018; 379:171–180

While many medicolegal decisions provide valuable insight into what not to do, the judgement in one particular case stunned GPs, in that if the lesson learned was to be universally applied, our system of referrals to nephrologists and endocrinologists would collapse under the strain.

Australian Doctor recently reported5 that a 66-year-old plaintiff with T2D successfully sued a Sydney GP for failing to refer him to a specialist after a once-off, random screening eGFR result of 54.

In this context, an eGFR of ≥60 would represent fairly normal kidney function, and many healthy 66-year-olds would occasionally measure 54 on a bad day. Indeed, in this case, just 11 days later a repeat eGFR came back at 84. Job done: time to move on to other health risks.

There would be few GP readers of DMJ who would not feel comfortable clinically managing an individual with T2D and slightly reduced or—at an eGFR of 84—normal kidney function. This edition’s feature article on diabetic kidney disease (see p8) should add to that confidence.

In the absence of any complicating factors (as was the case here), this is bread-and-butter GP work that requires evidence-based primary care interventions rather than any sprinkling of magic that only a nephrologist or endocrinologist can provide.

All the more perplexing, then, that the judge quoted an expert endocrinology opinion; “It certainly would have been helpful to have referred this matter a bit earlier to a kidney physician.” Really? Well, helpful to the tune of saving the unlucky GP a $210,000 negligence award, as it turns out.

Happily, the story doesn’t end with tens of thousands of extra nephrology referrals every year. In June, the Supreme Court of NSW quashed the original verdict, in a belated win for the GP and for Australia’s envied system of primary care gatekeeping the portal to specialist care.

5. Scholefield A. GP wins appeal as $200k negligence claim quashed. Australian Doctor, 11 June 2019. Avail at www.ausdoc.com.au/news/gp-wins-appeal-200k-negligence-claim-quashed

An extraordinary legal precedent

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Approximately one-third of people with diabetes will develop diabetic kidney disease (DKD).2 DKD is characterised

by the development of albuminuria, which advances over years from normoalbuminuria (albumin-creatinine ratio (ACR) <3mg/mmol), to microalbuminuria (ACR 3-30mg/mmol), and macroalbuminuria (ACR >30 mg/mmol). Glomerular filtration does not tend to fall until macroalbuminuria is well established, although concurrent renal damage due to co-morbid hypertension or vascular disease can cloud this picture.

Twenty years after diagnosis, 20% of those with T1D have overt DKD with macroalbuminuria, and one‐fifth of these eventually progress to end stage kidney disease (ESKD) requiring renal replacement therapy.5 At diagnosis, up to 20% of those with T2D already have albuminuric DKD.1 The time from macroalbuminuria to ESKD varies greatly, from as early as 4 years to over 18 years.3, 4 Although only a minority of

those with DKD ever reach ESKD, DKD is the leading cause of ESKD requiring dialysis or transplantation.6

PATHOGENESISHyperglycaemia damages renal tissue via multiple complex pathways. These include altered angiotensin signalling and decreased nitric oxide production, which results in increased glomerular blood flow and intracapillary pressure.2 The glomerulus is also affected by podocyte dysfunction, which leads to increasing levels of albuminuria. In parallel, oxidative stress and toxic advanced glycation end-products induce vascular injury, while accumulation of extracellular protein triggers transforming growth factor-beta (TGF-β) and renal fibrosis.7

Early on, these changes are reversible; however with sustained and/or repeated hyperglycaemia, the glomerular damage progresses and eventually becomes permanent. Moreover, the very complexity of mechanisms involved means that no single therapy (no ‘silver bullet’) is likely to be sufficient to halt the progression of established DKD.

PRESENTATION AND DIAGNOSISThe classic presentation of DKD is slowly progressing albuminuria, with gradual decline in eGFR beginning after the development of macroalbuminuria. However, individual presentations and progress are variable and additional causes of renal disease always need to be considered in those with diabetes who have renal abnormalities. Given the frequent co-existence of other comorbidities leading to renal pathology (atherosclerosis, hypertension and obesity), determining the relative contribution of diabetes may be difficult (and may not affect management).

It is reasonable to assume DKD as

being causative in those with a known (or suspected) long history of diabetes, slowly progressing albuminuria and a gradual decline in renal function. However, any deviation from this pattern, including rapid or relentless deterioration in eGFR, or nephrotic-range proteinuria (with or without nephrotic syndrome) cannot be attributed to DKD without a thorough investigation, which may include a renal biopsy. Haematuria (whether micro- or macroscopic) is not typical of DKD and warrants investigation, as in the general population.

INTERPRETING URINE ACR & EGFR People with diabetes should be screened at least annually for DKD, starting at the time of diagnosis. The key tests are urine ACR (UACR—a spot urine sample is sufficient) and estimated glomerular filtration rate (eGFR) calculated from serum creatinine.8

The risk of ESKD rises continuously with level of albuminuria. UACR exhibits a high degree of within-individual variability, meaning that change as great as a doubling or halving of ACR between two timepoints may occur despite stable renal disease.9 While variability is somewhat lessened by use of early morning samples, it remains important to consider trend and to interpret short-term fluctuations with caution.


FEATURE

Managing diabetic kidney disease is no longer just about ACE inhibitors. Risk reduction involves a broader approach, and some of the novel hypoglycaemic agents provide new treatment possibilities. Nephrology advanced trainee Dr Nasir Shah, nephrologist Dr Brendan Smyth, and The George Institute outgoing executive director Professor Vlado Perkovic have put together a very practical guide to management.


DIABETIC KIDNEY DISEASE:A PRACTICAL APPROACH

CLINICAL PEARL: A sudden increase in (or large amount of) proteinuria is not the usual pattern seen in diabetes, and warrants specific renal evaluation.

D I A B E T E S M A N A G E M E N T J O U R N A L A u g u s t 2 0 1 9 9

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DIABETIC KIDNEY DISEASE:

eGFR equations approximate an individual’s actual glomerular filtration rate based on known correlation between age, sex, serum creatinine, and direct measurement of glomerular filtration by radioisotope (or other means) in large population samples. Thus eGFR may be inaccurate in those at extremes of muscle mass for their age and/or sex, including malnourished or cachectic individuals.10 In such situations, a creatinine clearance (using the Cockroft-Gault formula) may be useful in assessing renal function as it has the advantage of including weight.

These limitations do not however


FEATURE

undermine the utility of sequential measurements of eGFR to monitor for changes in renal function. Although not as variable as UACR, changes of up to 15% in creatinine-based eGFR may not reflect real changes in renal function. Repeat testing is recommended to confirm changes and to establish trends.9

Using eGFR and UACR, those with DKD can be risk stratified. Consensus guidelines define chronic kidney disease (CKD) as either an eGFR <60ml/min/1.73m2 (with or without other evidence of renal disease) or any level of renal function with evidence of renal disease (e.g. albuminuria or glomerular haematuria).11 The pattern of eGFR stage and albuminuria stage can be used to predict progression to ESKD. See figure 1 below. In general, all high- or very-high risk individuals should be referred to a nephrologist, although in the presence of life-limiting comorbidities, frailty or clear conservative treatment goals this decision should be individualised.

MANAGEMENT Until recently, the only proven treatment to slow progression of DKD was renin-angiotensin system (RAS) inhibition (angiotensin converting enzyme [ACE] inhibitors or angiotensin receptor blockers [ARBs]).12-14 However, sodium-glucose co-transporter-2 inhibitors (SGLT2is) are now also proven to slow the progression of DKD and are likely to provoke important changes to treatment guidelines.15-18 Our overall approach to the management of DKD is provided in Box 1 opposite.

ANGIOTENSIN INHIBITIONIt is now 26 years since the Collaborative Study Group established the ability of ACE inhibitors to slow the progression of DKD in T1D.12-14 Further studies at the turn of the century confirmed similar benefits with ARBs in T2D.12, 14 RAS inhibition now forms the cornerstone of reno-protective therapy for those with albuminuric DKD. Repeat blood tests

2-3 weeks after commencing treatment are important to identify hyperkalaemia or excessive rises in creatinine. A moderate increase in creatinine (less than 30%) should be expected when starting angiotensin inhibition (as intraglomerular pressure is reduced) and this does not necessitate cessation of therapy. Combination ACE inhibitor and ARB is not recommended.19, 20

BLOOD PRESSURE CONTROLThe optimal blood pressure target for those with DKD continues to be debated. Key trials of intensive BP lowering (<120mmHg) have not clearly shown benefit21 in people with diabetes, but evidence from meta-analyses22 and trials in subjects without diabetes23 suggests that reductions in cardiovascular events are achievable with BP targets below the standard <140/90mmHg. Consistent with Australian guidelines,24 a target of <140/90mmHg has strong, level 1 evidence for CKD, and <120mmHg

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Figure 1.

KIDNEY DISEASE IMPROVING GLOBAL OUTCOMES11 ASSESSMENT OF RENAL FUNCTION:

Persistent albuminuria categoriesDescription and range

A1 A3

Prognosis of CKD by GRF and Albuminuria Categories:

KDIGO 2012

Normal to mildly increased

<30 mg/g<3 mg/mmol

Moderately increased

Severely increased

30-300 mg/g3-30 mg/mmol

>300 mg/g>30 mg/mmol

G1

G2

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G3b

G4

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Normal or high

Mildly decreased

Mildly to moderately decreased

Moderately to severely decreased

Severely decreased

Kidney failure

> 90

60 - 89

45 - 59

30 - 44

15 - 29

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Green: low risk (if no other markers of kidney disease, no CKD); Yellow: moderately increased risk; Orange: high risk; Red: very high risk.

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systolic should be considered in those at high absolute cardiovascular risk.

As the presence of diabetes and albuminuria (at any age) are sufficient to indicate high absolute cardiovascular risk,25 all those with DKD should be considered for tight blood pressure targets. However, this requires close monitoring and a frank discussion with the individual about the potential risks and benefits.

In practice it is reasonable to sequentially add each of the four cornerstone antihypertensives (ACE inhibitor or ARB; thiazide; beta-blocker; dihydropyridine calcium channel blocker), reassessing response and tolerability at each step. In those who respond well, continue until a target of <120mmHg is reached. However, it is essential that target BP be adjusted upwards if concern arises regarding side effects or medication regimen complexity. For such individuals (of whom there are many), a BP <140mmHg is still consistent with good practice, and higher targets may be appropriate for older or frailer individuals, or those with postural hypotension (particularly common in diabetes). Moreover, it is useful to remember that any reduction in blood pressure is associated with cardiovascular benefits, regardless of the absolute value achieved.

CARDIOVASCULAR RISK REDUCTIONIn addition to risk of ESKD, the presence of albuminuria and reduced eGFR are strong predictors of cardiovascular events.26 Measures to reduce the risk of cardiovascular events should be considered in all those with DKD. This includes a statin for all those with diabetes and micro- or macroalbuminuria, or reduced eGFR.27

As for everyone, those with DKD should exercise regularly and adopt a healthy diet. There is emerging evidence that diets rich in vegetables and fruit, and emphasising plant-protein over animal-protein may slow progression of kidney disease in those with eGFR <60 (especially those with metabolic acidosis).28 A plant-rich diet with reduced sodium intake is similar to the ‘DASH’ (Dietary Approaches to Stop Hypertension) diet, shown to lower blood pressure.29

DIABETES MANAGEMENTThe HbA1c target in those with DKD is mostly the same as the general population with T2D (HbA1c ≤ 7%), although if tolerated, a lower target (e.g. < 6.5%) may confer additional benefits. In individuals at risk of severe hypoglycaemia, a limited life expectancy, or advanced micro- or macrovascular disease (all of which are common in DKD), an HbA1c target above 7% should be considered.30, 31 As eGFR declines, dose adjustments or medication

cessation may be necessary – see Table 1 (page 12).

EVIDENCE BASED HYPOGLYCAEMIC THERAPIESThe key development in recent years is the emergence of two new classes of hypoglycaemic agents with evidence for cardiovascular and/or renal benefits: SGLT2i and GLP-1RA.15-18 As these studies are digested and new results are published, the Australian prescribing guidelines may evolve further.

SGLT2 inhibitorsSGLT2 inhibitors increase urinary glucose excretion and sodium delivery to the distal tubule, which (via tubuloglomerular feedback) results in a reduction in glomerular pressure, thus reducing proteinuria. This effect is independent of glycaemic control. In addition, the diuretic effect of increased glucose delivery to the distal tubule lowers blood volume and blood pressure, and the net loss of calories from sustained glucosuria contributes to weight loss. Most recently, the CREDENCE trial, which enrolled participants with eGFR as low as 30ml/min/1.73m2, showed a 30% reduction in the composite outcome of doubling creatinine, ESKD or death from renal or cardiovascular cause.17 In the wake of this study, SGLT2i should be considered for those with albuminuric DKD and an eGFR above 30 ml/min/1.73m2.

The most common side effect of SGLT2i is fungal genital infections (1-7% per year).17, 18 While euglycaemic ketoacidosis appears to be very rare in those with T2D, it is increased with SGLT2i and it is important that those taking medication and their clinicians are aware of this risk, and

that individuals may present with only mildly elevated blood glucose levels. They should be given a sick-day plan, whereby they are advised to withhold their SGLT2i during intercurrent illness.

GLP-1 receptor agonistsThe second class of novel hypoglycaemics, GLP-1RAs exert their glucose-lowering effect through activation of the incretin pathway. In addition to the favourable reductions in HbA1c, body weight, and systolic


THE A – F OF MANAGING PEOPLE WITH DIABETIC

KIDNEY DISEASE

A ACE inhibitor or ARB

B Blood pressure control (<120mmHg systolic if tolerated, otherwise <140/90mmHg)

C Cardiovascular risk reduction (exercise, diet and statin)

D Diabetes management (individualised HbA1c targets)

E Evidence based hypoglycaemics – SGLT2 inhibitor > GLP-1 agonist > other agents1

F Follow up regularly and refer to a nephrologist when at high risk of progression to ESKD

Abbreviations: ACE, angiotensin converting enzyme; ARB, angiotensin receptor blocker; SGLT2, sodium-glucose co-transporter 2; GLP-1, glucagon-like peptide-1; ESKD, end-stage kidney disease. 1. PBS subsidised supply of novel hypoglycaemic agents should adhere to prescribing criteria.

Box 1:

blood pressure, these agents have cardiovascular and renal benefits.32-34 At present, the renal benefits appear limited to reduced incidence of macroalbuminuria, without a clear signal that they significantly preserve renal function. Owing to partial renal clearance, GLP-1RAs were initially restricted to those with an eGFR of >30 mL/minute/1.73 m2; however, liraglutide is now approved in Australia for those with an eGFR > 15.

DPP-4 inhibitorsThe third class of novel hypoglycaemics, DPP-4 inhibitors, are associated with modest improvements in albuminuria.35-38

However, it is increasingly clear that these agents do not result in significant improvements in cardiovascular or renal events.37,39 As such, in the absence of contraindications or intolerances, it seems reasonable to use SGLT2i or GLP-1RA in preference to DPP-4i, so as to maximise the benefit to outcomes.

REGULAR FOLLOW UP AND REFERRAL The course of DKD can be unpredictable, so regular follow up is recommended. The frequency required depends on the severity and rate of progression of disease,

the need for review of treatment changes, on comorbidities, and on the individual’s priorities. In those with known DKD, referral to a nephrologist is recommended for all those with an eGFR <30, with macroalbuminuria, or with an eGFR <60 and a confirmed decline in eGFR >5ml/min in a 6 month period.40 Referral is also necessary for those in whom an alternative diagnosis is suspected, or where the diagnosis of DKD is uncertain. In suitable candidates, planning for renal replacement therapy (dialysis or transplantation) typically begins once the eGFR falls below 30. This preparatory time aids in ensuring that veins are preserved for vascular access and that individuals and their families are prepared for the transition.

CONCLUSIONFor most people with DKD, the two key issues will be cardiovascular risk minimisation and slowing the progression of their kidney disease. This requires establishing and achieving multiple individualised therapeutic goals. The recent emergence of novel hypoglycaemic agents with proven effects on important outcomes has expanded the tools available to general practitioners. The early identification and optimal treatment of DKD will result in longer and healthier lives for people with diabetes.

Vlado Perkovic is a member of steering committees for CREDENCE (Chair, Janssen), CARMELINA (co-chair, Boehringer-Ingelheim and Eli Lilly),

MARLINA (BI/Lilly), SONAR (Abbvie), TESTING (NHMRC/Pfizer), RESOLVE (NHMRC), and ASCEND (GSK) and has received honoraria from or participated on advisory boards for Abbvie, Astellas, Astra Zeneca, Bayer, BMS, Boehringer Ingelheim, Eli Lilly, Janssen, Merck, Novartis, Novo Nordisk, and Servier. Brendan Smyth has received travel funding from Roche.

For references go to www.diabetesaustralia.com.au/diabetes-management-journal.


FEATURE

CKD 3b CKD 4 ESKD

eGFR (ml/min/1.73m2) > 60 45-60 30-44 15-29 <15

Metformin

Sulfonylureas

SGLT2i

GLP-1RA

DPP-4i

Comments

Maximum 1g/day when eGFR 30-59. Only use with specialist consultation below eGFR 30.

Gliclazide and glipizide are preferred when eGFR <30. All sulfonylureas should be dosed cautiously in the presence of CKD given the possibility of prolonged hypoglycaemia.

Prescribing guidelines in Australia (MIMS) restrict dapagliflozin to eGFR ≥60 and empagliflozin and ertugliflozin to eGFR ≥45. Canagliflozin (not available presently in Australia) has been shown to be safe and beneficial with eGFR down to 30.

No CKDCKD 1-2

Liraglutide is approved for use in those with an eGFR ≥15. Dulaglutide is approved only for those with an eGFR ≥30.

Dose reductions are required for many DPP-4i when eGFR <45. Linagliptin is an exception and can be used even in those with ESKD.

Stage of CKD CKD 3b

Table 1

Dr Nasir Shah is a Nephrology Advanced Trainee at the Department of Renal Medicine, Wollongong Hospital, NSW.

Dr Brendan Smyth is a Nephrologist at the Department of Renal Medicine, St George Hospital, NSW.

Dr Vlado Perkovic is a Professorial Fellow at The George Institute for Global Health, UNSW Medicine.

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People with T2D are more likely to suffer from depression and anxiety, and these psychological conditions in turn affect the management of T2D and its complications. We teamed up psychiatrist Professor Sergio Starkstein and physician Professor David Bruce to examine the problem from both angles.

HOW DEPRESSION AND ANXIETY INTERACT WITH DIABETES

It has been consistently demonstrated that depression has a negative impact on type 2 diabetes (T2D). Compared to having T2D alone, the combination

with depression results in worse glycaemic management, poorer quality of life, increased health care costs, and increased risk of chronic complications and premature death.1

This association works both ways; depression in the general population increases the risk of diabetes, and the onset of T2D increases the rate of depression. Therefore, current guidelines for the treatment of T2D recommend regular screening for depression.1, 2

Prevalence of depression and anxiety in T2DWe examined the frequency and correlates of depression and anxiety in the context of the Fremantle Diabetes Study (FDS),1 an epidemiological cross-sectional and longitudinal study that included about 1,500 individuals with T2D living in the Fremantle catchment region, Western Australia.

One of the first questions was whether having depression and/or anxiety before the onset of T2D are associated with higher clinical and psychiatric morbidity. We found that both a lifetime history (i.e. any past history) of major depression disorder (L-MDD) and a lifetime history of Generalized Anxiety Disorder

(L-GAD) before the onset of diabetes were independently associated with more severe depression and anxiety at the time of psychiatric assessment at baseline during the study. L-MDD was also associated with higher HbA1c, a higher BMI, a greater likelihood of current smoking, and reduced self-monitoring of blood glucose.

In addition, the combination of both L-MDD and L-GAD was associated with increased HbA1c levels, and worse diabetes management during an increment of current depression.

These outcomes suggest that both anxiety and depression are early indicators of suboptimal diabetes management, and the combination

FEATURE


of L-MDD and L-GAD may confer additional risk for increased psychological symptoms. Comorbidity between depression and GAD occurs in 17% of that group3, and is associated with greater resistance to psychotherapy and more significant diabetes complications.

These findings imply that it is important to enquire about any previous history of depression when T2D is first diagnosed. Those individuals with depression before the onset of T2D may benefit from regular screening of depression, especially when complications arise.

Our group has validated the Brief Lifetime Depression Scale (BLDS) for use in T2D.4 This self-administered

questionnaire screens for a previous history of major depression. Using this instrument we found that a lifetime history of depression results in a 4-fold risk of depression in individuals with T2D, thus helping identify those with T2D at risk for future depression.

Diagnosing depression and anxiety in T2D Depression may be underdiagnosed in T2D due to the overlap of symptoms, such as fatigue, changes in weight and appetite, sleep disturbances and motor retardation. To clarify this overlap, our group calculated a latent class analysis in a large sample of individuals with T2D and found that depressive and

anxiety symptoms characterised four classes of individuals.5

When symptoms were analysed, their profile was construed into the following groups: (1) major anxious depression, (2) minor anxious depression, (3) subclinical anxiety, and (4) no anxious depression. One third of the sample were included in the classes of anxious depression (1 and 2), whereas only 12% had a DSM-IV diagnosis of minor or major depression, and 5% met DSM-IV criteria for GAD.

These findings suggest that using classes rather than DSM criteria defines a far larger number of people with T2D as having current psychopathology. The high frequency of anxiety present in individuals with T2D and depression


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HOW DEPRESSION AND ANXIETY INTERACT WITH DIABETES

suggests that specific criteria for depression in T2D should also include anxiety, which will help to identify those with more severe psychopathology who may benefit from more intensive therapy.

In terms of clinical correlates, we found that the major anxious depression group were significantly younger at onset of T2D, had higher HbA1c, higher serum triglycerides, and a higher frequency of insulin use as compared to the other classes.

Research conclusionsThe Fremantle Diabetes Study examined the longitudinal association between anxiety, depression and T2D, and provided novel findings that are relevant to primary care. An important finding was that people with a history of depression before the onset of T2D have reduced self-care behaviours and worse peripheral arterial disease than people with T2D who have never been depressed.

Those who developed depression after T2D onset showed the worst outcomes in terms of glycaemic management, requiring more intensive management and having more diabetes complications than those with T2D but not depression. Importantly, this group was less likely to be receiving antidepressants than people with T2D who developed depression before diabetes onset. We speculate that depression may be more difficult to detect in individuals with more complications and more complex treatment regimes.

The most frequent complication and cause of death in T2D is coronary heart disease (CHD). In the longitudinal FDS we found that 31% of participants had CHD at baseline and that a subsequent diagnosis of depression significantly contributed to micro- and macro-vascular disease over time. In a 4-year longitudinal study including the four classes identified using latent class analysis, we found that both major and minor anxious depression were independent predictors of cardiovascular mortality and incident CHD.

Another important finding in people with T2D was that those with GAD (but no depression) had a higher risk of CVD mortality than those with major

depression (but no GAD), which may be related to anxiety-related factors such as high blood pressure, increased frequency of smoking and low levels of physical activity. Given the clinical relevance of the class with anxious depression, future studies may propose specific diagnostic criteria for validation and use in T2D.

Treatment of depressionAntidepressants are frequently used to treat depression in T2D. Nevertheless, psychotherapy is the preferred modality to treat depression in T2D given the potential side effects and pharmacological interactions of psychoactive medication, and the finding that gains with psychotherapy may be maintained for up to one year after cessation of treatment.

Cognitive Behavioural Therapy (CBT) is the preferred type of psychotherapy for T2D with depression. A recent RCT showed that CBT was better than placebo in terms of decreasing depression scores, increasing adherence to diabetes treatment, reducing HbA1c and increasing self-monitoring of blood glucose. Moreover, these improvements lasted for at least 12 months.6

Recent studies developed a web-based intervention with specific programs for diabetes, such as the GET ON Mood Enhancer Diabetes, a minimally guided web-based self-help intervention for diabetes and comorbid depression symptoms. An RCT using this web-based treatment showed that active intervention was significantly more

effective than placebo in reducing depressive symptoms.7 A recent meta-analysis of randomised controlled trials of CBT for individuals with T2D and depression showed significant improvements in mood, fasting glucose levels, improved quality of life and anxiety in the long term, but no significant changes in HbA1c.8

ConclusionsIn busy clinics, depression in T2D should be assessed using the PHQ-9, a valid and reliable instrument to diagnose depression based on DSM-IV criteria and to measure the severity of depression. We developed the Generalized Anxiety Disorder Scale (GADS), which is structured in a similar way to the PHQ-9 and allows a DSM-IV diagnosis of GAD as well as measuring the severity of anxiety. Both instruments can be self-assessed and may take between 5-15 minutes to complete.

Both depression and anxiety have a significantly negative impact on relevant clinical variables of T2D, including higher mortality. The combination of depression and anxiety may indicate individuals who require more intensive management. Therefore, screening for both depression and anxiety are of great relevance in primary care. Once recognised, those with depression and/or anxiety should be referred for psychotherapy. Psychoactive medication may be used in severe cases of depression or when psychotherapy proves ineffective.

The Fremantle Diabetes Study was partially supported by grants from the NHMRC.

For references given in this article, go to www.diabetesaustralia.com.au/diabetes-management-journal.


Professor David Bruce is a Professor of Medicine at University of Western Australia and Consultant at Fremantle Hospital

Professor Sergio Starkstein is a Professor of Psychiatry at University of Western Australia and Consultant at Fremantle Hospital

FEATURE

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PBS Information: Authority required (STREAMLINED) for dual therapy, triple therapy or add-on to insulin therapy for Type 2 Diabetes. Refer to PBS Schedule for full Authority information. This product is not PBS listed for monotherapy

or in combination with a thiazolidinedione (glitazone), a glucagon-like peptide-1 or an SGLT2 inhibitor.

References: 1. Galvumet® Approved Product Information, 3 March 2017. 2. Bosi E et al. Diabetes Care 2007;30:890–95.Galvus is a registered trademark of Novartis AG. Copyright© 2018 Mylan N.V. All rights reserved. Mylan Health Pty Ltd, ABN 93 002 359 739, Level 1, 30 The Bond, 30–34 Hickson Road, Millers Point NSW 2000. Tel: 1800 274 276. www.mylan.com.au. GGT-2018-0006 May 2018 SHOW1376-DMJ. *Please note changes in Product Information.

Please review Approved Product Information before prescribing. Approved Product Information can be accessed at http://www.novartis.com.au/products_healthcare.html

Proven 1.1% HbA1c reduction in type 2 diabetes uncontrolled on metformin alone1,2*

*Galvumet (vildagliptin + metformin) vs placebo + metformin

WARNING: Life-threatening lactic acidosis can occur due to accumulation of metformin. The main risk factor is renal impairment, other risk factors include old age associated with reduced renal function and high doses of metformin above 2000 mg per day.

GALVUMET (vildagliptin/metformin hydrochloride): Indication: For patients with Type 2 diabetes mellitus: (a) as an adjunct to diet and exercise to improve glycaemic control in patients whose diabetes is not adequately controlled on metformin hydrochloride alone or who are already treated with the combination of vildagliptin and metformin hydrochloride, as separate tablets; treatment of type 2 diabetes should not be initiated with this fixed-dose combination; or (b) in combination with a sulfonylurea as an adjunct to diet and exercise in patients inadequately controlled with metformin and a sulfonylurea; or (c) as add-on to insulin as adjunct to diet and exercise to improve glycaemic control in patients when a stable dose of insulin and metformin alone do not provide adequate glycaemic control. Dosage and administration: Starting dose should be on the patient’s current regimen of vildagliptin and/or metformin hydrochloride: 50/500, 50/850 or 50/1000 twice daily. Do not exceed the maximum recommended daily dose of vildagliptin (100 mg). Should be given with meals. To minimise the risk of lactic acidosis, only one strength of Galvumet should be prescribed and used at any one time. Patients should also be advised to discard their previous metformin medication when initiated on Galvumet. When used in combination with a sulfonylurea or insulin, the selected dose should provide 50mg vildagliptin twice daily and metformin similar to the dose already being taken. Contraindications: Hypersensitivity to vildagliptin or metformin hydrochloride or to any of the excipients. Renal disease or dysfunction. Congestive heart failure. Acute or chronic metabolic acidosis including diabetic ketacidosis. Temporarily discontinuation recommended in patients undergoing radiologic studies involving intravascular administration of iodinated contrast materials. Precautions: Not for type 1 diabetes or diabetic ketoacidosis. Caution with concomitant use of medications that may affect renal function or metformin hydrochloride disposition. Renal function should be assessed and verified as normal before initiating Galvumet. Not recommended in patients with hepatic impairment including patients with a pre-treatment ALT or AST>2.5X the upper limit of normal; liver function tests (LFT) to be performed prior to treatment initiation, at three-month intervals during the first year and periodically thereafter; withdrawal of therapy is recommended if an increase in AST or ALT of 3X upper limit normal or greater persist; following withdrawal of treatment and LFT normalisation, treatment should not be reinitiated. Not recommended in patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption. Risk of lactic acidosis. Not recommended in paediatric patients. Discontinue treatment in case of hypoxemia. Temporary discontinuation in patients undergoing radiologic studies involving intravascular administration of iodinated contrast materials or surgical procedure. Excessive alcohol intake to be avoided. Risk of decreased vitamin B12 serum levels. Risk of hypoglycaemia. May be temporarily withhold in case of loss of glycaemic control. Pregnancy (Category C): Should not be used unless the potential benefit justifies the potential risk to the foetus. Breast-feeding: Should not be used. Interactions: Vildagliptin has a low potential for drug interactions. No clinically relevant interactions with other oral antidiabetics (glibenclamide, pioglitazone, metformin), amlodipine, digoxin, ramipril, simvastatin, valsartan or warfarin were observed after co-administration with vildagliptin. Interactions with metformin hydrochloride: furosemide, nifedipine, glyburide, cationic drugs, drugs tending to produce hyperglycaemia, alcohol. Side effects: Vildagliptin: Common: dizziness; Uncommon: headache, constipation, oedema peripheral; Rare: angioedema, hepatic dysfunction (including hepatitis); Metformin : Very common: flatulence, nausea, vomiting, diarrhoea, abdominal pain, loss of appetite; Common: metallic taste; Very rare: decrease of vitamin B12 absorption, lactic acidosis, liver function test abnormalities, hepatitis, skin reactions such as erythema, pruritus and urticaria. Common effects of vildagliptin and metformin combination: headache, tremor, dizziness. Triple combination with a sulfonylurea: Common: dizziness, tremor, asthenia, hypoglycaemia, hyperhidrosis. Add-on to insulin: Common: headache, chills, nausea, gastrooesophageal reflux disease, decreased blood glucose. Post-marketing experience: Rare: hepatitis (reversible with drug discontinuation); Unknown: pancreatitis, urticaria, bullous and exfoliative skin lesions, including bullous pemphigoid*.

MYL1376 Advert - metformin DMJ FAr2.indd 1 19/8/19 1:05 pm


PBS Information: Authority required (STREAMLINED) for dual therapy, triple therapy or add-on to insulin therapy for Type 2 Diabetes. Refer to PBS Schedule for full Authority information. This product is not PBS listed for monotherapy

or in combination with a thiazolidinedione (glitazone), a glucagon-like peptide-1 or an SGLT2 inhibitor.

References: 1. Galvumet® Approved Product Information, 3 March 2017. 2. Bosi E et al. Diabetes Care 2007;30:890–95.Galvus is a registered trademark of Novartis AG. Copyright© 2018 Mylan N.V. All rights reserved. Mylan Health Pty Ltd, ABN 93 002 359 739, Level 1, 30 The Bond, 30–34 Hickson Road, Millers Point NSW 2000. Tel: 1800 274 276. www.mylan.com.au. GGT-2018-0006 May 2018 SHOW1376-DMJ. *Please note changes in Product Information.

Please review Approved Product Information before prescribing. Approved Product Information can be accessed at http://www.novartis.com.au/products_healthcare.html

Proven 1.1% HbA1c reduction in type 2 diabetes uncontrolled on metformin alone1,2*

*Galvumet (vildagliptin + metformin) vs placebo + metformin

WARNING: Life-threatening lactic acidosis can occur due to accumulation of metformin. The main risk factor is renal impairment, other risk factors include old age associated with reduced renal function and high doses of metformin above 2000 mg per day.

GALVUMET (vildagliptin/metformin hydrochloride): Indication: For patients with Type 2 diabetes mellitus: (a) as an adjunct to diet and exercise to improve glycaemic control in patients whose diabetes is not adequately controlled on metformin hydrochloride alone or who are already treated with the combination of vildagliptin and metformin hydrochloride, as separate tablets; treatment of type 2 diabetes should not be initiated with this fixed-dose combination; or (b) in combination with a sulfonylurea as an adjunct to diet and exercise in patients inadequately controlled with metformin and a sulfonylurea; or (c) as add-on to insulin as adjunct to diet and exercise to improve glycaemic control in patients when a stable dose of insulin and metformin alone do not provide adequate glycaemic control. Dosage and administration: Starting dose should be on the patient’s current regimen of vildagliptin and/or metformin hydrochloride: 50/500, 50/850 or 50/1000 twice daily. Do not exceed the maximum recommended daily dose of vildagliptin (100 mg). Should be given with meals. To minimise the risk of lactic acidosis, only one strength of Galvumet should be prescribed and used at any one time. Patients should also be advised to discard their previous metformin medication when initiated on Galvumet. When used in combination with a sulfonylurea or insulin, the selected dose should provide 50mg vildagliptin twice daily and metformin similar to the dose already being taken. Contraindications: Hypersensitivity to vildagliptin or metformin hydrochloride or to any of the excipients. Renal disease or dysfunction. Congestive heart failure. Acute or chronic metabolic acidosis including diabetic ketacidosis. Temporarily discontinuation recommended in patients undergoing radiologic studies involving intravascular administration of iodinated contrast materials. Precautions: Not for type 1 diabetes or diabetic ketoacidosis. Caution with concomitant use of medications that may affect renal function or metformin hydrochloride disposition. Renal function should be assessed and verified as normal before initiating Galvumet. Not recommended in patients with hepatic impairment including patients with a pre-treatment ALT or AST>2.5X the upper limit of normal; liver function tests (LFT) to be performed prior to treatment initiation, at three-month intervals during the first year and periodically thereafter; withdrawal of therapy is recommended if an increase in AST or ALT of 3X upper limit normal or greater persist; following withdrawal of treatment and LFT normalisation, treatment should not be reinitiated. Not recommended in patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption. Risk of lactic acidosis. Not recommended in paediatric patients. Discontinue treatment in case of hypoxemia. Temporary discontinuation in patients undergoing radiologic studies involving intravascular administration of iodinated contrast materials or surgical procedure. Excessive alcohol intake to be avoided. Risk of decreased vitamin B12 serum levels. Risk of hypoglycaemia. May be temporarily withhold in case of loss of glycaemic control. Pregnancy (Category C): Should not be used unless the potential benefit justifies the potential risk to the foetus. Breast-feeding: Should not be used. Interactions: Vildagliptin has a low potential for drug interactions. No clinically relevant interactions with other oral antidiabetics (glibenclamide, pioglitazone, metformin), amlodipine, digoxin, ramipril, simvastatin, valsartan or warfarin were observed after co-administration with vildagliptin. Interactions with metformin hydrochloride: furosemide, nifedipine, glyburide, cationic drugs, drugs tending to produce hyperglycaemia, alcohol. Side effects: Vildagliptin: Common: dizziness; Uncommon: headache, constipation, oedema peripheral; Rare: angioedema, hepatic dysfunction (including hepatitis); Metformin : Very common: flatulence, nausea, vomiting, diarrhoea, abdominal pain, loss of appetite; Common: metallic taste; Very rare: decrease of vitamin B12 absorption, lactic acidosis, liver function test abnormalities, hepatitis, skin reactions such as erythema, pruritus and urticaria. Common effects of vildagliptin and metformin combination: headache, tremor, dizziness. Triple combination with a sulfonylurea: Common: dizziness, tremor, asthenia, hypoglycaemia, hyperhidrosis. Add-on to insulin: Common: headache, chills, nausea, gastrooesophageal reflux disease, decreased blood glucose. Post-marketing experience: Rare: hepatitis (reversible with drug discontinuation); Unknown: pancreatitis, urticaria, bullous and exfoliative skin lesions, including bullous pemphigoid*.

MYL1376 Advert - metformin DMJ FAr2.indd 1 19/8/19 1:05 pm

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MEDICATION

DRUG NAME DULAGLUTIDEGLP-1

EXENATIDEGLP-1

LIRAGLUTIDEGLP-1

GLARGINE BASAL Insulin

GLULISINERapid Insulin

DEGLUDEC DEGLUDEC / INS. ASPARTMixed

BRAND NAME(s) Trulicity Byetta, Bydureon Saxenda, Victoza Lantus, Optisulin, Toujeo Apidra Tresiba (not yet available) Ryzodeg

Duration of Action 7 days1 12hrs immediate release, 7 days extended release.1

24 hours.1 24 hours.4 ~4 hours.1 42 hours.4 Aspart: 3-5 hrs, degludec: 42 hrs.2,4

CV Risk No risk (PI).1 No risk17 13% risk CV death, non-fatal MI or CVA.13

No change.1-

In 65-74yo: non-inf to glargine, risk as age .3


CKD Adjustment OK if GFR>30ml/min. Limited data <30ml/min so not recommended. 1

OK if GFR>30ml/min. Should not be used if <30ml/min- clearance, so worse GI tolerability.1

Not recommended in ESRD.1 Δ may be required in renal clearance.2

Monitor: may need dose as GFR .1

Generally OK, but may need to dose as GFR .1


Dose cutoff risk of ADR if GFR.** 1 Use with caution and increase dose conservatively in patients ≥70years old.

Do not increase dose above 1.8mg/day.1

The usual individual insulin requirement is 0.5-1 units/kg/day. In meal-related treatment, 50 to 70% of this daily requirement may be provided by rapid acting insulin and the remainder provided by an intermediate-acting or long-acting insulin.1

Hypo Risk Only in combination with SU or prandial insulin. 1

Low; only if combined with SU or prandial insulin.1


risk.13 Higher due to rapid action.1 Lower nocturnal rate than glargine.21

Low from degludeg but high from aspart.1

Dosage Interval Weekly. (2-4 weeks to reach steady state). 1

BD (Byetta). Weekly (Bydureon- 6-7 weeks to reach steady state).1

Daily.1 Daily.2 With each meal.1 Daily.1 BD or daily.1

Missed dose Dose as long as next dose due ≥72 hours later. 1

Dose as long as next dose due ≥72 hours later.1

Have dose if <12 hours late, otherwise skip.

Caution; check BGL and seek advice.2




Contraindications (other than known hypersensitivity)

None. 1 Family or current history of medullary thyroid carcinoma.1

Not for NYHA Class IV (lack of experience).1

None, but careful in diabetic retinopathy.1

None.1 None.1 None.1

Special Warnings Not for T1D or DKA. Avoid if severe GI disease (potential GI side effects). Hypersensitivity in 0.3-0.5%. 1

Not for T1D or DKA. Avoid if severe GI disease. Watch dangerously rapid wt loss (>1.5kg/week). Increased thyroid tumours in rats.1

Thyroid adverse events (e.g. goitre) in clinical trials; caution with pre-existing thyroid disease.1

- - - -

Drug Interactions Unlikely. 1 Post marketing — spontaneous change in INR with warfarin, rare worsening renal function, especially concomitant with ACEi, NSAIDs, diuretics1

May warfarin INR. May HR. Caution with sympathomimetics.

Careful with all drugs that alter blood glucose levels, insulin levels or may mask the signs of hypoglycaemia.1

Pregnancy category B31 C1 B31 B32 B31 No data at this stage B31

Most frequent ADRs Nausea, vomiting, diarhhoea, appetite. 1

Nausea, vomiting, diarrhoea and constipation. Acute pancreatitis and acute renal failure have been reported rarely since exenatide has been marketed.1

Nausea, vomiting, diarrhoea and constipation.1

Hypoglycaemia, weight gain.1 Hypoglycaemia, local reaction, lipodystrophy.1

Nasopharyngitis, URTI, headache.16 Hypoglycaemia, nasopharyngitis, URTI, headache.1

Interesting May HR by 2-4bpm, and pancreatic enzymes by ≤20%. 1

US: extended release carris Boxed warning re thyroid C-cell tumours.9

May HR by 2-3bpm.- - - -

Reduction in HbA1c% as monotherapy

0.78-1.64% over 52-104 weeks. 12 0.8% after 26 weeks on 10mcg Byetta.7 0.84% with 1.2mg, 1.14% with 1.8mg over 1 yr.10 - - - -

Δ HbA1c% with metformin

1.1% after 1yr (1.08% with metformin + SU). 1

0.9% Byetta,1.6% Bydureon after 24 weeks.8

1.12% after 26 weeks.8- -

1.1% at 2 yrs +/- other agents.**21 0.39% after 2 years.20

Δ HbA1c% with metformin + SU

1.08% after 1 yr. 1 0.9% Byetta,1.6% Bydureon after 24 weeks.8 - - -

1.1% at 2 yrs +/- other agents.**21

-

Weight change Modest; 2-3kg loss after 1 yr .1 1.4kg loss Byetta, 2.3kg loss Bydureon after 24 weeks.7

3.24kg loss after 26 weeks8 Slight gain. 5, 21 Weight gain can occur.1 2.7kg gain over 2 yrs.21 0.9kg gain after 2 yrs.20

Immunogenicity May develop anti-drug antibodies, although no clear impact on HbA1c.1

May develop antibodies. Change agents if glycaemic control worsens.1

8.6% May develop antibodies, but no change in efficacy.1 - -

Low incidence of anti-insulin antibodies.21

Antibodies may necessitate dose changes (rare).1

** not significantly different

D I A B E T E S M A N A G E M E N T J O U R N A L A u g u s t 2 01918

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THE NEW INJECTABLES Seven new injectable medications for treating diabetes have appeared in recent times. Regular DMJ contributor and consultant clinical pharmacist in Sydney, Tim Perry has prepared this handy pull-out guide.

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DRUG NAME DULAGLUTIDEGLP-1

EXENATIDEGLP-1

LIRAGLUTIDEGLP-1

GLARGINE BASAL Insulin

GLULISINERapid Insulin

DEGLUDEC DEGLUDEC / INS. ASPARTMixed

BRAND NAME(s) Trulicity Byetta, Bydureon Saxenda, Victoza Lantus, Optisulin, Toujeo Apidra Tresiba (not yet available) Ryzodeg

Duration of Action 7 days1 12hrs immediate release, 7 days extended release.1

24 hours.1 24 hours.4 ~4 hours.1 42 hours.4 Aspart: 3-5 hrs, degludec: 42 hrs.2,4

CV Risk No risk (PI).1 No risk17 13% risk CV death, non-fatal MI or CVA.13

No change.1-



CKD Adjustment OK if GFR>30ml/min. Limited data <30ml/min so not recommended. 1

OK if GFR>30ml/min. Should not be used if <30ml/min- clearance, so worse GI tolerability.1

Not recommended in ESRD.1 Δ may be required in renal clearance.2

Monitor: may need dose as GFR .1



Dose cutoff risk of ADR if GFR.** 1 Use with caution and increase dose conservatively in patients ≥70years old.

Do not increase dose above 1.8mg/day.1

The usual individual insulin requirement is 0.5-1 units/kg/day. In meal-related treatment, 50 to 70% of this daily requirement may be provided by rapid acting insulin and the remainder provided by an intermediate-acting or long-acting insulin.1

Hypo Risk Only in combination with SU or prandial insulin. 1



risk.13 Higher due to rapid action.1 Lower nocturnal rate than glargine.21

Low from degludeg but high from aspart.1

Dosage Interval Weekly. (2-4 weeks to reach steady state). 1

BD (Byetta). Weekly (Bydureon- 6-7 weeks to reach steady state).1

Daily.1 Daily.2 With each meal.1 Daily.1 BD or daily.1

Missed dose Dose as long as next dose due ≥72 hours later. 1

Dose as long as next dose due ≥72 hours later.1

Have dose if <12 hours late, otherwise skip.





Contraindications (other than known hypersensitivity)

None. 1 Family or current history of medullary thyroid carcinoma.1

Not for NYHA Class IV (lack of experience).1

None, but careful in diabetic retinopathy.1

None.1 None.1 None.1

Special Warnings Not for T1D or DKA. Avoid if severe GI disease (potential GI side effects). Hypersensitivity in 0.3-0.5%. 1

Not for T1D or DKA. Avoid if severe GI disease. Watch dangerously rapid wt loss (>1.5kg/week). Increased thyroid tumours in rats.1

Thyroid adverse events (e.g. goitre) in clinical trials; caution with pre-existing thyroid disease.1

- - - -

Drug Interactions Unlikely. 1 Post marketing — spontaneous change in INR with warfarin, rare worsening renal function, especially concomitant with ACEi, NSAIDs, diuretics1

May warfarin INR. May HR. Caution with sympathomimetics.

Careful with all drugs that alter blood glucose levels, insulin levels or may mask the signs of hypoglycaemia.1

Pregnancy category B31 C1 B31 B32 B31 No data at this stage B31

Most frequent ADRs Nausea, vomiting, diarhhoea, appetite. 1

Nausea, vomiting, diarrhoea and constipation. Acute pancreatitis and acute renal failure have been reported rarely since exenatide has been marketed.1

Nausea, vomiting, diarrhoea and constipation.1

Hypoglycaemia, weight gain.1 Hypoglycaemia, local reaction, lipodystrophy.1

Nasopharyngitis, URTI, headache.16 Hypoglycaemia, nasopharyngitis, URTI, headache.1

Interesting May HR by 2-4bpm, and pancreatic enzymes by ≤20%. 1

US: extended release carris Boxed warning re thyroid C-cell tumours.9

May HR by 2-3bpm.- - - -

Reduction in HbA1c% as monotherapy

0.78-1.64% over 52-104 weeks. 12 0.8% after 26 weeks on 10mcg Byetta.7 0.84% with 1.2mg, 1.14% with 1.8mg over 1 yr.10 - - - -

Δ HbA1c% with metformin

1.1% after 1yr (1.08% with metformin + SU). 1

0.9% Byetta,1.6% Bydureon after 24 weeks.8

1.12% after 26 weeks.8- -

1.1% at 2 yrs +/- other agents.**21 0.39% after 2 years.20

Δ HbA1c% with metformin + SU

1.08% after 1 yr. 1 0.9% Byetta,1.6% Bydureon after 24 weeks.8 - - -

1.1% at 2 yrs +/- other agents.**21

-

Weight change Modest; 2-3kg loss after 1 yr .1 1.4kg loss Byetta, 2.3kg loss Bydureon after 24 weeks.7

3.24kg loss after 26 weeks8 Slight gain. 5, 21 Weight gain can occur.1 2.7kg gain over 2 yrs.21 0.9kg gain after 2 yrs.20

Immunogenicity May develop anti-drug antibodies, although no clear impact on HbA1c.1

May develop antibodies. Change agents if glycaemic control worsens.1

8.6% May develop antibodies, but no change in efficacy.1 - -

Low incidence of anti-insulin antibodies.21

Antibodies may necessitate dose changes (rare).1

** not significantly different

19D I A B E T E S M A N A G E M E N T J O U R N A L A u g u s t 2 019

For references go to www.diabetesaustralia.com.au/diabetes-management-journal and click on the link for August 2019 References.

THE NEW INJECTABLES


Proper injection technique (IT) by individuals using injectable diabetes medicines is essential for optimal diabetes management.1

However, despite the availability of IT guidelines, large studies have found that many are not following evidence-based recommendations for the administration of insulin.2,3 Health care professionals play a central role in educating individuals with diabetes regarding correct IT.1

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A growing number of Australians are injecting diabetes medicines. This is due to an increasing prevalence of diabetes, the move to earlier insulin use in T2D and the newer classes of non-insulin injectable medicines for T2D. However, research shows that many people with diabetes are not using the correct injection technique. Credentialled Diabetes Educator Dr Kate Marsh discusses the key considerations for injecting diabetes medications and why they matter.

INJECTION TECHNIQUE MATTERS

FEATURE


FIVE KEYS TO THE SAFE ADMINISTRATION OF INJECTABLE DIABETES MEDICATIONS:Correct needle lengthIn Australia, users of insulin and injectable medications currently have a choice of insulin pen needles ranging from 4mm to 12.7mm in length or syringes with needles from 6mm to 8mm. However, needles greater than 6mm are no longer recommended due to the higher risk of intramuscular (IM) injection,1 so while they are still available on the NDSS, their use should be discouraged. Shorter length pen needles (4-5mm) are recommended for children and adults of all sizes and younger children and slimmer individuals should be encouraged to use 4mm.1 Those using syringes should choose a 6mm needle length (currently the shortest available).1

Correct injection sitesThe abdomen is the most commonly recommended site for injections and these should be given at least 1cm above the symphysis pubis, 1cm below the lowest rib and 1cm away from the umbilicus.1 Other sites include the posterior lateral aspect of both upper buttocks and flanks, the upper third anterior lateral aspect of both thighs and the middle third posterior aspect of the upper arm.1 However, the risk of intramuscular injection is significantly higher in the arms and thighs, so these should be discouraged, particularly in young children and slimmer adults. Good site rotation is also important to reduce the risk of LH and each person with diabetes should be taught an easy-to-follow structured process for site rotation1. For those using older insulin types (e.g. regular and NPH), it is important to consider the variation in absorption from different sites.1

Correct injection device. Pen devices, rather than syringes, are now the standard choice for most people in Australia, and are the only option available for non-insulin injectables. Insulin pens have several advantages over syringes, including convenience, ease of

use, greater accuracy (particularly with small doses), reduced fear of needles and greater perceived social acceptance.4-6 However, some people still choose to use syringes. Several different brands and models of insulin pens are available in Australia, including pre-filled and refillable devices, and it is important to choose the device that best suits the needs of each individual (Box 1).

Correct use of injection device. Whether a pen device or syringe, education needs to be provided on the use of each injection device1. For pen devices this includes loading the cartridge (for refillable pens), attaching the pen needle, priming the pen, dialing and delivering the dose. For syringes, users need to be taught how to draw up their dose, remove air bubbles and mix insulins, if applicable. With either method, those using cloudy insulins must be shown how to resuspend these sufficiently prior to injection.1 It is also important to emphasise that syringes and pen needles are single-use. As well as the risk of infection, re-use of needles is associated with an increased risk of developing lipohypertrophy (Box 2).

Correct injection technique. IT, including the angle of insertion and use of a lifted skinfold, should be determined according to the needle length used, injection site and anticipated thickness of subcutaneous tissue. In general, longer needles should be inserted at 45 degrees with a lifted skinfold, while 4mm needles should be inserted at 90 degrees.1 However, an angled injection and/or skinfold may be needed in children or slim adults using 5mm or 6mm pen needles in areas with little subcutaneous tissue, to reduce the risk of intramuscular injection.1

EDUCATION: MORE THAN JUST GIVING AN INJECTIONComprehensive education is essential for anyone starting insulin or injectable medications.1,19 Research has shown that people with diabetes don’t always receive education about the injection of diabetes medications, and when they do,


Box 1

FACTORS TO CONSIDER WHEN CHOOSING AN INSULIN PEN DEVICE:7

• Insulin type (refillable pens must be matched to the correct insulin cartridge).

• The maximum dose of insulin that can be given (important for those taking large doses).

• Availability of 0.5 unit or 1.0 unit dosing increments (0.5 unit dosing may be helpful for children and those on smaller doses).

• Readability of the numbers for those who are vision impaired.

• Audible sound for dialing the dose for those who are vision impaired.

• Dexterity in dialing the dose.• The ease of use of the pen.• Choice of colour (some devices offer a choice of colours; someone taking two types of insulin with the same device type should use different colours to avoid confusion).

• Preference for disposable versus non-disposable.

• Additional features such as an inbuilt electronic memory of previous doses.

Injection sites and rotation

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not all essential topics are covered.3,20 In a large worldwide survey investigating IT in people with diabetes, many

participants didn’t recall a number of key topics being adequately covered during their education and training and 25% of participants reported wanting more education regarding IT.3 Consideration also

needs to be given to the many psychological barriers the person

with diabetes and their family/carers may face when commencing

insulin or injectable medications.21 Ideally, the person should be referred to a Credentialled Diabetes Educator, who can provide this individualised education and support (Box 3).

BINNING SHARPSMany people don’t dispose

of their sharps safely. In the 2014–2015 worldwide Injection Technique Questionnaire (ITQ) survey, only 20% of respondents

used a formal sharps container, and 40% placed their used sharps in their household garbage.2

Procedures for disposing of sharps safely vary from state to state and within local council areas. Health

professionals should be aware of their local guidelines.

REGULAR REVIEW ESSENTIAL IT should be reviewed at least annually, or when lipodystrophy has been identified1. A review of injection sites should also occur at least annually and preferably at every diabetes visit.1 Assessment should include the visual inspection and palpation of injection sites.1 This not only enables the healthcare professional to discover and address injection site problems but also reinforces to the person with diabetes the importance of correct IT to avoid such problems.3 Of concern, in the 2014–2015 ITQ survey, 39% of participants could not remember ever having their injection sites checked.22

FOR MORE INFORMATION The ADEA Clinical Guiding Principles for Subcutaneous Injection Technique provide an evidence base for the injection of diabetes medicines for health care professionals involved in the administration and teaching of

subcutaneous IT (SCIT) for diabetes therapies in various clinical settings7. They include information about the principles of SCIT, education of individuals in safe and accurate IT, evaluation of IT, and specific issues for health care settings and carers. This document can be downloaded from the ADEA website.

The author declares no conflict of interest. For references go to www.diabetesaustralia.com.au/diabetes-management-journal.

FEATURE


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Dr Kate MarshBSc, MNutrDiet, PhD, Grad Cert Diab Edn & Mgt, FADEA, FASLM is an Advanced Accredited Practising Dietitian, Credentialled Diabetes Educator,Health & Medical Writer and a DMJ Editorial Advisory Board member.

Lipohypertrophy (LH) is an area of thickened subcutaneous tissue which may be hard and scar-like, or soft like a rubber ball.8 LH is a common complication, associated with repeated injection into the same sites, inadequate site rotation and the re-use of needles.9–14 The incidence of LH is increased with duration of diabetes, duration of insulin use and the number of injections per day.9–14 A 2017 meta-analysis of 26 studies involving almost 12,500 people with diabetes using insulin found a pooled prevalence of LH of 38% although this varied widely between studies.15 Injecting into LH-affected sites may lead to greater variability in blood glucose levels due to delayed or erratic insulin absorption.16–18

Box 2 LIPOHYPERTROPHY

• The timing and action of the medicines and dose(s) required.

• Training in the use of the insulin pen device and/or syringe.

• Choice of injection sites and the importance of site rotation.

• Care and self-examination of injection sites.

• Choice of optimal needle length. • The importance of the single use of

pen needles and syringes.• IT including the angle of injection and

use of a lifted skin fold, where required.

• Injection complications and how to avoid these.

• Storage of injectable medicines according to manufacturers’ instructions.

• Safe disposal of sharps.• Preparation of skin prior to injecting. • Structured self-blood glucose

monitoring, including appropriate frequency and timing in relation to the injection regimen.

• Hypoglycaemia, including symptoms, prevention and treatment.

• Where required, discussion of the considerations for flying and travelling when taking injectable medicines.

• Sick-day management.

Box 3

KEY TOPICS FOR EDUCATION.1,7


The new BD Ultra-Fine™ PRO 4mm Pen Needle has been redesigned with patients in mind. Our new pen needle features the same EasyFlow™ Technology and 5-Bevel Comfort, with the added benefits of a wide outer cover, moulded ridges and additional grips for easier attachment and removal from a medication pen device.1-3#

BD, the BD logo and BD Ultra-Fine are trademarks of Becton, Dickinson and Company or its affiliates. © 2019 BD. All rights reserved. BD-11911

bd.com/anz/diabetes

Becton Dickinson Pty Ltd Australia. Toll Free: 1800 656 100

# Compared to BD standard hub, 3-bevel, thin wall pen needles. * Very slim adults and young children may need a lifted skin fold at all sites.

References: 1. Results from a BD sponsored, non-blinded, randomized, home-use, 2-period crossover, patient preference study with patients currently using 32G pen needles; 39.6% had no preference. Total of 225 paid participants; superiority was established with each subgroup. Data on file. 2. Aronson R, et al. Clin Ther. 2013;35(7):923-933. 3. Hirsch L, et al. J Diabetes Sci Technol. 2012;6(2):328-335. 4. Australian Diabetes Educators Association (ADEA). Clinical Guiding Principles for Subcutaneous Injection Technique, March 2017. https://www.adea.com.au/wp-content/uploads/2009 /10/Injection-Technique-FINAL_170323.docx.pdf. Accessed 18 July 2018.

Now available...Helping you support your patients with easier injections.1-3#

Easier to attach1#

Wider outer cover features a flat end and moulded ridges to support easier attachment and removal of the pen needle.

Easy, comfortable injections2-3#

Includes EasyFlow™ Technology and a 5-bevel needle tip for a more comfortable injection.

Easier to remove1#

The inner shield includes additional grips for easier handling.

Short 4mm needle length4

The short 4mm needle length is suitable for adults, children and people who are overweight.*

NDSS Code: 101

Available at leading pharmacies

The same BD Ultra-Fine™ 4mm Pen Needle now with easier handling and new packaging.1#

www.bd.com/anz/diabetes

www.bd.com/anz/diabetes

https://www.adea.com.au/wp-content/uploads/2009/10/Injection-Technique-FINAL_170323.docx.pdf

Please review Product Information before prescribing.The Product Information can be accessed at www.novonordisk.com.au

PBS Information: Ryzodeg® 70/30 is listed on the PBS for treatment of adult patients with diabetes mellitus where insulin treatment is necessary.

Ryzodeg® 70/30 (70% insulin degludec (rys) / 30% insulin aspart (rys)). Indication: To improve glycaemic control in adult patients with diabetes mellitus requiring basal and prandial insulin. Contraindications: Hypersensitivity to insulin degludec, insulin aspart or to any of the excipients. Precautions: Must be taken with a carbohydrate containing meal. Hypoglycaemia may occur due to omission of a meal, unplanned strenuous physical exercise, dose too high in relation to insulin requirement, co-administration with insulin secretagogues or GLP-1 agonists. The prolonged effect of Ryzodeg® 70/30 may delay recovery from hypoglycaemia. Hyperglycaemia may occur due to inadequate dosing and/or discontinuation of treatment or concomitant illness, and may potentially lead to diabetic ketoacidosis. Insulin administration may cause insulin antibodies to form. No clinical experience in pregnant women (Category B3) or breast-feeding. Not for use in children and adolescents below 18 years. Must not be mixed with other insulins. Interactions: OADs, GLP-1 receptor agonists. Cases of cardiac failure have been reported when thiazolidinediones were used in combination with insulin. Others, see Full PI. Adverse effects: Hypoglycaemia, injection site reactions. Dosage and method of use: Administered once- or twice-daily with the main meal(s). Flexibility in the timing of administration allowed as long as it is dosed with the main meal(s). In T2DM, use alone, in combination with OADs, and in combination with bolus insulin. Recommended starting dose for T2DM: 10 units with dose adjustments. In T1DM, use in combination with short-/rapid-acting insulin at the remaining meals. Recommended starting dose for T1DM: 60-70% of the total daily insulin requirements. Dosed in accordance with individual patients’ needs. See Full PI. Subcutaneous use only. Not for intravenous or intramuscular use. Must not be used in insulin infusion pumps. (Feb 2018).

References: 1. Ryzodeg® 70/30 Product Information. 2. Haahr H, Fita EG, Heise T. Clin Pharmacokinet. 2017; 56(4): 339-54.

Novo Nordisk Pharmaceuticals Pty Ltd. ABN 40 002 879 996 Level 3, 21 Solent Circuit, Baulkham Hills, NSW, 2153 NovoCare® Customer Care Centre (Australia)1800 668 626. www.novonordisk.com.au ®Registered trademark of Novo Nordisk A/S. AU19RZG00035. Date of Preparation: May 2019.

FOR TYPE 1 AND TYPE 2 DIABETES

FIRST-IN-CLASS:A co-formulation of an ultra-long acting insulin (degludec) and a mealtime insulin (aspart) in 1 pen1,2mealtime insulin (aspart) in 1 pen

UNRESTRICTEDPBS LISTED

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Theresa May, the former Prime Minister of the United Kingdom, has publically shared her story of being diagnosed

with adult-onset T1D in her fifties. Rather than letting the condition affect her demanding political career as Home

Secretary, just four years later May took on the nation’s top job. A/Prof Spiros Fourlanos discusses the surprisingly high

proportion of people whose T1D begins later in life.

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FEATURE

Contrary to previous teaching, adult-onset T1D is at least equally as common as juvenile-onset T1D. In Australia almost half of all people who develop T1D are diagnosed over the age of 30.1

IDENTIFYING ADULT-ONSET T1DT1D is a polygenic autoimmune disease and the age of onset is well known to be in part determined by the HLA genotype profile. Highest risk Class II HLA genotypes, DR3-DQ2 in combination with DR4-DQ8, bestow the greatest risk for earlier onset diabetes, while intermediate Class II HLA genotypes, DR3-DQ2 or DR4-DQ8 alone, can be associated with later onset of the condition.2

Adult-onset T1D may also have the immunologic characteristic of having only one autoantibody antigen specificity [typically glutamic acid decarboxylase (GAD), tyrosine phosphatase-like insulinoma-associated protein (IA2) or Zinc Transporter 8 protein (ZnT8)].

T1D, or autoimmune diabetes in adulthood, may not be recognised at diagnosis of diabetes given it is a less 27

Theresa May was diagnosed with diabetes following the London 2012 Olympic Games. When she organised to see her GP, after developing an episode of bronchitis, she had no idea that the visit would change her life. While seeing her doctor she mentioned she had lost a significant amount of weight which she attributed to “dashing about” in her role as Home Secretary.

The GP performed a blood test and suddenly Theresa May was diagnosed with diabetes. As one can understand this news came as a shock, although in retrospect she realised she had other classic symptoms including drinking more water than usual and making more frequent trips to the bathroom.

May’s initial diagnosed was T2D; however over time it became apparent her blood glucose management was not settling and

further investigations eventually resulted in a diagnosis of T1D.

May stated, “My very first reaction was that it’s impossible because at my age you don’t get it”, reflecting the popular misconception that only younger people are diagnosed with T1D. Her subsequent response was “Oh no, I’m going to have to inject” and the change in diagnosis meant switching from taking oral medication to insulin – first two and then four injections per day.

As the first world leader known to have T1D, the Prime Minister rapidly learnt to cope with her condition. “I go to a lot of functions where I am eating and I speak at dinners, so that brings an added complication. When I’m going to do a debate or speaking at a conference, I have to make sure that I’ve tested and know where I am, so I can adjust as necessary.”

Aiming to avoiding hypoglycaemia has led to Theresa May covertly breaking the House of Commons' strict no-eating rules in the Chamber. May recalls, “There was an occasion when I had a bag of nuts in my handbag and one of my colleagues would lean forward every now and then, so that I could eat some nuts without being seen by the Speaker.”

Despite being one of the busiest and most high profile people in the UK with diabetes she has maintained a pragmatic and open attitude to managing the condition. Her attitude to diabetes has been partly inspired by another prominent person with T1D, Olympic rower Sir Steve Redgrave. When she was first diagnosed, she was “very struck by” a quote on his website, in which he said that diabetes had to learn to live with him, rather than him living with diabetes.


FEATUREIm

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THERESA MAY’S STORY

common type of diabetes and clinicians may be distracted by taking a history of suboptimal nutritional choices and physical activity, and the presence of abdominal adiposity on examination.

Adult-onset T1D can present in many different ways: from a presentation with classical symptoms of diabetes in a lean adult to an asymptomatic overweight adult with an initial response to oral diabetes treatments who then develops persistent hyperglycaemia and progresses to needing insulin therapy more rapidly than anticipated. This latter pattern reflects Latent Autoimmune Diabetes in Adulthood (LADA).

LADA is defined as adult-onset diabetes with circulating islet antibodies but not requiring insulin therapy initially. Around 10% of adults with diabetes have LADA.3

The author helped develop a clinical screening tool to aid clinicians in identifying which adults might warrant islet

antibody testing in adult-onset diabetes.4 Box 1 lists five key clinical features which can alert a clinician to increase their level of suspicion that the diagnosis might not be T2D.

MANAGEMENTThe clinical course and management of adult-onset T1D shares similarities with managing adults with juvenile-onset T1D. The goals of treatment remain similar; to avoid hypoglycaemia and achieve target range glycaemia in order to minimise the

risk of vascular complications. However, adult-onset T1D can be characterised by a longer symptomatic period prior to diagnosis, better preservation of beta-cell function and thereby lesser treatment intensity, at least in the initial clinical course, compared to juvenile-onset T1D.5 The author declares no conflict of interest. For references go to www.diabetesaustralia.com.au/diabetes-management-journal

“ My Time in Range is up to over 80%! I spend a lot less timethinking about mydiabetes now...” MiniMed™ 670G Clinical Trial Participant1

THE MINIMED™ 670G SYSTEM GAME CHANGER

MORE TIME TO BE

Leanne

To find out more about the world’s first self-adjusting insulin pump system2 visit hcp.medtronic-diabetes.com.au or talk to your Medtronic Representative today.1Leanne was a participant in an Australian MiniMed™ 670G clinical study. The study was supported with a product grant from Medtronic Inc. The patient is a member of the Medtronic Patient Ambassador Program. This patient testimonial relates an account of an individual’s response to the treatment. The account is genuine, typical and documented. However, the individual’s response does not provide any indication, guide, warranty or guarantee as to the response other persons may have to the treatment. The response other persons have to the treatment could be different. Responses to the treatment discussed can and do vary and are specific to the individual patient.2Some user interaction required. 6071-052019

MDA0155_MDJ HPC.indd 1 8/5/19 11:50 am

RED FLAGS FOR LATENT AUTOIMMUNE DIABETES IN ADULTHOOD (LADA) IN THE OLDER PERSON WITH NEWLY DIAGNOSED DIABETES

The author found five common distinguishing features on retrospective interview of 102 Australian adults with LADA (age at diagnosis 30-75 years). When these features were prospectively applied to 130 adults with newly diagnosed diabetes, the presence of two or more features had a positive predictive value of 21% (i.e. islet antibody testing would be worthwhile) while the presence of one or no features had a negative predictive value of 99% (i.e. islet antibody testing probably not warranted).4

Five Clinical Features:

1. Classical symptoms of diabetes (unintentional weight loss, polydipsia, polyuria).

2. Absence of overweight or obesity (i.e. BMI <25 kg/m2).

3. Age at diagnosis <50 years.4. Past history of autoimmune disease

(e.g. autoimmune thyroid disease, autoimmune gastritis, coeliac disease).

5. Family history of autoimmune disease.

Assoc Professor Spiros Fourlanos is Director, Dept of Diabetes & Endocrinology, Royal Melbourne Hospital. He is a member of the DMJ Editorial Advisory Board.

Box 1.


www.hcp.medtronic-diabetes.com.au


As a GP who provides antenatal shared care it’s frustrating dealing with guidelines which tell you slightly different things in regard to screening in pregnancy. The changes

recommended following the HAPO (2008) trial have resulted in more women being diagnosed with gestational diabetes mellitus (GDM).1 This has made it more imperative that screening is done.

As a GP I am very aware of the impacts of undiagnosed diabetes and gestational diabetes on pregnancy, neonatal/ maternal morbidity and mortality. At the coal face however, it’s a much harder ask. The pregnant women I see are a bit bewildered by all their antenatal screening tests. I wrestle with selecting from the range of RACGP2, state guidelines3 and ADIPS guidelines4; all are guides, not rules.

SANDRA’S CASE Sandra (not her real name), a 25-year-old happy to be pregnant with baby number four, has booked

Evidence-based practice involves three steps; the evidence, how that evidence applies to the individual, and the individual’s preferences. Darwin GP Dr Meredith Hansen-Knarhoi runs antenatal GTT screening through its paces, and discovers that well-intentioned evidence guidelines often stumble at the next two hurdles.

WHY THIS GP DOESN’T LIKE GLUCOSE TOLERANCE TESTS

today to ‘get her bloods and scan done’. Her 18-month-old is careering madly round the room while the three-year-old is occupied with chips and gravy on the floor. I secretly hope the chips last long enough for the consult.

Sandra is eight weeks’ gestation and feeling quite nauseated; she has vomited a few times this morning, but is managing her Powerade now. After reviewing her obstetric history of GDM (the last pregnancy required metformin and insulin) I’m just thinking that all the pregnancy guidelines recommend a GTT when she says ‘Geez doctor, do I have to do that sugar drink again? That always makes me chuck!’ I sigh internally, but she’s right; here we go again!

Sandra is a casual care assistant in a nursing home. Things are financially tight – she works six early shifts a week to cover the mortgage. Her partner has left her (once he found out she was pregnant again) so her mother has moved in to help. She is emotionally drained, juggling lots of balls in the air and is now pregnant again. So, what to do?

REALITY CHECK

Dr Meredith Hansen-Knarhoi BMBS (Hons) FRACGP MPH&TM is a GP who lives and works in the Top End, currently working for Danila Dilba Health Service, an ACCHO in Darwin, NT.




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job. Do I settle for the fasting reading and add on an HbA1c?

Sandra declares ‘I’m not doing this stupid test that makes me chuck again.’ The told-you-so look is quite justified. My internal monologue worries about my therapeutic alliance and the need for open communication during this pregnancy, when she will need support as she is having a hard time physically and psychologically. Decisions, decisions.

GUIDELINES, NOT TRAMLINESWe all use various guidelines; RACGP Diabetes guidelines, ADIPS, and for us in the NT the SA Perinatal Guidelines. HbA1c is now a validated screening tool in adults for T2D, but not in pregnancy. This is where I get stuck ethically and professionally.

Ideally Sandra should have a GTT now and at 26-28 weeks. But this is not an ideal world and I am a pragmatist at heart. Sandra is doing it tough; she

needs someone to listen and support her, not to enforce a guideline. Realistically there

is little chance of her getting the test done accurately.

Will an HbA1c help in this situation and at what level is she likely to be classed as a T2D? If it turns out to be 6 % then the grey void of murkiness descends upon you with no clear guidance. Depending

on who your local obstetrician and endocrinologist is that cut off

number will vary again, from 5.7%, 5.9% up to 6.5%.

Some obstetricians seem to be pushing lower thresholds than the RACGP and other evidence-based guidelines, and it is the obstetric units that decide whether GPs can participate in shared care. Yet if the threshold is set too low, the harms of diabetes treatment will outweigh the benefits and I’ll risk pushing unhelpful treatment onto a reluctant Sandra.

I am aware that if I insert an HbA1c >5.9% into the referral letter, Sandra might not thank me for the obstetric unit response – QID finger pricks, bringing in her book every week, insulin and super-tight control.

I don’t know which particular obstetric response is right or wrong, but I know the whole area is fraught. I wish the evidence boffins would agree on where the goalposts stand, taking into account all the negative consequences that can accompany screening for and managing GDM.

As the chips and gravy spill and the toddler climbs into the bin, I know that best practice demands a screening GTT, as Sandra will likely have GDM again in this pregnancy. But actually working with her to get an accurate GTT is going to be logistically difficult. Right now the test is not her priority.

AN INCONVENIENT TRUTHRACGP and ADIPS guidelines recommend GTT screening early in pregnancy for women with BMI >30 (or >35),4 high risk ethnicities, previous GDM, PCOS, previous baby >4.5kg, and various other factors. The guidelines do mention HbA1c, but the diagnostic level is variable, depending on your local endocrinologist. Women previously diagnosed with GDM are also supposed to attend for a 6-week GTT but I often wonder how many actually get it done. Sandra, like many women, did not do the test as she was busy recovering from the birth of the last baby and did not have the time.

The GTT is an inconvenient test. It is designed for organised people who have at least two hours to sit in a waiting room watching morning TV or looking at very old magazines while the toddler goes crazy. For unpaid carers, shift workers, casual employees or contractors (like many GPs), and women who have small children, morning sickness, or are fasting for other reasons (like Ramadan), obtaining an early pregnancy GTT can be diabolical.

SANDRA IS STILL WAITINGThe GTT guidelines are blissfully unaware of Sandra’s preferences. She is sitting in front of me feeling pretty ordinary—literally ‘sick and tired’. My internal monologue tells me that an HbA1c might be helpful, but has not been validated in pregnancy.

After a lot of discussion I arrange for her to have the GTT next week; this is the earliest she can do it, given she has to work to cover her bills and requires child care during the test. I cross my fingers.

A week later the collection centre next door phones. Sandra just vomited 10 minutes after the drink and is feeling very queasy—will you come over and review? I pop my head around the door. Sandra is okay, but the sugar drink is in the sick bag, rather than in Sandra. What to do?

She clearly cannot complete this test today, and she has taken a day off work, unpaid in her casual

“I don’t know which particular

obstetric response is right or wrong, but I know the whole area

is fraught.”



PATIENT POINT-OF-VIEW

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Dad is a bit of a living legend not only in the economic world, but also the medical one, having survived a series of ‘near misses’ over the years.

One of the scariest was back in the 1970s when his anaesthetist put him under just enough so he couldn’t move or respond. He felt every cut of the surgeon’s knife across his thin belly; the scar is at least 15cm long. Since having an equally impressive vertical scar from another operation, Dad likes to joke that now he wears a cross!

Dad has treatment for an underactive thyroid and injections into his left eye to prevent blindness. A couple of years ago the aftermath of his hernia repair, gave us a bit of scare.

A week after the operation while recovering at

Professor Geoff Harcourt, AC is an Australian economist, a leading member of the post-Keynesian school, and Emeritus Reader in the History of Economic Theory, University of Cambridge. He and his daughter Rebecca Harcourt both have late-onset T1D. Rebecca, who went on to become an Ambassador of Diabetes NSW & ACT, describes the health struggles of a man who has reached the pinnacle of his field.

Living with T1D is a challenge for many, not least as we get older and inevitably frailer.Our 88-year-old father has lived with T1D since first diagnosed in his 60s, which is very late in life. It was a bit of a shock for all of us

to be honest as Dad has always kept very fit, running barefoot three miles a day since he was a teenager, way before running was on trend – as he often reminds us!

He played AFL until he was 47 and cricket well into his late sixties. Despite two hip replacements he still does daily press ups, swims laps, walks and climbs stairs. He still misses running tremendously.

A decade after Dad’s diagnosis, I was myself diagnosed with T1D in my early thirties…much younger than Dad, although still older than most people assume.

Dad and I have had various health issues related to our whole endocrinology system, such as my recent thyroidectomy. I’m not a doctor but like Dad I learn and understand more about biology through my various medical conditions and interesting yarns with our medical practitioners. We are a naturally gregarious family, interested in people and their expertise.

Rebecca Harcourt is a writer, facilitator, teacher and Program Manager at Indigenous Business Education at UNSW, Sydney. She is also a Diabetes NSW & ACT Ambassador.

HIS BRILLIANT CAREER: MY FATHER’S T 1D COULDN’T STOP HIM

probably more productive than most of us! Stress and excitement play havoc with Dad’s and

my glucose readings. A big event makes our glucose levels go sky high. Dad, being both a popular and high achieving soul, is often asked to speak at local, national and overseas events. He and Mum returned to live in Australia less than a decade ago, having left in the 1950s for Cambridge, England.

Dad loves people, and although his travelling has greatly reduced he and Mum often attend 2-3 key events each week. As an Honorary Professor where where I work at UNSW, he comes in here every week day, much to the delight of many!

Dad’s deteriorating eyesight means it’s harder for him to double-check his insulin and test if his pen is working. As a technophobe he has no interest in trying out the pump or new scanners. However, he is incredibly diligent at monitoring his BGLs and insulin doses, and regularly attends his GPs and specialists. He is frailer, finding walking great distances hard, and his hearing is deteriorating.

Dad and I both use humour to deflect; this helps us cope with the myriad of challenges from living with a chronic condition. We build good repartee with our medical practitioners and others, but we probably don’t let on too much. Our fierce independence is a great strength, although both

of us have had to learn to let others help us out. Ironically, we are the first to insist that others

seek help when they need it! When Dad and I are stressed we can get

defensive, and to be fair it’s so important we (and medical practitioners) don’t patronise Dad because of his age. I have the utmost respect for our specialists because we have

open and frank conversations where I’m informed of my options. We highly value the respect we’re given and

recognise that so much depends on our daliy self care. It is our responsibility to respond to our own health needs. Equally crucial is that we’re not in the self-blame game; living with diabetes is not an exact science (how much easier it would be if it was!)

With gratitude, my advice to medical practitioners is to continue to respect us all as intelligent individuals. Inform us – we want to know – assist and guide us with our medical care to make a joint decision in the same way we defer to your medical expertise and experience.

Listen to us and continue to treat each of us as our own person, including people such as Dad who is living independently in his late eighties whilst grappling with the inevitable frustrations and physical restrictions of living with T1D. All of us have so much wisdom and knowledge to learn.

31

home, something didn’t seem right and so after encouragement from Mum and me, stoic Dad who doesn’t like to make a fuss, reluctantly agreed to revisit the hospital. He required a second emergency operation, which I’m relieved to share all went well.

Some of the T1D challenges I observe in Dad are similar to mine, but others are harder with his age. We are both brittle in relation to our BGLs, with many swings. Dad regularly checks in with his diabetes educator and doctors to try and rectify his swings. The high sugars particularly frustrate Dad, as they make reading and thinking harder. Although Dad is officially retired, he is still writing, editing, publishing and in much demand. By his standards he has slowed down a lot though Dad’s slow down is


Rebecca (left) with father Geoff, mother Joan and

brother Professor Rob Harcourt at Government House Canberra for the investiture ceremony at

which Geoff received an AC in 2018.

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FOOD STUFF


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A growing group of health professionals is attempting to change the concept of dieting by adopting a ‘weight-neutral’ approach to health. While ‘health at

every size’ may initially appear counterintuitive for people with diabetes and higher body weights, Accredited Practising Dietitian and

nutritionist Zoe Nicholson explains the concepts behind it.

NON-HUNGRY EATING

WHAT IS NON-HUNGRY EATING AND WHEN IS IT A PROBLEM?Non-hungry eating refers to eating for reasons other than physical hunger cues. Physical hunger refers to any physical sensation in the body due to release of the hunger hormone ghrelin.

Non-hungry eating can be a perfectly normal and healthy part of the human experience with food. It is natural to eat for reasons other than physical hunger; including social interaction, entertainment, celebrations, tiredness, mood changes, or for the simple pleasure of food itself. Sometimes eating before hunger appears is necessary when there is knowledge that food may not be available for a certain period.

The familiar term ‘emotional eating’ is a form of non-hungry eating involving eating in response to a (usually) heightened emotion. This can also be a normal part of eating.

Non-hungry eating is not problematic if eating involves an awareness of the food and the reason behind choosing to eat. For the self-aware person, eating outside of physical hunger can delay or reduce the amount of food eaten at the next point of hunger, preventing excessive energy intake. A key point here is the capacity to feel physical hunger as a clear sensation and to differentiate between other non-physical hunger cues.

Unfortunately, many people struggle with this, so some non-hungry eating can lead to an intake of superfluous food. Non-hungry eating can also cause psychological distress—anxiety and shame around food—or lead to prolonged over-consumption of a particular food or quantity of food. For the person with diabetes, both psychological distress and over-consumption can hinder glucose management.

WHAT INFLUENCES NON-HUNGRY EATING?Non-hungry eating affects everybody. If you are human, you will at times eat for reasons other than physical hunger, either in response to an emotional state or a social situation.

In my 15 years of practice I have seen thousands of people who struggle with non-hungry eating. I explain how two key areas drive this eating—heightened emotions (or unmet needs) and food restriction.

Food restriction can result from physical or mental restriction around certain foods, or simply not eating enough food to meet energy requirements (which usually results from dieting or pursuing weight loss). Physical restriction is not allowing yourself to eat food you want to eat, whereas mental restriction is eating the food but thinking you shouldn’t be eating it, or that you need to compensate in some way.

Of course people can choose not to eat a food and be perfectly comfortable with that decision. However, people commonly experience an active struggle with

factors described that drive the desire to eat more.

THE ‘INTUITIVE EATING’ APPROACHWhere non-hungry eating has become problematic, the first step is to ensure the individual is adequately fed; i.e. that they consistently get enough food energy.

One way to do this is using an intuitive eating approach2 where people learn to tune into appetite and satisfaction. For the most part, we choose to eat in response to physical hunger; we eat food we enjoy that satisfies our hunger, and stop eating when comfortably full. People with a history of dieting, weight cycling, disordered eating, eating disorders, or trauma, or who can no longer clearly sense their appetite signals, can benefit from a professional trained in using a non-diet or intuitive eating approach.

Many of these health professionals work within the Health At Every Size (HAES) paradigm, which is a weight-neutral approach to health. HAES practitioners advocate that a focus on healthy behaviours, rather than a focus on reducing body size, is the most useful way to support people of all sizes to take care of their health. The website https://haesaustraliainc.wildapricot.org/ has further information, including how to find a practitioner.

The intuitive eating approach works on a person’s psychology around food to reduce the excitement factor (dopamine response) to certain foods. Common thinking patterns are, ‘I’ve blown it now, may as well write off the rest of today and be good tomorrow’ and ‘I’ll just finish this packet so it’s not in the house and then never buy it again.’

This diet mentality nearly always leads to over-eating or non-hungry eating, often of the very food a person was trying to limit. It also increases a person’s shame around food and their body. Health related shame has significant impacts on the health of people with diabetes. An interesting article3 includes discussion of this impact on metabolic risk factors such as blood glucose.

An approach to non-hungry eating should acknowledge shame and address it; both health professionals and health campaigns need to reconsider the way health advice is provided.

The author declares no conflict of interest. For references go to www.diabetesaustralia.com.au/ diabetes-management-journal

restriction that then leads to distress or shame when the food is eaten or over-eaten.

A PSYCHOLOGICAL, PHYSIOLOGICAL AND SOCIAL PHENOMENONFor people struggling with non-hungry or emotional eating, often the first area to address is food restriction.

It is human nature to desire more of what you can’t have; the ‘forbidden fruit’ effect. We want to consume something with much greater intensity when we are aware it is off limits or unavailable. This is partly due to the complex role of dopamine and other neurotransmitters in the drive and desire to eat.

Receiving a diagnosis of diabetes does not change this basic human trait, nor suddenly alter one’s brain chemistry to reduce the dopamine response to a perceived reward. So while it may seem like sound advice to recommend reducing intake of sweet foods, very often this backfires and can result in an increased desire for sweets and/or over-eating them when the opportunity arises.

Actively pursuing weight loss nearly always involves physical food restriction to reduce calories. As the need for calories is one of our most basic human needs, the human brain is hard wired to seek out these calories from food.

When energy intake is insufficient—as with most diets or weight loss programs—the brain releases more neuropeptide Y, triggering our drive to eat carbohydrates. Most people with T2D are advised to lose weight, and some of those will respond by not eating enough. This intake deficit drives the desire to eat more; particularly more carbohydrate and/or sweet food. This genuine need for food is mistakenly seen as ‘eating more than one should’, which can then lead to sense of failure and the ‘I’ve blown it now’ effect.

A significant factor exacerbating non-hungry eating is our culture’s diet mentality. It has become mainstream thinking to label food as either good or bad, and to claim that foods will either heal you or harm you.

There is an assumption that pursuing weight loss is the key to improving health and that dieting or restricting food is necessary.1 Diet culture emphasises and encourages food restriction whereby either a person is not getting enough food energy or is having to restrict food they enjoy. For many people, this triggers both the psychological and physiological


FOOD STUFF

Zoe Nicholson is an Accredited Practising Dietitian and nutritionist, and Chair of the Victorian Private Practice Dietitians Networking Group.

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https://haesaustraliainc.wildapricot.org/


XIGDUO® XR (dapagliflozin/metformin XR) is bioequivalent to co-administration of approved doses of individual components.3 Comparable glycaemic control has been shown between metformin immediate (IR) and extended-release (XR) formulations.5

MINIMUM PRODUCT INFORMATION (COMBINED): FORXIGA (dapagliflozin) 10mg, QTERN 5/10 (saxagliptin/dapagliflozin) 5mg/10mg and XIGDUO XR (dapagliflozin/metformin extended release) 10mg/500mg, 10mg/1000mg and 5mg/1000mg tablets. INDICATIONS: FORXIGA Monotherapy: in patients with type 2 diabetes as an adjunct to diet and exercise use where metformin is otherwise indicated but was not tolerated. Initial Combination: use as initial combination therapy with metformin, as an adjunct to diet and exercise, to improve glycaemic control in patients with type 2 diabetes mellitus when diet and exercise have failed and there are poor prospects for response to metformin monotherapy. Add-on Combination: in patients with type 2 diabetes mellitus to improve glycaemic control in combination with other anti-hyperglycaemic agents, when these together with diet and exercise do not provide adequate control (Refer to full PI for available data on different combinations); QTERN is indicated as an adjunct to diet and exercise, in combination with metformin, to improve glycaemic control in adults with type 2 diabetes mellitus when treatment with both saxagliptin and dapagliflozin is appropriate. XIGDUO XR is indicated as an adjunct to diet and exercise to improve glycaemic control in adults with type 2 diabetes mellitus when treatment with both dapagliflozin and metformin is appropriate. DOSAGE AND ADMINISTRATION: Tablets must be taken whole. FORXIGA 10mg once daily at any time of the day regardless of meals. Monotherapy and Add-On Combination Therapy: 10mg once daily as monotherapy or as add-on to combination therapy with metformin, a sulfonylurea, DPP4 inhibitor (with or without metformin), *a GLP-1 receptor agonist (extended release exenatide), when initiated concomitantly with FORXIGA (with metformin) or insulin (alone or with one or both of metformin or a sulfonylurea). In add-on therapy, a lower dose of insulin or sulfonylurea may be considered to reduce the risk of hypoglycaemia. Initial Combination Therapy: Starting doses of 10mg FORXIGA plus 500mg metformin once daily. Patients with inadequate glycaemic control on this starting dose should have their metformin dose increased according to metformin Product Information; QTERN One 5mg/10mg tablet once daily at any time of day with or without food. XIGDUO XR One tablet (10mg/500mg or 10mg/1000mg) or two tablets 5mg/1000mg once daily with the evening meal with gradual dose titration to reduce gastrointestinal side effects associated with metformin. In add-on therapy, a lower dose of insulin or sulfonylurea may be considered to reduce the risk of hypoglycaemia. For initial combination therapy, start with one tablet 10mg/500mg once daily. Patients with inadequate glycaemic control on this starting dose should further have their metformin dose increased to one tablet 10mg/1000mg or two tablets 5mg/1000mg once daily. XIGDUO XR maximum dose is 10mg/2000mg taken as two 5mg/1000mg tablets once daily. FORXIGA, QTERN and XIGDUO XR are not to be taken together in combination.CONTRAINDICATIONS: FORXIGA, QTERN and XIGDUO XR hypersensitivity to any of the ingredients; moderate or severe renal impairment (CrCl persistently <60mL/min or eGFR persistently <60mL/min/1.73m2). QTERN anaphylaxis or angioedema following exposure to any DPP-4 inhibitor. XIGDUO XR Diabetic ketoacidosis, diabetic pre-coma; acute conditions with the potential to alter renal function; diseases causing tissue hypoxia; during or immediately following surgery; elective major surgery; hepatic impairment; acute alcohol intoxication, alcoholism; lactation. PRECAUTIONS: FORXIGA, QTERN and XIGDUO XR Not for type 1 diabetes mellitus or diabetic ketoacidosis. Monitoring of renal function recommended – prior to initiation and at least yearly thereafter, prior to initiation of concomitant medicines that may reduce renal function and periodically thereafter, for renal function approaching moderate renal impairment at least 2–4 times yearly. Patients receiving loop diuretics or at risk for volume depletion, hypotension and electrolyte imbalance; patients for whom dapagliflozin induced blood pressure drop could pose a risk; *ketoacidosis; *surgery; urinary tract infections; *Necrotising fasciitis of the perineum (Fournier’s gangrene); *lower limb amputations, counsel patients on routine preventative foot care; hypoglycaemia when used in combination with insulin or sulfonylurea; children; elderly; patients treated with pioglitazone; limited or no experience in cardiac failure; severe hepatic impairment; pregnancy (Category D); lactation; interference with 1,5-anhydroglucitol (1,5-AG) assay; avoid hypoglycaemia while driving or using machinery if used with sulfonylurea or insulin. QTERN hypersensitivity reactions; caution if used in patients with known risk factors for hospitalisation for heart failure; dizziness; monitor for skin disorders; pancreatitis; *bullous pemphigoid; arthralgia; not studied in combination with GLP-1 analogues, insulin and sulfonylureas; immunocompromised patients. XIGDUO XR Impaired hepatic function; lactic acidosis; administration of iodinated contrast agent; hypoxic states; vitamin B12 levels; alcohol intake; loss of glycaemic control; change in clinical status in previously well controlled patients. INTERACTIONS: XIGDUO XR Metformin: frusemide, nifedipine, careful patient monitoring and dose adjustment of metformin and/or the interfering drug in patients who are taking cationic medications excreted by renal tubular secretion (e.g. amiloride, digoxin, morphine, procainamide, quinidine, quinine, ranitidine, cimetidine, triamterene, trimethoprim, or vancomycin). FORXIGA or QTERN no clinically meaningful interactions expected. (See full PI). ADVERSE REACTIONS: FORXIGA, QTERN and XIGDUO XR Genital infections; urinary tract infections; back pain; polyuria; hypoglycaemia; headache; volume depletion; events related to decreased renal function; malignancies; ketoacidosis; pyelonephritis; urosepsis; *necrotising fasciitis of the perineum (Fournier’s gangrene); rash. QTERN upper respiratory tract infection; dysuria; diarrhoea; nausea; cough; dyslipidaemia; pancreatitis; arthralgia; *bullous pemphigoid. XIGDUO XR Taste disturbance; mild gastrointestinal symptoms including diarrhoea; nausea; vomiting; abdominal pain and loss of appetite. Date of first approval: FORXIGA 22 October 2012; QTERN 25 October 2016; XIGDUO XR 18 July 2014. Date of revision: FORXIGA 3 January 2019; QTERN 3 January 2019; XIGDUO XR 3 January 2019.

*Please note changes to Product Information DPP4i = dipeptidyl peptidase 4 inhibitor; HbA1c = glycated haemoglobin; SGLT2i = sodium glucose co-transporter 2 inhibitor. References: 1. Rosenstock J et al. Arch Endocrinol Metab 2018; 62(4):424–430. 2. FORXIGA® Approved Product Information. 3. XIGDUO® XR Approved Product Information. 4. QTERN® Approved Product Information. 5. Fujioka K et al. Clin Ther 2003; 25(2):515–525. FORXIGA,® XIGDUO,® and QTERN® are registered trademarks of the AstraZeneca group of companies. Registered user AstraZeneca Pty. Ltd. ABN 54 009 682 311. 66 Talavera Road, Macquarie Park, NSW 2113. www.astrazeneca.com.au. For Medical Information enquiries: 1800 805 342 or [email protected]. To report an adverse event: 1800 805 342 or via https://aereporting.astrazeneca.com. AU-6573. 15685_DMJ. August 2019.

BEFORE PRESCRIBING PLEASE REVIEW FULL PRODUCT INFORMATION AVAILABLE ON REQUEST FROM ASTRAZENECA ON 1800 805 342 OR www.astrazeneca.com.au/PI

WARNING: Life-threatening lactic acidosis can occur due to accumulation of metformin. The main risk factor is renal impairment, other risk factors include old age associated with reduced renal function and high doses of metformin above 2g per day.

PBS Information: FORXIGA, XIGDUO XR and QTERN: Authority Required (STREAMLINED). Type 2 Diabetes. Refer to PBS Schedule for full Authority Required Information.

(dapagliflozin)(dapagliflozin) (dapagliflozin/metformin HCl extended-release) tablets(dapagliflozin/metformin HCl extended-release) tablets

(saxagliptin/dapagliflozin) 5mg/10mg tablets(saxagliptin/dapagliflozin) 5mg/10mg tablets

^

^QTERN® is indicated with metformin when treatment with both saxagliptin and dapagliflozin is appropriate.

FORXIGA® I N PAT I E N T S W I T H T Y P E 2 D I A B E T E SVERSUS DPP4i (SAXAGLIPTIN), WHEN ADDED TO METFORMIN XR, AT 24 WEEKS IN A POST-HOC ANALYSIS HAS SHOWN:

ADDITIONAL BENEFITS OF:

HbA1c

Significant reductions1*

-1.20% decrease from baseline (vs -0.88%)1

WeightSignificant reductions1†

Systolic blood pressure reductionson top of background anti-hypertensive therapy1^

-2.4kg decrease in body weight (vs no decrease)1

-3.3mm Hg reduction from baseline (vs +0.5mm Hg gain) P=0.0008 Dapa + Met vs Saxa + Met1

D A P A G L I F L O Z I N

*Statistically significant; P<0.005 †Statistically significant; P<0.0001. Dapagliflozin is not indicated for

weight loss. Secondary endpoint.1–4

^Dapagliflozin is not indicated for blood pressure reduction.

Safety assessment.1–4

15685_Forxiga_Qualifier_DMJ_FullPage_275x210mm_AD_FA.indd 1 15/8/19 5:34 pm

http://www.astrazeneca.com.au/PI

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https://aereporting.astrazeneca.com

The National Diabetes Services Scheme is an initiative of the Australian Government administered with the assistance of Diabetes Australia.

NDSS Helpline 1300 136 588 ndss.com.au

NDSS FactsheetsFree diabetes information just one click

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Understanding type 1 diabetes

Understanding type 2 diabetes

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Sick days and type 1 diabetes

These factsheets are available in Arabic, Greek, Italian, Korean, Samoan, Spanish, Simplified Chinese, Traditional Chinese, Turkish, Urdu and Vietnamese. The“Understanding Gestational Diabetes” fact sheet is also availablein Hindi, Samoan and Bengali.

Sick days and type 2 diabetes

Steroid medications

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Adjusting to life with diabetes

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Concerns about starting insulin

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Diabetes and depression

Disordered eating

Caring for someone with diabetes

ndss.com.au

NDSS Helpline 1300 136 588


Gestational diabetes is a form

of diabetes that occurs during

pregnancy. About 12–14% of

pregnant women will develop

gestational diabetes, usually

around the 24th to 28th week

of pregnancy.

In most cases, blood glucose

levels return to target ranges after

the baby is born and the woman

no longer has diabetes. However,

some women will continue to have

high blood glucose levels after

delivery, leading to a diagnosis

of type 2 diabetes.

Diabetes is a condition where there

is too much glucose (sugar) in the

bloodstream.

Glucose is an important source of energy

for your body. It comes from carbohydrate

foods that you eat, such as bread, pasta,

rice, cereals, fruits, starchy vegetables,

milk and yoghurt. Your body breaks down

carbohydrates into glucose, which then

enters your bloodstream.

Insulin is needed to allow glucose from

the bloodstream to enter the body cells

and be used for energy. Insulin is made

in the body by your pancreas.

During pregnancy, some of the hormones

produced by the placenta reduce the action

of insulin. The pancreas then needs to

produce extra insulin to keep blood

glucose levels in the target range. If the

pancreas is unable to produce enough

insulin, blood glucose levels rise and

gestational diabetes develops.

Understanding gestational

diabetes

Managing gestational

diabetes can help

keep blood glucose

levels in the target

range for a healthy

pregnancy.

ndss.com.auNDSS Helpline 1300 136 588


Diabetes-related complications

Looking after your diabetes is important for long-term health. If your diabetes is well managed and you take care of your general health, you can reduce the risk of diabetes-related complications.

What are the most common complications of diabetes?

Diabetes-related complications can include

damage to:

» the large blood vessels (macrovascular/

cardiovascular complications), leading

to heart attack, stroke or circulation

problems in the lower limbs

» the small blood vessels (microvascular

complications), causing problems in the

eyes, kidneys, feet and nerves

» other parts of the body, including the

skin, teeth and gums.

Large blood vessels

The main cause of large blood vessel

damage in people with diabetes is

atherosclerosis. Atherosclerosis occurs

when plaque – made up of cholesterol and

other fats – builds up inside the walls of

blood vessels. This causes a narrowing of

the vessels, reducing the blood flow to

organs and other parts of the body.

If the plaque ruptures, this can form a

blood clot that can totally block the

blood supply to organs and other parts

of the body. This can affect the blood

vessels that supply blood to the heart,

brain and lower limbs.

ndss.com.au

NDSS Helpline 1300 136 588 The National Diabetes Services Scheme is an initiative of the Australian Government administered with the assistance of Diabetes Australia.

Blood glucose monitoring Regularly checking your blood glucose levels (also called self-monitoring) can help you manage

your diabetes. Your diabetes health

professionals can help you with information and advice about blood glucose monitoring. Regular monitoring can help you see

the effects of food, exercise, medication

and illness on your blood glucose levels.

It can also help you identify any patterns

or changes that you should discuss

with your doctor or diabetes health

professionals.

Why monitor? Monitoring your blood glucose levels

help you to: » know immediately if your levels are in the

target range » gauge whether your diabetes medication

is helping you to achieve target levels

» better understand how physical activity,

food, stress, travel and illness influence

your blood glucose levels » look for any patterns at different times of

the day to help you identify when you have

high or low blood glucose levels » identify and treat low blood glucose levels

(hypoglycaemia or hypo) quickly if you

are using insulin or other types of blood

glucose-lowering medications » feel more confident about managing

your diabetes » know when you need to seek support

from your doctor or diabetes health

professionals to adjust your medications

or insulin, or for advice on meal planning

or physical activity.Your diabetes health professionals, especially

your credentialled diabetes educator, can:

» help you choose a blood glucose meter

that best suits you » give you information about how to check

your blood glucose levels » work with you to decide how often and at

what times you should check your levels

» help you learn how to interpret your

readings.

ndss.com.au



Alcohol

Most people can enjoy a small

amount of alcohol. However, drinking

too much alcohol can be harmful

to your health. When you have

diabetes, there are some extra things

to consider when you drink alcohol.

Alcohol can have many different effects on

your body, including:

Weight gain – alcohol has very little

nutritional value and is high in kilojoules/

calories. If you drink alcohol in large

amounts, or on a regular basis, it can lead

to weight gain.

Making it difficult to manage your diabetes

– drinking alcohol can cause both high and

low blood glucose levels. Alcohol may also

affect your judgement when looking after

your diabetes.

Damage to the body – drinking large

amounts of alcohol can be extremely

dangerous. It can affect many different

parts of your body, including your brain,

nerves, liver and pancreas. Too much

alcohol can also increase your risk of

developing heart disease and some

cancers.

Risk of complications – too much alcohol

can increase the risk of developing

complications related to diabetes. This is

because alcohol can contribute to weight

gain, increase triglycerides (blood fats) and

raise blood pressure.

Alcohol and hypoglycaemia

If you are taking insulin or certain diabetes

tablets, you are at risk of alcohol-related

hypoglycaemia (hypos). A hypo is when

blood glucose levels drop below 4mmol/L.

Hypos can occur while drinking alcohol

– or many hours afterwards – and can be

dangerous.

Normally, the liver releases stored glucose

if your blood glucose level drops too low.

However, when you drink alcohol, the liver

always processes the alcohol first, instead of

releasing stored glucose. This can increase

the risk of a hypo. Alcohol can also make it

harder to recognise the symptoms of, and to

treat, a hypo.

When drinking, it’s important that your

friends and family understand the signs of a

hypo and what the symptoms are.

Ask your doctor or diabetes health

professional whether you might be at

increased risk of alcohol-related hypos.

ndss.com.au



Diabetes can be really tough to

live with. Sometimes people feel

distressed, which can include feeling

frustrated, guilty, sad, or worried.

It is understandable if you feel this way

from time to time, – but you are not

alone. There are many things you

that can be donecan do to reduce

your diabetes distress.

“I think the hardest thing was as soon

as you start testing your sugars and you

don’t watch them go down, that just

becomes blow after blow every day. It’s

not something you deal with every three

months when you get your blood test

result, it’s something you’re dealing with

on a daily basis, so it’s taken me a long

time to get used to doing sugar readings

and accepting them.”Marianne, 62, person with diabetes

Diabetes distress

What is diabetes distress?

Diabetes distress is the emotional burden

of living with and managing diabetes.

For example, you may feel:

» overwhelmed by the demands of living

with diabetes» concerned that you are ‘failing’ with your

diabetes management

» worried about your risk of long-term

complications» frustrated that you can’t predict or

‘control’ diabetes from one day to the next

» guilty when your diabetes management

gets ‘off track’.Diabetes distress becomes a serious

problem when these emotions start to

affect daily life, including work, school,

relationships and diabetes management.

If severe diabetes distress is not managed,

it can get worse over time. It may lead

to ‘burnout’. This is when a person feels

emotionally exhausted and overwhelmed by

the demands of their diabetes. They try to

cope with this by giving up on taking care of

their diabetes.If you experience diabetes distress, talk to

your health professional. They will assess the

problem and help you work out strategies to

manage your distress.

www.ndss.com.au

https://www.ndss.com.au/about-diabetes/resources/

https://www.ndss.com.au/about-diabetes/resources/

Diabetes · 2019-09-10 · Diabetes Management Journal 4 DIABETES MANAGEMENT JOURNAL August 2019...

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Transcript of Diabetes · 2019-09-10 · Diabetes Management Journal 4 DIABETES MANAGEMENT JOURNAL August 2019...