Vitamin d deficiency
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04/15/23 Dr. M. S. Prasad 1
Vitamin-D DeficiencyVitamin-D Deficiency
Dr. M. S. PrasadDr. M. S. PrasadRetired Consultant & HeadDepartment of Pediatrics
VM Medical College & Safdarjung HospitalNew Delhi
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04/15/23 Dr. M. S. Prasad 2
S Balasubramanian, K Dhanalakshmi and Sumanth Amperavani:
Vitamin-D Deficiency in Childhood – A Review of Current Guidelines on Diagnosis and Management.
Indian Pediatrics, Vol. 50 – July 15, 2013 pp 669 – 675.
Indian Pediatrics, Volume 51, April 15, 2014.
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IntroductionIntroduction
• Most common nutritional deficiency,
• One of the most common undiagnosed medical conditions in the world.
• Vitamin-D has evolved into a hormone.
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FunctionsFunctions
• Regulates calcium and bone metabolism,
• Reduce the risk of chronic diseases:– Auto-immune diseases,– Malignancies,– Cardiovascular, and– Infectious diseases.
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Facts!!Facts!!• It has been estimated that 1 billion people
worldwide have vitamin-D deficiency or insufficiency.
• Though majority of population in India lives in areas with ample sunlight throughout the year, vitamin-D deficiency is very common in all the age groups and both the sexes across the country.
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Facts!!!Facts!!!
• Nutritional Rickets has recently re-emerged as a problem in many countries where it was thought to have been eradicated.
• Hospitalization rates for rickets in England are now the highest in 5 decades.
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EtiologyEtiology
• Prevalence: 50-90% in India,
• Low dietary intake of calcium, skin color and changing life-style.
• Deficiency of dietary calcium is more responsible for rickets than deficiency of vitamin-D.
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EtiologyEtiology (continued)
• Vitamin-D insufficiency + decreased calcium intake or high phytate intake combine to induce rickets.
• Common in infancy:– Decreased dietary intake,– Decreased cutaneous synthesis,– Increased rate of exclusive breastfeeding, and – Low maternal vitamin-D.
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EtiologyEtiology (continued)
• Decreased vitamin-D synthesis,
• Decreased nutritional intake of vitamin-D,
• Age & Physiology related,
• Decreased maternal vitamin-D stores,
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Etiology Etiology (continued)
• Malabsorption,
• Decreased metabolic conversion to active form,
• Increased degradation of 25(OH)D.
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Decreased vitamin-D synthesisDecreased vitamin-D synthesis
• Skin pigmentation,
• Physical agents blocking UVR exposure,
• Clothing,
• Latitude,
• Season,
• Air-pollution,
• Cloud cover,
• Altitude.
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MalabsorptionMalabsorption
• Celiac disease,
• Pancreatic insufficiency (cystic fibrosis),
• Biliary obstruction (Biliary Atresia)
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Decreased metabolic conversionDecreased metabolic conversion
• Chronic Liver Disease,
• Chronic Renal Failure.
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Increased degradation of 25(OH)DIncreased degradation of 25(OH)D
• Drugs such as:– Rifampicin,
– Isoniazid,
– Anticonvulsants,
– Glucocorticocoids.
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OthersOthers• Decreased nutritional intake:
– Strict Vegan Diet.
• Age & Physiology related:– Elderly,– Obese,– Institutionalized.
• Decreased maternal vitamin-D stores:– Exclusive Breastfeeding.
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Definition of vitamin-D statusDefinition of vitamin-D status
• Debated by clinicians and researchers,
• Defined as serum level of 25(OH)D less than 20 ng/dL.
• Less than 15 ng/dl: Definite Deficiency.
• Less than 5 ng/dL: Severe Deficiency.
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Serum vitamin-D levelsSerum vitamin-D levels
• Sufficient data are not available to define the upper level of normal or dose levels above which toxicity occurs.
• Previous thought: intoxication does not occur until serum levels of 25(OH)D reach 100 to 200 ng/dL.
• Recently, risks identified at higher levels above 50 ng/dL.
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Vitamin-D levels Vitamin-D levels (continued)
• 25(OH)D:– Major circulating vitamin-D,– Half-life 2-3 weeks,– Best available indicators of vitamin-D status.
• 1,25(OH)2D (calcitriol):– Active form,– Half-life only 4 hours.
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When to treat?When to treat?
• Symptomatic:– Signs & symptoms of
hypocalcaemia,– Signs & symptoms of Rickets.
• Asymptomatic:– When vitamin-D levels are in the
deficient range even if asymptomatic.
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Treatment RegimenTreatment Regimen
• D3: 2000 IU daily or D2: 50000 IU weekly.
• Stoss Therapy: 6 lakh units once, or
• D3: 1000 – 5000 IU/day for weeks, or
• D2: 50000 units/wk for 8 weeks.
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TreatmentTreatment
GroupDaily regimen(8-12 weeks)
Weekly regimen
(8-12 weeks)
Stoss Therapy (Oral or IM)
Maintenance
<1 mo old 1000 IU 50000 IU 400-1000 IU
1-12 mo 1000-5000 IU 50000 IU1 – 6 lakh units over 1-5 days
400-1000 IU
1-18 y old 5000 IU 50000 IU3-6 lakh units over 1-5 days
600-1000 IU
>18 y old 6000 IU 50000 IU3-6 lakh units over 1-5 days
1500-2000 IU
Obese, Malabsorption 6000-10000 IU 3000-6000 IU
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Treatment Treatment (continued)
• A single dose of 300, 000 IU is not inferior to double of this dose (600, 000 IU).
• The dose is effective orally.
• Intramuscular dose is painful and unnecessary.
• I. M. reserved for cases with malabsorption only.
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DiscussionDiscussion• Lack of compliance lack of response.
• Solution: Administer high dose of 100000 to 600000 IU over 1-5 days (Stoss Therapy).
• Advantage of Stoss therapy: Vitamin-D is efficiently stored in adipose tissue and muscle and is continuously converted into active form.
• Shah and Finberg successfully administered 1 lakh IU every 12 hours over 12 hour period.
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MaintenanceMaintenance
• After completion of treatment, continue vitamin-D at 800-1000 IU/day till serum alkaline phosphatase returns to normal.
• D3 is 3 times more potent than D2.
• Provide Calcium supplement throughout treatment and maintenance. (elemental calcium 30-75 mg/kg/day in 3 divided doses).
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Indian Pediatrics: Volume 51, April 15, 2014Indian Pediatrics: Volume 51, April 15, 2014
• Both 3 lakh and 6 lakh IU vitamin D3 as single day doses are equally effective in treating children between 6 months and 5 years of age with vitamin D deficiency rickets.
• Neither dose is able to normalize the vitamin D status of the children 3 months after the administered dose.
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How to screen?
SAP
Normal ElevatedElevated
1. 25(OH)D2. Calcium3. Phosphorus4. PTH and5. Radiology.SAP =Serum Alkaline Phosphatase
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Whom to screen?Whom to screen?• Dark skinned infants who live at higher
altitude and infants born to vitamin-D deficient mothers.
• In the presence of non-specific symptoms like poor growth, gross motor developmental delay and unusual irritability.
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Whom to screen?
• Children with suspected rickets, those with osteopenia.
• Chronic Kidney Disease.
• Hepatic Failure.
• Hyperparathyroidism.
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Whom to screen?
• Malabsorption syndrome:– Cystic Fibrosis,– IBD (Inflammatory Bowel Disease),– Crohn’s Disease
• Medications:– Anticonvulsants,– Glucocorticosteroids,– AIDS medication,– Antifungal (ketoconazole).
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Whom to screen?
• Obese children and adults (BMI>30 kg/M2)
• Granuloma forming disorders:– Sarcoidosis,– Tuberculosis,– Histoplasmosis.
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PreventionPrevention
• Improve maternal vitamin-D status,
• Administration of high dose of vitamin-D (400-6400 IU) daily to breastfeeding mothers increases anti-rachitic activity of breastmilk without causing hypervitaminosis in the mother.
• Vitamin-D supplementation to preterm babies since birth (400-800 IU/day)
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Sources of vitamin-DSources of vitamin-D
• Sunlight,
• Diet:– Oily fish (salmon, mackerel and sardine),– Cod liver oil,– Liver and organ meat.
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