SAT740& DESIGN GUIDE TYPE(B(INSULIN ... - Poster Talks · without any antidiabetic treatment...
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RESEARCH POSTER PRESENTATION DESIGN © 2012 www.PosterPresentations.com The type B insulin resistance syndrome is an autoimmune disease of low prevalence. It is due to the presence of antibodies against the insulin receptor (1) and its relationship with Lupus Erythematosus is low, having an incidence of 2.6% (2). Although in some cases it manifests with hypoglycemia, it more often presents with severe hyperglycemia with high insulin requirements and exaggerated insulin resistance (3). The immunomodulatory treatment may be the best strategy to achieve metabolic control and can even turn the antibodies negative (3). Background 23 year old, thin, female patient, diagnosed with Systemic Lupus Erythematosus since 2010, undergoing therapy with prednisolone 5 mg daily, chloroquine and azathioprine. In August 2013 she presented diabetic ketoacidosis; steroids were suspended and treatment with insulin was begun. During her stay at the hospital she had high insulin requirements (glargine insulin 90 units every 12 hours and aspart insulin 70 preprandial units). Due to poor metabolic control, she needed to change from a basal-bolus scheme to an insulin pump plus additional bolus, persisting poor metabolic control with glucometric measurements of 600mg / dl or greater, requiring progressive increases in doses up to 300 units of insulin per day through the infusion pump plus a basal-bolus insulin scheme of glargine and glulisine, with total doses of up to 600 units per day. (Fig.1) Clinical Case Discussion Some patients with these antibodies evidence an association with an autoimmune disorder, mainly Systemic Lupus Erythematosus (SLE) and, to a lesser degree, with other undifferentiated autoimmune disorders, although a low incidence of the presence of insulin antibodies in SLE patients has been reported (2). Often these patients have high insulin requirements associated with signs of insulin resistance as acanthosis nigricans, amenorrhea and hyperandrogenism (4). Treatment of Type B insulin resistance has been largely empirically based on immunotherapies such as corticosteroids, cyclophosphamide, cyclosporine, azathioprine, mycophenolate rituximab and plasmapheresis, associated with high doses of insulin (1). In this particular case, management with prednisolone, azathioprine and mycophenolate for the lupus activity resulted in a progressive insulin requirement decrease, and eventually in withdrawal of all antidiabetic therapy, achieving a complete resolution of hyperglycemia. Conclusions Type B insulin resistance syndrome should be suspected in a patient with autoimmune disease presenting severe hyperglycemia with very high insulin requirements. The study should include anti insulin antibodies and anti insulin receptor; the absence of these antibodies does not rule out disease but allows confirmation with positive reports. In this patient the positivity for anti-insulin antibodies was confirmed at levels only slightly above the normal upper limit, but the complete resolution of severe hyperglycemia in response to immunomodulators allowed us to confirm the diagnosis and to prevent severe complications of prolonged uncontrolled hyperglycemia. References 1. Kawashiri S., Kawakami A. 1, Fujikaw K,.Et al. Type B Insulin Resistance Complicated with Systemic Lupus Erythematosus. Inter Med 49: 487-490, 2010 2. Elliot D. Rosenstein, Sonoo Advani, Richard E. Reitz , Et al. The Prevalence of Insulin Receptor Antibodies in Patients with Systemic Lupus Erythematosus and Related. Conditions. J ClinRheumatol 2001;7:211–2. 3. Arioglu E, Andewelt A, DiaboC, Bell M, Taylor SI, Gorden P. Clinical course of the syndrome of autoantibodies to the insulin receptor (type B insulin resistance): a 28-year perspective. Medicine (Baltimore) 2002;81:87- 100 4. Gehi A., Webb A., Nolte M. Et al. Treatment of Systemic Lupus Erythematosus–Associated Type B Insulin Resistance Syndrome With Cyclophosphamide and Mycophenolate Mofetil. ARTHRITIS & RHEUMATISM Vol. 48, No. 4, April 2003, pp 1067–1070 Mejia MG* Rivera A** Medina A*** Rojas W**** * Internist – Endocrinologist, Professor FUCS-Hospital San José **Internist, Endocrinology resident. FUCS-Hospital San José *** Internist - Endocrinologist, Professor FUCS-Hospital San José **** Internist, Endocrinologist. Professor FUCS-Hospital San José Non conflict of interest TYPE B INSULIN RESISTANCE SYNDROME IN PATIENT WITH SYSTEMIC LUPUS ERYTHEMATOSUS, ANTI – INSULIN POSITIVE AND A SUBSEQUENT RESOLUTION WITH INMUNOMODULATORY TREATMENT Fig 2. A 23 year old, thin, female pa/ent with acanthosis nigricans (a marker of insulin resistance) Tab 1. Laboratory results table During monitoring she presented lupus activation with Lupus Nephritis class IV, handled with immunomodulatory therapy, reset of azathioprine and prednisolone, obtaining an adequate response. The results of anti-insulin antibodies were positive, the other antibodies were negative and complete sequencing of the INSR gene was inconclusive. A short time after beginning the immunomodulators the patient started to lower her glucose measurements allowing sequential reductions in insulin dosage until the withdrawal of the infusion pump and the reduction of the basal-bolus scheme. In March 2015, she received the last dose of insulin; since that time maintaining an adequate glucometric control with liraglutide 1.2mg / day as mono-therapy. In September 2015, mycophenolate was initiated for the management of her renal impairment allowing further withdrawal of liraglutide. Since then, the patient has been without any antidiabetic treatment showing good glycemic control and HbA1c: 5.6%. ( Fig.3) Due to clinical signs of severe insulin resistance in a young woman with high glycemic variability (180 and 480 mg/dl) and HbA1c:14%, diabetes type MODY was suspected; as a result 850 mg of metformin and sulfonylurea every 8 hours were added showing partial improvement of the hyperglycemia. (Fig.2) Subsequent management with a GLP-1 analogue (liraglutide 1.8 mg daily) was required and an evaluation of genetic or immunological origin of the insulin resistance was initiated (anti-insulin antibodies, anti- insulin receptor, anti-GAD, anti B cells, C-peptide, and sequencing of the INSR gene). (Table 1) Fig 3. Glucose monitoring post immunotherapy Fig 1. Glucose monitoring prior to immunotherapy Discussion The Type B insulin resistance syndrome, is an autoimmune condition characterized by production of antagonistic antibodies against the insulin receptor; this leads to hyperglycemia and insulin resistance. Sometimes anti insulin antibodies may have insulin-like effect and cause hypoglycemia (4). SAT 740 TEST SCORES DATE LABORATORY RESULT REFERENCE VALUE October 2014 An/bodies to glutamic acid decarboxylase 0,47 U/ML Nega/ve Insuline An/bodies 1,3 U/ML Up to 0,4 U/ML November 2014 Complete sequencing of the Gene INSR Inconclusive. The patient is not a carrier of pathologic changes in the analyzed sequence of the INSR gene. The results do not allow to confirm or exclude the clinical diagnosis.
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The type B insulin resistance syndrome is an autoimmune disease of low prevalence. It is due to the presence of antibodies against the insulin receptor (1) and its relationship with Lupus Erythematosus is low, having an incidence of 2.6% (2). Although in some cases it manifests with hypoglycemia, it more often presents with severe hyperglycemia with high insulin requirements and exaggerated insulin resistance (3). The immunomodulatory treatment may be the best strategy to achieve metabolic control and can even turn the antibodies negative (3).
Background
23 year old, thin, female patient, diagnosed with Systemic Lupus Erythematosus since 2010, undergoing therapy with prednisolone 5 mg daily, chloroquine and azathioprine. In August 2013 she presented diabetic ketoacidosis; steroids were suspended and treatment with insulin was begun. During her stay at the hospital she had high insulin requirements (glargine insulin 90 units every 12 hours and aspart insulin 70 preprandial units). Due to poor metabolic control, she needed to change from a basal-bolus scheme to an insulin pump plus additional bolus, persisting poor metabolic control with glucometric measurements of 600mg / dl or greater, requiring progressive increases in doses up to 300 units of insulin per day through the infusion pump plus a basal-bolus insulin scheme of glargine and glulisine, with total doses of up to 600 units per day. (Fig.1)
Clinical Case
Discussion
Some patients with these antibodies evidence an association with an autoimmune disorder, mainly Systemic Lupus Erythematosus (SLE) and, to a lesser degree, with other undifferentiated autoimmune disorders, although a low incidence of the presence of insulin antibodies in SLE patients has been reported (2). Often these patients have high insulin requirements associated with signs of insulin resistance as acanthosis nigricans, amenorrhea and hyperandrogenism (4). Treatment of Type B insulin resistance has been largely empirically based on immunotherapies such as corticosteroids, cyclophosphamide, cyclosporine, azathioprine, mycophenolate rituximab and plasmapheresis, associated with high doses of insulin (1). In this particular case, management with prednisolone, azathioprine and mycophenolate for the lupus activity resulted in a progressive insulin requirement decrease, and eventually in withdrawal of all antidiabetic therapy, achieving a complete resolution of hyperglycemia.
Conclusions
Type B insulin resistance syndrome should be suspected in a patient with autoimmune disease presenting severe hyperglycemia with very high insulin requirements. The study should include anti insulin antibodies and anti insulin receptor; the absence of these antibodies does not rule out disease but allows confirmation with positive reports. In this patient the positivity for anti-insulin antibodies was confirmed at levels only slightly above the normal upper limit, but the complete resolution of severe hyperglycemia in response to immunomodulators allowed us to confirm the diagnosis and to prevent severe complications of prolonged uncontrolled hyperglycemia.
References
1. Kawashiri S., Kawakami A. 1, Fujikaw K,.Et al. Type B Insulin Resistance Complicated with Systemic Lupus Erythematosus. Inter Med 49: 487-490, 2010 2. Elliot D. Rosenstein, Sonoo Advani, Richard E. Reitz , Et al. The Prevalence of Insulin Receptor Antibodies in Patients with Systemic Lupus Erythematosus and Related. Conditions. J ClinRheumatol 2001;7:211–2. 3. Arioglu E, Andewelt A, Diabo C, Bell M, Taylor SI, Gorden P. Clinical course of the syndrome of autoantibodies to the insulin receptor (type B insulin resistance): a 28-year perspective. Medicine (Baltimore) 2002;81:87- 100 4. Gehi A., Webb A., Nolte M. Et al. Treatment of Systemic Lupus Erythematosus–Associated Type B Insulin Resistance Syndrome With Cyclophosphamide and Mycophenolate Mofetil. ARTHRITIS & RHEUMATISM Vol. 48, No. 4, April 2003, pp 1067–1070
Mejia MG* Rivera A** Medina A*** Rojas W**** * Internist – Endocrinologist, Professor FUCS-Hospital San José **Internist, Endocrinology resident. FUCS-Hospital San José *** Internist - Endocrinologist, Professor FUCS-Hospital San José **** Internist, Endocrinologist. Professor FUCS-Hospital San José
Non conflict of interest
TYPE B INSULIN RESISTANCE SYNDROME IN PATIENT WITH SYSTEMIC LUPUS ERYTHEMATOSUS, ANTI – INSULIN POSITIVE AND A SUBSEQUENT RESOLUTION WITH INMUNOMODULATORY TREATMENT
Fig 2. A 23 year old, thin, female pa/ent with acanthosis nigricans (a marker of insulin resistance)
Tab 1. Laboratory results table
During monitoring she presented lupus activation with Lupus Nephritis class IV, handled with immunomodulatory therapy, reset of azathioprine and prednisolone, obtaining an adequate response. The results of anti-insulin antibodies were positive, the other antibodies were negative and complete sequencing of the INSR gene was inconclusive. A short time after beginning the immunomodulators the patient started to lower her glucose measurements allowing sequential reductions in insulin dosage until the withdrawal of the infusion pump and the reduction of the basal-bolus scheme. In March 2015, she received the last dose of insulin; since that time maintaining an adequate glucometric control with liraglutide 1.2mg / day as mono-therapy. In September 2015, mycophenolate was initiated for the management of her renal impairment allowing further withdrawal of liraglutide. Since then, the patient has been without any antidiabetic treatment showing good glycemic control and HbA1c: 5.6%. ( Fig.3)
Due to clinical signs of severe insulin resistance in a young woman with high glycemic variability (180 and 480 mg/dl) and HbA1c:14%, diabetes type MODY was suspected; as a result 850 mg of metformin and sulfonylurea every 8 hours were added showing partial improvement of the hyperglycemia. (Fig.2) Subsequent management with a GLP-1 analogue (liraglutide 1.8 mg daily) was required and an evaluation of genetic or immunological origin of the insulin resistance was initiated (anti-insulin antibodies, anti- insulin receptor, anti-GAD, anti B cells, C-peptide, and sequencing of the INSR gene). (Table 1)
Fig 3. Glucose monitoring post immunotherapy Fig 1. Glucose monitoring prior to immunotherapy
Discussion
The Type B insulin resistance syndrome, is an autoimmune condition characterized by production of antagonistic antibodies against the insulin receptor; this leads to hyperglycemia and insulin resistance. Sometimes anti insulin antibodies may have insulin-like effect and cause hypoglycemia (4).
SAT 740
TEST SCORES
DATE LABORATORY RESULT REFERENCE VALUE
October 2014 A n / b o d i e s t o g l u t a m i c a c i d decarboxylase
0,47 U/ML Nega/ve
Insuline An/bodies 1,3 U/ML Up to 0,4 U/ML
November 2014 Complete sequencing of the Gene INSR
Inconclusive. The patient i s not a carr ier of pathologic changes in the analyzed sequence of the INSR gene. The results do not allow to confirm or exclude the clinical diagnosis.
