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Insulin Antibodies Hypoglycemia

Insulin Autoimmune Syndrome: A Rare Cause Of Postprandial Hypoglycemia

Insulin Autoimmune Syndrome: A Rare Cause Of Postprandial Hypoglycemia

Division on Endocrinology and Metabolic Medicine and Department of Internal Medicine, St Vincent Hospital, Worcester, Massachusetts, USA Summary A 65-year-old obese Caucasian woman presented with symptomatic postprandial hypoglycemic episodes, resolution of symptoms with carbohydrate intake and significantly elevated anti-insulin antibody levels. She did not have any evidence for the use of oral antidiabetic medications, insulin, herbal substances, performing strenuous exercise or history of bariatric surgery. Fingerstick blood glucose readings revealed blood sugar of 35 mg/dL and 48 mg/dL, when she had these symptoms. Her medical history was significant for morbid obesity, hypothyroidism and gastro esophageal reflux disease. Her home medications included levothyroxine, propranolol and omeprazole. A blood sample obtained during the symptoms revealed the following: fingerstick blood sugar 38 mg/dL, venous blood glucose 60 mg/dL (normal (n): 70–99 mg/dL), serum insulin 202 IU/mL (n: <21), proinsulin 31.3 pmol/L (n: <28.9), C-peptide 8 ng/mL (n: 0.9–7), beta-hydroxybutyrate 0.12 mmol/L (n: 0.02–0.27) anti-insulin antibody >45.4 U/mL (n: <0.4). The result obtained while screening for serum sulfonylurea and meglitinides was negative. The repeated episodes of postprandial hypoglycemia associated with significantly elevated anti-insulin antibodies led to a diagnosis of insulin antibody syndrome (IAS). Significant improvement of hypoglycemic symptoms and lower anti-insulin antibody levels (33 U/mL) was noted on nutritional management during the following 6 months. Based on a report of pantoprazole-related IAS cases, her omeprazole was switched to a H2 receptor blocker. She reported only two episodes of hypoglycemia, and anti-insulin antibody levels were significantly lowe Continue reading >>

Insulin Antibodies

Insulin Antibodies

Antibodies to exogenously delivered insulin are common with insulin treatment but are not often clinically significant. IgG antibodies are the most common while IgE antibodies are the cause of insulin allergy[10]. At high titers, IgG antibodies may limit insulin action which could delay or diminish insulin action. Rarely, antibodies can be agonists to the insulin receptor and cause hypoglycemia (usually postprandial hypoglycemia)[11]. The development of antibodies depends on the purity, molecular structure, and storage conditions of the insulin administered as well as patient factors such as age, HLA type, and delivery route[10]. Most common when patients are exposed to beef or pork insulin, rather than only to human or analog insulins[9]. Insulin auto-antibodies, in people not previously treated with insulin, are an indication of developing type 1 diabetes (See Insulin Initiation in Type 1 Diabetes and to LADA for more information). React equally to analog insulin and unmodified human insulins. Radioligand binding (RLB) assays are the most common assay used for measurement of insulin antibodies[10]. Standard immunoprecipitation and agglutination analytic methods cannot measure insulin antibodies since insulin antibody immune complexes do not precipitate[10]. High sensitivity is required for evaluating autoantibodies, which are in much lower concentration than antibodies to exogenous insulin[13]. Gel filtration chromatography can identify insulin immunocomplexes with addition of exogeneous insulin to diagnose insulin autoimmune syndrome without necessarily using radiolabelled reagants[1]. The presence of insulin antibodies does not prove that they are causing insulin resistance or hypoglycemia. More soluble insulins, such as regular and semilente are less allergenic tha Continue reading >>

Autoimmune Hypoglycemia In A Type 2 Diabetic Patient With Anti-insulin And Insulin Receptor Antibodies

Autoimmune Hypoglycemia In A Type 2 Diabetic Patient With Anti-insulin And Insulin Receptor Antibodies

There are two types of autoimmune hypoglycemia, one due to autoantibodies acting against the insulin receptor and the other due to autoantibodies acting against insulin itself in individuals who have or have never received exogenous insulin, respectively (1). Both types are rare and can produce fasting and postprandial reactive hypoglycemia. A 72-year-old woman with frequent severe hypoglycemia was admitted to the emergency room, presenting with loss of consciousness. Three weeks before her admission, she was diagnosed with diabetes and received insulin at a local hospital. In the emergency room, her blood glucose level was 40 mg/dl. She had been in good general health, except for hypertension for 30 years and postmenopausal osteoporosis 10 years before admission. She has no evidence of other diseases associated with altered immunity. Three weeks ago, her biceps tendon ruptured when she slipped and fell, and during treatment, her blood glucose levels were >400 mg/dl. She was treated with insulin. However, she stopped insulin treatment because of frequent hypoglycemic events. Although she had had intravenous glucose injections, she had frequent hypoglycemic attacks, such as disorientation, loss of consciousness, palpitation, and diaphoresis. Her blood glucose levels had been <40 mg/dl on every hypoglycemic event, especially during fasting hypoglycemia. Physical examination revealed normal vital signs except for a chronically ill appearance. Her HbA1c was 6.3% (range 3–6%), plasma glucose 40 mg/dl, insulin 103.7 μU/ml, C-peptide 4.1 ng/ml, GAD autoantibody levels 0.01 units/ml (normal range 0–1.45 units/ml; RSR, Cardiff, U.K. ), and insulinoma-associated protein 2 autoantibody 0.01 units/ml (normal range 0–1.1 units/ml; RSR). Her thyroid, liver, and adrenal functio Continue reading >>

Spontaneous Hypoglycemia Due To Insulin Antibody After Insulin Treatment Of Diabetic Ketoacidosis

Spontaneous Hypoglycemia Due To Insulin Antibody After Insulin Treatment Of Diabetic Ketoacidosis

Your browser does not support the NLM PubReader view. Go to this page to see a list of supporting browsers. Spontaneous Hypoglycemia due to Insulin Antibody after Insulin Treatment of Diabetic Ketoacidosis Endocrinol Metab. 2010 Sep;25(3):217-220. Endocrinol Metab. 2010 Sep;25(3):217-220. English. Published online September 30, 2010. Copyright 2010 Korean Endocrine Society Spontaneous Hypoglycemia due to Insulin Antibody after Insulin Treatment of Diabetic Ketoacidosis Jin Ook Chung,Dong Hyeok Cho,Dong Jin Chung and Min Young Chung Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea. Corresponding author: Min Young Chung. Department of Internal Medicine, Chonnam National University Medical School, Hak-dong, Dong-gu, Gwangju 501-757, Korea. Tel: +82-62-220-6500, Fax: +82-62-225-8578, Email: [email protected] Received November 24, 2009; Accepted March 16, 2010. This article has been cited by GoogleScholar. Hypoglycemia in diabetic patients is usually caused by excessive exogenous insulin or the administration of an insulin secretagogue relative to the prevailing glucose concentration. Thus, the clinical manifestations of hypoglycemia are usually not observed in diabetic patients after either insulin or an oral hypoglycemic agent is discontinued. In contrast, diabetic ketoacidosis results from relative or absolute insulin deficiency. Although about 40% of diabetic patients who inject human insulin have insulin antibodies, these antibodies seldom significantly affect the glycemic control. It has not been reported in the literature that insulin antibody in the setting of human insulin therapy is associated with diabetic ketoacidosis and subsequent hypoglycemia. We describe here a rare case of spontaneous hypoglycemia due to insuli Continue reading >>

Insulin Autoimmune Syndrome Treated With Rituximab

Insulin Autoimmune Syndrome Treated With Rituximab

Insulin Autoimmune Syndrome Treated with Rituximab The patient was diagnosed with insulin autoimmune syndrome (HealthDay News) In a case report published online May 1 in Diabetes Care, resolution of hypoglycemia and cardiovascular dysfunction after rituximab treatment of insulin autoimmune syndrome is described. David Church, from the University of Cambridge Metabolic Research Laboratories in the United Kingdom, and colleagues report on the case of a 37-year-old female who presented to the emergency department after having collapsed. She had reported recurrent dizziness since the birth of her fifth child, and when symptomatic had recorded low capillary blood glucose. During her most recent pregnancy she had gestational diabetes, which was treated with insulin aspart, insulin glargine, and metformin. The authors note that the patient had early-morning hypoglycemia and postprandial hyperglycemia. The patient had high circulating insulin during hypoglycemia. An insulin assay was performed and serum anti-insulin immunoglobulin G concentration was 171 mg/L; insulin autoimmune syndrome was diagnosed. The patient was fitted with continuous glucose monitoring (CGM) with a hypoglycemia alarm, and was prescribed frequent low-glycemic index carbohydrate meals. Prednisone was commenced as significant hypoglycemia continued, and rituximab was given to reduce anti-insulin antibodies. After six weeks, repeat CGM demonstrated intermittent hypoglycemia and sustained daytime hyperglycemia. There were reductions in total insulin, anti-insulin antibody concentration, and antibody-bound insulin over the following months. Hypoglycemia was rare and postprandial hyperglycemia had improved by six months. Continue reading >>

Insulin Autoimmune Syndrome: The Highs And Lows Of Hyperinsulinemic Hypoglycemia

Insulin Autoimmune Syndrome: The Highs And Lows Of Hyperinsulinemic Hypoglycemia

Abstract: Background Insulin autoimmune syndrome (IAS) is characterized by hyperinsulinemic hypoglycemia associated with high titers of insulin antibodies in the absence of functional beta-cell disorders, insulinoma and insulin secretagogue use.1 This syndrome is extremely rare in Western countries, with approximately 75 cases reported in patients of non-Asian descent. We report the oldest patient to-date who presented with hypoglycemia and was found to have IAS. Case presentation 92-year old man with a past medical history of hypertension, hyperlipidemia, coronary artery disease, systolic heart failure, chronic kidney disease, and amiodarone induced hypothyroidism, was referred to endocrinology for hypoglycemia. These episodes occurred primarily after a high carbohydrate meal and included hyperglycemia, one to two hours postprandially, with glucose values in the 400’s mg/dL, followed by hypoglycemia. Symptoms included diaphoresis and confusion, occurred four to six hours after the meal, concurred with glucose values in the 30’s mg/dL and resolved with dextrose. The patient was admitted for a 72 hour fast. Initial labs included a morning cortisol of 13.8 ug/dL, a TSH of 13.85 uIU/MI (normal range 0.34-5.60 uIU/MI), an A1C of 5.5%, capillary glucose 46 mg/dL, preserved glucose 104 mg/dL, insulin 927 uU/mL (1.9-23 uU/mL), insulin antibodies >50 U/mL (< 0.4 U/ml), beta-hydroxybutyrate 1 mg/dL (0-3 mg/dL), pro-insulin 4.9 pmol/L (<8 pmol/L) and c-peptide 5.6 ng/mL (0.9-7.1 ng/mL). Screening for oral hypoglycemic agents was negative. At 48 hours of fasting, the patient became hypoglycemic with a capillary glucose of 52 mg/dL. Concomitant labs included glucose of 54 mg/dl and total insulin of 48 uIU/mL. He received intravenous dextrose and glucagon with an improvement of Continue reading >>

Syndromes Of Autoimmunity And Hypoglycemia. Autoantibodies Directed Against Insulin And Its Receptor.

Syndromes Of Autoimmunity And Hypoglycemia. Autoantibodies Directed Against Insulin And Its Receptor.

Abstract Humoral autoimmunity plays an important role in the pathogenesis of two forms of hypoglycemia. In one syndrome, antireceptor autoantibodies bind to the insulin receptor, mimic insulin action, and cause fasting hypoglycemia. In most patients with autoantibodies to the insulin receptor, there is other evidence of autoimmune disease as well. Interpretation of the standard tests used in evaluation of hypoglycemia may be confusing in these patients. For example, antireceptor antibodies may inhibit insulin binding, thereby inhibiting insulin clearance and elevating levels of plasma insulin. Nevertheless, because hypoglycemia suppresses beta-cell secretion, C-peptide levels are usually low. This constellation of data is consistent with surreptitious insulin injection. The most important laboratory test in the differential diagnosis is a direct assay for the presence of antibodies directed against the insulin receptor. Therapy with prednisone appears to alleviate the hypoglycemia rapidly, usually within 24 hours. This effect of prednisone appears to result from antagonism of the effects of antireceptor antibodies without actually lowering their titer. The natural history of this syndrome is that the antireceptor antibodies disappear and the syndrome resolves over a time course of several months to several years. In North America, the presence of anti-insulin antibodies in a hypoglycemic patient most commonly suggests that the patient has been immunized with exogenous insulin. However, some patients--especially in Japan--develop spontaneous autoantibodies directed against insulin. These antibodies can cause hypoglycemia, which is generally reactive in that it occurs several hours after a meal or a glucose challenge rather than in a fasting state. The most effective ther Continue reading >>

Autoimmune Hypoglycaemia [ndash] When And How To Look For Anti-insulin And Anti-insulin Receptor Antibodies

Autoimmune Hypoglycaemia [ndash] When And How To Look For Anti-insulin And Anti-insulin Receptor Antibodies

Endocrine Abstracts (2013) 31 CMW4.4 | DOI: 10.1530/endoabs.31.CMW4.4 Autoimmune hypoglycaemia [ndash] when and how to look for anti-insulin and anti-insulin receptor antibodies After secretion from the pancreatic cells, insulin exerts its pleiotropic effects by binding to its widely expressed cell surface receptor and triggering a cascade of intracellular signalling events, suppressing hepatic glucose production and inducing glucose uptake into fat and muscle among many other effects. Insulin is also cleared rapidly from the circulation, with a half-life of around 5 min, a process which is partly mediated by insulin receptor binding. This rapid clearance is critical to normal glucose homeostasis. Autoantibodies may perturb the highly dynamic glucose-insulin negative feedback loop in two major ways, both of which may lead to severe hypoglycaemia and/or hyperglycaemia. First, antibodies against the insulin receptor often have the ability to activate the receptor inappropriately irrespective of circulating insulin levels. This may produce severe hypoglycaemia, although the chronic presence of these antibodies more commonly desensitizes the receptors, producing severe type B insulin resistance. Second, high affinity, high capacity antibodies against insulin itself may perturb insulin kinetics sufficiently to produce severe hypoglycaemia associated with the presence of macroinsulin complexes. Either pathological anti insulin receptor or pathological anti-insulin antibodies may arise either spontaneously or in the context of pre-existing diabetes, which may complicate interpretation of diagnostic tests. Rapid diagnosis is important, and in some cases may lead to use of potent multimodal immunosuppression to correct the severe metabolic disorder. How to select appropriate pa Continue reading >>

Hypoglycemia Due To Insulin Autoimmune Syndrome: A Rare Cause Not To Be Forgotten

Hypoglycemia Due To Insulin Autoimmune Syndrome: A Rare Cause Not To Be Forgotten

Highlights • Insulin Autoimmune Syndrome (IAS) is a rare cause of hypoglycemia. • Most cases of IAS have been reported from Japan and this is the fourth case from India. • It should be considered among the differential diagnosis of hypoglycemia to avoid unnecessary investigations and surgery. • It runs a benign course and can be managed on a diet of frequent small meals and withdrawal of offending drugs. Most cases of recurrent hypoglycemia occur in patients with diabetes mellitus and can be prevented by changes in medications, diet or activity. However, a person with unexplained hypoglycemia can indicate potentially grave, often treatable underlying disorders such as insulinoma, Addison's disease or hypopituitarism. Medication is another cause of unexplained hypoglycemia. A focused laboratory work-up is essential, often a plasma/serum glucose, insulin and C-peptide. Normal or high insulin and C-peptide levels indicate excessive endogenous insulin production. We are reporting a case of Insulin Autoimmune Syndrome (IAS) in a 38-year-old Indian female who presented to us with recurrent episodes of spontaneous hypoglycemia. On evaluation, the patient was found to have Endogenous Hyperinsulinemic Hypoglycemia (EHH). As no obvious cause of EHH was found on abdominal imaging, we further evaluated her for insulin antibodies which were found to be raised. A diagnosis of IAS was made and the patient was put on a diet of frequent small meals and she improved. Most cases of this syndrome have been reported from Japan and very few case reports of IAS exist in India. Thus IAS, though rare, should be kept in the differential diagnosis of spontaneous hypoglycemia. Continue reading >>

Hyperinsulinemic Hypoglycemia Associated With Insulin Antibodies Caused By Exogenous Insulin Analog

Hyperinsulinemic Hypoglycemia Associated With Insulin Antibodies Caused By Exogenous Insulin Analog

Go to: Insulin antibodies (IA) associated with exogenous insulin administration seldom caused hypoglycemia and had different characteristics from insulin autoantibodies (IAA) found in insulin autoimmune syndrome (IAS), which was first described by Dr Hirata in 1970. The characteristic of IAS is the presence of insulin-binding autoantibodies and related fasting or late postprandial hypoglycemia. Here, we report a patient with type 1 diabetes mellitus under insulin glargine and insulin aspart treatment who developed recurrent spontaneous post-absorptive hyperinsulinemic hypoglycemia with the cause probably being insulin antibodies induced by exogenous injected insulin. Examinations of serial sera disclosed a high titre of insulin antibodies (33%, normal <5%), high insulin concentration (111.9 IU/mL) and undetectable C-peptide when hypoglycemia occurred. An oral glucose tolerance test revealed persistent high serum levels of total insulin and undetectable C-peptide. Image studies of the pancreas were unremarkable, which excluded the diagnosis of insulinoma. The patient does not take any of the medications containing sulfhydryl compounds, which had been reported to cause IAS. After administering oral prednisolone for 3 weeks, hypoglycemic episodes markedly improved, and he was discharged smoothly. Insulin autoimmune syndrome (IAS) or IAS-like situation should be one of the differential diagnosis in patients with hyperinsulinemic hypoglycemia. Although less reported, insulin antibodies (IA) caused by exogenous insulin analog should be considered as the cause of hypoglycemia. Patients with suspected insulin autoimmune syndrome (IAS) should be screened for drugs related to autoimmunity to endogenous insulin. Go to: Background Hyperinsulinemic hypoglycemia can be caused by exog Continue reading >>

Insulin, Insulin Antibodies And Insulin Autoantibodies

Insulin, Insulin Antibodies And Insulin Autoantibodies

Recently we have been queried about the relationship of insulin antibodies (IA) and the development of either hypoglycemia or hyperglycemia in various persons with type 1 diabetes mellitus (T1DM). As opposed to IA, which are induced by any type of exogenous insulin, insulin autoantibodies (IAA) occur spontaneously in the plasma of some patients (predominantly children) prior to the diagnosis of T1DM and prior to exposure to exogenous insulin.1,2 In general, IA are in much higher concentration than IAA. A not uncommon inquiry is as follows: “A patient with T1DM is suffering recurrent and possibly severe hypoglycemia. Could this be due to insulin autoantibodies and/or the ‘insulin autoimmune syndrome’ (IAS; also known as Hirata disease)?”3 The other question is: “A patient with T1DM is taking his insulin but is in poor metabolic control. Could he be resistant to injected insulin? Should we measure his insulin levels?” In terms of hypoglycemia that required hospital admission, often insulin and C-peptide were measured at the time of the hypoglycemic episode. Insulin present in the circulation could be endogenous or exogenous. However, the only source of C-peptide is the patient’s own pancreatic beta cells. So how are the C-peptide and insulin measurements interpreted in such clinical scenarios? Insulin measurements First, let’s address the question of the insulin measurement. Measuring insulin in insulin-treated patients is conceptually complex because many patients treated with insulin injections develop IA.4 This is true regardless of the type of insulin injected. Recombinant DNA insulins appear to be more immunogenic than animal insulins.5 Even exogenous human insulin is immunogenic.6 The literature reports IA frequencies of 78 percent to 97 percent in i Continue reading >>

Immunological Hypoglycemia Associated With Insulin Antibodies Induced By Exogenous Insulin In 11 Chinese Patients With Diabetes

Immunological Hypoglycemia Associated With Insulin Antibodies Induced By Exogenous Insulin In 11 Chinese Patients With Diabetes

Journal of Diabetes Research Volume 2015 (2015), Article ID 746271, 9 pages Department of Endocrinology and Metabolism, West China Hospital of Sichuan University, Chengdu, Sichuan 610041, China Academic Editor: Mitsuhiko Noda Copyright © 2015 Heng Quan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Aims. To investigate the characteristics of immunological hypoglycemia associated with insulin antibodies (IAbs) induced by exogenous insulin in Chinese patients with diabetes. Methods. The clinical data of patients with immunological hypoglycemia due to IAbs were retrospectively analyzed by screening patients with diabetes discharged from West China Hospital from 2007 to 2013. Results. A total of 11 patients (eight men and three women) were identified. Insulin-C-peptide separation was found in all patients via insulin and C-peptide release test. Previous insulin use was ceased after admission and was switched to oral hypoglycemic agents (OHAs) (8/11), lifestyle modification only (2/11), or regular human insulin (1/11). Hypoglycemia was ameliorated after a median of 20 days (interquartile range [IQR], 11–40), while IAbs turned negative after a median of 17 months (IQR, 4–19), and serum immunoreactive insulin (IRI) levels dropped substantially after a median of 22 months (IQR, 9–32) in these cases. Conclusions. In insulin-treated patients with unexpected and refractory hypoglycemia even after insulin therapy was gradually reduced or even withdrawn, IAbs induced by exogenous insulin should be considered, and insulin withdrawal might be promptly needed. The course of immunological hypoglycemia was Continue reading >>

Hypoglycemia Due To An Insulin Binding Antibody In A Patient With An Iga-κ Myeloma

Hypoglycemia Due To An Insulin Binding Antibody In A Patient With An Iga-κ Myeloma

Context: Autoantibodies to insulin have been described to cause spontaneous hypoglycemia in nondiabetic subjects. There have been occasional reports of spontaneous hypoglycemia due to monoclonal anti-insulin antibodies. We present the first report of a patient with an IgA-κ myeloma in whom frequent hypoglycemia resulted from the ability of the monoclonal IgA-κ to bind insulin. Objectives: The aim of this study was to describe the occurrence of profound hypoglycemia in a patient with IgA-κ myeloma, characterize biochemically the nature of the IgA:insulin complex present, and place this case in the context of the published literature on hypoglycemia resulting from autoantibodies to insulin. Design: A case study was performed. Patients: A single case of profound hypoglycemia associated with IgA-κ myeloma was studied. Intervention: There were no interventions. Main Outcome Measures: A case study was performed. Results: Polyethylene glycol precipitation and gel filtration chromatography were used to demonstrate high-molecular weight insulin immunoreactivity in the patient’s plasma. This was characterized as an insulin binding IgA-κ paraprotein present at 4200 mg/dl (42 g/liter) with a relatively high insulin dissociation constant of 0.32 μm/liter using radiolabelled insulin binding studies. Conclusions: We present the first case of hypoglycemia due to IgA binding insulin antibodies in a patient with an IgA-κ paraprotein myeloma. The hypoglycemia was associated with high-plasma insulin levels and relatively low C-peptide levels. A plausible mechanism for the hypoglycemia is the delayed clearance of insulin. This case broadens the spectrum of monoclonal gammopathies that have been associated with anti-insulin reactivity and spontaneous hypoglycemia. Context: Altered v Continue reading >>

Recurrent Hypoglycemia From Insulin Autoimmune Syndrome

Recurrent Hypoglycemia From Insulin Autoimmune Syndrome

Go to: CASE REPORT A 45-year-old Caucasian woman presented to clinic with a 6-week history of recurrent hypoglycemic symptoms consisting of fatigue, lightheadedness, blurry vision, and diaphoresis. The episodes were triggered by fasting and exercise, and alleviated with food intake. She also reported a 10-pound weight gain during this period. There was no history of diabetes mellitus in the patient or her family, and she had no access to insulin and/or insulin secretagogues. Past medical history was significant for endometriosis requiring multiple pelvic surgeries, von Willebrand disease, hepatic steatosis, gastroesophageal reflux disease, and patellofemoral syndrome. The patient took esomeprazole occasionally but no other prescription or over-the-counter medications. She did not smoke, drink alcohol, or use recreational drugs. Family history was negative for any endocrine tumors or autoimmune diseases. Vital signs were normal and her physical examination was non-contributory. Laboratory investigations revealed normal renal and liver function. Hemoglobin A1c was 5.4 %. Adrenocorticotropic hormone (ACTH) stimulation test indicated an adequate cortisol response. Blood work was collected during a spontaneous symptomatic hypoglycemic event (Table 1). The markedly increased insulin level and the non-suppressed connecting peptide (C-peptide) result, along with the corresponding insulin to C-peptide molar ratio of 13.4, were incompatible with exogenous insulin administration as the cause of hypoglycemia. Computed tomography (CT) of the abdomen did not identify any masses in the pancreas or in the retroperitoneum. Magnetic resonance imaging (MRI) of the abdomen was aborted due to feelings of claustrophobia in the patient. Selective arterial calcium stimulation was performed to Continue reading >>

Hypoglycemia Associated With Antibodies To The Insulin Receptor

Hypoglycemia Associated With Antibodies To The Insulin Receptor

Abstract Antibodies to the insulin receptor are insulinomimetic in vitro, although they generally induce insulin resistance in vivo. We report the novel case of a patient who presented with fasting hypoglycemia as the sole manifestation of autoantibodies to the insulin receptor. Prednisone therapy (120 mg per day) produced a rise in fasting glucose to more than 100 mg per deciliter (6 mmol per liter) within 48 hours, although there was no detectable change in the titer of antireceptor antibodies. After 10 weeks of therapy, the titer of antireceptor antibodies had fallen approximately 100-fold, and prednisone could be discontinued without recurrence of hypoglycemia. This case demonstrates that antireceptor antibodies must be considered in the differential diagnosis of hypoglycemia, especially in patients with other manifestations of autoimmunity. (N Engl J Med. 1982; 307:1422–6.) Presented in part at the 39th annual meeting of the American Federation for Clinical Research, May 8, 1982. We are indebted to Dr. Jesse Roth for valuable discussions and to Ms. Laurie Tuchman for assistance in preparing the manuscript. Note added in proof: Since submission of this manuscript, Rossetti et al. have described a similar patient with hypoglycemia resulting from autoantibodies to the insulin receptor.24 From the Diabetes Branch, National Institute of Arthritis, Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, and the Department of Medicine, University of Alabama, Birmingham. Address reprint requests to Dr. Taylor at Bldg. 10, Rm. 8S–243, National Institutes of Health, Bethesda, MD 20205. Continue reading >>

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