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Anti-insulin Antibodies Type 1 Diabetes

Anti-insulin Antibodies And Retinopathy In Juvenile Onset Type-1 Diabetes

Anti-insulin Antibodies And Retinopathy In Juvenile Onset Type-1 Diabetes

Dr. Rajendra Prasad Centre for Ophthalmic Sciences, Department of Medicine, Department of Anatomy, All Institute of Medical Sciences, New Delhi, India Correspondence Address: K Sharma Department of Neuro-Ophthalmology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Raebareli Road, Post Box 375, Lucknow - 226001 India Source of Support: None, Conflict of Interest: None PMID: 1810880 Juvenile diabetics have severe loss of beta cell function and require replacement therapy with insulin. Insulin antigenicity can produce anti-insulin antibodies resulting in allergic reactions and insulin resistance. The role of insulin-anti-insulin antibody complexes in the development and progress of chronic diabetic complications like microangiopathy is not very clear. In the present study, there was statistically a significant trend of higher insulin antibody binding levels in IDDM patients who developed retinopathy. Though there was a trend of higher insulin antibody in IDDM patients with retinopathy, there was no association between insulin antibody and HLA antigen which some authors have reported. How to cite this article: Sharma K, Khosla P K, Tiwari H K, Sharma R K, Bajaj J S. Anti-insulin antibodies and retinopathy in juvenile onset type-1 diabetes. Indian J Ophthalmol 1991;39:174-5 Juvenile diabetics have severe loss of beta cell function and require replacement therapy with insulin. Insulin antigenicity can produce anti-insulin antibodies resulting in allergic reactions [1] and insulin resistance [2] The role of insulin-anti-insulin antibody complexes in the development and progress of chronic diabetic complications like microangiopathy is not very clear. The present study investigates the relationship between anti-insulin antibody and retinopathy in insulin dependent Continue reading >>

Anti-insulin Receptor Antibodies Related To Hypoglycemia In A Previously Diabetic Patient

Anti-insulin Receptor Antibodies Related To Hypoglycemia In A Previously Diabetic Patient

We report the case of a 47-year-old woman who was referred to our unit for hypoglycemia. She was diagnosed with diabetes at age 30 years and was previously treated with metformin, sulfonylureas, and glucagon-like peptide 1 agonists. Despite interruption of her treatments, she had for 1 month clinical features evoking hypoglycemic spells, with adrenergic and neuroglycopenic symptoms subsiding after glucose administration. Her BMI was 23.8 kg/m2. She had axillary acanthosis nigricans but no lipodystrophy. Continuous glucose monitoring showed hypoglycemia down to 2.1 mmol/L, mostly during fasting periods, and hyperglycemia up to 13.7 mmol/L in the absence of any treatment. HbA1c was 15%. During a fasting test, venous glucose concentration dropped to 2.5 mmol/L with concomitant low serum levels of C-peptide, insulinemia, and proinsulinemia: <1.40, <3, and 3.6 pmol/L, respectively (reference ranges in healthy subjects 17.8–173, 370–1,470, and 3.3–28 pmol/L, respectively). Plasma levels of cortisol, somatostatin, IGF-1, and Western blot analysis of IGF-2 and its precursors were normal. Thoraco-abdominal computed tomography and whole-body F-18-fluorodeoxyglucose positron emission tomography scan did not reveal any abnormality. We evaluated the presence of anti-insulin receptor antibodies (AIRAs) using a radioreceptor assay (1). The patient’s total serum and purified immunoglobulin fractions inhibited the binding of a tracer concentration of radiolabeled insulin, consistent with significant titers of AIRAs. Patient’s serum and purified immunoglobulins activated proximal (tyrosine phosphorylation of insulin receptor β-subunit and insulin receptor substrate-1) and distal (phosphorylation of Akt/PKB) insulin-signaling pathways in vitro in a dose-dependant manner, mimick Continue reading >>

Anti-insulin Antibody Test

Anti-insulin Antibody Test

Insulin antibodies - serum; Insulin Ab test; Insulin resistance - insulin antibodies; Diabetes - insulin antibodies The anti-insulin antibody test checks to see if your body has produced antibodies against insulin. Antibodies are proteins the body produces to protect itself when it detects anything "foreign," such as a virus or transplanted organ. How the Test is Performed How to Prepare for the Test No special preparation is necessary. How the Test will Feel When the needle is inserted to draw blood, some people feel moderate pain. Others feel only a prick or stinging. Afterward, there may be some throbbing or a slight bruise. This soon goes away. Why the Test is Performed This test may be performed if: Normal Results Normally, there are no antibodies against insulin in your blood. Normal value ranges may vary slightly among different laboratories. Some labs use different measurements or test different samples. Talk to your health care provider about the meaning of your specific test results. What Abnormal Results Mean If you have IgG and IgM antibodies against insulin, your body reacts as if the insulin in your body is a foreign protein that needs to be removed. This may make insulin less effective, or not effective at all. This is because the antibody prevents the insulin from working the right way in your cells. As a result, your blood sugar can be unusually high. The antibodies can also prolong the effect of insulin by releasing some insulin long after your meal has been absorbed. This can put you at risk for low blood sugar. If the test shows a high level of IgE antibody against insulin, your body has developed an allergic response to the insulin. This could put you at risk for skin reactions where you inject insulin. You can also develop more severe reactions tha 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 >>

Impact Of Anti-glutamic Acid Decarboxylase-65, Anti-insulin And Anti-tyrosine Phosphatase Autoantibodies On Disease Activity In Type 1 Diabetes Patients

Impact Of Anti-glutamic Acid Decarboxylase-65, Anti-insulin And Anti-tyrosine Phosphatase Autoantibodies On Disease Activity In Type 1 Diabetes Patients

Jalees Farhan1, Abdullah Alghasham2, Uzma Zafar3, Abdel-Raheim MA. Meki1 and Zafar Rasheed1* *Correspondence: Zafar Rasheed [email protected] 1. Department of Medical Biochemistry, College of Medicine, Qassim University, Buraidah, Saudi Arabia. Abstract Background: Type 1 diabetes mellitus (T1D) is a chronic autoimmune disease with autoantibodies against glutamic-aciddecarboxylase (GAD)65, insulin and tyrosine phosphatase (TP) as a feature of disease. The correlations of these autoantibodies with disease severity remain to be explored. Here we investigate the status and contribution of autoantibodies against GAD65, insulin and TP in T1D patients and to explore whether these antibodies have a role in T1D progression and in T1D associated neuropathy. Methods: Sera from 57 T1D patients with varying levels of disease activities and 42 age- and sex-matched healthy controls were evaluated for anti-GAD65-antibodies, anti-insulin-antibodies and anti-TP-antibodies. Results: Serum analysis showed T1D patients contain 42% of anti-GAD65-antibodies, 76% of anti-insulin-antibodies and 34% of anti-TP-antibodies. Interestingly, not only was there an increased number of subjects positive for these antibodies, but also levels of these antibodies were significantly higher among T1D patients whose ages were >35 years as compared with younger T1D patients (age ≤35 years). In addition, significant correlation was observed between the levels of these antibodies and glycosylated haemoglobin (HbA1c). Furthermore, T1D neuropathic patients had higher levels of these antibodies compared with T1D patients without neuropathy. Conclusions: Our data support an association between these markers autoantibodies and severity of T1D. The stronger response observed in patients with uncontrolled T1 Continue reading >>

Analytical And Clinical Challenges In A Patient With Concurrent Type 1 Diabetes, Subcutaneous Insulin Resistance And Insulin Autoimmune Syndrome

Analytical And Clinical Challenges In A Patient With Concurrent Type 1 Diabetes, Subcutaneous Insulin Resistance And Insulin Autoimmune Syndrome

Harrogate District Hospital, Harrogate HG2 7SX, UK [1] Leeds Children's Hospital NHS Trust, Leeds, UK [2] Wellcome Trust, Cambridge University Hospital, Cambridge, UK [3] Clinical Biochemistry Department, Addenbrooke's Hospital, Cambridge, UK [4] SAS Peptides Hormone Section, Royal Surrey County Hospital, Surrey, UK [5] Blood Sciences Department, Leeds Teaching Hospitals NHS Trust, Leeds, UK Summary A lean 15-year-old girl was diagnosed with type 1 diabetes based on symptomatic hyperglycaemia and positive anti-islet cell antibodies. Glycaemia was initially stabilised on twice-daily mixed insulin. After 11 months from the time of diagnosis, she complained of hyperglycaemia and ketosis alternating with hypoglycaemia. This progressively worsened until prolonged hospital admission was required for treatment of refractory hypoglycaemia. A high titre of anti-insulin antibodies was detected associated with a very low recovery of immunoreactive (free) insulin from plasma after precipitation with polyethylene glycol, suggesting the presence of insulin in bound complexes. Insulin autoimmune syndrome was diagnosed and metabolic fluctuations were initially managed supportively. However, due to poor glucose control, immunosuppressive therapy was initiated first with steroids and plasmapheresis and later with anti-CD20 antibody therapy (Rituximab). This treatment was associated with a gradual disappearance of anti-insulin antibodies and her underlying type 1 diabetes has subsequently been successfully managed with an insulin pump. Learning points Anti-insulin antibodies may result in low levels of free insulin. Polyclonal anti-insulin antibodies can interfere with the pharmacological action of administered insulin, resulting in hypoglycaemia and insulin resistance, due to varying aff Continue reading >>

Islet Autoantibodies And Type 1 Diabetes: Does The Evidence Support Screening?

Islet Autoantibodies And Type 1 Diabetes: Does The Evidence Support Screening?

Type 1 diabetes (T1D)3 is a chronic progressive autoimmune disorder with complex polygenic susceptibility, usually associated with certain HLA alleles (IDDM1 locus). Environmental factors, which are poorly defined, also contribute to the pathogenesis. T1D is characterized by lymphocyte infiltration into the islets of Langerhans in the pancreas, leading to inflammation and selective destruction of the insulin-producing β-cells, resulting in hyperglycemia (1). Patients with T1D fail to produce insulin and are dependent on exogenous insulin to maintain life. Although it is considerably less common than type 2 diabetes, the worldwide prevalence of T1D is increasing by approximately 3% per annum. The incidence varies widely among countries. In Americans under the age of 20 years, the prevalence of T1D rose by 23% between 2001 and 2009, and >30 000 people are diagnosed annually in the US with T1D. Progression to T1D is typically marked by the presence of islet-specific autoantibodies in the serum. In humans, autoantibodies are present months to years before disease onset, and a similar trend is seen in the nonobese diabetic (NOD) mouse model of autoimmune diabetes (2). The rate of T1D development varies among individuals, possibly due to non-HLA genetic factors and/or environmental factors beyond the initial trigger. Most of the current information on the pathogenesis of T1D from the initial triggers to the final effector stages of β-cell destruction has been derived from animal models that mimic the human disease (3). T lymphocytes are central determinants for β-cell destruction in T1D. Nevertheless, autoantibodies and B lymphocytes are components of some autoimmune diseases and may contribute to the pathogenesis of T1D. Multiple studies have documented the role of autoan Continue reading >>

Anti-insulin Antibody Test

Anti-insulin Antibody Test

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Pro-insulin; A “primary” Target Of Autoantibodies In Type 1 Diabetes

Pro-insulin; A “primary” Target Of Autoantibodies In Type 1 Diabetes

Insulin autoantibodies (IAA) were first convincingly demonstrated by Palmer and co-workers in 1983. These autoantibodies appear prior to insulin treatment and are present in approximately 70% of children and adolescents at the diagnosis of type 1 diabetes. The levels of IAA show a strong inverse correlation with age, being found in more than 90% of children under the age of 5 years at diagnosis. The early appearance of IAA makes them particularly useful for diabetes prediction in young children. Induction of insulin antibodies to exogenous insulin means that IAA measurement is no longer informative once insulin therapy has been given for more than 2 weeks. Of the major islet antigens, proinsulin and glutamate decarboxylase (GAD) are currently the best candidates as primary autoantigens; i.e. those that could play a role in the initiation of the autoimmune response that leads to beta cell destruction and type 1 diabetes. Proinsulin is favoured by many, since autoantibodies to insulin are often the first to be detected in young children at increased genetic risk of type 1 diabetes. Proinsulin, unlike GAD is expressed almost exclusively in beta cells, which is consonant with the specific targeting of beta cells by T-cells infiltrating the pancreatic islets. The very high frequency of insulin autoantibodies (IAA) found in young children at diabetes onset shows that loss of tolerance to proinsulin is common in those who progress rapidly [1][2]. Insulin autoantibodies are also found in the non-obese diabetic (NOD) mouse model of spontaneous autoimmune diabetes [3], which further supports a role for proinsulin as a primary autoantigen. Age effects Birth cohort studies have shown that IAA can be detected from 6 months of age in children at increased genetic risk of type 1 diabe 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 >>

Test Id: Inab Insulin Antibodies, Serum

Test Id: Inab Insulin Antibodies, Serum

Predicting the future development of type 1 diabetes in asymptomatic children, adolescents, and young adults, when used in conjunction with family history, HLA-typing, and other autoantibodies, including GD65S/81596 Glutamic Acid Decarboxylase (GAD65) Antibody Assay, Serum and islet cell antigen 2 (IA-2) antibodies Differential diagnosis of type 1 versus type 2 diabetes Evaluating diabetics with insulin resistance in patients with established diabetes (type 1 or type 2) Investigation of hypoglycemia in nondiabetic subjects The onset of autoimmune diabetes mellitus (type 1 diabetes mellitus) is preceded (and accompanied) by the appearance of autoantibodies to a variety of pancreatic islet cell antigens in serum, including insulin. The level of these autoantibodies is generally low and may even fall during follow-up. In genetically predisposed, but disease-free, individuals (first degree relatives of patients with type 1 diabetes or individuals with permissive HLA alleles), detection of multiple islet cell autoantibodies is a strong predictor for subsequent development of type I diabetes. Once type 1 diabetes has become fully manifest, insulin autoantibody levels usually fall to low or undetectable levels. However, after insulin therapy is initiated, autoantibody production may recur as a memory response. Insulin autoantibody production is more common when therapeutic insulin of animal origin is used (rarely used in contemporary practice). Larger therapeutic doses may be required because of antibody-induced insulin resistance. Insulin antibodies may be found in nondiabetic individuals complaining of hypoglycemic attacks. In this setting their presence can be an indicator of "factitious hypoglycemia" due to the surreptitious injection of insulin, rather than to a clinical Continue reading >>

The Importance Of Anti-insulin Antibody In Patients With Type 1 Diabetes Mellitus Treated With Continuous Subcutaneous Insulin Infusion Or Multiple Daily Insulin Injections Therapy.

The Importance Of Anti-insulin Antibody In Patients With Type 1 Diabetes Mellitus Treated With Continuous Subcutaneous Insulin Infusion Or Multiple Daily Insulin Injections Therapy.

Abstract To investigate the influence of two insulin administration modalities, continuous subcutaneous insulin infusion (CSII) and multiple daily insulin injections (MDI) therapy with insulin analogues, on the development of insulin antibodies (IAs) in patients with type 1 diabetes mellitus and to assess the impact of IAs on glucose control and hypoglycaemia. 96 patients with type 1 diabetes mellitus treated with CSII (n = 48) or MDI (n = 48) were included in the study. Age, duration of diabetes, A1c, preprandial and postprandial blood glucose and hypoglycaemic events were compared between IA positive and negative patients. IA levels were higher in the CSII group (% 24.6 ± 14.2) than the MDI group (% 13.2 ± 9.9). Duration of diabetes and age were not associated with IA positiveness. While A1c, preprandial blood glucose and the frequency of hypoglycaemic events were similar in two groups, postprandial blood glucose was lower in IA positive group (P = 0.03). Patients with type 1 diabetes mellitus treated with CSII with insulin analogues had higher IA levels when compared to MDI therapy. However, the development of IAs did not impair the glycaemic control. Continue reading >>

Diabetes-related Autoantibodies

Diabetes-related Autoantibodies

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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 >>

Why Is My Doctor Checking For Antibodies

Why Is My Doctor Checking For Antibodies

I Have Diabetes, not an Infection! By Armand A. Krikorian, MD Insulin is the main hormone that controls your blood sugar (glucose). Cells in the pancreas called islet [EYE-let] cells secrete insulin. Antibodies are proteins made by your immune system to defend against foreign substances. Sometimes antibodies can be directed against your own body organs. This results in diseases that are called “autoimmune.” Type 1 diabetes is one such disease where antibodies are made against the body’s own islet cells. These antibodies can be detected by blood tests. Several antibodies against the pancreas are islet-cell antibodies (ICA), anti-glutamic [anti-gloo-TAM-ic] acid decarboxylase [dee-kahr-BOK-suh-leyz] antibodies (anti-GAD) and Insulin autoantibodies (IAA). Type 1 diabetes results from the destruction of insulin producing pancreatic islet cells. The pancreatic antibodies, however, do not cause type 1 diabetes. They simply happen to be present in people at risk of developing type 1 diabetes. They can be detected years before diabetes begins. Doctors can use the antibody levels in the blood to predict who will develop type 1 diabetes. This is still mostly done in research studies, especially in research aimed at preventing the onset of type 1 diabetes. Not all people with type 1 diabetes have these antibodies, because these antibodies can disappear after years of diabetes being present. So not having these antibodies doesn’t mean you don’t have type 1 diabetes. Presence of the antibodies can help doctors distinguish between type 2 diabetes or type 1 diabetes. This is particularly true in people who might seem to have type 2 diabetes (develop diabetes later in life, have a family history of diabetes, have had diabetes during pregnancy) but do not have the typical body Continue reading >>

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