Check GAD antibody positivity with the Diamyd anti-GAD RIA plate*

GAD Antibodies and LatentAutoimmune Diabetes of theAdult (LADA)TA.G. Unnikrishnan and S. K. Singhhe prevalence of Type 2 diabetesis rapidly increasing in theIndian subcontinent.While themajority of subjects with Type2 diabetes in developed countriesare obese, those fromIndia are mostly non-obese, and many of them arelean (1). The proposed hypotheses to explain thisinclude coexistent malnutrition, autoimmunityand metabolic abnormalities.Recent research from North India shows thatone-fourth of the recently diagnosed Type 2 diabeticswho are lean (i.e with a body mass index ofless than 18.5 kg/m 2 ) have positivity to GADantibodies. These adult subjects with autoimmunitywere significantly younger, had a lower waisthip ratio and beta cell function (HOMA) as comparedto lean Type 2 diabetics without antibodypositivity. Hence they had a clinical profile consistentwith latent autoimmune diabetes of theadult (LADA) . They also had lower insulinresistance (HOMA), showing that reduced betacell function is the predominant metabolic abnormalityin these subjects (2).The above study included only adult-onsetType 2 diabetes, which is seen commonly in India.There is also evidence that 23% of emaciated, veryyoung subjects with a ketosis-resistant form ofdiabetes, a phenotype which is rare yet peculiar toIndia, are positive for GAD antibodies (3). Thisform of diabetes has also been termed malnutritionmodulated diabetes mellitus (MMDM).Exciting work is in progress to unravel the geneticbasis of Indian diabetics with GAD65 antibodypositivity. It has been reported that MHC-relatedgenes can discriminate between acute-onset andslow-onset Type 1 diabetes in India, and can alsodistinguish the MMDM phenotype (4).Clearly, it is important to avoid the misclassificationof these lean diabetic subjects, as some ofthem could have LADA. The detection of GADantibodies could predict the early onset of insulindependency, prompting more aggressive glucoseloweringtherapy. This could prevent unneccessaryexposure to hyperglycemia. Further Indian studiesare needed to assess the prevalence of eventualbeta cell failure in these subjects, and the speed ofprogression.References1. Mohan V, et al,Clinical Profile of lean NIDDM in South India.Diabetes Res Clin Pract 38(2): 101-8, 1997.2. Unnikrishnan AG, et al,Clinical and immunological profile of underweightType 2 diabetes in north India.( Abstract number: A-03-255-EASD). Accepted for presentationat the 18th International Diabetes FederationCongress, 24 - 29 August 2003, Paris, France.3. Singh AK, et al,Role of islet autoimmunity in the aetiology of differentclinical subtypes of diabetes mellitus in young northIndians.Diabet Med Apr;17(4):275-80, 2000.4. Sanjeevi CB, et al,MHC class I chain-related gene a alleles distinguishmalnutrition-modulated diabetes, insulin-dependent diabetes,and non-insulin- dependent diabetes mellitus patientsfrom eastern India.Ann N Y Acad Sci Apr 958:341-4, 2002.A.G. Unnikrishnan 1 , S. K. Singh 21 Asst. Professor, Department of Diabetesand Endocrinology, Amrita Institute ofMedical Sciences, Kochi, India, 2 Reader,Department of Endocrinology, Institute ofMedical Sciences, Banaras Hindu University,Varanasi, India.dmccad june 2003page 37