Background: Insulin resistance is a major cause for developing type 2 diabetes but is not synonymous with the type 2 diabetes. Pancreatic beta cell dysfunction probably needs to be sets in for clinical occurrence of type 2 diabetes. So knowledge regarding residual beta cell function and degree of insulin resistance is essential.
Aims and Objectives: The objectives are as follows: (1) To estimate degree of insulin resistance (HOMA-IR) and pancreatic beta cell functional capacity (HOMA-B %) among newly detected Type 2 diabetics and (2) to identify different clinical phenotypic presentations of type 2 diabetes on the basis of these parameters.
Materials and Methods: This present study was conducted in newly diagnosed type 2 diabeticpatients. After obtaining informed consent, anthropometric and clinical examination was carried out in all patients. Venous blood samples were drawn for fasting plasma glucose,c-peptide,fasting insulin level,HbA1c,lipid profile, etc.HOMA-IR and HOMA-B% were calculated with HOMA 2 calculator.
Results: A total 100 newly diagnosed type 2 diabetic patients were studied. About 71% pt of study population had HOMA-B% value below 50% and half of study population had significant amount of insulin resistance. Three distinct clinical phenotypes had identified. Insulin resistance predominant group (30%), beta cell dysfunction predominant group (45%), and both abnormalities coexist group (25%).
Conclusion: By the time of diagnosis of Type 2 diabetes, more than two-third study population had <50% residual beta cell function left and more than half had significant degree of insulin resistance. Hence,this functional assessment needs to be done for appropriate antidiabetic drug selection and for identification of different clinical phenotypes.
Background: Insulin resistance is a major cause for developing type 2 diabetes. However, simultaneously pancreatic beta-cell dysfunction must coexist in for clinical occurrence of type 2 diabetes (T2D). Hence, knowledge regarding residual beta-cell function and degree of insulin resistance is required while treating type 2 diabetic patients.
Aims and Objectives: The present study was done to estimate degree of insulin resistance (homeostatic model assessment insulin resistance - HOMA-IR) and pancreatic beta-cell functional capacity (HOMA-B%) among newly detected type 2 diabetics and correlation of these with anthropometric, glucose, and lipid parameters.
Materials and Methods: This was an observational cross-sectional study conducted in 100 newly diagnosed type 2 diabetic patients. Detailed anthropometric and clinical examination were carried out. Venous blood samples were drawn for fasting plasma glucose, c-peptide, fasting insulin level, hemoglobin A1C (HbA1C), lipid profile, and postprandial glucose. HOMA-IR and HOMA-B% were calculated using HOMA 2 calculator and correlations were calculated between the study variables.
Results: The mean age of the study population was 45.55±11.64 years and 58% of study participants were male. The mean HOMA-IR and HOMA-B% were 2.55±1.75 and 40.67±23.55%, respectively. HOMA-IR positively correlated with abdominal circumference, triglyceride to HDLc ratio, and negatively correlated with HDLc. There were statistically significant negative correlations between HOMA-B% and fasting glucose(r=−0.48, P<0.001), 2 hr post prandial glucose (r=−0.37, P<0.001 and HbA1C (r=−0.24, P=0.01).
Conclusion: This study found more reduced beta-cell function compared to reduced insulin sensitivity in new T2D mellitus patients. Hence, this kind of functional assessment needs to be done while selecting appropriate anti-diabetic drugs for a particular patient.
We reported cases of Graves’ ophthalmopathy who presented solely with symptoms of the eyes and normal thyroid function tests, negative TSH receptor autoantibody (TRAb). These cases were referred to our hospital for unilateral or bilateral eye swelling with painful eye movements, with or without double vision, without any signs or symptoms of hyper- or hypothyroidism. Serum thyroid function tests and 99mTc uptake studies were within the normal range. Anti-thyroid autoantibodies (TRAb) were negative in all the cases. Since orbital CT scan and MRI gave typical results compatible with Graves’ ophthalmopathy and after exclusion of other possibilities, these patients were treated with corticosteroid pulse therapy and orbital radiation therapy, leading to a partial improvement of the symptoms. We followed up those cases with serial thyroid profile testing and TRAb estimation and they were subsequently developed clinical & biochemical hyperthyroidism within the next 18 months follow-up. At that time, they also became TRAb positive. These cases give us insight into the potential pathophysiologic mechanism underlying Graves’ ophthalmopathy and cast light upon the difficulties of establishing the diagnosis in biochemically euthyroid & thyroid autoantibody negative cases. Clinicians should be aware of the variable temporal relationship between the clinical expression of thyroid dysfunction and orbital disease in the natural course of Graves’ disease.
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