RESUMO
Background The clinical impact of body mass index (BMI), residual beta cell function and estimated glucose disposal rate (eGDR) in the development of double diabetes (DD) and microvascular complications are largely unknown. We aimed to assess whether BMI, residual beta cell function measured by plasma "C" peptide and insulin resistance measured by eGDR have any impact on the development of DD and microvascular complications in patients with type 1 diabetes mellitus (T1DM). Methods It is a cross-sectional observational study involving 113 T1DM patients of more than five years duration who were classified into two groups: normal BMI (18.5-22.9 kg/m2) and overweight/obese group (≥ 23kg/m2) based on Asian BMI classification. Based on their eGDR values, they were grouped into four categories: ≥ 8, 6-7.99, 4-5.99, and < 4 mg/kg/min. The prevalence of DD based on eGDR values was determined. Their BMI and different eGDR categories were compared with the prevalence of diabetic retinopathy and nephropathy and their odds ratio (OR) was calculated. Results The median and interquartile range (IQR) of the eGDR of the overweight/obese group was significantly lower than the normal BMI group (5.3 [3.96-8.15] vs 8.72 [6.50-9.77 mg/kg/min], p < 0.001). The prevalence of DD in the overweight/obese T1DM group and normal BMI group was 75% and 33.3% respectively. The OR of retinopathy and nephropathy in the overweight/obese group was 3.28 (p = 0.007) and 3.01 (p = 0.015) respectively when compared to the normal BMI group. The OR of retinopathy and nephropathy in T1DM patients with eGDR < 4 mg/kg/min was 17.13 (p = 0.001) and 18.5 (p = 0.001) respectively. The lower the eGDR values, the higher the prevalence of retinopathy and nephropathy regardless of HbA1c levels. Conclusion As overweight and obesity are increasingly becoming more prevalent in T1DM, the eGDR will better predict the development of DD and microvascular complications irrespective of HbA1c levels. It is more useful as a variable and easily inducted into routine clinical practice. However, residual beta cell function was not useful in predicting the development of microvascular complications.
RESUMO
Fahr's disease is an idiopathic basal ganglia calcification with autosomal dominant inheritance. Prior to diagnosing Fahr's disease based on computed tomography (CT) and/or magnetic resonance imaging (MRI) of the brain, one should rule out hypoparathyroidism (HP), and pseudohypoparathyroidism (PHP). Treatments of these conditions are entirely different. HP- and PHP-related hypocalcemia requires calcium, calcitriol, and vitamin D therapy in a long run to avoid recurrent seizures whereas Fahr's disease is treated with an antiepileptic alone.
