Autoimmune thyroid disease (AITD), a common organ specific autoimmune disorder is seen mostly in women between 30-50 yrs of age. Thyroid autoimmunity can cause several forms of thyroiditis ranging from hypothyroidism (Hashimoto's thyroiditis) to hyperthyroidism (Graves'Disease). Prevalence rate of autoimmune mediated hypothyroidism is about 0.8 per 100 and 95% among them are women. Graves' disease is about one tenth as common as hypothyroidism and tends to occur more in younger individuals. Both these disorders share many immunologic features and the disease may progress from one state to other as the autoimmune process changes. Genetic, environmental and endogenous factors are responsible for initiation of thyroid autoimmunity. At present the only confirmed genetic factor lies in HLA complex (HLA DR-3) and the T cell regulatory gene (CTLA 4). A number of environmental factors like viral infection, smoking, stress & iodine intake are associated with the disease progression. The development of antibodies to thyroid peroxidase (TPO) thyroglobulin (TG) and Thyroid stimulating hormone receptor (TSH R) is the main hallmark of AITD. Circulating T Lymphocytes are increased in AITD and thyroid gland is infiltrated with CD4+ and CD8+ T Cells. Wide varieties of cytokines are produced by infiltrated immune cells, which mediate cytotoxicity leading to thyroid cell destruction. Circulating antibodies to TPO and TG are measured by immunofluorescense, hemagglutination, ELISA & RIA. TSHR antibodies of Graves' disease can be measured in bioassays or indirectly in assays that detect antibody binding to the receptor.

A 35-year-female presented with generalized weakness, weight loss, and progressive pigmentation was worked up for suspicion of Addisons disease. On examination hyper pigmentation was noted on both palmar and dorsal aspect of hands involving knuckles, creases, feet, tongue, oral mucosa and gluteal region. There was no evidence of hypocortisolemia as initially suspected, and literature search revealed a possibility of vitamin B12 deficiency. She had megaloblastic anemia with a low serum vitamin B12, mostly due to poor dietary intake. Her hyper pigmentation resolved with vitamin B12 supplementation. Skin biopsy showed increased pigmentation at stratum spinosum and basal-layer. The mechanism of hyper pigmentation in vitamin B12 deficiency was due to an increase in melanin synthesis.

Aim of the Study:This study aimed to compare the different adiposity parameters, namely visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) between patients with polycystic ovary syndrome (PCOS) and controls. In addition, it aimed to correlate these adiposity indices with hormonal parameters as well as cardiovascular (CV) risk factors in patients with PCOS.Materials and Methods:Newly diagnosed PCOS patients of reproductive age group according to Rotterdam criteria were included. Age- and body mass index (BMI)-matched healthy females with normal menstrual cycles were taken as controls. All the study participants underwent detailed clinical, biochemical, and hormonal evaluation. Transabdominal ultrasound (US) was performed for detailed ovary imaging and assessment of adiposity (SAT and VAT) parameters.Results:A total of 58 PCOS patients and 40 age- and BMI-matched controls were included. PCOS patients had significantly higher levels of androgens (P < 0.001), elevated highly sensitive C-reactive protein (P = 0.007), and higher degree of insulin resistance (P < 0.001) than controls. PCOS patients had a mean SAT of 2.37 ± 0.7 cm and mean VAT of 8.65 ± 1.78 cm. These parameters were significantly higher than controls who had a mean SAT of 2.01 ± 0.7 cm (P = 0.014) and mean VAT of 7.4 ± 1.89 cm (P = 0.003), despite both groups having similar BMI. Among PCOS cohort, VAT correlated positively with total testosterone (r = 0.295, P = 0.025) and negatively with dehydroepiandrosterone sulfate (r = −0.210, P = 0.114). However, no significant correlation was observed between SAT and androgens in PCOS group.Conclusion:PCOS patients, whether obese or nonobese, had elevated visceral adiposity than controls. VAT correlated positively with adverse CV risk factors and testosterone in PCOS patients. Hence, a simple and inexpensive ultrasonography screening of visceral fat may identify women who have adverse metabolic profile and enhanced CV risk.

Aims and Objective: We aimed to compare serum vitamin D level in new onset Graves' disease versus age and sex matched controls. Furthermore, we assessed the correlation of vitamin D with hormonal parameters and antibody titers in Graves' disease. Materials and Methods: In total, 84 patients of new onset Graves' disease and 42 age and sex matched healthy individuals were recruited. Biochemical and hormonal investigations that included serum calcium, phosphorous, free triiodothyronine (FT3), free thyroxine (FT4), thyroid stimulating hormone (TSH), 25 hydroxy vitamin D (25(OH) D), and parathyroid hormone (PTH) were done for all subjects. Thyrotropin receptor antibody (TRAb) was measured only for Graves' disease patients. Results: The patients with Graves' disease had significantly lower 25(OH) D levels (19.2 ± 8.9 ng/ml) as compared to control subjects (23.8 ± 12.5 ng/ml) ( P = 0.019). Thyroid hormone levels, thyroid volume, and TRAb titers did not differ significantly between vitamin D deficient Graves' disease group (25(OH)D <20 ng/ml) and vitamin D non deficient Graves' disease group (25(OH)D ≥20 ng/ml). Furthermore, serum vitamin D level did not correlate significantly with thyroid hormones, thyroid volume, or TRAb titers among Graves' disease. The odds ratio (OR) for association of vitamin D deficiency (VDD) state and Graves' disease was 1.62 (95% CI 0.77–3.41). Vitamin D sufficiency state was associated significantly with lower risk of Graves' disease (OR = 0.38, 95% CI 0.15–0.95). Conclusion: Serum vitamin D levels are significantly lower in new onset Graves' disease. No significant correlation between vitamin D and thyroid hormones, thyroid volume, or TRAb titers was found in these patients. VDD state is not associated with Graves' disease.