Global Warming and Endocrinology: The Hyderabad Declaration of the South Asian Federation of Endocrine Societies.

Global warming and endocrine disorders are intertwined issues posing significant challenges. Greenhouse gases emanating from human activities drive global warming, leading to temperature rise and altered weather patterns. South Asia has experienced a noticeable temperature surge over the past century. The sizable population residing in the region heightens the susceptibility to the impact of global warming. In addition to affecting agriculture, water resources, and livelihood, environmental changes interfere with endocrine functioning. Resulting lifestyle changes increase the risk of metabolic and endocrine disorders. Individuals with diabetes face heightened vulnerability to extreme weather due to impaired thermoregulation. A high ambient temperature predisposes to heat-related illnesses, infertility, and nephropathy. Additionally, essential endocrine drugs and medical devices are susceptible to temperature fluctuations. The South Asian Federation of Endocrine Societies (SAFES) calls for collaboration among stakeholders to combat climate change and promote healthy living. Comprehensive approaches, including the establishment of sustainable food systems, promotion of physical activity, and raising awareness about environmental impacts, are imperative. SAFES recommends strategies such as prioritizing plant-based diets, reducing meat consumption, optimizing medical device usage, and enhancing accessibility to endocrine care. Raising awareness and educating caregivers and people living with diabetes on necessary precautions during extreme weather conditions are paramount. The heat sensitivity of insulin, blood glucose monitoring devices, and insulin pumps necessitates proper storage and consideration of environmental conditions for optimal efficacy. The inter-connectedness of global warming and endocrine disorders underscores the necessity of international collaboration guided by national endocrine societies. SAFES urges all stakeholders to actively implement sustainable practices to improve endocrine health in the face of climate change.

Diagnosis and Management Considerations in Steroid-Related Hyperglycemia in COVID-19: A Position Statement from the Endocrine Society of India.

The current coronavirus disease (COVID-19) pandemic is showing no signs of abatement and result in significant morbidity and mortality in the infected patients. Many therapeutic agents ranging widely between antivirals and anti-inflammatory drugs have been used to mitigate the disease burden. In the deluge of the drugs being used for COVID-19 infection, glucocorticoids (GCs) stand out by reducing mortality amongst in-hospital severe-to-critically ill patients. Health-care practitioners have seen this as a glimmer of hope and started using these drugs more frequently than ever in clinical practice. The fear of mortality in the short term has overridden the concern of adverse long-term consequences with steroid use. The ease of availability, low cost, and apparent clinical improvement in the short term have led to the unscrupulous use of the steroids even in mild COVID-19 patients including self-medication with steroids. The use of GCs has led to the increasing incidence of hyperglycemia and consequent acute complications of diabetic ketoacidosis and mucormycosis in COVID-19 patients. There is an urgent need to dissipate information about optimum management of hyperglycemia during steroid use. In view of this, the Endocrine Society of India has formulated this position statement about the diagnosis and management of hyperglycemia due to the use of GCs in patients with COVID-19 infection.

Pregnancy outcomes with thyroxine replacement for subclinical hypothyroidism: Role of thyroid autoimmunity.

OBJECTIVE: To study pregnancy outcomes in relation to thyroid peroxidase antibody (TPOAb) status with optimum thyroxine replacement for subclinical hypothyroidism. MATERIALS AND METHODS: Ninety-eight women with subclinical hypothyroidism were followed up until the end of their pregnancy. TPO antibody status was performed for 59 women (positive 20, negative 39). Levothyroxine was supplemented to maintain TSH between 0.3-3 mIU/l in all patients, irrespective of TPOAb status. Pregnancy outcomes were noted as pregnancy-induced hypertension (PIH), antepartum or postpartum hemorrhage, preterm delivery, and spontaneous abortion. Outcomes were compared between 3 groups as per TPO antibody status (positive, negative, and undetermined), which were matched for age and gestational period. RESULTS: Thyroid autoimmunity was noted in 34% of women screened for TPO antibody. A total of 11 adverse pregnancy outcomes were recorded (4 spontaneous abortions, 4 preterm deliveries, 3 PIH) with no significant difference between the groups. CONCLUSION: Adverse pregnancy outcomes were not different in the 3 groups with adequate thyroxine replacement for pregnant women with subclinical hypothyroidism targeting TSH in euthyroid range, irrespective of thyroid autoimmunity status.

Central hypothyroidism.

A 15-mth-old male child of consanguineous parents, presented with classical features of congenital hypothyroidism. Serum total thyroxine (T4), total triiodothyronine (T3) and TSH were low. There was no evidence of deficiency of other pituitary hormones. Magnetic resonance imaging of the pituitary was normal. TSHB gene sequencing revealed a homozygous missense mutation due to single base substitution G?A at codon 85 resulting in change from Glycine to Arginine. This mutation in TSHB gene has been reported earlier in three cases with similar phenotype from Japan.

Nerve, muscle or bone disease? Look before you leap.

Severe muscle weakness in osteomalacia may mimic a primary neuromuscular disorder like spinal muscular atrophy. A 32-year-old woman, initially diagnosed as a case of spinal muscular atrophy based on clinical presentation, electromyography and muscle biopsy, was later found to have osteomalacic myopathy due to primary hyperparathyroidism complicated by vitamin D deficiency. Before diagnosing a progressive, inevitably fatal degenerative condition like spinal muscular atrophy, one must rule out all possible treatable conditions with a similar presentation.

Symptomatic primary hyperparathyroidism: a retrospective analysis of fifty one cases from a single centre.

OBJECTIVE: Widely prevalent vitamin D deficiency and delayed diagnosis contributes to severe symptomatic primary hyperparathyroidism in India. We analysed fifty one consecutive patients of primary hyperparathyroidism managed at our centre. All of them were symptomatic. DESIGN: Retrospective analysis. MATERIAL AND METHODS: Fifty one consecutive cases of symptomatic primary hyperparathyroidism, presenting to our centre from January 1994 to May 2007 were retrospectively analyzed. Clinical presentation, biochemical, radiological and details of underlying parathyroid lesion were noted. RESULTS: A total of 51 cases of primary hyperparathyroidism were studied. Mean age was 39.5 +/- 11.5 yrs (Range 13 to 70 years, Female: Male 2:1). Mean duration of symptoms was 35.8 + 29.1 months. Bone pains and painful proximal myopathy were the commonest presentation (24/51), followed by pathological fractures in 12 cases. Distal Renal tubular acidosis was diagnosed in 4 cases, 3 of whom normalized after surgery. At initial evaluation, twenty one patients had elevated alkaline phosphatase with normal calcium levels indirectly suggesting associated vitamin D deficiency. Low serum levels of 25-hydroxy vitamin D were documented in five of them. Parathyroid carcinoma was diagnosed in 3 patients. Ectopic parathyroid adenoma was seen in 7 cases (3 mediastinal, 3 intrathyroidal, 1 near left carotid sheath). All the cases responded well to surgical excision. CONCLUSION: Lack of universal screening for hypercalcemia, normocalcemia contributed by associated vitamin D deficiency and lack of awareness about unusual presentations of primary hyperparathyroidism led to delayed diagnosis in our patients. Delayed diagnosis and associated vitamin D deficiency in our patients contributed to greater severity of symptomatic primary hyperparathyroidism.