The classical approach to treating Graves’ hyperthyroidism involves rapid control of the symptoms, generally with a beta adrenergic blocker, and reduction of thyroid hormone secretion by antithyroid drugs (ATDs) and/or using one of the several modalities available, including radioactive iodine therapy (RAI), and surgery; the selection of the treatment modalities often varies according to different guidelines, patient preferences and local traditions. Thionamides are invariably used as first-line medication to control hyperthyroidism and induce remission of the disease, thereby relieving the symptoms. In case of failure of the medical therapy, which is not uncommon, definitive treatment with surgery or RAI is the standard modality of management after due consideration and discussion with the patients. However, the therapeutic options available for patients with Graves’ hyperthyroidism have remained largely unchanged for the past several decades despite the current treatments having either limited efficacy or significant adverse effects. The clinical demand for new therapeutic regimens of Graves’ disease has led to the emergence of several new therapeutic ideas/options like biologic, peptide immunomodulation and small molecules, currently under investigations which may lead to the restoration of a euthyroid state without the requirement for ongoing therapy, but the potential risk of immunocompromise and cost implications needs careful consideration.

Introduction: It is well known that marked hypokalemia manifest as muscle weakness, but rhabdomyolysis is a rare presentation of hypokalemia. Case Description: Here we report a case of primary hyperaldosteronism due to unilateral aldosterone producing adenoma in a 15yr old girl who developed rhabdomyolysis following hypokalemia. Aldosterone producing adenoma are rare in children with less than 20 cases reporting in literature. We present a 15year female who presenting with polyurea and proximal muscle weakness, investigation revealed hypokalemia, raised creatinine phosphokinase suggesting of hypokalemia induced rhabdomyolysis, further patient’s investigations showed raised aldosterone and suppressed renin and CT abdomen was suggesting of left adrenal adenoma which was removed laparoscopically. Discussion: Potassium depletion from any cause may produce muscle weakness, but hypokalemic rhabdomyolysis is a rare presentation of hypokalemia. Rhabdomyolysis from any cause leads to increase in free ionized calcium in the sarcoplasm. This increased sarcoplasmic calcium initiates a series of complex intracellular processes leading to the clinical manifestation of rhabdomyolysis. On initial assessment our patients presented with rhabdomyolysis including weakness of lower limb, increased creatinine phosphokinase and mild tubulopathy including polyurea and hypokalemia. Tubulopathy might be secondary tom hypokalemia or rhabdomyolysis in our patient rhabdomyolysis may cause renal tubular damage and tubulopathy either by free radical mediated injury or directly by effect of lipid peroxidation on tubular cells. Chronic hypokalemia can also induce tubulointerstitial damage consisting of vacuolization of epithelial tubular cells and interstitial fibrosis; called as hypokalemic nephropathy, which is quite rare. Primary hyperaldosteronism due to an adrenal tumor is rare in childhood; however, it should be considered in the presence of hypokalemia in a hypertensive child with normal renal function, even if the clinical presentation is unusual, such as severe rhabdomyolysis, of which early recognition is crucial for interventions directed to preserve renal function.

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