Repeated blood transfusions in transfusion dependent thalassemia (TDT) leads to iron overload-related endocrine complications. Hypoparathyroidism (HPT) with severe signs of hypocalcemia is a recognized complication among these patients. A 14-year-old thalassaemic boy, on regular transfusion and on anticonvulsant therapy with a presumptive diagnosis of epilepsy for the last 1 year, was admitted with high fever and severe muscle cramps with positive Trousseau’s sign. He was diagnosed as a case of primary HPT and magnesium deficiency on the basis of low serum calcium, high phosphate, normal alkaline phosphates, very low intact parathyroid hormone (iPTH), normal serum vitamin D and very low serum magnesium level. His calcium, magnesium and phosphate level normalised following treatment with intravenous magnesium and calcium. His iPTH improved but remained at low normal. He was discharged from hospital with oral calcium, calcitriol, and magnesium supplementation. The anticonvulsant (Phenobarbitone) was successfully withdrawn gradually over the next six months without any recurrence of seizure in the subsequent 3 years of follow up. Acquired HPT (apparently from hemosiderosis) is a common cause of hypocalcemia; and magnesium depletion further complicated the situation leading to severe hypocalcemia with recurrent episodes of convulsion. Magnesium replacement improved the parathyroid hormone (PTH) value proving its role in acquired HPT. Very high phosphate level on admission and poor PTH response with respect to the low serum calcium, indicates intrinsic parathyroid pathology. Metabolic abnormalities should always be evaluated in thalassaemic subject with seizure disorder and it appears that the initial convulsive episodes were due to hypocalcemia. Muscle pain, cramps or convulsion may occur from HPT and simultaneous magnesium deficiency in transfusion dependent thalassaemic subjects. Metabolic correction is more important than anticonvulsant medication. Calcium and magnesium should both be assessed routinely in transfusion dependent thalassemic patients.
Hemosiderosis ; Hypoparathyroidism ; Thalassemia

Myxedema coma is associated with decreased mental status and hyponatremia among patients with diagnosed or undiagnosed hypothyroidism. The diagnosis is challenging in the absence of universally accepted diagnostic criteria, but should be considered as a differential even in cases with competing established diagnoses. All patients should receive intensive care level treatment. Even with optimal treatment, mortality is very high.
Myxedema ; Coma

Graves' disease (GD) and Guillain-Barre syndrome (GBS) are both autoimmune disorders and are triggered by interactions between genetic and environmental factors. GBS in patients who suffer from other autoimmune diseases is rarely reported, and the development of atypical GBS with cranial nerve involvement in a patient with GD has never been previously reported. Herein, we report a patient with GD and a rare form of pharyngo-cervico-brachial variety of GBS.

We report a case of diabetes mellitus in a middle-aged female who subsequently developed primary hyperparathyroidism and underwent parathyroidectomy. Prior to surgery, she was hospitalized several times since 1988 for vomiting, pain abdomen and dehydration. On none of these occasions hypercalcaemia could be documented. Yet she developed pancreatic calcification and diabetes in 1991 and was diagnosed as fibrocalculous pancreatic diabetes (FCPD) and treated with insulin. Nephrolithiasis developed in 2003. Hypercalcaemia with high PTH was detected in 2004 and a solitary right parathyroid adenoma was identified and surgically removed. Following surgery, gastrointestinal symptoms disappeared but diabetes remained unaltered on follow up for 8 years. The cause of multi-organ calcification which started well before development of hypercalcaemia is not known.
Parathyroid Neoplasms

We report a case of a 38-year-old Indian male who presented with severe throbbing headache spreading diffusely from occipital to nuchal regions. He was detected to have superior cerebral (sagittal) venous sinus thrombosis (CVST) with severe hypertriglyceridemia without any coagulation abnormalities or autoimmune disease. Our case highlights the need for clinicians to consider CVST among patients with uncontrolled hypertriglyceridemia. New prognostic measures may become necessary having an implication on the risk of recurrence and duration of anticoagulant therapy in CVST.
Hypertriglyceridemia ; Venous Thrombosis ; Headache