Distal renal tubular acidosis, hypokalemic paralysis, nephrocalcinosis, primary hypothyroidism, growth retardation, osteomalacia and osteoporosis leading to pathological fracture: a case report

Renal tubular acidosis [RTA] is a constellation of syndromes arising from different derangements of tubular acid transport. Recent advances in the biology of urinary acidification have allowed us to discern various molecular mechanisms responsible for these syndromes. RTA often presents as renal stone disease with nephrocalcinosis, ricket/osteomalacia and growth retardation in children with ultimate short stature in adulthood. The case reported here has features of distal renal tubular acidosis [dRTA], hypokalemic paralysis, primary hypothyroidism, growth retardation, osteomalacia and osteopenia leading to stress fracture. All these features presenting in a single case [as in our case] is a rare occurrence, so far other cases of distal renal tubular acidosis [dRTA] have been reported

case of severe primary hyperthyroidism, secondary hyperparathyroidism, adrenal insufficiency and osteoporosis with multiple fractures

Osteoporosis is generally known to be one of the most serious adverse effects of long-term corticosteroid administration. Recently it was discovered that corticosteroid-induced osteoporosis occurs not only in trabecular bone but also in cortical bone, leading to the reduction in the strength of bones and subsequent fracture. We report a case of severe hyperthyroidism, secondary hyperparathyroidism, adrenal insufficiency and osteoporosis with multiple fractures [mostlikely collectively due to chronic steroid intake because of steroid dependant bronchial asthma, hyperparathyroidism and hyperthyroidism] which was treated appropriately and made an uneventful recovery

case report of basal ganglia calcification - a rare finding of hypoparathyroidism

Physiological intracranial calcification occurs in about 0.3-1.5% of cases. It is asymptomatic and detected incidentally by neuroimaging. Pathological basal ganglia calcification is due to various causes, such as: metabolic disorders, infectious and genetic diseases. Hypoparathyroidism and pseudohypoparathyroidism are the most common causes of pathological basal ganglia calcification. Besides tetany and seizures this condition is presented by parkinsonism and dementia. Such parkinsonism does not respond to drugs containing levodopa. Infections [toxoplasmosis, rubella, cytomegalovirus, cysticercosis, AIDS] give multiple and asymmetric intracranial calcification. Inherited and neurodegenerative diseases cause symmetrical, bilateral basal ganglia calcification which is not related to metabolic disorders. Since adequate treatment of hypoparathyroidism may lead to marked clinical improvement, serum concentration of calcium, phosphorus, and parathyroid hormone [PTH] is suggested to be determined in all individuals with calcification of the basal ganglia to rule out hypoparathyroidism

Autoimmune polyglandular syndrome [type - 111]: case report

Autoimmune poly glandular syndromes are constellations of multiple glandular insufficiencies. There are four types - 1, 11, 111 and IV. Type 11 is the commonest. The case reported here has features of type 111, which is a rare occurrence