Cardiac beriberi: often a missed diagnosis.

Thiamine deficiency leads to various manifestations due to dysfunction of nervous or cardiovascular system, commonly known as dry and wet beriberi, respectively. The latter, also known as cardiac beriberi is usually missed in clinical practice because of the absence of classically described symptoms such as pedal edema/anasarca. We investigated 55 such infants and prospectively followed their clinical course. All the babies were exclusively breast-fed and their mothers belonged to low socio-economic status with their staple diet consisting of non-parboiled polished rice. Majority presented with tachypnea, chest indrawing and tachycardia and cardiomegaly with dilatation of right heart and pulmonary hypertension on 2D-echocardiography. Low levels of erythrocyte transketolase activity suggested thiamine deficiency that was confirmed by reversion of several clinical features including cardiologic abnormalities to normalcy on thiamine supplementation. We recommend thiamine therapy for infants with unexplained congestive cardiac failure or acute respiratory failure from precarious socio-economic background since it is life-saving in many instances.

Secondary hypertension. An overview of its causes and management.

Primarily hypervolaemic, high output forms of hypertension, with features indicating or strongly suggesting fluid overload as the cause of elevated cardiac output, resulting from renal disease with reduced glomerular filtration rate causing sodium retention, renal tubular causes of sodium retention, greatly excessive sodium intake and low renin hypertension, can be treated by reduction of sodium intake and potentiation of its excretion by diuretic therapy, removal of the cause (e.g. aldosteronoma), and calcium antagonists. Excessive vasoconstriction resulting from noradrenaline (norepinephrine) in neurogenic hypertension, phaeochromocytoma, orthostatic hypertension and alpha-adrenergic drug administration; angiotensin excess due to renal ischaemia brought about by aortic coarctation, renal arterial and arteriolar stenosis, intraluminal obstruction, external renal compression, renin-producing tumours, intrinsic kidney diseases and excessive renin substrate; and vascular structural disorders such as atherosclerosis, arteriolitides and fibrosis with or without calcification of major arteries may also induce hypertension. Secondary hypertension of uncertain mechanism may occur in hyperparathyroidism, hyper-or hypothyroidism, or acromegaly. All are best treated by appropriate correction of the endocrine excess or deficiency. It may also occur in pregnancy, where the mechanism may involve prostaglandin-thromboxane imbalance or calcium deficiency; calcium deficiency with some evidence of benefit from calcium supplements; and the recumbent hypertension paradoxically associated with autonomic failure. Excellent responses to specific correction of the underlying cause or pathogenetic mechanism is usual in young individuals but less frequent in older patients.