Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a 56-year-old normotensive white male subject with a 12-year history of hypokalemic alkalosis, hyperreninemia, and aldosteronism, the diagnosis of Bartter's syndrome was established on the basis of an impaired maximal renal diluting capacity and decreased distal fractional chloride absorption [CH2O/(CH2O+CCl)]. Negative urine analysis for diuretics suggested that this renal tubular defect was not secondary to diuretic (ab)use. In this normotensive patient with hyperreninemia and secondary aldosteronism, significant cardiovascular remodeling could be observed. Thus, in spite of normal arterial blood pressure and normal left ventricular systolic function (ejection fraction > 70%), impaired left ventricular diastolic function was observed using pulsed-wave Doppler echocardiography. Moreover, duplex analysis of the common carotid artery revealed significant intima-media hypertrophy with an average intima-media diameter of 0.9 mm (normal < or = 0.6 mm). Also, forearm venous occlusion plethysmography revealed an abnormally high minimal forearm vascular resistance following a 10-min period of forearm ischemia handgrip exercise suggesting remodeling within the peripheral arterioles. Thus, in a patient with Bartter's syndrome and activated neurohormonal systems such as the renin-angiotensin system, cardiac and vascular remodeling can be observed in the absence of hypertension. In analogy to the results of experimental studies showing that angiotensin II and noradrenaline act as growth factors on cardiac and vascular cells, cardiovascular remodeling present in our patient with Bartter's syndrome may be explained by increased activity of angiotensin II and/or noradrenaline.
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PMID:Evidence for cardiovascular remodeling in a patient with Bartter's syndrome. 789 15

Pheochromocytomas cause the most dramatic life-threatening crises in all of endocrinology. Pheochromocytoma is an explosive clinical syndrome that may be characterized by either severe hypertension associated with cerebral, cardiac, and renal complications or hypotension, or even shock and sudden death. Other emergencies include lactic acidosis, hypoglycemia, hypercalcemic crisis, severe hypokalemic alkalosis, and acute bowel obstruction due to bowel ischemia, necessitating prompt surgical intervention. Better understanding of the mechanisms of catecholamine action and the pathophysiology of pheochromocytoma and the availability of various treatment modalities have made successful management more promising than ever before.
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PMID:Pheochromocytoma. 832 90