SUMMARY A 40-year-old man was admitted to the hospital with pulmonary edema without signs of left ventricular failure. Noncardiogenic pulmonary edema was diagnosed, and a subsequent workup identified a pheochromocytoma as the cause of this condition. The clinical picture could be mimicked by infusion of exogenous norepinephrine. It is concluded that surges of catecholamines from a pheochromocytoma may provoke pulmonary edema in a manner similar to that by which neurogenic pulmonary edema related to cerebral disorders occurs. (Hypertension 8: 810-812, 1986) KEY WORDS • catecholamines • heart failure * hypertension P RESSOR crises, excessive sweating, and headache are among the most frequent symptoms of pheochromocytoma. 1 Furthermore, pulmonary edema may develop as a result of cardiac failure. The latter usually is due to a sudden or sustained rise in arterial pressure or the result of catecholamine-induced cardiomyopathy.1 ' 2 We report on a patient with pheochromocytoma in whom several episodes of pulmonary edema occurred in the absence of hypertension and without signs of left ventricular dysfunction.Case Report A 40-year-old man was admitted to the coronary care unit because of acute, severe dyspnea and production of blood-stained sputum. He had been well until 8 years earlier when he was involved in a car accident and remained comatose for 24 hours. Since that time he had had several bouts of mild dyspnea accompanied by feelings of unease and restlessness. Although such episodes were short-lived, the patient had noticed an increased frequency over the previous 2 or 3 months.On examination he appeared tachypneic, cyanotic, and clammy. Supine blood pressure was 80/60 mm Hg, and the heart rate was 115 beats/min. The heart was normal, and no ventricular gallop was heard, but numerous rales were audible in both lungs. No other abnormalities were evident. Laboratory investigation disclosed slightly elevated hemoglobin levels (12 mmol/L), hematocrit (59%), and creatinine levels (135 /xmol/L). The levels of serum glutamic-oxalacetictransaminase, serum glutamic-pyruvate transaminase, and lactic dehydrogenase were modestly increased, but the creatinine kinase level was normal. A chest roentgenogram showed massive pulmonary edema but a normal-sized heart; an electrocardiogram revealed sinus tachycardia and signs of right ventricular strain with no evidence of myocardial infarction. After a Swan-Ganz thermodilution catheter had been introduced, the following hemodynamic data were obtained: pulmonary artery pressure, 21/3 mm Hg (mean, 12 mm Hg); pulmonary capillary wedge pressure, 2 mm Hg; right atrial pressure, 0 mm Hg. Cardiac output was 3.45 L/min, while intra-arterial pressure was still low: 75/55 mm Hg. All measurements were done while the patient was still recumbent. Calculated systemic vascular resistance was normal, but pulmonary vascular resistance was increased. Treatment consisted of oxygen by mask and infusion of plasma and the patient recovered within a few hours. Cardiac output then stabilized at 7 L/min...

Identification by serology of asymptomatic patients with advanced GBA in primary care is adequately possible and useful in selecting for endoscopy.

The aim of this double-blind parallel-group study was to compare the effects of doxazosin, a selective alpha 1-adrenoceptor antagonist with a long plasma half-life, with nitrendipine, a long-acting calcium-entry blocking drug. Following a 4-week placebo period, 26 patients with mild-to-moderate essential hypertension were randomly allocated to treatment with either doxazosin (n = 12) or nitrendipine (n = 14). Over a period of 10 weeks, doses were titrated to obtain a standing diastolic pressure below 90 mmHg. Thereafter, optimal doses were continued for another 4 weeks. Both drugs were administered once daily; median doses were 4 mg/day for doxazosin and 10 mg/day for nitrendipine. During the titration period three patients in the doxazosin group and one in the nitrendipine group dropped out from the study; one patient on doxazosin was considered a nonresponder. Twenty-one patients completed the study. The percentage of patients showing an adequate hypotensive effect (standing diastolic pressure below 90 mmHg) at the end of the study was similar in the two groups (42% vs. 50% in the intention-to-treat analysis and 56% vs. 54% in the per-protocol analysis). Casual, basal, and standing blood pressure and heart rate did not differ between groups throughout the study; serum lipids and blood glucose remained unchanged. We conclude that doxazosin and nitrendipine given as monotherapy are equally effective in mild to moderate hypertension.