Pseudopheochromocytoma.

Abstract

A 52-year-old man was admitted to the Brigham and Women's Hospital (BWH) on August 21, 1984, for evaluation of a possible pheochromocytoma. He was first told of his hypertension at age 43 and was treated with /3-blockers, most recently nadolol (40 mg p.o q.d.) with "good control." On August 12, 1984, he was awakened from sleep with spasmotic midepigastnc pain, strong pulsations in his head, a feeling of generalized warmth, nausea, and diaphoresis. He induced vomiting, which did not improve his symptoms, and had an episode of watery diarrhea. He then went to a local hospital, where a blood pressure (BP) of 152/130 mm Hg was noted. He was treated for abdominal pain with 15 mg of morphine sulfate and 10 mg of prochlorperazine maleate (Compazine). Nadolol (40 mg daily) was continued. Results of an upper gastrointestinal series and a sulfobromophthalein function test were normal, and an abdominal ultrasono- He was transferred to BWH on August 21, 1984 He denied any history of palpitations, chest discomfort, or weight loss. On further questioning, the patient stated that he had had a premonition before each episode occurred. Past medical history included the passage of a kidney stone in 1981. Family history included a father and four siblings with onset of high BP in their midthirties. The patient was experiencing stress because of an ongoing divorce and his work as an executive in a computer company. He smoked no cigarettes, drank alcohol socially, and used no other medications On admission, the following BP measurements were recorded: supine, right arm, 190/110 mm Hg, left arm, 170/110 mm Hg, pulse, 60 beats/min; standing, 96/50 mm Hg, pulse, 100 beats/min. Fundi showed artenolar narrowing; lungs were normal. The carotid arteries were without bruits, and examination of the heart revealed no murmur or gallop. Results of an abdominal examination were normal. The ECG was normal. Results of laboratory studies (Tables 1 and 2) were normal except for serum glutamic-oxaloacetic transaminase levels of 128 U/L, serum glutamic-pyruvic transaminase levels of 216 U/L, and alkaline phosphatase levels of 148 U/L. While at the BWH, the patient had no further episodes.

Pheochromocytoma and Paraganglioma

“…Moreover, micturition or bladder distension in the case of a pheochromocytoma of the urinary bladder can cause clinical symptoms and signs of catecholamine excess. These episodes should be differentiated from pseudopheochromocytoma, which refers to the large majority of individuals (often women) with severe paroxysmal hypertension, whether normotensive or hypertensive between episodes, (Kuchel, 1985), related to a short-term activation of the sympathetic nervous system. In contrast to pheochromocytoma, patients with pseudopheochromocytoma more often present with panic attacks or anxiety, flushing, nausea and polyuria (Kuchel, 1985(Kuchel, , 2004White and Baker, 1986).…”

“…These episodes should be differentiated from pseudopheochromocytoma, which refers to the large majority of individuals (often women) with severe paroxysmal hypertension, whether normotensive or hypertensive between episodes, (Kuchel, 1985), related to a short-term activation of the sympathetic nervous system. In contrast to pheochromocytoma, patients with pseudopheochromocytoma more often present with panic attacks or anxiety, flushing, nausea and polyuria (Kuchel, 1985(Kuchel, , 2004White and Baker, 1986).Less common clinical manifestations include fever of unknown origin (hypermetabolic state) and constipation secondary to catecholamine-induced decrease in intestinal motility (Bouloux and Fakeeh, 1995). Observed flushing is rare, but can follow the vasoconstrictive episode of pallor or Raynaud's phenomenon, associated with the attack (Manger and Gifford, 1996).…”

Pheochromocytoma and Paraganglioma

“…Moreover, micturition or bladder distension in the case of a pheochromocytoma of the urinary bladder can cause clinical symptoms and signs of catecholamine excess. These episodes should be differentiated from pseudopheochromocytoma, which refers to the large majority of individuals (often women) with severe paroxysmal hypertension, whether normotensive or hypertensive between episodes, (Kuchel, 1985), related to a short-term activation of the sympathetic nervous system. In contrast to pheochromocytoma, patients with pseudopheochromocytoma more often present with panic attacks or anxiety, flushing, nausea and polyuria (Kuchel, 1985, 2004; White and Baker, 1986).…”

Paroxysmal hypertension due to sinoaortic baroreceptor denervation in humans.

“…There was no evidence for carcinoid syndrome or other causes of paroxysmal hypertension, as described by Kuchel. 21 The mechanism of the paroxysmal hypertension appeared to be spontaneous fluctuations in sympathetic activity that were inadequately buffered by the arterial baroreceptor reflex system. Unfortunately, we were not able to directly measure sympathetic nerve activity during a paroxysm, but the elevation of plasma norepinephrine during an episode suggests enhanced sympathetic drive.…”