Plasma free metanephrines provide the best test for excluding or confirming pheochromocytoma and should be the test of first choice for diagnosis of the tumor.

Recent studies of acetaminophen-induced liver damage in animals indicate 676vital hepatocellular macromolecules. 9 , 18 Pretreatment with inducers of metabolism, such as phenobarbital, increases the rate of metabolism of acetaminophen, the extent of hepatic binding of radio labeled metabolite, and the severity of hepatic necrosis.!" 13. 15. 18 Conversely, pretreatment with inhibitors of metabolism markedly decreases the metabolism of acetaminophen, the covalent binding, and the hepatic necrosis.!)' 1:1, 15, 18 A direct relationship has also been demonstrated between the formation of an acetaminophen-gluthathione conjugate, arylation of hepatic macromolecules, and hepatic damage after administration of acetaminophenY, 16·18 After nontoxic doses of

Measurements of plasma normetanephrine and metanephrine provide a highly sensitive test for diagnosis of pheochromocytoma, but false-positive results remain a problem. We therefore assessed medication-associated false-positive results and use of supplementary tests, including plasma normetanephrine responses to clonidine, to distinguish true- from false-positive results. The study included 208 patients with pheochromocytoma and 648 patients in whom pheochromocytoma was excluded. Clonidine-suppression tests were carried out in 48 patients with and 49 patients without the tumor. Tricyclic antidepressants and phenoxybenzamine accounted for 41% of false-positive elevations of plasma normetanephrine and 44-45% those of plasma and urinary norepinephrine. High plasma normetanephrine to norepinephrine or metanephrine to epinephrine ratios were strongly predictive of pheochromocytoma. Lack of decrease and elevated plasma levels of norepinephrine or normetanephrine after clonidine also confirmed pheochromocytoma with high specificity. However, 16 of 48 patients with pheochromocytoma had normal levels or decreases of norepinephrine after clonidine. In contrast, plasma normetanephrine remained elevated in all but 2 patients, indicating more reliable diagnosis using normetanephrine than norepinephrine responses to clonidine. Thus, in patients with suspected pheochromocytoma and positive biochemical results, false-positive elevations due to medications should first be eliminated. Patterns of biochemical test results and responses of plasma normetanephrine to clonidine can then help distinguish true- from false-positive results.

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Combination chemotherapy with cyclophosphamide, vincristine, and dacarbazine is effective for advanced malignant pheochromocytoma. Urinary catecholamines are useful to ascertain biochemical response to therapy.

Measurements of plasma normetanephrine and metanephrine are useful in screening for pheochromocytomas in patients with a familial predisposition to these tumors.

Pheochromocytomas occur in a small but defined number of patients with von Recklinghausen's disease, and can be associated with significant morbidity and mortality if not detected. Screening of patients with von Recklinghausen's disease and hypertension or before provocative procedures or pregnancy seems to be indicated.

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