The clonidine suppression test for pheochromocytoma. A review of its utility and pitfalls.

OBJECTIVE: The intent of this study is to retrospectively evaluate our experience, as well as all published information, regarding the clonidine suppression test to determine its utility, accuracy, and safety in the diagnosis of pheochromocytoma. PATIENTS AND METHODS: All 22 patients (including four with pheochromocytoma) evaluated at a major military referral hospital with the clonidine suppression test for suspected pheochromocytoma for more than 6 years were retrospectively reviewed. All published series of patients similarly evaluated were also critically reviewed. RESULTS: All studies confirm that a nonstressed plasma norepinephrine of more than 2000 pg/mL is diagnostic of pheochromocytoma. In those patients with a plasma norepinephrine of less than 2000 pg/mL, the clonidine suppression test is 92% accurate in diagnosing pheochromocytoma when the normal response to clonidine is defined as total plasma catecholamines of less than 500 pg/mL. Its accuracy diminishes in patients with low baseline plasma catecholamine levels, who may better be tested with a stimulatory test (ie, glucagon). The use of diuretics, beta-blockers, and antidepressants may cause false-positive results or severe hypotension during the clonidine suppression test. Those previously treated with clonidine or with baroreceptor dysfunction may also be prone to severe hypotension, but this complication is otherwise uncommon after acute clonidine ingestion. CONCLUSION: Although it is rarely necessary for the diagnosis of pheochromocytoma, the clonidine suppression test is an accurate and safe test in a select group of patients.

Crossover comparison of maximum dose glyburide and glipizide.

Patients with non-insulin-dependent diabetes mellitus (NIDDM) failing to respond to therapy with a maximum dose of glyburide (GB) or glipizide (GZ) are often given a trial of the alternate second-generation sulfonylurea (SGS) before insulin therapy is considered. The efficacy of this therapeutic maneuver has not been thoroughly tested. We studied 26 subjects with fasting serum glucose (FSG) levels greater than 8.3 mmol/L (150 mg/dL) despite maximum doses of either GB (20 mg/day) or GZ (40 mg/day). Group 1 consisted of 16 subjects taking GB (mean FSG = 12.7 mmol/L [228 mg/dL]) and group 2 included 10 subjects taking GZ (mean FSG = 13.0 mmol/L [234 mg/dL]). Subjects continued taking their original SGS for 8 weeks then switched to a maximum dose of the alternate agent for an additional 8 weeks. Values for FSG, hemoglobin A1c, and lipids were recorded before the study and after 8 weeks on each SGS trial. No significant changes were noted for any variable in either group. When maximum dose GB therapy was compared to maximum dose GZ therapy in the combined study group (n = 26), no advantage was noted for either agent. We conclude that metabolic control in NIDDM patients failing to respond to therapy with maximum dose GB or GZ is not improved by switching to the alternate SGS.

Massive extracapsular hemorrhage from a parathyroid cyst.

A 32-year-old man had a giant cervical mass, dysphagia, dyspnea, and severe hypercalcemia. A computed tomographic scan showed the mass to extend from the left mandible to the level of the aortic arch. Exploratory surgery of the neck revealed a ruptured parathyroid cyst complicated by massive hemorrhage into the cervical tissues and mediastinum. The postoperative course was uncomplicated with prompt resolution of the hypercalcemia. Although a rare occurrence, extracapsular parathyroid hemorrhage should be considered in the differential diagnosis of all rapidly evolving cervical and mediastinal masses, especially when hypercalcemia is present.