James H. Mersey

Plasma norepinephrine and epinephrine responses to glucagon in patients with suspected pheochromocytomas

Plasma norepinephrine and epinephrine levels were measured before and after glucagon administration in 28 patients suspected of having a pheochromocytoma: three patients were subsequently found to have tumors. The norepinephrine response predicted the presence or absence of a tumor in 27 of the 28 patients. Epinephrine levels doubled, on the average, in patients who did not have pheochromocytomas, and were not useful in distinguishing the patients with or without tumors. A comparison of the response to glucagon and a placebo indicated that changes in plasma catecholamine levels were hormone-related and not the result of side-effects accompanying injection. The glucagon provocation test, with measurement of plasma norepinephrine and epinephrine levels, may be a useful adjunctive tool for evaluating patients suspected of having a pheochromocytoma when performed according to a standardized protocol and interpreted in relation to appropriate controls.

Adrenal Vein Epinephrine Levels: A Useful Aid in Venous Sampling for Primary Aldosteronism

We evaluated the usefulness of adrenal vein epinephrine levels as an indicator of adrenal venous dilution in seven patients with primary aldosteronism who had venous sampling. In six patients adrenal vein epinephrine levels greater than 1500 pg/mL confirmed that relatively undiluted adrenal efflux had been obtained. In another patient a low value of left adrenal vein epinephrine indicated that the sample was markedly diluted with nonadrenal blood. Measurement of epinephrine levels appears to be a useful tool for verifying successful venous sampling, particularly when cortisol and aldosterone levels from the same adrenal vein are not elevated or when deep adrenal vein cannulation cannot be confirmed radiologically.

Withdrawal phenomena in subjects with essential hypertension on clonidine or tiamenidine

The incidence and pathogenesis of withdrawal phenomena with the centrally acting drugs clonidine (CLON) and tiamenidine (TIAM) were evaluated. Thirty subjects with hypertension on hydrochlorothiazide (HCTZ) were randomized to TIAM or CLON. Blood pressure and integrated plasma catecholamine levels fell equally in response to both drugs. On withdrawal, blood pressure and pulse rose in both groups with no difference between them. Three subjects had symptoms of withdrawal, four had blood pressure overshoot above pretreatment levels of 10 mm Hg or more, and eight had a rise in blood pressure of 30 mm Hg systolic or 20 mm Hg diastolic. There was no difference between TIAM and CLON in these effects. There was a direct correlation between blood pressure rise and increase in integrated plasma norepinephrine levels. We conclude that the incidence of withdrawal phenomena in subjects on TIAM or CLON is infrequent and that there is a direct relationship between the rise in blood pressure and the loss of suppression of catecholamines by these drugs.

Evidence for Elevated Glucose Threshold in Patients With Impaired Glucose Tolerance and Symptoms of Hypoglycemia During OGTT

We evaluated the relationship between hypoglycemic symptoms, glucose nadir levels, and hormone changes in patients with impaired glucose tolerance (IGT) after an oral glucose tolerance test (OGTT). The peak counterregulatory hormone response was determined at the glucose nadir identified by continuous glucose monitoring. Eight patients with IGT who had symptoms and signs typical of hypoglycemia at the glucose nadir were compared with completely asymptomatic subjects (5 IGT patients and 13 patients who had normal glucose tolerance [NGT]). The mean glucose nadir of symptomatic IGT patients was 3.50 ± 0.46 mM, which was not statistically different from the mean of asymptomatic NGT patients (4.10 ± 0.56 mM) but was significantly lower than that for asymptomatic IGT patients (5.10 ± 0.81 mM, P < 0.001). Seven of 8 symptomatic IGT patients had glucose levels that never fell below the range of glucose nadirs for asymptomatic NGT patients. However, the symptomatic IGT group had significantly higher levels of growth hormone, cortisol, epinephrine, and norepinephrine than the asymptomatic groups in response to the nadir. We conclude that patients with IGT are capable of experiencing signs and symptoms of hypoglycemia at physiological glucose levels during OGTT with reflex stimulation of counterregulatory hormone release. This may indicate that symptomatic IGT patients have a higher glucose threshold for eliciting characteristic hypoglycemic symptom episodes than individuals with NGT.