Herbal therapy for management of obesity: observations from a clinical endocrinology practice.

OBJECTIVE: To assess the effectiveness and safety of two herbal therapies for weight reduction. METHODS: A nonrandomized group of 128 patients seen in my office who had received one of two herbal treatments for obesity were retrospectively analyzed for their weight loss response. No control group was studied or analyzed in conjunction with these patients. All these patients had been unsuccessful losing weight with use of diet and exercise modalities alone. Of the 128 patients, 90 were treated with the herbal product BioLean, and 38 were treated with the combination of prescription phentermine and the herbal product Satiete. Both herbal products are manufactured under the highest standards of purity, consistency, and quality control, and both are listed in the Physicians' Desk Reference for Nonprescription Drugs and Dietary Supplements. RESULTS: The patients receiving BioLean were treated for a mean of 18.7 weeks and lost a mean of 0.73 lb/wk. The patients receiving phentermine and Satiete were treated for a mean of 12.4 weeks and lost a mean of 0.87 lb/wk. Overall, 79% of the BioLean-treated patients and 87% of the phentermine- and Satiete-treated patients lost a mean of at least 0.5 lb/wk. No significant adverse reactions to either treatment were noted. Comparable data from a matched control group were not available for further analysis of these results. CONCLUSION: Herbal products for weight reduction in motivated patients may be effective in helping to treat clinically significant obesity, which is an important public health problem in the United States. The consistency and safety of a bioavailable active herbal product for weight reduction, as well as its efficacy, remain important factors in the consideration of such therapy for weight reduction.

Reversal of diuretic-induced secondary hyperaldosteronism and hypokalemia by enalapril (MK-421): a new angiotensin-converting enzyme inhibitor.

The study reported here prospectively evaluated the prevention of diuretic-induced secondary hyperaldosteronism and hypokalemia by a converting enzyme inhibitor, enalapril (MK 421). Eighteen normal subjects were randomized into three groups: (1) a HCTZ group (hydrochlorothiazide (HCTZ) 50 mg/day); (2) a MK-421 group (MK-421 10 mg/day); and (3) a HCTZ + MK-421 group [HCTZ 50 mg/day plus MK-421 10 mg/day]. Following a five-day control and a 28-day treatment period, the HCTZ group demonstrated an attenuated but persistent secondary hyperaldosteronism and hypokalemia, the MK-421 group manifested a gradual decline in aldosterone secretion, and the HCTZ + MK-421 group had a delayed but effective correction of secondary hyperaldosteronism and hypokalemia at 28 days but not before. In conclusion, MK-421 reversed diuretic-induced secondary hyperaldosteronism and hypokalemia after 28 days of hydrochlorothiazide therapy. Therefore, converting enzyme inhibitors, such as enalapril, provide useful adjunctive therapy in diuretic-treated patients, but potassium supplementation may be required before the start of four weeks of combined therapy.

The superiority of the metyrapone test versus the high-dose dexamethasone test in the differential diagnosis of Cushing's syndrome.

Differentiating the cause of Cushing's syndrome traditionally has depended upon measuring the response of 24-hour urine samples of cortisol or glucocorticoid metabolites to the high-dose (8 mg per day) dexamethasone test. The metyrapone test, however, is more convenient because it is a shorter test and requires the obtainment of serum samples, which can be collected more simply and more reliably than 24-hour urine samples. The usefulness of these two tests has not been adequately evaluated in a large series of patients with Cushing's syndrome. This study prospectively evaluated the accuracy of the dexamethasone and metyrapone tests in determining the cause of Cushing's syndrome in a series of 25 unselected patients. The diagnostic accuracy of these tests was calculated as follows: diagnostic accuracy = true positives and true negatives/study population X 100. Results of this study demonstrated that the metyrapone test was more accurate than the dexamethasone test in differentiating Cushing's disease from adrenocortical neoplasm (diagnostic accuracy, 100 percent versus 81 percent). All patients with Cushing's disease had a normal postmetyrapone 11-deoxycortisol concentration (greater than 10 micrograms/dl), while all patients with adrenocortical neoplasm had a suppressed 11-deoxycortisol concentration (less than 10 micrograms/dl). Thus, this study demonstrates that the metyrapone test is superior to the high-dose dexamethasone test in the differential diagnosis of Cushing's syndrome.

Temporal enhancement of renin-aldosterone blockade by enalapril, an angiotensin-converting enzyme inhibitor.

Interruption of the renin-aldosterone system with angiotensin-converting enzyme inhibitors (CEI) should result in a low aldosterone secretion, but most investigators have measured aldosterone production only indirectly by plasma aldosterone (PA) levels or urinary metabolites. We evaluated the effects of CEI of the aldosterone secretion rate (ASR) and compared them with PA, urinary tetrahydroaldosterone (THA), plasma renin activity (PRA), and electrolyte balance in six normotensive subjects in a metabolic unit during a control period (5 days) and during administration of 10 mg/day enalapril for 28 days. Our results demonstrated that (1) the ASR did not decline until after 1 wk of CEI therapy and this was reflected by a corresponding decline in the urine potassium:sodium ratio, (2) upright PA levels at day 1 declined, but supine PA levels were unchanged, (3) THA excretion remained essentially unchanged and the THA:ASR ratio rose progressively during therapy, (4) PRA rose and was maximal on day 3, but subsequently declined. In conclusion, enalapril-induced hypoaldosteronism required several days to become demonstrable and this was not accurately assessed by PA or THA--possibly due, in part, to altered aldosterone metabolism. The simultaneous decline in both PRA and ASR could be due to a decrease in renin substrate. Caution is therefore warranted when assessing aldosterone secretion indirectly by either PA levels or urinary metabolites during CEI therapy.

The effect of amiloride on the renin-aldosterone system in primary hyperaldosteronism and Bartter's syndrome.

Amiloride is a potassium-sparing diuretic which has been advocated for the treatment of hypokalemic disorders. This agent was prospectively evaluated in hypokalemic patients with either primary hyperaldosteronism (ten patients) or Bartter's syndrome (five patients). Vital signs, electrolytes, and ambulatory hormonal studies were assessed during a control period and treatment period with amiloride therapy at 10 to 40 mg/day over two to 24 weeks. During the treatment period the systolic and diastolic blood pressure fell significantly in primary hyperaldosteronism but remained unchanged in Bartter's syndrome. In summary, amiloride therapy (1) increased plasma potassium in both diseases; (2) increased plasma renin activity (PRA) in primary hyperaldosteronism but decreased PRA in Bartter's syndrome; and (3) increased plasma aldosterone in both diseases. Since potassium is known to suppress renin production and stimulate aldosterone secretion, correction of the hypokalemia in this study probably accounts for the decreased PRA and increased plasma aldosterone observed in Bartter's syndrome. The increase in both PRA and plasma aldosterone in primary hyperaldosteronism, however, may be evidence of either a direct activation of the renin-aldosterone system or, alternatively, may be due to the mild natriuretic effects of amiloride.

Primary empty sella syndrome, ACTH hypersecretion, and normal adrenocortical function. Report of two cases.

Although the primary empty sella syndrome (PESS) is associated with normal endocrine function or subtle pituitary insufficiency, pituitary hormone hypersecretion associated with PESS has also been recognized. ACTH hypersecretion and primary empty sella syndrome have previously been reported in patients with either Cushing's disease or Addison's disease. This report describes two unique patients with ACTH hypersecretion, primary empty sella syndrome, and normal cortisol dynamics. The investigators speculate that this association may have resulted from infarction of hyperplastic adenohypophyseal corticotrophes due to production of an ACTH peptide with reduced biologic activity. These two cases emphasize that primary empty sella syndrome may be associated with ACTH hypersecretion and normal adrenocortical function.

Amiloride in Bartter's syndrome.

Hypokalemia in Bartter's syndrome (BS) is often difficult to correct despite all measures. Amiloride is a new potassium-sparing diuretic that blocks sodium channels in distal renal tubular cells, independent of aldosterone. Four patients with BS were studied, in an outpatient clinic, while on amiloride therapy (10 to 40 mg/day). Before receiving amiloride the patients were treated with combinations of prostaglandin synthetase inhibitors, potassium-sparing diuretics, and potassium supplements. After a baseline observation period, the potassium-sparing diuretics were discontinued and amiloride therapy was instituted. Cumulative mean plasma potassium level rose after amiloride (0.5 mEq/l; P less than 0.05). The mean plasma potassium levels in three of the patients rose and one of these patients eventually became normokalemic. There were very few adverse reactions and none could be attributed to amiloride alone. Amiloride may be a useful and safe drug for the treatment of the hypokalemia of BS.

Amiloride in primary hyperaldosteronism.

Amiloride is a potassium-sparing diuretic used in spontaneous and diuretic-induced hypokalemia. The effect of amiloride was studied prospectively in 12 patients with primary hyperaldosteronism. Four patients had unilateral adrenal adenomas and eight had bilateral adrenal hyperplasia. All patients were hypertensive and their mean plasma potassium levels were low. Amiloride, 10 to 40 mg daily, was given for 6 mo. Mean plasma potassium levels rose (0.96 mEq/l, P less than 0.001) and remained normal throughout the study without potassium supplementation. Mean blood pressure was lowered by amiloride (22/10 mm Hg, P less than 0.001) but normotension required concomitant antihypertensive therapy in most patients. No significant adverse clinical or laboratory experiences could be directly attributed to amiloride therapy. There was no correlation between the response to therapy and the plasma aldosterone levels, aldosterone secretion rate, or presence of a unilateral adrenal adenoma. Our study demonstrates the efficacy of amiloride in the correction of hypokalemia and amelioration of hypertension in primary hyperaldosteronism.