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Background: Fluctuations in lipid and lipoprotein levels are encountered quite often in hyperlipidemic patients. We examined the possibility that lipid and lipoprotein levels fluctuate due to the different effects of estrogen and progestogen in postmenopausal hyperlipidemic women receiving combined hormonal replacement therapy., Methods: In an open-label study conducted during 3 consecutive hormonal cycles (3 months), levels of fasting total cholesterol, triglycerides, and low (LDLC)- and high-density lipoprotein cholesterol (HDLC) were determined in 36 postmenopausal hyperlipidemic women on day 13 of conjugated equine estrogen (1.25 mg/d) therapy and on day 25 after 12 days of receiving estrogen plus medroxyprogesterone acetate (5 mg/d)., Results: While receiving estrogen and combined therapies, means +/- SD total cholesterol levels increased from 6.50 +/- 0.97 mmol/L (251 +/- 37 mg/dL) to 6.88 +/- 1.42 mmol/L (266 +/- 54 mg/dL) (P<.001); LDLC levels, from 4.05 +/- 1.14 mmol/L (156 +/- 44 mg/dL) to 4.62 +/- 1.36 mmol/L (178 +/- 52 mg/dL) (P<.001). Mean +/- SD HDLC cholesterol levels decreased from 1.44 +/- 0.32 mmol/L (55 +/- 12 mg/dL) to 1.29 +/- 0.28 mmol/L (50 +/- 10 mg/dL) (P<.001); triglyceride levels, from 2.23 +/- 1.03 mmol/L (197 +/- 91 mg/dL) to 2.06 +/- 1.04 mmol/L (182 +/- 92 mg/dL) (P<.001)., Conclusions: Hyperlipidemic postmenopausal women receiving combined sequential estrogen and progestogen replacement therapy demonstrate very significant fluctuations in their lipid and lipoprotein levels. These fluctuations depend on the hormonal phase, ie, estrogen alone or combined with progestogen.

Calcium-entry blockers have proven efficacy in a variety of cardiovascular disorders. The effects of these agents on ionic calcium fluxes and, thus, on smooth-muscle contraction suggest that several noncardiac conditions involving smooth-muscle dysfunction may be managed with calcium antagonists. Beneficial therapeutic results have been reported in various forms of hypertension and Raynaud's phenomenon. The results of preliminary studies in treating pulmonary hypertension, cerebral arterial spasm, migraine headache, esophageal motility disorders, and myometrial hypercontractile states are encouraging. Carefully designed, large-scale and long-term clinical trials are needed to establish the therapeutic value of calcium-entry blockers in these disorders.

In three cases of attempted suicide by massive digoxin ingestion, a therapeutic attempt was undertaken to shorten the duration of toxicity of the drug by accelerating the removal of the glycoside from the body. Early administration of intravenous (IV) furosemide and fluids appeared to increase digoxin excretion in one case, which resulted in a substantially shortened digoxin half-time of eight hours. In two cases this therapy, initiated after a delay of 12 and eight hours was ineffective. The half-times were 51 and 43 hours, respectively. At an early preequilibrium stage, higher serum-tissue ratios of digoxin are present; thus, greater amounts of free digoxin are available for glomerular filtration and excretion. The prompt treatment by IV furosemide may be beneficial in the management of massive digitalis overdose.

Cholestatic jaundice developed in four patients after the administration of prajmalium bitartrate. The clinical, histologic, ultrastructural, and immunologic findings were determined. In all patients, the clinical and morphologic features indicated idiosyncrasy. Two antibodies distributed in a granular pattern along the bile canaliculi were detected by immunofluorescence in all patients. In one patient, autoimmune markers were found in the serum, and in two instances, the migration-inhibition factor assay against the offending drug was found to be positive. The data support the concept that immunologic processes may participate in the production of the cholestatic syndrome.

The effect of low doses (25 mg three times a day) of captopril was evaluated in 16 patients with mild to moderate essential hypertension, previously uncontrolled by hydrochlorothiazide. After a no-treatment period, mean eight-hour seated diastolic blood pressure (SDBP, mm Hg) was 103 +/- 5 on placebo, 95 +/- 8 after a single dose of captopril, 96 +/- 4 after two weeks of captopril alone, and 90 +/- 6 after its combination with hydrochlorothiazide. Though nine patients had at least a 10% fall in SDBP after the initial dose of captopril, only three had a comparable fall after two weeks; after captopril and hydrochlorothiazide, however, 12 patients had such a response. Captopril decreased mean angiotensin-converting enzyme activity and plasma aldosterone, though to a lesser extent with continued therapy. Because its side effects appear dose related, low doses of captopril combined with a diuretic are effective and may be better tolerated.