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Fifty-one patients with urgent hypertension were treated in the emergency department with either oral nifedipine or oral clonidine in a randomized double-blind prospective study. Nifedipine was administered as a single dose of 20 mg. Clonidine was administered as an initial dose of 0.1 mg with hourly doses of 0.1 mg. Nifedipine was successful in reducing diastolic blood pressure in 83% of the patients within 45 minutes and in 96% of the patients within two hours, with a mean reduction in systolic blood pressure of 47 mm Hg and diastolic blood pressure of 29 mm Hg. Thirty percent of those who initially responded to nifedipine experienced a subsequent increase in diastolic blood pressure to pretreatment levels within three hours. Clonidine was successful in reducing diastolic blood pressure in 79% of the patients within four hours, with a mean reduction in systolic blood pressure of 51 mm Hg and diastolic blood pressure of 30 mm Hg. Our results indicate that both nifedipine and clonidine are safe and effective in the treatment of urgent hypertension. Nifedipine had a much more rapid onset of action with a greater initial success rate, and it was free from the sedative side effects of clonidine. We believe that either nifedipine or clonidine may be used as first-line therapy in the treatment of urgent hypertension.

Patients with active Schistosoma mansoni infection attending a medical clinic in an endemic area, 100 miles from Cairo, were asked to participate in this study. Ninety-six patients are reported, 72 of whom presented with musculoskeletal complaints. Nine of these presented with an enthesitis alone; 16 had an inflammatory peripheral polyarthritis alone; the remaining 47 were suffering from the combination of both an arthritis and an enthesitis. Alpha-1-acid glycoprotein was significantly lowered in those patients with musculoskeletal manifestations.

1. Adjuvant-induced arthritis in rats is accompanied by a loss of activity of the drug-metabolizing enzyme system and a decrease in hepatic cytochrome P-450. 2. Arthritic rats have normal serum and liver cholesterol concentrations. 3. The rate of biogenesis of cholesterol in vivo and in vitro from either [(14)C]acetate or [(14)C]mevalonate in arthritic rats was the same as or greater than that found in control rats. 4. Treatment of rats with carbon disulphide (1ml/kg) resulted in a loss of drug-metabolizing-enzyme activity and increased cholesterol biogenesis. 5. The activity of cholesterol 7alpha-hydroxylase in adjuvant-induced arthritic rats did not differ significantly from that in control rats. 6. Rats fed with cholestyramine had an elevated hepatic cholesterol 7alpha-hydroxylase activity, but neither the concentration of cytochrome P-450 nor the activity of the drug-hydroxylating enzyme, aminopyrine demethylase, was affected. 7. The relationships between drug hydroxylation and cholesterol metabolism are discussed.

1. Non-saponifiable lipid from the livers of rats treated with 1-dodecylimidazole contained an unidentified compound that was not present in the livers from untreated animals. 2. Treated rats had lower serum cholesterol concentrations than control rats. 3. 1-Dodecylimidazole, when added to rat liver slices, inhibited the incorporation of [1-(14)C]acetate and [2-(14)C]mevalonate into digitonin-precipitable sterols and resulted in the accumulation of a labelled compound, which was chromatographically identical with the unknown compound described in 1 above. 4. Rats treated with 1-dodecylimidazole incorporated less [(14)C]mevalonate into liver digitonin-precipitable sterols than untreated animals and accumulated the unknown compound as a labelled intermediate. 5. The unknown intermediate had the same chromatographic properties, n.m.r. and mass spectra as authentic 2,3-oxidosqualene. 6. The identity of the intermediate as 2,3-oxidosqualene was further established by showing that it was incorporated into sterols by rat liver homogenates under anaerobic conditions. In addition, incubation of [(14)C]squalene with rat liver homogenates resulted in trapping of the radioactivity by the added intermediate. 7. It is suggested that the hypocholesterolaemic activity of 1-dodecylimidazole results in part from the inhibition of cholesterol biosynthesis at the level of 2,3-oxidosqualene sterol cyclase.