Weight gain, improvement in metabolic profile, and CD4 count with insulin administration in an AIDS patient.

Malnutrition with muscle wasting, weight loss, and decreased immunogenicity is a hallmark of Acquired Immune Deficiency Syndrome (AIDS). Several anabolic agents have been utilized for retarding or preventing progressive wasting with limited success. However, insulin, with its most effective anabolic properties, has not been tried in an attempt to prevent or reverse cachexia in AIDS or any other wasting disorders. We report here the effect of using subcutaneous (s.c.) daily administration of insulin 0.3 U/kg (BW) for 6 months in a subject with AIDS. We noted a marked weight gain, improvement in metabolic profiles, that is, lowering of triglyceride, liver enzymes, glycohemoglobin concentrations, as well as 24-hour urinary excretion of urea nitrogen, protein, and creatinine suggestive of positive energy balance. Simultaneously, a marked rise in CD4 counts and an improvement in the thyroid hormone profile were also noted. A deterioration in these parameters occurred during the period of insulin withdrawal following completion of the study protocol. Resumption of insulin administration, on patient's request, once again resulted in the marked improvement similar to that noted during the study period. No adverse effects, including hypoglycemic episodes, were noted during either phase of insulin administration. The possibility that insulin administration may improve the wasting associated with AIDS may warrant further evaluation.

Lovastatin use and muscle damage in healthy volunteers undergoing eccentric muscle exercise.

We did a double-blind, placebo-controlled crossover study of 10 healthy young men taking no medications to determine if ingesting lovastatin is associated with more severe muscle damage after exercise. Five men in the first group took 40 mg of lovastatin daily for 30 days while those in the second group took an identical-appearing placebo. Each volunteer then walked downhill on a -14-degree incline on a treadmill at 3 km per hour for an hour. After a 2-week rest, the subjects were crossed over. Serial serum creatine kinase activity was measured immediately before and 8, 24, 48, 72, 120, and 144 hours after each treadmill session. With each subject serving as his own control, peak mean serum creatine kinase activity (/+- SEM) following treadmill after lovastatin therapy was similar to that following placebo (168.4 +/- 25.8 U per liter versus 146.7 +/- 14.7 U per liter, respectively [P = .9]). With an alpha value of .05, we had greater than a 99% chance of detecting a difference in the rise of serum creatine kinase activity of 200 U per liter between groups. Our data suggest that lovastatin is not an independent risk factor for developing exercise-induced muscle damage using this model of exercise in our study population.