Comparison of the efficacy of Questran Light, a new formulation of cholestyramine powder, to regular Questran in maintaining lowered plasma cholesterol levels.

Sixty-one men with known hypercholesterolemia (plasma cholesterol greater than 265 mg/dl), most of whom were previous participants in the Coronary Primary Prevention Trial of the U.S. Lipid Research Clinic Program, were chosen to take part in this study to test the effectiveness of a new low-calorie (Questran Light) cholestyramine formulation against the proven effectiveness of the currently marketed formulation Questran in maintaining lowered plasma cholesterol levels. The study recorded changes in fasting plasma lipids, total cholesterol, high-density lipoprotein cholesterol, triglycerides, and calculated low-density lipoprotein cholesterol. After establishing baseline lipid/lipoprotein levels in a 3-week period during which all participants received the currently marketed formulation, the men were randomized into 2 groups, 1 group (n = 31) taking the new Questran Light formulation of 4 g of cholestyramine in 5 g of powder per pack, while the other group (n = 30) continued to take the marketed Questran formulation of 4 g of cholestyramine in 9 g of powder per pack. Each group consumed a total of 24 g/day of cholestyramine in 2 divided doses. At the end of the maintenance phase of the study there were no statistically significant mean changes in percentage from baseline to end-point lipid/lipoprotein levels within either group, nor were there any significant differences between the Questran Light group or the currently marketed Questran formulation group. The new low-calorie cholestyramine formulation appears to be equally as effective in maintaining lowered plasma cholesterol levels as the currently marketed formulation.

Sensory/mixability preference evaluation of cholestyramine powder formulations.

This double-blind, crossover trial compared the sensory and product preparation characteristics of two cholestyramine powder preparations. The study involved 100 healthy volunteers, aged 22-65 (mean 42 years). Questran, a currently marketed product containing sucrose as a sweetener, was compared with Questran Light, a new formulation substituting aspartame for 90 percent of the sucrose. Comparisons were conducted with the two products mixed in water and orange juice. The subjects expressed a significant overall preference for the new formulation mixed in either water (77 percent) or orange juice (80 percent) (p less than 0.01 in both comparisons). Subjects expressed an overwhelming preference for the old product (99 percent) with respect to ease of preparation, although the ratings of the new product were generally neutral rather than negative. The new product is somewhat more difficult to prepare compared with the old cholestyramine preparation, but offers significantly increased patient acceptance based on sensory evaluations.

Platelet aggregation. II. Adenyl cyclase, prostaglandin E1, and calcium.

PIP: In exploration of the proposal that prostaglandin E1 (PGE1) inhibits platelet aggregation via stimulation of adenyl cyclase, the temporal relationship of adenosine cyclic 3',5' monophosphate (cyclic AMP) synthesis and inhibition of ADP-induced aggregation in response to PGE1 was studied. The requirement for calcium in aggregation led to the investigation of the effects of calcium ions on platelet adenyl cyclase activity. PGE1 stimulated the synthesis of cyclic AMP from adenosine-5'-triphosphate-8-14-C by platelet membrane fractions and also increased cyclic AMP synthesis in intact platelets previously incubated for 2 hours with adenosine-14-C. The accumulation of cyclic AMP increased signficiantly at low concentrations of PGE1 and reached a maximum at about 1 mug. Regardless of the inducing agent, calcium ions are an absolute requirement for the aggregation of platelets.^ieng

Platelet aggregation. I. Regulation by cyclic AMP and prostaglandin E1.

PIP: Platelet aggregation plays a major role in thrombogenesis. This study was undertaken to examine the inhibition of platelet aggregation induced by adenosine diphosphate. It is known that cyclic AMP (adenosine monophosphate) and its dibutyryl derivative inhibit platelet aggregation. This study showed that prostaglandin E1 (PGE1) also inhibits platelet aggregation and stimulates cyclic AMP synthesis by stimulation of adenyl cyclose. Caffeine, on the other hand, inhibits platelet phosphodiesterase, and increases cyclic AMP levels. PGA1 and PGF1 alpha can also inhibit platelet aggregation but only at very high concentrations.^ieng