Treatment of acute, non-traumatic pain using a combination of diclofenac-cholestyramine, uridine triphosphate, cytidine monophosphate, and hydroxycobalamin.

This randomized, controlled, double-blind clinical study in parallel groups evaluated the safety and efficacy of an oral combination diclofenac-cholestyramine, nucleotides (uridine and cytidine) and vitamin B12 versus the oral combination of nucleotides and vitamin B12 in the treatment of acute, non-traumatic pain. Subjects received twice-daily, 10-day oral administration of diclofenac-cholestyramine + uridine + cytidine + vitamin B12 (Group DN, n=40) or uridine + cytidine + vitamin B12 (Group NB, n=41). The primary study endpoint was the number of subjects with VAS reduction of >30mm after 10 days of treatment. Secondary endpoints included the number of patients with improvement >5 points in the Patient Functionality Questionnaire after 10 days of treatment, and the number of subjects presenting adverse events. Treatment with the combination of diclofenac-cholestyramine, nucleotides and Vitamin B12 resulted in a higher number of subjects with VAS score reductions >30mm after 10 days of treatment (87.5% subjects) than in the control group administered nucleotides and Vitamin B12 (51.23% of subjects), (p>0.0006). A significantly higher number of subjects in the DN group (80%) had a score reduction of >5 points in the Patient Functionality Questionnaire at after 10 days of treatment compared to Group NB (29.3%), (p<0.001). The number of subjects presenting AEs did not vary significantly between treatment groups (p=0.587). The combination of diclofenac-cholestyramine with uridine, cytidine and vitamin B12 was well-tolerated over a 10-day treatment period. The combination reduced pain and improved functionality among subjects presenting acute, non-traumatic pain in the lower back, hips, and neck.

[Combined therapy with cholestyramine and HMG-CoA reductase inhibitors in secondary prevention of coronary disease]. / Terapia combinada de colestiramina e inibidores da HMG-CoA redutase na prevenção secundária da Doença coronária.

PURPOSE: To evaluate lipid profile changes associated with cholestyramine addition in hypercholesterolemic patients with established coronary heart disease under treatment with HMG-CoA reductase inhibitors that had not achieved the ideal value of LDL-cholesterol. METHODS: Twenty patients with coronary heart disease, (12 submitted to coronary artery bypass grafts, 3 to coronary angioplasty and 5 maintained under clinical management) with mean age of 60.78 years old, who were under hypolipemic diet and were medicated with lovastatin 20 mg/d or simvastatin 10 mg/d, received cholestyramine, doses ranging from 8 to 16 g/day during 8 weeks, aiming to reduce LDL-cholesterol to values less than 100 mg/dL. RESULTS: There was a significant reduction of total cholesterol, from initial mean value of 239.52 mg/dL to final mean value of 199.00 mg/dL, with a mean reduction of 16.92%. The mean value of LDL-cholesterol was also reduced significantly from 172.73 mg/dL to 118.26 mg/dL, with a mean reduction of 31.53%. Mean triglyceridemia increased, still within the normal reference values, from 145.05 mg/dL to 162.00 mg/dL, and the mean difference was 11.69%. There was a significant increase of HDL-cholesterol fraction from an initial mean value of 38.00 mg/dL to a final mean value of 48.21 mg/dL, mean difference of 26.87%. Side effects were not frequent, and did not interfere in the duration of the study. CONCLUSION: The association of cholestyramine to HMG-CoA reductase inhibitors, both in low doses, in patients with primary hypercholesterolemia and high coronary risk is a good therapeutic option that can reach benefits on the lipid profile similar to those obtained when these drugs are used in association or separately in higher doses.

Use of cholestyramine in the treatment of children with familial combined hyperlipidemia.

We studied the effectiveness of and compliance with the use of cholestyramine in children with heterozygous familial hypercholesterolemia (FH) and familial combined hyperlipidemia (FCHL). During a 10-year period, 673 children (aged 10.5 +/- 4.0 years) were referred for evaluation of hyperlipidemia, of whom 87 (36 with FH; 51 with FCHL) were treated with cholestyramine (8 to 24 gm/day). In both groups, total cholesterol, low-density lipoprotein (LDL)-cholesterol, and apolipoprotein B levels were significantly reduced after cholestyramine use. In those with FH, plasma LDL-cholesterol levels decreased from 258 +/- 35 mg/dl (6.67 +/- 0.90 mmol/L) to 190 +/- 31 mg/dl (4.91 +/- 0.80 mmol/L); in those with FCHL, LDL-cholesterol levels dropped from 207 +/- 40 mg/dl (5.35 +/- 1.03 mmol/L) to 141 +/- 35 mg/dl (3.64 +/- 0.90 mmol/L). High-density lipoprotein-cholesterol levels were not significantly changed after cholestyramine use in either group. In the FCHL group, plasma triglyceride levels increased significantly from 81 +/- 35 mg/dl (0.92 +/- 0.40 mmol/L) to 134 +/- 42 mg/dl (1.52 +/- 0.48 mmol/L). Seven patients were lost to follow-up; 18 discontinued the medication within 1 month. Of the remaining 62 children, 59 had a good response to the drug. Of the 62 patients, 52 discontinued the medication after 21.9 +/- 10 months. Adverse effects included foul taste (73%), nausea with bloating (18%), and constipation. Cholestyramine is effective in reducing LDL-cholesterol levels in children with inherited hyperlipidemia, but the majority of children will not comply with its long-term use.

[The efficacy of cholestyramine as a hypocholesterolemic agent and its tolerance in a Mexican population]. / Eficacia como agente hipocolesterolemiante y tolerancia de la colestiramina en población mexicana.

The tolerance and efficacy of cholestyramine (12-16 gr/day) was evaluated in 19 patients with primary type-IIa hyperlipoproteinemia. All patients were on an isocaloric low-cholesterol diet that began at least one month before entry, and was continued during the eight weeks of the study. Cholestyramine significantly (p less than 0.001) lowered the plasma levels of cholesterol and of low density lipoprotein cholesterol from means of 288 +/- 46 mg/dl to 244 +/- 44 mg/dl and from 221 +/- 50 mg/dl to 171 +/- 46 mg/dl respectively. These were reductions of 15 and 22%. The magnitude of response to cholestyramine was unrelated to age, sex, cause of the hypercholesterolemia (familial or polygenic) or basal cholesterol levels. The drug was well tolerated. Only one patient was excluded because gastrointestinal discomfort. Because of its safety and efficacy, cholestyramine can be recommended as a first choice drug in the treatment of hypercholesterolemia.