Subcutaneous enoxaparin for outpatient anticoagulation therapy in a patient with an aortic valve replacement.

Low-molecular-weight heparins have been administered for a variety of clinical conditions. A patient with a mechanical aortic valve replacement patient underwent elective transurethral prostatectomy. Anticoagulation was managed with unfractionated heparin immediately preoperatively and postoperatively. Warfarin was begun on postoperative day 1. The patient had a prolonged hospitalization due to subtherapeutic international normalized ratios (INR) despite warfarin administration. Because he intended to leave the hospital against medical advice before therapeutic INR was achieved, enoxaparin 1 mg/kg subcutaneously every 12 hours was prescribed to provide anticoagulation, facilitating discharge and improving the patient's quality of life. Enoxaparin was associated with an approximate saving of $4500 over warfarin. The only adverse event reported was bruising at the injection site.

Drug-use review program for concurrent histamine H2-receptor antagonist-sucralfate therapy.

The effect of drug-use review on concomitant histamine H2-receptor antagonist-sucralfate therapy at a 600-bed, university-affiliated Veterans Affairs medical center was studied. In an effort to curtail the concomitant use of H2-antagonist plus sucralfate therapy, the department of pharmacy, in conjunction with the gastroenterology service, developed and introduced criteria for the appropriate use of combination therapy. The extent of prescribing of concomitant histamine H2-receptor antagonist-sucralfate therapy before and after implementation of criteria-based guidelines and the appropriateness of current H2-receptor antagonist-sucralfate combination therapy, based on the guidelines, were assessed. The effectiveness of the intervention process was evaluated, and cost savings associated with intervention were calculated. After intervention, the number of treatment courses of histamine H2-receptor antagonist-sucralfate combination therapy decreased by 30%. However, of the 109 evaluable postintervention combination treatment courses, only one complied with both the indication and the duration of treatment criteria. This review of prescribing patterns and the implementation of criteria-based guidelines proved an effective means of reducing inappropriate combination therapy and resulted in annual cost savings of $25,000.

Influence of antihistamine pretreatment on vancomycin-induced red-man syndrome.

Twelve adult male volunteers participated in a double-blind study to determine the effect of pretreatment with histamine and/or histamine2 receptor antagonists on the incidence and severity of vancomycin-induced "red-man syndrome." Subjects received hydroxyzine, 50 mg, ranitidine, 300 mg, hydroxyzine plus ranitidine, or placebo at weekly intervals 2 h before a l-h infusion of vancomycin, 1,000 mg. The extent of erythema was evaluated by burn chart and pruritus was assessed by each subject using a rank scale; symptoms were thus classified a priori as mild, moderate, or severe and their summation determined a global severity score for red-man syndrome. There was no significant intrasubject variation between area under the concentration-time curves for histamine and vancomycin (P greater than .05). Pretreatment with hydroxyzine alone provided significant protection against vancomycin-induced erythema and pruritus (P less than .05) whereas the effect of ranitidine did not differ significantly from placebo. The combination of hydroxyzine and ranitidine offered no advantage over hydroxyzine alone. Similar results were observed for global severity scores. Thus in normal volunteers prior administration of a histamine antagonist (hydroxyzine) provided significant protection against vancomycin-induced red-man syndrome compared to that afforded by placebo. There was no significant benefit from the histamine antagonist alone or by its addition to a histamine antagonist.

Misoprostol: a prostaglandin E1 analogue.

The pharmacology, pharmacokinetics, clinical efficacy, contraindications and precautions, adverse effects, dosage, and cost of misoprostol are reviewed. Misoprostol is a synthetic analogue of natural prostaglandin E1. It produces a dose-related inhibition of gastric acid and pepsin secretion and enhances mucosal resistance to injury. Misoprostol is extensively absorbed from the stomach and undergoes rapid de-esterification to its biologically active metabolite, misoprostol acid. The average absorption after an oral dose is 88%; peak plasma concentrations of misoprostol acid are achieved in less than 30 minutes. Clinical trials have demonstrated ulcer healing rates of approximately 60-80% in patients with duodenal ulcers who received misoprostol 800 micrograms daily for four weeks. Misoprostol was generally no more efficacious than conventional therapy with the H2-receptor antagonists cimetidine and ranitidine. The healing rate observed for gastric ulcers was less than that observed for duodenal ulcers. In trials involving healthy volunteers and patients with arthritis receiving aspirin, naproxen, tolmetin, ibuprofen, or piroxicam, misoprostol was consistently superior to placebo, cimetidine, and sucralfate in the prevention of nonsteroidal anti-inflammatory drug (NSAID)-induced gastropathy. The majority of these studies have been of short duration; however, long-term studies (up to three months) have corroborated superiority over placebo. Misoprostol is an abortifacient and is contraindicated in pregnant women and women of childbearing potential not using effective contraception. The most common adverse effect of misoprostol therapy is diarrhea, which is often mild and self-limiting and can be minimized by administration of misoprostol after meals and at bedtime. The cost (based on retail price) of four weeks of therapy with misoprostol is comparable to that of other antiulcer agents. Misoprostol has been shown to be an effective agent for the prevention of NSAID-induced gastric ulcers. However, there is no evidence that it offers any clinical advantage over H2-receptor antagonists for the treatment of gastric or duodenal ulcer disease.