Withdrawal Syndrome In Patients Research Articles

Treatment of alcoholic liver disease

With advances in our understanding of the pathophysiology of alcoholic liver disease, pharmacological treatments of some of the basic disease processes are now in sight. The most notable development has been the introduction of propylthiouracil for the treatment of alcoholic hepatitis. In a recent trial the mortality rate of patients treated with this drug was 62% lower than that of a control group. Its beneficial effects may stem not from its anti-thyroid properties but rather from other actions such as free radical scavenging. Corticosteroids now appear to have no place in the treatment of alcoholic liver disease. Anabolic steroids, however, show promise, though longer term trials are required before this can be confirmed. Colchicine, too, has been reported to improve survival in patients with established cirrhosis. More experience is required with this and other anti-inflammatory and anti-fibrogenic drugs. β Adrenergic blocking drugs, such as propranolol, reduce portal venous pressure. In a trial among patients with alcoholic cirrhosis who had oesophageal varices, 39% of those receiving propranolol had not experienced a haemorrhage by 2 years compared with 74% in the control group. The mortality rates at this time were 28% and 49% respectively. Results of treatment once the first haemorrhage has occurred are less impressive. Treatment of the alcohol withdrawal syndrome in patients with liver disease is often problematic. The dose of any sedative should be reduced to 25–50% of the usual dose and sedatives should be avoided in patients who are encephalopathic. Once the patient has recovered from the acute illness, abstinence from alcohol remains the single most important factor that determines long term survival.

Efficacy and safety of verapamil in patients with angina pectoris after 1 year of continuous, high-dose therapy

The long-term efficacy and safety of high-dose verapamil therapy (480 mg/day) was assessed in 26 patients with chronic stable angina pectoris during a 3-phase protocol: Phase 1—an initial, 6-week placebo-controlled, double-blind crossover assessment; Phase 2—an open label, 1-year follow-up; and Phase 3—a final drug withdrawal and rechallenge 10-week study. Three patients withdrew during Phase 2(1 had hepatitis and 2 underwent coronary bypass surgery). Adverse effects during Phase 2 were mild, consisting of constipation (6 patients) and prolongation of the P-R interval (5 patients); however, no patient required alteration of the 480 mg/day dosage. At the end of Phase 2, 10 patients underwent the Phase 3 study, commencing with a 2-week period in which verapamil was either tapered gradually or abruptly discontinued. This was followed by an 8-week double-blind, placebo-controlled crossover rechallenge study with verapamil. The clinical and exercise responses to verapamil compared with placebo were similar during the Phase 3 protocol and the initial Phase 1 study (treadmill time increased by 55% and anginal attacks per week decreased by 63% during Phase 3, compared with a 28% increase and a 42% decrease, respectively, during Phase 1, p = not significant [NS]). Withdrawal of verapamil produced a similar return of anginal symptoms whether the drug was abruptly discontinued or its administration tapered. No patient had unstable angina pectoris or acute myocardial infarction.These investigations demonstrate that verapamil is safe and effective when evaluated after 1 year of continuous therapy using a dosage of 480 mg/day. There is no evidence of drug tachyphylaxis, nor does verapamil appear to cause an abrupt withdrawal syndrome in patients with chronic stable angina pectoris.