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The long term course of alcohol dependence often includes one or several relapses, which can be divided into low (< 5 standard drinks = lapse, slip) and high intake of alcohol with loss of control (relapse). The biological etiology of relapse is derived from different phenomena such as alcohol craving, psychosocial reasons, development of withdrawal symptoms, different primary psychiatric diseases and "addiction memory". Moreover, the metabolism of alcohol itself substantially contributes to alcohol dependence. For about 100 years different definitions for subgroups of alcohol dependence have been described, of which the Lesch typology is internationally acknowledged, especially for medical treatment. This typology differentiates between four types of alcohol dependent patients in which prevention and treatment of relapse should be specific to the primary psychiatric disease of the patient and to alcohol related disabilities. The aim is a long term improvement of sobriety rates of alcohol dependent patients as well as quality of life and life expectancy.

Even though alcohol dependence is not often found in the elderly, alcohol consumption and alcohol abuse are both common. As the elderly also often take medication on a regular basis, this group is at particularly high risk for problems resulting from the concurrent use of these substances. Physical changes as a result of the aging process (e.g. reduction of body water, decrease of hepatic blood flow) and alcohol related diseases can influence the pharmacokinetics and pharmacodynamics of both ethanol as well as other drugs. Alcohol dehydrogenase (ADH), acetaldehydede hydrogenase (ALDH) and cytochrome P450 2E1 are the enzymes responsible for the metabolism of ethanol. These enzymes are also the sites of direct pharmacological interaction between ethanol and other drugs, however, altered effects of medication can also be caused by ethanol adding to or reducing the drug's effect. Although some of these effects result from heavy use of alcohol, others can also occur with moderate use. Interactions have most frequently been described for analgetics, psychopharmacologically active drugs, antihistamines, anticoagulants antihypertensive drugs and antibiotics.

Background: Hepatitis G (GBV-C/HGV) is an RNA-virus belonging to the flavivirus family and is capable of inducing hepatitis in rare cases. Its importance as a co-factor in the pathogenesis of liver disease needs to be clarified., Aims: To determine the prevalence of HGV in chronic alcoholics with and without liver cirrhosis., Patients: 86 alcoholics, 44 with liver cirrhosis and 42 without liver cirrhosis, were investigated; 93 healthy individuals served as controls., Methods: Serum was tested for GBV-C/HGV-RNA by reverse-transcription polymerase chain reaction (RT-PCR) and for anti-E2, a marker of resolved GBV-C/HGV infection, by ELISA. GBV-C/HGV-RNA positive samples were sequenced and the GBV-C/HGV subtype determined., Results: Eight out of 86 (9.3%) alcoholics were GBV-C/HGV-RNA positive, as compared to 2 out of 93 (2.2%) healthy controls (n. s.). Twenty-one (24.4%) alcoholics had anti-E2 in serum, whereas this antibody was found in 12 (12.9%) healthy persons only (n. s.). However, significantly more alcoholic patients (33.7%) than healthy controls (15.1%) had past or present contact with GBV-C/HGV (p = 0.006). 11.4% of alcoholic patients with liver cirrhosis and 7.1% of alcoholic patients without liver cirrhosis showed GBV-C/HGV-RNA. 34.1% of alcoholic patients with liver cirrhosis and 16.6% of alcoholic patients without liver cirrhosis had anti-E2. Among the 44 patients with liver cirrhosis, 8 out of 11 (72.7%) patients with variceal bleeding, but only 11 of 33 patients without bleeding had contact with GBV-C/HGV (p = 0.05). Seven out of 8 GBV-C/HGV-RNA positive alcoholics had genotype 2a, 1 had type 1a of GBV-C/HGV., Conclusion: Alcoholic patients have a significantly higher contact rate with GBV-C/HGV as compared to healthy controls. Alcoholics with liver cirrhosis tend to be more frequently infected than alcoholic patients without liver cirrhosis. A previous variceal bleeding episode is significantly associated with GBV-C/HGV infection.

The role of drug abuse as a risk factor for cerebrovascular events has been underestimated, particularly in patients with juvenile stroke. The drug most often associated with acute cerebrovascular events is cocaine. After cocaine hydrochloride abuse intracerebral hemorrhages or subarachnoid hemorrhages--predominantly caused by ruptured aneurysms or arteriovenous malformations--are by far the most frequently observed cerebrovascular complications, whereas on abuse with the alkaloidal form ("crack") intracranial hemorrhages and ischemic strokes are encountered with equal frequency. In most cases, the time interval between drug abuse and the cerebrovascular event is less than 3 hours. Several pathophysiological mechanisms are discussed as serving as triggers for the cerebrovascular event, either alone or in combination. No specific antidote to cocaine is known. Nevertheless drug screening (urine analysis) should be performed immediately to allow optimal management of patients with drug-associated acute cerebrovascular events, especially in cases with juvenile stroke.

Alcoholism is usually understood as ethanolism. There is some evidence that its oxidation product acetaldehyde may condense with endogenous amines to form tetrahydroisoquinoline (TIQ) and - tetrahydro-beta-carboline (THBC) alkaloids which ultimately might be responsible for addiction. In most animal experiments pure ethanol solutions were fed, but chronic alcoholics prefer normal alcoholic beverages, and it is widely ignored that all these beverages without exception also contain methanol. Its metabolite formaldehyde is a much more potent reaction partner for TIQ and THBC formation than acetaldehyde. As our findings in chronic alcoholics proved that these persons in contrast to healthy subjects are able to oxidize methanol despite high ethanol levels, there must be a continuous leakage of formaldehyde. And it seems possible that methanol plays a more significant role in the pathophysiology and possibly the etiology of chronic alcoholism than ethanol.

Arterial hypertension is the most important risk factor in all types of stroke. The significance of alcohol in the pathogenesis of stroke is less well defined. Chronic alcoholism leads to an elevation of blood pressure. Thus, the association between alcohol and stroke might be the blood pressure effect of alcohol. However, some studies have shown a significant influence of alcohol on the incidence of stroke--especially of intracerebral haemorrhage and subarachnoid haemorrhage--even after adjustment for blood pressure. Many possible pathomechanisms are discussed. Alcohol inhibits aggregation of thrombocytes, and chronic alcohol abuse may induce thrombocytopenia, which could lead to a haemorrhagic stroke. Alcohol withdrawal leads to rebound thrombocytosis. Acute alcohol ingestion induces a decrease in fibrinolytic activity and an increase in factor VIII activity, which enhances the thrombotic potential. Additionally, alcohol increases plasma osmolarity, erythrocyte aggregability, haematocrit and blood viscosity, and decreases deformability of erythrocytes. The effects of alcohol on cerebral blood flow are still under debate; there is a deterioration in autoregulation of cerebral blood flow anyway. In animal studies alcohol induced dose-dependent vasospasm of the cerebral blood vessels, which could be a possible pathomechanism in ischaemic, as well as in haemorrhagic stroke. Chronic alcoholism is the most common cause of secondary non-ischaemic cardiomyopathy, which can lead to cerebral embolism via rhythm disorders or intracardiac thrombus formation.(ABSTRACT TRUNCATED AT 250 WORDS)

Patients resistant to therapy with lithium or lithium plus tricyclic antidepressants were included in our study. They had shown no curtailment of depression, no lessening of the depth of depression nor any improvement in the manic symptoms. Therapeutic medication with lithium, lithium plus tricyclics, neuroleptics and/or tranquilizer had been tried out for at last three years and the episodes of the manic-depressive illness were documented over this period. The diagnosis in the case of these patients was manic-depressive illness, type bipolar I or II. We report one case covering three years of treatment showing the following trend: Psychopathology did not change after quitting anciliary medication and tricyclic antidepressants while lithium intake was continued. A low-dose MAO inhibitor (tranylcypromine 13.7 mg/die) in addition to lithium led to shortened and less pronounced depressive and manic episodes and more prolonged normorhythmic periods. This trend emerged with even greater clarity during the course of the study.