Physical Complications of Substance Abuse: What the Psychiatrist Needs to Know

Michael F Baigent


Curr Opin Psychiatry. 2003;16(3) 

In This Article


Adding to the literature in this area are a number of studies that examined the harms related to alcohol in terms of mortality, end organ pathology and dose effects.

In their prospective study, Kristenson et al.[7*] found that those men who drink more than 40 g alcohol/day and who have a raised -glutamyltransferase in the top decentile due to alcohol may be at increased risk for premature death. Similarly, a representative sample of over 4000 US men over the age of 50 years was followed up over 6 years.[8*] 'Heavy drinkers' (i.e. those who consumed five or more drinks per day) at the outset were twice as likely to die by the end of the study than were those who drank one or two drinks per day. Interestingly, 'heavy drinking' was not associated with an increase in adverse health outcomes such as angina, cancer, heart failure, diabetes, myocardial infarction, lung disease or stroke. A similar lack of associations was found by Kristenson et al..[7*]

Even moderate alcohol intake (20-40 g/day) can cause right upper quadrant pain, which is a common presentation among patients with liver disease. It may be the result of fatty liver or alcohol hepatitis, both of which are reversible. Cirrhosis occurs in 10-20% of chronic alcohol dependent patients (consuming >120-180 g alcohol/day) and is not reversible.[9] Chronic alcohol consumption, along with hepatitis C and hepatitis B, are risk factors for hepatocellular carcinoma. One mediating factor for this may be low levels of hepatic vitamin A, which is a consequence of chronic alcohol consumption. High rates of hepatitis C are found among patients with alcoholic liver disease. The rates of cirrhosis in these patients are doubled if the daily alcohol consumption exceeds 40 g.[10]

Alcohol abuse is also associated with an increased risk for cancers of the gastrointestinal system, once again by reducing available vitamin A and encouraging tobacco products to promote cancerous change.[9] One study[11] detected that heavy drinkers (mean alcohol intake 117 g/day, mean duration 22 years) were significantly more likely to have precancerous adenomas than were control individuals, but there appeared to be no control for cigarette smoking. Smoking is a strong confounding variable in research of cancer and cardiovascular illnesses in alcoholic persons because of its over-representation in this group. A very large retrospective study based on the Swedish Inpatient Register[12] established a statistically significant 40% elevated risk for pancreatic cancer among alcoholic persons. When the attributable risk was calculated for smoking, alcohol was unlikely to play a causal role.

Hypertension in patients is due to alcohol in 5-10% of cases. This may mediate the increased risk for cerebrovascular accident. Cardiac arrhythmia can occur because of alcohol and is most often atrial fibrillation.[9]

Heavy alcohol intake is associated with impaired left ventricular functioning but the research suggests that one need not advise complete abstinence. The Framingham Heart Study[13**] offered an opportunity to investigate the effects of differing levels of self-reported alcohol consumption in a prospective observational design over a number of years (the original cohort were recruited in 1948 and then additional subjects were recruited in 1971). The risk for cardiac failure was not increased for any level of consumption in men or women; in men it was lower at all levels of alcohol intake than it was in nondrinkers.

In a study of patients with alcoholic cardiomyopathy, those who achieved abstinence and those who reduced their intake to 60 g/day or less had similar improvement in their cardiac functioning.[14**] Those who drank more than 80 g/day exhibited deterioration in their cardiac functioning during the first year and accounted for all 10 of the deaths over the 4 years of follow up. As the authors pointed out, relying on self-reports of alcohol intake can lead to inaccuracies, but the tendency is toward under-reporting.[15]

Up to 75% of heavy alcohol users may have bone marrow suppression, which is typically due to the direct alcohol effects and related folate deficiency. Anaemia can be further contributed to by iron deficiency. Long-term leukopaenia and thrombocytopaenia are markers of chronic alcoholism.[9] Alcohol alters cellular immunity in such a way that it increases the risk for respiratory infection among those with alcohol abuse.[16*]

Amenorrhoea, dysfunctional uterine bleeding and infertility have all been described.[9] Hypocalcaemia is often found in alcohol-dependent patients. The mechanism proposed is through magnesium depletion and faulty parathormone release and resistance.[17] Of patients with alcohol-related hepatic cirrhosis 50-100% have associated glomerulonephropathy, which tends to remain quiescent clinically.[18]

Deficiencies in thiamine and other B-group vitamins are the cause of peripheral neuropathy. Myopathy can occur suddenly following a binge or may evolve slowly.[9] Alcohol should always be considered in presentations with neurological and odd neuropsychiatric presentations. Marchiafava-Bignami disease is a rare and fatal central demyelination of the corpus callosum that is usually associated with red wine consumption.[19*] It can present with gradual psychomotor retardation and negativism, progressing to catatonia and fits.

White matter is preferentially affected in chronic alcoholism. Using advanced magnetic resonance imaging techniques, Pfefferbaum and Sullivan[20**] examined the white matter of alcoholic women for microstructural changes. The women had greater disruption in the white matter of the genu and centrum semiovale of the corpus callosum than did control individuals. There were no macrostructural changes visible on routine magnetic resonance imaging, leading the authors to speculate that they may be early or potentially reversible changes.

There is real sex bias in research into the effects of alcohol,[21**] which is evident in the research presented in the present review. Women take less time than do men to progress from the start of problem drinking to adverse consequences. Women are more vulnerable to cognitive impairment and alcohol-induced liver disease than are men. Intervention in women clearly needs to be early to prevent adverse health consequences.[21**]


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