Complications and comorbidities

Older patients with long-standing alcoholism are at high risk for development or aggravation of many medical problems, especially liver disease, several cancers, disorders of glucose, fat and uric acid metabolism, osteoporosis, anaemias, congestive heart failure, aspiration pneumonia, and accidental injuries. (7) Control of hypertension and diabetes mellitus is compromised by heavy drinking. Acute doses of alcohol compete with many medications (e.g. warfarin, phenytoin, most benzodiazepines, propanolol) for hepatic drug metabolizing enzymes in the cytochrome P-450 system, which can produce higher than desired drug blood levels, while chronic alcohol dosing induces the cytochrome P-450 system and can lead to more rapid metabolism of the same medications, with resulting lower than desired drug blood levels.(8) Inhibition of hepatic alcohol dehydrogenase by such drugs as chlorpromazine and isoniazid, or inhibition of gastric alcohol dehydrogenase by histamine receptor antagonists (e.g. cimetidine, ranitidine, nizatidine) can reduce alcohol metabolism and lead to higher blood alcohol levels. Alcohol acts in the central nervous system to intensify the depressant effects of opioids and sedative-hypnotic agents. When regular heavy drinking accompanies use of non-steroidal anti-inflammatory drugs, bleeding times may be increased and the risk of gastrointestinal haemorrhage is higher.

Alcohol becomes an increasingly potent neurotoxin with age.(4) Alcohol intoxication and withdrawal can both be more severe in elderly people than in younger adults. Cognition is often impaired in recently detoxified alcoholics of all ages, but deficits are greater and more long lasting in older patients, with improvements noted as long as 5 years after initiation of abstinence. In non-amnesic chronic alcoholics, alcohol neurotoxicity is suggested by a number of deficits in neuropsychological performance and by brain imaging studies demonstrating atrophy of both grey and white matter in the cerebral cortex, especially in frontal areas. (9,19 Cortical changes occur in older alcoholic individuals beginning in about the fifth decade, and are over and above the changes associated with normal ageing. Dementia associated with chronic alcoholism accounts for as many as 20 to 25 per cent of cases in dementia cohorts. It lacks the dense amnesia found in Wernicke-Korsakoff syndrome and may be distinguishable from Alzheimer's disease when the following features predominate: history of heavy alcohol use, presence of peripheral polyneuropathy and/or gait ataxia, sparing of naming ability (e.g. absence of dysnomia or anomia), presence of other alcohol-related disorders (e.g. cirrhosis), evidence on MRI of cerebellar atrophy (especially of the vermis), and evidence after a period of abstinence of either stabilization or improvement in cognitive functioning or cerebral atrophy seen on MRI/l!!)

Depressive symptoms are widespread in newly admitted, recently drinking alcoholics of all ages, including elderly people, and are much more common than comorbid depressive disorders, which occurred in 12 per cent of one large hospital admitted series of elderly patients. (19 Depression in recently drinking patients resolves in a majority of cases during the first 3 to 4 weeks of abstinence without specific antidepressant therapy, and probably represents an alcohol-induced mood disorder. Continuing depression after 3 weeks of sobriety suggests a comorbid mood disorder. Functional impairment caused by heavy drinking ranges from mild to very severe, presenting in extreme cases as senile squalor or Diogenes syndrome. The major comorbid substance use disorder in elderly alcoholics is tobacco dependence, with current smoking reported in 50 to 70 per cent of cases, four to five times the rate of tobacco dependence found in the general elderly population.

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