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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
|
| pubmed:dateCreated |
1978-12-2
|
| pubmed:abstractText |
Alcoholic patients frequently have evidence of nutritional deficiency the consequences of which may be seen in all systems of the body. Alcoholism is theoretically a completely preventable disorder which requires more attention by the general public, practising physicians and research workers. Rehabilitation of the established alcoholic will sometimes be limited by failure to modify behaviour or because of nutritionally induced brain damage but we are beginning to understand some of the mechanisms by which malnutrition evolves (Figure 2). Better methods must be developed to limit alcohol-induced tissue injury in patients whose drinking cannot be controlled. The final mechanisms of liver injury remain to be established. Cirrhosis may be induced in animals ingesting a good diet but this does not ensure adequate delivery and utilization of nutrients at the subcellular level. Cirrhosis takes a long time to evolve and the natural history, including longitudinal nutritional profiles in man, has not been established. Therefore, although normal liver morphology is sometimes seen in alcoholics with gross stigmata of malnutrition suggesting that factors other than malnutrition are important, it may be that critical nutrients have not been deficient for long enough in these individuals or severe depletion has been intermittent. Whether or not malnutrition is of decisive importance in the toxicity of alcoholic liver injury in man, adequate replacement is essential for protection and repair of liver cells. Established daily minimal requirements are not adequate for patients with active liver disease. Hepatocyte injury reduces the capacity of this major storage site and causes release of vitamins (co-enzymes) into the circulation in the form of holoenzymes. Liver damage reduces the conversion of nutrients into their metabolically useful forms required for catabolic processes and to meet increased needs for DNA/RNA synthesis necessary for repair of damaged cells and to replace necrotic cells. The choice and route of therapy must take account of the patient's metabolic needs and their absorptive defects. The effects of alcohol and maternal undernutrition on the fetus/neonate may cause intra-uterine death or varying degrees of brain damage, thus limiting the potential of the next generation.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jul
|
| pubmed:issn |
0300-595X
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
7
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
405-28
|
| pubmed:dateRevised |
2004-11-17
|
| pubmed:meshHeading |
pubmed-meshheading:688685-Alcoholism,
pubmed-meshheading:688685-Cations, Divalent,
pubmed-meshheading:688685-Enzymes,
pubmed-meshheading:688685-Fatty Liver, Alcoholic,
pubmed-meshheading:688685-Female,
pubmed-meshheading:688685-Hepatitis, Alcoholic,
pubmed-meshheading:688685-Humans,
pubmed-meshheading:688685-Liver Cirrhosis, Alcoholic,
pubmed-meshheading:688685-Magnesium,
pubmed-meshheading:688685-Nervous System Diseases,
pubmed-meshheading:688685-Nutrition Disorders,
pubmed-meshheading:688685-Pregnancy,
pubmed-meshheading:688685-Vitamins
|
| pubmed:year |
1978
|
| pubmed:articleTitle |
Alcohol and nutrition.
|
| pubmed:publicationType |
Journal Article
|