Alcohol gastrointestinal effects

It is a pure antagonist and chemically related to naloxone. It is more potent than naloxone and because of its longer duration of action, it can be used as maintenance drug for morphine addicts. It has no euphoric effect and no physical dependence liability. It is effective orally. It is also claimed to be beneficial in decreasing craving for alcohol in alcoholics. Side effects include gastrointestinal disturbances and muscular pain. 

Naltrexone Nonselective competitive antagonist of opioid receptors Reduced risk of relapse in individuals with alcoholism Available as an oral or long-action parenteral formulation Toxicity Gastrointestinal effects and liver toxicity will precipitate a withdrawal reaction in individuals physically dependent on opioids and will prevent the analgesic effect of opioids... 

Acamprosate Poorly understood NMDA receptor Reduced risk of relapse in individuals with alcoholism Toxicity Gastrointestinal effects and rash... 

Podophyllum peltatum (may apple, or American mandrake) and P. emodi are. respectively, American and Himalayan plants, widely separated geographically but used in both places as cathartics in folk medicine (94). An alcoholic extract of the rhizome known as podophyllin was included in many pharmacopoeias for its gastrointestinal effects it was included in the U.S.P., for example, from 1820 to 1942. At about this time the beneficial effect of podophyllin, applied topically to benign tumors known as condylomata acuminata, was demonstrated clinically (96). This usage was not inspirational, given that there are records of topical application in the treatment of cancer by the Penobscot Indians of Maine and, subsequently, by various medical practitioners in the United States from the 19th century (96). The crude resinous podophyllin is an irritant and unpleasant mixture unsuited to systemic administration. 

Toxicity and drug interactions Unpleasant taste and gastrointestinal effects may occur, sometimes with dizziness or headache. Some preparations have a high alcohol content, but no dmg interactions have been reported. 

Like most halogenated hydrocarbon pesticides, very little of the chlordecone or its metabolites is excreted via the urine. Because of the apparent enterohepatic recirculation of chlordecone and chlordecone alcohol, most experimental approaches to chlordecone detoxification have focused on limiting reabsorption from the gastrointestinal tract using cholestyramine (Boylan et al. 1978 Cohn et al. 1978), liquid paraffin (Richter et al. 1979), and chlorella and chlorella- derived sporopollenin (Pore 1984). No information was found that indicated that mirex undergoes enterohepatic recirculation, so it is not known whether use of these therapies would be effective in reducing absorption of mirex. 

All of the above examples are acetates of active alcohols. Here, we also mention the acetate of a phenol, namely the provitamin a-tocopheryl acetate, whose natural enantiomer of absolute configuration (2R,47 ,87 ) is shown as 8.73. a-Tocopheryl acetate is a substrate of cholesterol esterase (EC 3.1.1.13), and was hydrolyzed in rats faster than its (2S,47 ,87 )-epimer. In vitro experiments required a-tocopheryl acetate to be dispersed as a micellar pseudosolution, and the nature of the bile salt used to prepare micelles had a profound effect on the substrate stereoselectivity of the reaction [95] [96], Only when the micelle composition approximated that of the gastrointestinal tract did the in vitro substrate stereoselectivity resemble that seen in vivo. 

The main limitation to the clinical use of the MAOIs is due to their interaction with amine-containing foods such as cheeses, red wine, beers (including non-alcoholic beers), fermented and processed meat products, yeast products, soya and some vegetables. Some proprietary medicines such as cold cures contain phenylpropanolamine, ephedrine, etc. and will also interact with MAOIs. Such an interaction (termed the "cheese effect"), is attributed to the dramatic rise in blood pressure due to the sudden release of noradrenaline from peripheral sympathetic terminals, an event due to the displacement of noradrenaline from its mtraneuronal vesicles by the primary amine (usually tyramine). Under normal circumstances, any dietary amines would be metabolized by MAO in the wall of the gastrointestinal tract, in the liver, platelets, etc. The occurrence of hypertensive crises, and occasionally strokes, therefore limited the use of the MAOIs, despite their proven clinical efficacy, to the treatment of atypical depression and occasionally panic disorder. 

Other portions of the gastrointestinal tract can also be injured. Chronic alcohol ingestion is by far the most common cause of chronic pancreatitis in the Western world. In addition to its direct toxic effect on pancreatic acinar cells, alcohol alters pancreatic epithelial permeability and promotes the formation of protein plugs and calcium carbonate-containing stones. 

Alcohol indirectly affects hematopoiesis through metabolic and nutritional effects and may also directly inhibit the proliferation of all cellular elements in bone marrow. The most common hematologic disorder seen in chronic drinkers is mild anemia resulting from alcohol-related folic acid deficiency. Iron deficiency anemia may result from gastrointestinal bleeding. Alcohol has also been implicated as a cause of several hemolytic syndromes, some of which are associated with hyperlipidemia and severe liver disease. 

Nontolerant individuals who consume alcohol in large quantities develop typical effects of acute sedative-hypnotic drug overdose along with the cardiovascular effects previously described (vasodilation, tachycardia) and gastrointestinal irritation. Since tolerance is not absolute, even chronic alcoholics may become severely intoxicated if sufficient alcohol is consumed. 

---