Abacavir Alcohol

A study in 24 EHV-positive patients found that alcohol 0.7 g/kg increased the AUC of a single 600-mg dose of abacavir by 41%. The half-life of abacavir was increased by 26%, from 1.42 to 1.79 hours. The pharmacokinetics of alcohol were not affected by abacavir. Alcohol may inhibit the formation of abacavir carboxylate resulting in a trend towards increased abacavir glucuronide formation and reduced abacavir metabolism. The increase in exposure to abacavir was not considered to be clinically significant, since it is within levels seen in other studies using higher doses, which demonstrated no additional safety concerns at doses of up to three times the recommended daily dose of abacavir. No special precautions therefore appear to be necessary. 

Abacavir (ABC) 300-mg tab 1 50 mg bid or None None Potentially fatal Alcohol... 

Walsh JS, Reese MJ, Thurmond LM. The metabolic activation of abacavir by human liver cytosol and expressed human alcohol dehydrogenase isozymes. Chem Biol Interact 2002 142(1-2) 135-154. 

Abacavir NRTT1 300 mg bid Testing to rule out the presence of the HI A-B 5701 allele is recommended prior to the initiation of therapy Rash, hypersensitivity reaction, nausea. Possible increase in myocardial infarction Avoid alcohol... 

After oral administration, abacavir is rapidly absorbed, and its bioavailability is about 83%. Food does not interfere with its absorption, and it is metabolized by alcohol dehydrogenase to 5 -carboxylic acid derivative and to S -glucuronidc by glucuronidation. Abacavir does not affect the cytochrome P-450 system. In combination with other antiretroviral drugs, abacavir is indicated for the treatment of HIV-1 infection. It is more potent than other nucleoside reverse transcriptase inhibitors in reducing HIV plasma concentration and increasing CD4+ count. 

In contrast to earlier NRTIs, abacavir is a guanosine analog. It is well absorbed following oral administration (83%), is unaffected by food, and is about 50% bound to plasma proteins. In singledose studies, the elimination half-life was 1.5 hours. Cerebrospinal fluid levels are approximately one-third those of plasma. The drug is metabolized by alcohol dehydrogenase and glucuronosyltransferase to inactive metabolites that are eliminated primarily in the urine. 

Phenols and aliphatic alcohols abacavir, APAP, almokalant, carvedilol, chloramphenicol, epirubicin, l -OH-estragole, 5-OH-rofecoxib, lorazepam, menthol, 4-methylumbelliferone, 1-naphthol (low), 4-nitrophenol, octyl-gallate, R-oxazepam, propranolol, temazepam, ZDV... 

The most important adverse effect of abacavir is a unique and potentially fatal hypersensitivity syndrome. This syndrome is characterized by fever, abdominal pain, and other gastrointestinal complaints a mild maculopapular rash and malaise or fatigue. Respiratory complaints (cough, pharyngitis, dyspnea), musculoskeletal complaints, headache, and paresthesias are reported less commonly. Abacavir is rapidly absorbed and is metabolized to inactivate metabolites by alcohol dehydrogenase and glucuronyl transferase. Alcohol decreases the elimination of abacavir and prolongs its half-life. 

Pharmacokinetics and clinical uses There is good oral bioavailability, with metabolism via alcohol dehydrogenase and glucuronosyltransferase. Abacavir has been used in combinations with zidovudine and lamivudine. 

Heavy alcohol intake may affect the virological response to HAART. Theoretically, alcohol consumption may induce liver enzymes, which interfere with the metabolism of some antivirals such as the protease inhibitors. Alcohol rednces the metabolism of abacavir but this does not appear to be clinically significant. 

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