Should a lower treatment line be used when treating XXXX @entity4968 in @entity1 with chronic alcoholism?: a case for.

@entity1 @entity167 @entity4313 @entity2041 @entity898 @entity4968 @entity26483 @entity33309 @entity1443 @entity1445 @entity5321
A lower threshold for treatment of @entity1443 ( @entity1443 ) @entity4968 has been advocated in chronic heavy users of @entity167 , based originally on animal studies indicating that chronic @entity167 ingestion increased hepatotoxicity. This was attributed to increased production of the toxic metabolite, @entity33309 , by @entity5321 induction. The clinical evidence for increased risk is limited to four retrospective studies with potential for referral and reporting bias and conflicting results. No study has specifically addressed the issue of the treatment threshold for acute @entity1443 @entity1445 in chronic @entity167 users. However, animal studies in multiple species have consistently shown a lower dose of @entity1443 is required to produce hepatotoxicity after chronic @entity167 use. The knowledge of potential mechanisms has expanded to include effects of other @entity4313 , such as @entity26483 , induction of CYP enzymes other than @entity5321 and @entity2041 depletion. There are no convincing reasons or data to suggest these findings do not apply to @entity1 . However, further @entity1 toxicokinetic and clinical research is required to quantify the extent of the interaction. Arguments about treating @entity1445 should not be confused with those about whether there is an @entity167 - @entity1443 interaction at therapeutic doses. Halving the threshold dose/concentration for treatment is a conservative educated guess that has been widely adopted. In @entity1445 , the potential benefits of treatment at this lower threshold clearly outweigh the minimal risks of @entity898 .
