www.meddean.luc.edu/.../ orfpath/images/8-4-1.jpg www.meddean.luc.edu/.../ orfpath/images/8-4-1.jpg
In the United States, the American Association if Poison Control reported that in 1991 there were 2656 cases of hepatotoxicity and 6 deaths. Ingestion of 1.5 g of INH may result in mild toxicity while 6 g to 10 g can result in death. Ingestion of 15 g is almost always fatal if not properly treated.
Mortality rate for acute toxicity is estimated to be ast high as 19 percent, but from regular INH prophylaxsis, the overal death rate is only .001 percent.
The rate in which one's liver acylates INH influences susceptibility to hepatotoxicity. Although slow acylators are more prone to INH induced hepatitis and neuropathy with regular use, acute toxicity seems to have no correlation. Slow acylators are disproportionately represented among African Americans and whites, as high as 60 percent of the population are slow acylators.INH induced hepatitis also seems to be influenced by age and race. 69% of women made up cases of INH induced hepatitis fatalities from 1969 to 1989, and there is an upward trend of hepatitis with increased aging. A recent study suggests that African American and Hispanic women are at the greatest risk.
To avoid heptatotoxicity there are certain precautions doctors may take. First a patients history must be properly documented with any previous adverse reaction to iNH, consuming long term medications, daily alcohol consumption, or current liver disease being closely monitered. Monthly interviews with patients should document symptoms of appetite loss, fatigue, malaise, nausea, vomiting, and abdominal discomfort as signs of hepatic damage or brown urine or icterus of conjunctivae or skin which could be consistent with liver damage.