01771nas a2200205   4500008004100000245010600041210007100147260001900218300001200237490000600249520113400255653001301389653002001402653001501422653001301437653001401450100002701464700002901491856004501520       2015                        eng d00aIsoniazid induced Acute Metabolic Acidosis and Neurotoxicity–A Case Report and Review of Literature0 aIsoniazid induced Acute Metabolic Acidosis and Neurotoxicity–A C  c16th July 2015  a121-1230 v13 a<p class="rtejustify">Isoniazid (INH) is a crucial drug in the prevention and treatment of tuberculosis. INH is commonly known to cause derangements in liver function tests and peripheral neuropathy due to pyridoxine deficiency in slow acetylators. However, in toxic doses it is known to cause severe neurologic manifestations and acute metabolic acidosis. INH toxicity is characterized by the clinical triad of repetitive seizures unresponsive to the usual anticonvulsants, metabolic acidosis with a high anion gap and coma. Hence, the diagnosis of INH overdose should be considered in any patient who presents to Emergency medical services (EMS) with the triad. Though accidental overdose of anti-tuberculosis drugs have been reported in children and adults, acute toxicity is rare. When recognized, intravenous pyridoxine and correction of acidosis with sodium bicarbonate and supportive treatment is effective. The condition is easily treated with intravenous pyridoxine but if not treated in time could prove fatal. Unlike other poisonings, serum INH levels do not co-relate with either symptomatology or liver injury.</p>
10aAcidosis10aINH (Isoniazid)10aPyridoxine10aSeizures10aToxicity.1 aMirgh, Sumeet, Prakash1 aSorabjee, Jehangir, Soli  uhttp://ptbreports.org/article/2015/1/3-0