Aminotransferases poisons

Isoniazid Adults S mg/kg (300 mg) Children 1 0-1 S mg/kg (300 mg) Asymptomatic elevation of aminotransferases, clinical hepatitis, fatal hepatitis, peripheral neurotoxicity, CNS system effects, lupus-like syndrome, hypersensitivity, monoamine poisoning, diarrhea LFT monthly in patients who have preexisting liver disease or who develop abnormal liver function that does not require discontinuation of drug Dosage adjustments may be necessary in patients receiving anticonvulsants or warfarin... 

Hepatic Effects. Two days after a man was splashed with a phenol-water solution over his face, chest wall, hand, and both arms, serum bilirubin increased 2-fold (Horch et al. 1994). After 5 days, serum bilirubin returned to normal. An enlarged and tender liver and increased liver enzymes in the serum were reported in a case of chronic phenol poisoning (Merliss 1972). Lactate dehydrogenase was about 2-fold greater than normal, aspartate aminotransferase was about 21-fold greater than normal, and alanine aminotransferase was about 100-fold greater than normal. The man worked in a laboratory for 13.5 years where he distilled phenol several times a day. During the process, heavy odors were detectable, phenol was often spilled on his clothes, and he noted skin irritation. 

Hepatomegaly, jaundice, and altered liver function tests have been reported in accidental poisonings with DME An outbreak of toxic liver disease was associated with DME exposure at a fabric coating factory. Thirty-six of 58 workers had elevations of either aspartate aminotransferase or alanine aminotransferase. Serological tests excluded known infectious causes of hepatitis in all but two cases. After modification of work practices and removal of the most severely affected from exposure, improvement in liver enzyme abnormalities and symptoms occurred in most patients. Medical surveillance of the working population for 14 months revealed no further cases of toxic liver... 

Acute inorganic lead poisoning is uncommon today. It usually results from industrial inhalation of large quantities of lead oxide fumes or, in small children, from ingestion of a large oral dose of lead in the form of lead-based paint chips small objects, eg, toys coated or fabricated from lead or contaminated food or drink. The onset of severe symptoms usually requires several days or weeks of recurrent exposure and manifests as signs and symptoms of encephalopathy or colic. Evidence of hemolytic anemia (or anemia with basophilic stippling if exposure has been subacute), and elevated hepatic aminotransferases may be present. 

Pattern of serum alanine aminotransferase (ALT) and bilirubin in the plasma, following poisoning with the toxic mushroom Amanita phalloides. 

Milk thistle has been used to treat acute and chronic viral hepatitis, alcoholic liver disease, and toxin-induced liver injury in human patients. Milk thistle has most often been studied in the treatment of alcoholic hepatitis and cirrhosis. In both of these disorders, outcomes have been mixed and reports include significant reductions in markers of liver dysfunction and in mortality, as well as no effect. In acute viral hepatitis, studies have generally involved small sample sizes and have shown mixed outcomes of improved liver function (eg, aminotransferase values, bilirubin, prothrombin time) or no effect. Studies in chronic viral hepatitis and toxin-induced injury have also been of small size but have reported mostly favorable results. Parenteral silybin is marketed and used in Europe as an antidote in Amanitaphalloides mushroom poisoning, based on favorable outcomes reported in case-control studies. 

Massano G, Ciocatto E, Rosabianca C, et al. Striking aminotransferase rise after chlorhexidine self-poisoning [letter]. Lancet 1982 i 289. 

AAPCC-TESS American Association of Poison Control Centers-Toxic Exposure Surveillance System ALT Alanine aminotransferase ARDS Adult respiratory distress syndrome AST Aspartate aminotransferase BUN Blood urea nitrogen ECG Electrocardiogram INR International normalization ratio NAPQI A-acetyl-/>-benzoquinone-imine PPPA Poison Prevention Packaging Act (of 1970)... 

Paracetamol poisoning provides a useful human model to compare the effectiveness of plasma GST with aminotransferase measurements because in such patients there is often a wide spectrum of the severity of liver damage encountered. In addition, damage to the liver initially occurs in the centrilobular hepatocytes, where phase I drug metabolizing enzymes produce the toxic metabolite (J3). 

Besides this main effect, which leads to suffocation, carbon monoxide also exerts other effects. They are, however, of a lower importance in a comparison with the effect on haemoglobin. It is possible to consider effects on myoglobin and on the other tetrapyrol substances. Many enzymes containing trace elements modify their activity by the action of carbon monoxide [41]. An increase of the activity of aspartate-aminotransferase and of the lactate concentration can be used for the indication of acute poisoning [42]. 

A young man mistakenly consumed tea made from an unknown amount of arnica flower and leaf. Two hours later he experienced myalgia, headache, chills, and developed hyperthermia, tachycardia, hypotension, and elevated serum levels of creatinine, aspartate aminotransferase, and alanine aminotransferase (Topliff and Grande 2000). Stomach cramping followed by death was reported in a man who had consumed 70 g of arnica tincture (Blaschek et al. 2002). Poisoning with arnica has been reported to cause death due to circulatory paralysis with secondary respiratory arrest (product and dose not specified) (Hansel et al. 1993). 

Watson and his colleagues examined 50 autopsy reports of children poisoned with Impila [17]. Upon presentation to hospital, 80 % of patients showed a disturbed level of consciousness (confusion, stupor, or coma), and in 52 %, this was associated with convulsions. Other conmum symptoms included abdominal pain, vomiting and diarrhea. Hypoglycemia (blood glucose <2.5 mmol/L) was found in 93 % of cases, metabolic acidosis (serum bicarbonate <19 nunol/L) in 87 %, uremia (elevated blood urea >6.64 mmoI/L) in 60 %, hyperkalemia (serum potassium >5.3 mmol/L) in 63 %, hyponatremia (serum sodium <130 nunoI/L) in 45 %, and leukocytosis (total white cell count >11 x 10 /L) in 80 %. In patients who survived more than 24 h, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactic dehydrogenase (LDH) were elevated up to 5—10 times the normal levels, and the prothrombin time was elevated up to 50 % of upper limit of normal. In all cases documented to date, concomitant jaundice has rarely been observed in the patients with hepatotoxicity, and the progression to death was very rapid. 

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