Proudfoot A T, Wright N
Br Med J. 1970 Sep 5;3(5722):557-8. doi: 10.1136/bmj.3.5722.557.
Of 41 cases of acute paracetamol poisoning one died of gastrointestinal haemorrhage and acute massive necrosis of the liver, three became jaundiced, and 13 others had biochemical evidence of hepatocellular damage. Liver damage is a toxic effect which is present in most patients who ingest more than 15 g. of paracetamol. One patient with liver damage survived renal failure due to acute tubular necrosis. It is suggested that the renal lesion was also the result of paracetamol overdosage.Profound hypoglycaemia and metabolic acidosis may also complicate severe poisoning. Plasma levels of para-aminophenol fall rapidly, and procedures currently used to enhance the elimination of the drug cannot be expected to prevent development of hepatic damage.
在41例急性扑热息痛中毒病例中，1例死于胃肠道出血和急性大面积肝坏死，3例出现黄疸，另有13例有肝细胞损伤的生化证据。肝损伤是一种中毒效应，大多数摄入超过15克扑热息痛的患者都会出现这种情况。1例肝损伤患者在急性肾小管坏死导致肾衰竭后存活下来。提示肾脏病变也是扑热息痛过量所致。严重低血糖和代谢性酸中毒也可能使严重中毒复杂化。对氨基酚的血浆水平迅速下降，目前用于促进药物排泄的方法无法预期防止肝损伤的发生。
