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食用掺假食用油导致的中毒性流行综合征中的肝损伤(西班牙,1981年)

Hepatic injury in the toxic epidemic syndrome caused by ingestion of adulterated cooking oil (Spain, 1981).

作者信息

Solis-Herruzo J A, Castellano G, Colina F, Morillas J D, Muñoz-Yagüe M T, Coca M C, Jelavic D

出版信息

Hepatology. 1984 Jan-Feb;4(1):131-9. doi: 10.1002/hep.1840040123.

Abstract

We describe the clinico-pathological characteristics of hepatic injury associated with the toxic-epidemic syndrome caused by the consumption of adulterated rapeseed oil. Of 842 toxic-epidemic syndrome patients admitted to our hospital between May, 1981, and January, 1982, 24.1% showed signs of liver involvement which was more frequent in women and in the fourth decade of life. No statistical significance was found in relation to alcohol consumption, treatment with potentially hepatotoxic antibiotics, or adult respiratory distress syndrome. Most (91.6%) patients with hepatic injury were asymptomatic; jaundice or abdominal pain was rarely noted. One patient died of acute liver failure following Budd-Chiari syndrome. Serum gamma-glutamyl transpeptidase activity was raised in all cases, alkaline phosphatase in 94.6%, and less frequently lactate dehydrogenase (80%), SGPT (84.7%), and SGOT (76%). Serum total bilirubin was usually normal (89.2%). The histologic lesion was similar to drug-induced cholestatic hepatitis. Lamellar inclusions, canalicular injury, giant mitochondria, and hyperplasia of the smooth endoplasmic reticulum were seen by electron microscopy. Ultrastructural signs of cholestasis were common (78.9%). The pathogenesis of this lesion is unknown; however, because of similarities with chlorpromazine-induced cholestatic hepatitis, we suggest that a combination of hypersensitivity and intrinsic hepatoxicity is a possible mechanism.

摘要

我们描述了食用掺假菜籽油所致中毒性流行综合征相关肝损伤的临床病理特征。在1981年5月至1982年1月期间入住我院的842例中毒性流行综合征患者中,24.1%出现肝脏受累迹象,女性及40岁左右人群中更为常见。在饮酒、使用可能具有肝毒性的抗生素治疗或成人呼吸窘迫综合征方面未发现统计学意义。大多数(91.6%)肝损伤患者无症状;很少有黄疸或腹痛症状。1例患者在布-加综合征后死于急性肝衰竭。所有病例血清γ-谷氨酰转肽酶活性均升高,94.6%的患者碱性磷酸酶升高,乳酸脱氢酶(80%)、谷丙转氨酶(84.7%)和谷草转氨酶(76%)升高的频率较低。血清总胆红素通常正常(89.2%)。组织学病变与药物性胆汁淤积性肝炎相似。电镜下可见板层小体、胆小管损伤、巨大线粒体和平滑内质网增生。胆汁淤积的超微结构征象常见(78.9%)。该病变的发病机制尚不清楚;然而,由于与氯丙嗪所致胆汁淤积性肝炎相似,我们认为超敏反应和内在肝毒性的联合作用可能是一种机制。

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