Horney J T, Galambos J T
Gastroenterology. 1977 Oct;73(4 Pt 1):639-45.
Within 5 to 14 days of onset of grade 3 or 4 coma, liver biopsies were obtained in 14 of 15 consecutive patients who recovered from fulminant hepatitis. In 9 patients, follow-up biopsy was obtained 6 to 60 months after acute hepatitis and autopsy was performed in 2 patients who died in 4 months from complications of hepatitis (aplastic anemia) or of corticosteroid therapy (sepsis). During fulminant illness the biopsy findings were: multilobular necrosis in 4 patients, confluent (bridging) necrosis in 9, and only portal inflammation in 1. The duration or the grade of coma did not correlate with the severity of necrosis on the biopsy. Follow-up biopsy showed development of chronic (active) hepatitis in 3 of 9 patients (with cirrhosis in one of these). Chronic liver disease was not found in the two autopsies. If fulminant hepatitis is the result of vigorous cell-mediated immune attack on hepatocytes, then this process cannot always eradicate chronic hepatitis B surface antigenemia, nor can it always prevent the development of chronic (active) hepatitis or cirrhosis.
在15例从暴发性肝炎中康复的连续患者中,有14例在3或4级昏迷发作后的5至14天内接受了肝活检。9例患者在急性肝炎发作后的6至60个月接受了随访活检,2例因肝炎并发症(再生障碍性贫血)或皮质类固醇治疗并发症(败血症)在4个月内死亡的患者接受了尸检。在暴发性疾病期间,活检结果如下:4例为多小叶坏死,9例为融合性(桥接)坏死,1例仅为门管区炎症。昏迷的持续时间或分级与活检时坏死的严重程度无关。随访活检显示,9例患者中有3例发展为慢性(活动性)肝炎(其中1例伴有肝硬化)。在两次尸检中均未发现慢性肝病。如果暴发性肝炎是对肝细胞的强烈细胞介导免疫攻击的结果,那么这个过程并不总能消除慢性乙型肝炎表面抗原血症,也不能总是预防慢性(活动性)肝炎或肝硬化的发展。