Giostra F, Manzin A, Lenzi M, Francesconi R, Solforosi L, Manotti P, Muratori L, Zauli D, Clementi M, Bianchi F B
Cattedra di Medicina Interna I, Università di Bologna, Italy.
J Hepatol. 1996 Oct;25(4):433-8. doi: 10.1016/s0168-8278(96)80201-7.
BACKGROUND/AIMS: The majority of adult patients positive for anti-liver-kidney microsomal antibody are also positive for anti-hepatitis C virus and serum HCV RNA. In these patients the role played by hepatitis C virus infection in the progression of liver damage and its relationship with anti-liver-kidney microsomal antibody are, however, still a matter of debate.
To clarify this point we have compared hepatitis C viremia in sera from 31 hepatitis C virus-related chronic hepatitis patients positive for anti-liver-kidney microsomal antibody with that of 31 patients with hepatitis C virus-related chronic hepatitis without autoantibodies using a newly developed competitive reverse transcription-polymerase chain reaction technique. Reverse transcription-polymerase chain reaction was performed using a synthetic competitor of a length similar to that of wild template (71 bp vs 86 bp).
The results obtained have been related to hepatitis C virus genotypes. Anti-liver-kidney microsomal antibody/anti-HCV positive patients show a median value of hepatitis C virus genome molecules (626829/ml, range 9780-25651424), significantly lower than anti-liver-kidney microsomal antibody negative/anti-HCV positive patients (10158314/ml, range 101822-67429974) (p < 0.001). No hepatitis C virus genotype was significantly associated with anti-liver-kidney microsomal antibody, although a predominance of genotype 1 (subtypes a and b) has been observed in these patients.
Since a low hepatitis C viremia has been observed in anti-liver-kidney microsomal antibody positive patients with disease severity comparable to that of patients without autoantibodies, it is conceivable that in them autoimmune mechanisms may cooperate with viral infection in sustaining disease activity.
背景/目的：大多数抗肝肾微粒体抗体阳性的成年患者抗丙型肝炎病毒及血清HCV RNA也呈阳性。然而，在这些患者中，丙型肝炎病毒感染在肝损伤进展中所起的作用及其与抗肝肾微粒体抗体的关系仍存在争议。
为阐明这一点，我们采用新开发的竞争性逆转录-聚合酶链反应技术，比较了31例抗肝肾微粒体抗体阳性的丙型肝炎病毒相关性慢性肝炎患者血清中的丙型肝炎病毒血症与31例无自身抗体的丙型肝炎病毒相关性慢性肝炎患者的情况。使用与野生模板长度相似的合成竞争物（71 bp对86 bp）进行逆转录-聚合酶链反应。
所得结果与丙型肝炎病毒基因型有关。抗肝肾微粒体抗体/抗HCV阳性患者的丙型肝炎病毒基因组分子中位数（626829/ml，范围9780 - 25651424）显著低于抗肝肾微粒体抗体阴性/抗HCV阳性患者（10158314/ml，范围101822 - 67429974）（p < 0.001）。虽然在这些患者中观察到基因型1（a和b亚型）占优势，但没有丙型肝炎病毒基因型与抗肝肾微粒体抗体显著相关。
由于在抗肝肾微粒体抗体阳性且疾病严重程度与无自身抗体患者相当的患者中观察到低丙型肝炎病毒血症，因此可以设想，在他们当中自身免疫机制可能与病毒感染协同维持疾病活动。
