Ali Hasan, Rizvi Taqi, Niazi Mumtaz, Galan Mark, Pyrsopoulos Nikolaos
Department of Internal Medicine, Rutgers University New Jersey Medical School, Newark, NJ, USA.
Edward Via College of Osteopathic Medicine, Spartanburg, SC, USA.
J Clin Transl Hepatol. 2022 Feb 28;10(1):174-177. doi: 10.14218/JCTH.2020.00178. Epub 2021 May 31.
We present a unique case of biopsy-proven syphilitic hepatitis which presented as severe acute liver injury with significant elevation in aminotransferases and bilirubin, and improved with antibiotic therapy. However, the patient returned weeks after initial presentation with new-onset acute liver injury and had developed hypergammaglobulinemia, positive autoantibody titers, and repeat liver biopsy demonstrating interface hepatitis, supporting a diagnosis of autoimmune hepatitis. He had an otherwise unrevealing etiologic workup, and responded to glucocorticoid therapy. We believe that syphilitic hepatitis and its treatment subsequently triggered an immunogenic response, leading to autoimmune hepatitis. Autoimmune hepatitis is a chronic liver disease thought to manifest as a result of predisposing genetic factors in combination with environmental insults, especially hepatotropic pathogens. Syphilis is a sexually transmitted disease caused by that has been associated with autoimmunity and the development of autoantibodies. We propose that in the setting of syphilitic hepatitis, a molecular mimicry event resulting from structural similarities between and liver antigens, as well as impaired regulatory T-cell function, led to the breakdown of immune tolerance and the onset of autoimmune hepatitis. To support this hypothesis, further molecular analyses and case series are necessary to determine if syphilitic hepatitis and its treatment are risk factors for the onset of autoimmune hepatitis. Autoimmune hepatitis should be considered early as the cause of acute liver injury in susceptible patients with risk factors for the disease, as prompt recognition and appropriate treatment may prevent progression of liver injury and result in improved outcomes.
我们报告了一例经活检证实的梅毒性肝炎的独特病例，该病例表现为严重的急性肝损伤，转氨酶和胆红素显著升高，并通过抗生素治疗得到改善。然而，患者在初次就诊数周后因新发急性肝损伤再次就诊，出现了高球蛋白血症、自身抗体滴度阳性，再次肝活检显示界面性肝炎，支持自身免疫性肝炎的诊断。他的病因学检查结果无其他异常，对糖皮质激素治疗有反应。我们认为梅毒性肝炎及其治疗随后引发了免疫原性反应，导致了自身免疫性肝炎。自身免疫性肝炎是一种慢性肝病，被认为是由遗传易感性因素与环境因素（尤其是嗜肝病原体）共同作用导致的。梅毒是一种由[此处原文缺失病原体名称]引起的性传播疾病，与自身免疫和自身抗体的产生有关。我们提出，在梅毒性肝炎的情况下，由于[此处原文缺失病原体名称]与肝脏抗原之间的结构相似性以及调节性T细胞功能受损导致的分子模拟事件，导致了免疫耐受的破坏和自身免疫性肝炎的发生。为了支持这一假设，需要进一步的分子分析和病例系列研究来确定梅毒性肝炎及其治疗是否是自身免疫性肝炎发病的危险因素。对于有该疾病危险因素的易感患者，应尽早考虑自身免疫性肝炎是急性肝损伤的病因，因为及时识别和适当治疗可能会阻止肝损伤的进展并改善预后。
