Kaspar Matthew B, Sterling Richard K
Department of Internal Medicine , Virginia Commonwealth University Medical Center , Richmond, Virginia , USA.
Department of Internal Medicine, Virginia Commonwealth University Medical Center, Richmond, Virginia, USA; Section of Hepatology, Virginia Commonwealth University Medical Center, Richmond, Virginia, USA; Division of Infectious Disease, Virginia Commonwealth University Medical Center, Richmond, Virginia, USA.
BMJ Open Gastroenterol. 2016 Mar 2;3(1):e000072. doi: 10.1136/bmjgast-2015-000072. eCollection 2016.
Hyperbilirubinaemia (HB) is common in HIV and hepatitis C virus (HIV-HCV) co-infected patients and poses a unique challenge in management as it may be due to medications such as the protease inhibitors (PIs) or to hepatic dysfunction. There are no data on the relationship of HB to liver histology and PI use in this population. Clinicians caring for these patients are faced with the difficult task of determining whether increasing serum bilirubin is due to drug effects or progression of liver disease.
To address this gap in knowledge, we performed a retrospective analysis of 344 consecutive HIV-HCV co-infected patients undergoing liver biopsy to identify factors associated with HB. Demographic, clinical, laboratory data were collected. Advanced fibrosis was defined as bridging fibrosis or cirrhosis. Those with hepatitis B virus, hepatic decompensation or hepatocellular carcinoma were excluded.
The prevalence of HB (range 1.3-9.4) was 33% and more common in those on a PI (46%) than those who were not (10%; p≤0.001) and mostly in those on indinavir (40%) or atazanavir (46%). Of the patients on these PIs, HB was not associated with fibrosis grade, demographics, or other clinical variables. Conversely, in those not on a PI, HB was associated with fibrosis grade (p≤0.0001) after adjusting for other clinical and demographic variables.
In the setting of indinavir or atazanavir use, HB is common and unrelated to underlying disease severity and the medications can be continued safely. Conversely, HB in HIV-HCV co-infected patients not on a PI is due to their underlying liver disease and suggests these patients require closer monitoring.
高胆红素血症（HB）在人类免疫缺陷病毒（HIV）与丙型肝炎病毒（HCV）合并感染的患者中很常见，在治疗方面带来了独特的挑战，因为它可能是由蛋白酶抑制剂（PI）等药物引起的，也可能是由于肝功能障碍。目前尚无关于该人群中HB与肝脏组织学及PI使用之间关系的数据。照顾这些患者的临床医生面临着一项艰巨的任务，即确定血清胆红素升高是由药物作用还是肝病进展所致。
为了填补这一知识空白，我们对344例连续接受肝活检的HIV-HCV合并感染患者进行了回顾性分析，以确定与HB相关的因素。收集了人口统计学、临床和实验室数据。重度纤维化定义为桥接纤维化或肝硬化。排除了患有乙型肝炎病毒、肝失代偿或肝细胞癌的患者。
HB的患病率（范围为1.3 - 9.4）为33%，服用PI的患者中更常见（46%），而未服用PI的患者中则为10%（p≤0.001），且主要发生在服用茚地那韦（40%）或阿扎那韦（46%）的患者中。在服用这些PI的患者中，HB与纤维化分级、人口统计学或其他临床变量无关。相反，在未服用PI的患者中，在调整了其他临床和人口统计学变量后，HB与纤维化分级相关（p≤0.0001）。
在使用茚地那韦或阿扎那韦的情况下，HB很常见且与潜在疾病严重程度无关，这些药物可以安全地继续使用。相反，未服用PI的HIV-HCV合并感染患者中的HB是由其潜在的肝脏疾病引起的，这表明这些患者需要更密切的监测。
