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Abstract：
Hepatitis C virus (HCV) infection is the most common blood-borne chronic infection in the United States. Chronic lymphocytic sialadenitis and sicca syndrome have been reported in chronic HCV infection. Up to 55% of these patients may have xerostomia; the mechanisms of the xerostomia and salivary gland (SG) hypofunction remain controversial. The objectives of this project are to establish if xerostomia associates with SG and HCV infection and to characterize the structural changes in SG and saliva composition. Eighteen HCV-infected patients with xerostomia were evaluated for SG dysfunction; 6 of these patients (patients 1-6) were further evaluated for SG histopathological changes and changes in saliva composition. The techniques used include clinical and laboratory assessment, SG ultrasonography, histological evaluation, sialochemical and proteomics analysis, and RNA in situ hybridization. All the HCV patients had low saliva flow, chronic sialadenitis, and SG fibrosis and lacked Sjögren syndrome (SS) characteristic autoantibodies. Further evaluation of a subgroup of 6 HCV patients (patients 1-6) demonstrated diffuse lymphocytic infiltrates that are predominantly CD8+ T cells with a significant increase in the number of inflammatory cells. Alcian Blue/periodic acid-Schiff staining showed significant changes in the ratio and intensity of the acinar secretory units of the HCV patients\' minor SG. The submandibular glands showed significant ultrasonographic abnormalities in the parenchyma relative to the parotid glands. Significant changes were also observed in the concentration of sodium and mucin 5b. Although no significant correlation was observed between the lymphocytic infiltrates and the years of HCV chronic infection, a positive correlation was observed between HCV RNA-positive epithelial cells and the years of HCV infection. Consistent with the low saliva flow and xerostomia, patients showed changes in several markers of SG acinar and ductal function. Changes in the composition of the saliva suggest that HCV infection can cause xerostomia by mechanisms distinct from SS.
摘要：
丙型肝炎病毒（HCV）感染是美国最常见的血源性慢性感染。慢性淋巴细胞性唾液腺炎和干燥综合征已在慢性HCV感染中报道。这些患者中多达55％可能患有口干症；口干症和唾液腺（SG）功能减退的机制仍存在争议。该项目的目的是确定口干症是否与SG和HCV感染相关，并表征SG和唾液成分的结构变化。评估了18例HCV感染的口干症患者的SG功能障碍；进一步评估了其中6例（患者1-6）的SG组织病理学变化和唾液组成变化。使用的技术包括临床和实验室评估，SG超声检查,组织学评估，唾液化学和蛋白质组学分析，和RNA原位杂交。所有的HCV患者唾液流量都很低,慢性唾液腺炎,和SG纤维化，缺乏干燥综合征（SS）特征性自身抗体。对6名HCV患者（患者1-6）的亚组的进一步评估表明，弥漫性淋巴细胞浸润主要是CD8T细胞，炎性细胞数量显着增加。AlcianBlue/高碘酸-Schiff染色显示HCV患者的腺泡分泌单位的比例和强度发生了显着变化。相对于腮腺，下颌下腺在实质上显示出明显的超声异常。钠和粘蛋白5b的浓度也观察到显著变化。尽管在淋巴细胞浸润和HCV慢性感染的年份之间没有观察到显着的相关性，HCVRNA阳性上皮细胞与HCV感染年限呈正相关.与低唾液流量和口干症一致，患者显示SG腺泡和导管功能的几种标志物发生变化。唾液组成的变化表明HCV感染可通过不同于SS的机制引起口干症。
