SMALL INTESTINAL STRUCTURE AND FUNCTION IN PATIENTS INFECTED WITH HUMAN IMMUNODEFICIENCY VIRUS (HIV) - EVIDENCE FOR HIV-INDUCED ENTEROPATHY
SMALL INTESTINAL STRUCTURE AND FUNCTION IN PATIENTS INFECTED WITH HUMAN IMMUNODEFICIENCY VIRUS (HIV) - EVIDENCE FOR HIV-INDUCED ENTEROPATHY
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DOI：
10.7326/0003-4819-111-1-15
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发表时间：
1989-07-01
影响因子：
39.2
通讯作者：
RIECKEN, EO
中科院分区：
文献类型：
--
作者：
ULLRICH, R;ZEITZ, M;RIECKEN, EO
本研究的目的是确定人类免疫缺陷病毒（HIV）感染患者的小肠粘膜结构和功能。采用前瞻性连续样本研究。在一个城市和一所大学的医疗中心的转诊医疗诊所进行了研究，45名HIV感染者（44名男性，1名女性）患有胃肠道疾病。所有患者均行食管胃镜检查。远端十二指肠活检标本进行形态测定和定量酶组织化学技术。进行免疫组织学研究以确定是否存在HIV抗原p24。检查活检和粪便样本中的肠道病原体，并评估患者的吸收不良。吸收不良在HIV感染者中很常见。在15至38例患者的粘膜中发现感染HIV的单核细胞。在25名患者中的15名中，没有检测到乳糖酶（β-葡萄糖苷酶）活性;当可测量时，乳糖酶（β-葡萄糖苷酶）活性在十二指肠刷状缘葡萄糖苷酶活性降低（P < 0.02）。碱性磷酸酶活性正常。与对照组相比，HIV感染者的腺窝深度更大（P < 0.05），绒毛表面积稍小，每个腺窝的核分裂像没有差异。无肠道感染的患者，每个隐窝核分裂像数减少（P < 0.05），隐窝深度正常。在粘膜HIV抗原p24的患者中，有丝分裂像的减少最为明显。有胃肠道症状的HIV感染者表现为轻度小肠萎缩和肠上皮细胞成熟缺陷，这可能完全由HIV引起。额外的肠道感染可以掩盖这种粘膜萎缩。
The study objective was to determine small intestinal mucosal structure and function in patients with human immunodeficiency virus (HIV) infection. A prospective, consecutive sample study was used. Referral-based medical clinics at a municipal and a university medical center studied, forty-five HIV-infected patients (44 men, 1 woman) with gastrointestinal complaints. All patients had esophagogastroduodenoscopy. Distal duodenal biopsy samples were examined morphometrically and by quantitative enzyme histochemical techniques. Immunohistologic studies were done to determine whether HIV antigen p24 was present. Biopsy and stool samples were examined for enteric pathogens and patients were evaluated for malabsorption. Malabsorption was common in HIV-infected patients. In 15 to 38 patients mononuclear cells infected with HIV were found in the mucosa. In 15 of 25 patients there was no detectable lactase (.beta.-gulcosidase) activity in the duodenal brush border; when measurable, lactase (.beta.-glucosidase) activity was decreased (P < 0.02). Alkaline phosphatase activity was normal. Crypt depth was greater (P < 0.05), villous surface area was slightly smaller, and mitotic figures per crypt were not different in HIV-infected patients compared with controls. Patients without additional intestinal infection had a reduced number of mitotic figures per crypt (P < 0.05) and normal crypt depth. The reduction im mitotic figures was most pronounced in patients with mucosal HIV antigen p24. The HIV-infected patients with gastrointestinal symptoms show low-grade small bowel atrophy and a maturational defect in enterocytes, which may be caused exclusively by HIV. An additional intestinal infection can mask this mucosal atrophy.