Department of Pathology, Government Medical college, Srinagar, Kashmir, India.
BMC Gastroenterol. 2011 Apr 11;11:36. doi: 10.1186/1471-230X-11-36.
Nodular lymphoid hyperplasia of gastrointestinal tract is a rare disorder, often associated with immunodeficiency syndromes. There are no published reports of its association with Helicobacter pylori infection.
From March 2005 till February 2010, we prospectively followed all patients with diffuse duodenal nodular lymphoid hyperplasia (DDNLH). Patients underwent esophagogastroduodenoscopy with targeted biopsies, colonoscopy, and small bowel video capsule endoscopy. Duodenal nodular lesions were graded from 0 to 4 based on their size and density. Patients were screened for celiac sprue (IgA endomysial antibody), immunoglobulin abnormalities (immunoglobulin levels & serum protein electrophoresis), small intestine bacterial overgrowth (lactulose hydrogen breath test), and Helicobacter pylori infection (rapid urease test, and histological examination of gastric biopsies). Patients infected with Helicobacter pylori received sequential antibiotic therapy and eradication of infection was evaluated by 14C urea breath test. Follow up duodenoscopies with biopsies were performed to ascertain resolution of nodular lesions.
Forty patients (Males 23, females 17; mean age ± 1SD 35.6 ± 14.6 years) with DDNLH were studied. Patients presented with epigastric pain, vomiting, and weight loss. Esophagogastroduodenoscopy showed diffuse nodular lesions (size varying from 2 to 5 mm or more) of varying grades (mean score ± 1SD 2.70 ± 0.84) involving postbulbar duodenum. Video capsule endoscopies revealed nodular disease exclusively limited to duodenum. None of the patients had immunoglobulin deficiency or small intestine bacterial overgrowth or positive IgA endomysial antibodies. All patients were infected with Helicobacter pylori infection. Sequential antibiotic therapy eradicated Helicobacter pylori infection in 26 patients. Follow up duodenoscopies in these patients showed significant reduction of duodenal nodular lesions score (2.69 ± 0.79 to 1.50 ± 1.10; p < 0.001). Nodular lesions showed complete resolution in 5 patients and significant resolution in remaining 21 patients. Patients with resistant Helicobacter pylori infection showed no significant reduction of nodular lesions score (2.71 ± 0.96 to 2.64 ± 1.15; p = 0.58). Nodules partially regressed in score in 2 patients, showed no interval change in 10 patients and progressed in 2 patients.
We report on a large cohort of patients with DDNLH, etiologically related to Helicobacter pylori infection.
胃肠道结节性淋巴组织增生是一种罕见的疾病，常与免疫缺陷综合征有关。目前尚无其与幽门螺杆菌感染相关的报道。
从 2005 年 3 月至 2010 年 2 月，我们前瞻性地随访了所有弥漫性十二指肠结节性淋巴组织增生（DDNLH）患者。患者接受了食管胃十二指肠镜检查，并进行了靶向活检、结肠镜检查和小肠视频胶囊内镜检查。根据其大小和密度，将十二指肠结节病变分为 0 至 4 级。对患者进行了乳糜泻（IgA 肌内膜抗体）、免疫球蛋白异常（免疫球蛋白水平和血清蛋白电泳）、小肠细菌过度生长（乳果糖氢呼气试验）和幽门螺杆菌感染（快速尿素酶试验和胃活检组织学检查）筛查。感染幽门螺杆菌的患者接受了序贯抗生素治疗，并通过 14C 尿素呼气试验评估感染的根除情况。进行了后续的十二指肠镜检查和活检，以确定结节病变的缓解情况。
研究了 40 名患者（男性 23 名，女性 17 名；平均年龄 ± 1SD 35.6 ± 14.6 岁）的 DDNLH。患者表现为上腹痛、呕吐和体重减轻。食管胃十二指肠镜检查显示弥漫性结节病变（大小从 2 至 5 毫米或更大），病变程度不一（平均评分 ± 1SD 2.70 ± 0.84），累及球后十二指肠。视频胶囊内镜检查显示结节病仅局限于十二指肠。所有患者均无免疫球蛋白缺乏或小肠细菌过度生长或 IgA 肌内膜抗体阳性。所有患者均感染了幽门螺杆菌。序贯抗生素治疗根除了 26 名患者的幽门螺杆菌感染。在这些患者中进行的后续十二指肠镜检查显示，十二指肠结节病变评分显著降低（2.69 ± 0.79 至 1.50 ± 1.10；p < 0.001）。5 名患者的结节病变完全缓解，21 名患者的结节病变明显缓解。对幽门螺杆菌感染耐药的患者的结节病变评分无显著降低（2.71 ± 0.96 至 2.64 ± 1.15；p = 0.58）。2 名患者的结节部分消退，10 名患者的结节无间隔变化，2 名患者的结节进展。
我们报告了一大群与幽门螺杆菌感染相关的 DDNLH 患者。
