Gastric reactive lymphoid hyperplasia

　　(I) Etiology

　　The etiology of gastric reactive lymphoid hyperplasia is not yet clear. Some people believe it is similar to intestinal lymph node hyperplasia, while most scholars believe that it is gradually developed into gastric reactive lymphoid hyperplasia under the continuous stimulation of the environment and/or antigens. That is to say, it may be a reactive hyperplasia of gastric ulcer or gastritis, or an organ reaction to some antigenic stimulation. Recent studies have shown that it is related to Helicobacter pylori (Hp) infection.

　　(II) Pathogenesis

　　Helicobacter pylori and its products as antigenic stimuli can activate the human mononuclear-macrophage system, causing an increase in the secretion of cytokines such as reactive oxygen species, interleukin-1, and tumor necrosis factor-α in the gastric mucosa, leading to an inflammatory response of the mucosa. Moreover, in the histological study of gastric reactive lymphoid hyperplasia, lymphoid follicles formation and the proliferation of lymphocytes and plasma cells were found, which can also be seen in Hp-related gastritis. After the eradication of Hp, these changes can gradually disappear, indicating that the occurrence of the disease may be related to Hp infection. However, there is no report confirming the role of Hp in the occurrence and development of gastric reactive lymphoid hyperplasia.

　　The main pathological change of this disease is the infiltration of a large number of lymphocytes in the固有层of the gastric mucosal layer, with germinal centers, and often mixed with macrophages, plasma cells, polymorphonuclear granulocytes, and other cells, which are different from lymphoma. It is divided into 3 types according to its gross morphology: nodular type, ulcerative type, and erosive type. Pathological histology shows that the lesion invades the muscular layer of the mucosa and the submucosa, even the serosa layer. The infiltration of lymphatic tissue is clear from the normal tissue, and the affected mucosal surface can develop erosions and superficial ulcers. A large number of mature lymphocytes can be found in the gastric juice, with consistent size and shape. The lymph nodes in the whole body are not invaded. In the late stage of the lesion, extensive lymphatic infiltration, fibrosis, thinning of the gastric wall, and weakening of gastric motility function can occur.

　　The main characteristics of nonspecific reactive lymphoid follicular hyperplasia are lymph node enlargement, lymphoid follicular hyperplasia, and a significant expansion of germinal centers. The number of lymphoid follicles increases, not only distributed in the cortex of lymph nodes, but also scattered at the junction of the cortex and medulla and within the medulla. The size and shape of the follicles are different, with clear boundaries. The germinal centers are significantly expanded and hyperplastic, containing a large number of variously transformed lymphocytes, with large nuclei, with or without cleavage, and mitotic figures are common, along with a large number of phagocytes containing phagocytosed cell debris. There are small lymphocytes surrounding the germinal centers. In the lymphatic tissue between the follicles, there are plasma cells, histiocytes, and a few neutrophils and eosinophils. The reticular cells and endothelial cells in the lymph sinuses are hyperplastic. Reactive lymphoid follicular hyperplasia is easily confused with follicular lymphoma, where the lymph node structure is destroyed, the size and shape of the follicles are similar, and the boundaries are not clear. The cells hyperplastic within the follicles show heterogeneity, but the types are relatively consistent, with fewer mitotic figures, and macrophages that do not phagocytose foreign matter are generally not seen. The hyperplastic lymphocytes are monoclonal; whereas during reactive lymphoid follicular hyperplasia, the hyperplastic lymphocytes are polyclonal.

　　The symptoms of reactive lymphoid hyperplasia of the stomach include: nausea, abdominal discomfort, bloating, melena, ulcers, lymphoid hyperplasia, weight loss, dyspepsia, and anorexia.

　　Most patients have non-specific symptoms, often with chronic dyspepsia for more than 1 year, such as discomfort in the upper abdomen, loss of appetite, bloating, nausea, vomiting, and weight loss. The medical history also often has symptoms similar to peptic ulcer disease, such as pain, hematemesis, and melena.

　　(1) Try to speak less, especially do not shout loudly.

　　(2) Strictly prohibit smoking, drinking, and spicy foods.

　　(3) Keep the living and working environment fresh, and prevent colds.

　　(4) Eat less cold drinks.

　　(5) Avoid overly salty, sweet, dry, and greasy foods, and do not overeat.

　　(6) Be cautious about using the voice during the voice change period, menstrual period, and cold season.

　　The examinations for reactive lymphoid hyperplasia of the stomach should include: gastroscopy, abdominal plain film, fiberoptic gastroscopy, CT examination, gastric mucosal biopsy, and gastric ultrasound examination.

　　The identification of lymphocyte surface markers by monoclonal antibodies can find that this disease is different from malignant lymphoma. Lymphocytes are polyclonal systems. In addition, immunohistochemistry, immunofluorescence technology, and other techniques may help with correct diagnosis. Hp examination should not be ignored and should be listed as routine.

　　This disease is often misdiagnosed as malignant lymphoma and type II C early gastric cancer by gastroscopy and X-ray. The differential diagnosis relies on multiple-point biopsy of the stomach, deep biopsy, and large-loop biopsy, and histological biopsy with lymphoid follicles is conducive to benign diagnosis. The immunohistochemical staining of tissue sections sometimes can distinguish from malignant lymphoma. Malignant lymphoma is monoclonal cells, and this disease is polyclonal cells, but not absolute.

　　When eating, patients with gastric reactive lymphoid hyperplasia should pay attention to:
　　1. Avoid smoking, alcohol, coffee, cocoa, etc.
　　2. Avoid刺激性 food, such as scallion, garlic, ginger, chili, Sichuan pepper, cassia, etc.
　　3. Avoid moldy and charred food.
　　4. Avoid greasy, fried, grilled, smoked, and other hot foods, such as lamb, ham, smoked meat, fatty meat, etc.

　　(I) Treatment

　　Many scholars advocate surgical treatment, which can provide clear diagnosis and treatment, but it also has surgical complications and mortality. Some scholars advocate regular follow-up, endoscopic examination, and histological examination, but this observation method may allow the disease to develop into malignant lymphoma. Sigal et al. believe that the disease develops gradually from continuous antigenic and environmental stimulation, eventually forming lymphoma. They speculate that if the antigenic stimulation can be eliminated, the process is reversible. This provides an alternative treatment strategy for gastric reactive lymphoid hyperplasia. Weston et al. propose that for early gastric reactive lymphoid hyperplasia, clinical immunological stimulation factors (such as Hp infection) should be sought, and then eradication should be carried out, and the lesions can usually disappear completely. If the endoscopy and histological, X-ray examination suggest that there is progression of gastric reactive lymphoid hyperplasia or the diagnosis of gastric reactive lymphoid hyperplasia cannot be clearly defined, then surgical treatment should be performed.

　　(II) Prognosis

　　Patients with Hp-positive should receive routine radical treatment after surgery. Long-term follow-up and monitoring Hp are very important. The prognosis of this disease is good.