[Gastric lymphoid hyperplasia: anatomic and immunologic study of a case followed for seven years (author's transl)].
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Lymphoid hyperplasia
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Morphological and morphometrical study is performed on serial and stepped sections of the lungs surgically removed from patients with bronchoectatic disease. As compared to healthy persons, hyperplasia of all structural components with formation of lymphoid and lymphoepithelial follicles was detected. The degree of lymphoid tissue hyperplasia in bronchoectatic disease is determined by inflammation activity and does not depend on the age. The number of interepithelial lymphocytes is significantly increased as well as that of peribronchial and peribronchiolar lymphoid accumulations, and the degree of diffuse infiltration. However, the number of periglandular and periductal lymphoid accumulations and lymphoid follicles is significantly reduced. Bronchoectatic disease with high active inflammation as compared to low activity is characterized by more pronounced hyperplasia with formation of lymphoid and lymphoepithelial follicles with clear centers.
Lymphoid hyperplasia
Infiltration (HVAC)
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Histopathological analysis of reactive lymphoid hyperplasia (RLH) and malignant lymphoma (ML) of the stomach was made based on the observations of lymphoid follicles appearing in gastric mucosa. The materials used for study consisted of 28 stomachs without RLH or tumor obtained from either operation or autopsy, 18 stomachs with RLH, and 46 stomachs with ML. Lymphoid follicles appeared soon after birth, increased with mucosal atrophy, and decreased in mucosa with intestinal metaplasia. They possessed a sinusoidal structure and appeared in the muscularis mucosae intimately related to the lymphatic flow. Excepting for the significant proliferative nature, the structural evolution of lymphoid follicles in RLH was similar to that in atrophic mucosa. They showed, however, a wide spectrum of changes containing cases with simple reactive changes to those with prelymphomatous changes. As to ML, the large cell type demonstrated a destructive proliferation, while both small and medium‐sized cell types showed proliferation and infiltration preserving their original structure. In the superficial type, ML was frequently accompanied by RLH and mucosal atrophy. The histological features of ML consisted of not only the characteristics of tumor cells but also the proper mucosal changes including lymphoid follicles.
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Intestinal metaplasia
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True thymic hyperplasia (enlarged gland composed of histologically unremarkable cortical and medullary parenchyma) and lymphoid hyperplasia (medullary lymphoid follicles in the clinical setting of autoimmunity) usually develop as independent pathologic processes. We reviewed the clinical features and gross and microscopic pathology of 2 hyperthyroid patients with features of both thymic hyperplasia and lymphoid hyperplasia. The diagnosis of thymic hyperplasia was supported by thymic weights greater than two standard deviations above the mean weight for age and histologic evidence of expanded cortical and medullary parenchyma. The diagnosis of lymphoid hyperplasia was supported by the increased number and size of medullary lymphoid follicles and the association with Grave's disease. This unusual combination results from two separate pathogenic mechanisms operating simultaneously in hyperthyroid patients. Elevated thyroid hormones directly stimulate the proliferation of thymic epithelium, producing thymic hyperplasia. The immune abnormalities underlying Grave's disease can also result in lymphoid hyperplasia of the thymus.
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Follicular hyperplasia
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Nodular lymphoid hyperplasia of the stomach is a rare lymphoproliferative disorder. Here, we report a 38-year-old man who presented with multiple submucosal tumors of the stomach. Histologically, the lesions were characterized by multiple discrete submucosal nodules of lymphoid cells. The infiltrates between the lymphoid follicles were composed mainly of medium-sized lymphoid cells with abundant clear cytoplasm, as well as a few large cells with vesicular nuclei. The gastric mucosa exhibited multifocal lymphoid aggregates and some of the epithelial cells were infiltrated by small lymphocytes mimicking lymphoepithelial lesions. Histopathology was consistent with mucosa-associated lymphoid tissue lymphoma. However, the infiltrating lymphoid cells were positive for CD2, CD3, CD5, and CD7. In addition, polymerase chain reaction analysis of the immunoglobulin heavy chain and T-cell receptor gene rearrangements demonstrated polyclonality. This case was diagnosed as reactive lymphoid hyperplasia of the stomach.
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CD5
Histopathology
Mucosa-associated lymphoid tissue
Pseudolymphoma
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Nodular lymphoid hyperplasia is a reaction of the intestinal lymphatic tissue to specific inflammatory stimuli and may be probably of no clinical significance, but it may evolve to primary gastrointestinal lymphoma in more severe cases. Recently, several cases of nodular lymphoid hyperplasia complicated by primary gastrointestinal lymphoma have been reported, and which suggested that nodular lymphoid hyperplasia could not be considered as simple benign colon disease any more. We also experienced a case of primary jejunal malignant lymphoma associated with nodular lymphoid hyperplasia, and report this case with a brief review of relevant literatures.
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We propose dividing histologically reactive lymphoid hyperplasia (RLH) of the stomach into two categories: atypical lymphoid hyperplasia (ALH), characterized by abnormal follicular architecture and infiltration of atypical lymphoid cells, and benign lymphoid hyperplasia (BLH), where normal follicular patterns are preserved and no atypical cells are found. Using twenty RLH cases (10 ALHs and 10 BLHs), both categories were compared front histopathological and immunohistochemical aspects. Macroscopic division into superficial, thick‐walled and nodular types revealed most ALH (80%) to be superficial in character whereas in BLH superficial and thick‐walled types were almost equally represented. Lesion size tended to be larger in ALH (> 6.1 cm) than in BLH (6.0 cm >) cases. As for prognosis after gastrectomy, both categories were favorable. On immunohistochemistry, ALH tended to be strongly labeled by B lymphocyte markers as compared to BLH, where only a weakly positive reaction was expressed. Infiltration of cells labeled by T lymphocyte markers was less conspicuous in ALH than in BLH. From these data, we concluded that ALH and BLH are two distinctive categories of lesion and that ALH has characteristics similar to these demonstrated by malignant lymphoma.
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Pseudolymphoma
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Follicular hyperplasia
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The relatively rare pseudotumoral lymphoid hyperplasia (benigh lymphoid or reactive lymphoreticular hyperplasia; pseudolymphoma; Castleman's disease) arises from the lymph nodes, usually in the mediastinum. The disease assumes tow histologically and clinically different forms: the first, angiofollicular, is often symptomless, while the second, lymphoplasmocytic, is sometimes associated with a marked chronic inflammatory syndrome. The etiology is unknown, but is probably a reaction of the lymphoplasmocytic system to an antigen, possibly of viral origin. Diagnosis is based on histology. Surgical treatment is curative. A rare form of this unusual disease is reported with reference to the morphological differential diagnosis; the similarities with immunoblastic lymphadenopathy are emphasized.
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Pseudolymphoma
Etiology
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Rare disease
Lymphoid hyperplasia
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Pulmonary nodular lymphoid hyperplasia is an uncommon reactive lymphoproliferative disorder that presents as an asymptomatic lung mass. The histopathologic diagnosis of pulmonary nodular lymphoid hyperplasia may be challenging because of its morphologic overlap with other diseases, such as extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue and immunoglobulin G4-related sclerosing disease. Despite the similarities, there are distinctive morphologic and phenotypic features that allow for the correct diagnosis in the majority of cases. This review aims to discuss the clinicopathologic features of pulmonary nodular lymphoid hyperplasia and contrast them with its histopathologic mimickers.
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Lymphoid hyperplasia
Pseudolymphoma
Lymphoproliferative Disorders
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