Primary Immunodeficiency Syndromes and Their Manifestations in Lymph Nodes

Cottier, H.; Kraft, Rainer; Meister, F.

doi:10.1007/978-3-642-75522-4_4

Cited by 8 publications

(3 citation statements)

References 318 publications

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“…The histology of lymphoid tissue from antibody deficiency patients without suspected malignancy varies from being microscopically normal to grossly abnormal. Stimulation by an infection may result in an atypical lymphoid hyperplasia often indistinguishable from lymphoma by ordinary light microscopy [33].…”

Section: Lymphoma In Common Variable Immunodeficiencymentioning

confidence: 99%

Lymphoma in common variable immunodeficiency: interplay between immune dysregulation, infection and genetics

Chua

Quinti

Grimbacher

2008

Current Opinion in Hematology

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There are several reasons for an increased risk of lymphoma in common variable immunodeficiency patients. These include genetics, immune dysregulation, radiosensitivity and chronic infections such as Helicobacter pylori, human herpes virus type 8 and cytomegalovirus. Chronic infections may enhance the development of lymphoma in an antigen specific manner. The interaction between chronic infections and the development of lymphoma is still unclear but studies to clarify this may lead to prevention measures and lymphoma reduction strategies.

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Section: Lymphoma In Common Variable Immunodeficiencymentioning

confidence: 99%

Lymphoma in common variable immunodeficiency: interplay between immune dysregulation, infection and genetics

Chua

Quinti

Grimbacher

2008

Current Opinion in Hematology

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“…The histology of lymphoid tissue from antibody deficiency patients without suspected malignant change varies from being microscopically normal to grossly abnormal. Where the histology is abnormal the germinal centres can be absent or poorly developed, and there are none of the features of the normal reactive lymph node [5]. Furthermore, stimulation by an infection can result in an atypical lymphoid hyperplasia which, together with the lack of germinal centres, can be indistinguishable from lymphoma on ordinary light microscopy.…”

Section: Introductionmentioning

confidence: 99%

Lymphoproliferative disease in antibody deficiency: a multi-centre study

Gompels

Hodges

Lock

et al. 2003

Clinical and Experimental Immunology

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SUMMARYWe have undertaken a retrospective study of antibody deficient patients, with and without lymphoma, and assessed the ability of specific polymerase chain reaction (PCR) primers to determine if the detection of clonal lymphocyte populations correlates with clinical and immunohistochemical diagnosis of lymphoma. We identified 158 cases with antibody deficiency presenting during the past 20 years. Paraffin-embedded biopsy specimens or slides were available for analysis in a cohort of 34 patients. Of these patients, 29 had common variable immunodeficiency, one X-linked agammaglobulinaemia, one Xlinked immunoglobulin deficiency of uncertain cause and three isolated IgG subclass deficiency. We have confirmed that lymphoma in antibody deficiency is predominantly B cell in origin. Clonal lymphocyte populations were demonstrated in biopsies irrespective of histology (16/19 with lymphoma and 11/15 without). Isolated evidence of clonality in biopsy material is therefore an insufficient diagnostic criterion to determine malignancy. Furthermore, our data suggest that clonal expansions are rarely the result of Epstein-Barr virus-driven disease.

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“…The diagnosis is complicated by the fact that lymphoid tissue from all patients with CVID can be histologically abnormal because germinal centres are frequently absent or poorly developed, so that stimulation by infection can result in histologies that are difficult to differentiate from lymphoma. 127 Lymphomas of B cell type predominate in CVID, although T cell types have been reported 128 The interpretation of clonality in this group of patients is complex. Although clonal rearrangements are the hallmark of lymphoid tumours, monoclonal proliferations have been reported in patients without progression.…”

Section: Infectionmentioning

confidence: 99%

Tumour suppressor genes do not regulate the cell cycle

2003

Journal of Clinical Pathology

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Primary Immunodeficiency Syndromes and Their Manifestations in Lymph Nodes

Cited by 8 publications

References 318 publications

Lymphoma in common variable immunodeficiency: interplay between immune dysregulation, infection and genetics

Lymphoma in common variable immunodeficiency: interplay between immune dysregulation, infection and genetics

Lymphoproliferative disease in antibody deficiency: a multi-centre study

Tumour suppressor genes do not regulate the cell cycle

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