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Lymphoproliferative disease in antibody deficiency: a multi-centre study
M M Gompels1, E Hodges, R J Lock
1Immunology and Immunogenetics, Southmead Hospital, North Bristol NHS Trust, Bristol, UK. mark.gompels@north-bristol.swest.nhs.uk
Clinical and Experimental Immunology
|November 18, 2003
Summary
In antibody deficiency patients, detecting clonal lymphocyte populations via PCR in biopsies does not reliably diagnose lymphoma. Lymphoma in these patients is primarily B-cell in origin and not typically Epstein-Barr virus-driven.
Area of Science:
- Immunology
- Oncology
- Molecular Diagnostics
Background:
- Antibody deficiency disorders increase lymphoma risk.
- Distinguishing lymphoma from reactive lymphocyte expansions can be challenging.
- Polymerase chain reaction (PCR) is used to detect clonal lymphocyte populations.
Purpose of the Study:
- To assess if PCR detection of clonal lymphocyte populations correlates with lymphoma diagnosis in antibody deficient patients.
- To investigate the origin and potential drivers of lymphoma in this cohort.
Main Methods:
- Retrospective study of 158 antibody deficient patients over 20 years.
- Analysis of paraffin-embedded biopsy specimens from 34 patients using specific PCR primers.
- Correlation of PCR results with clinical and immunohistochemical diagnoses.
Main Results:
- Lymphoma in antibody deficiency is predominantly B-cell.
- Clonal lymphocyte populations were detected in biopsies from patients both with (16/19) and without (11/15) lymphoma.
- Isolated clonality in biopsies is insufficient for malignancy diagnosis.
- Epstein-Barr virus was rarely implicated in clonal expansions.
Conclusions:
- PCR detection of clonality alone is not a definitive diagnostic criterion for lymphoma in antibody deficient individuals.
- Further diagnostic methods are necessary to confirm malignancy.
- The pathogenesis of lymphoma in antibody deficiency may involve mechanisms other than Epstein-Barr virus infection.