Primary cutaneous B-cell lymphoma associated with actinic prurigo

Perrett, Conal M.; Harwood, Catherine A.; Khorshid, M.; Cerio, R.; McGregor, Jane

doi:10.1111/j.1365-2133.2005.06611.x

Cited by 11 publications

(3 citation statements)

References 19 publications

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“…Both clonal B‐ and T‐cell populations have been observed 109 . Rare reports of patients with actinic prurigo developing B‐cell lymphoma in the setting of chronic UV‐induced antigen stimulation have been described 110 …”

Section: Non‐neoplastic Inflammatory Conditions With Clhmentioning

confidence: 99%

Cutaneous reactive B‐cell lymphoid proliferations

Khalil

Donthi²,

Gru

2022

J Cutan Pathol

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Cutaneous lymphoid hyperplasia (CLH), also known as cutaneous pseudolymphoma, is a spectrum of benign conditions characterized by reactive B‐ and T‐cell cutaneous lymphocytic infiltrates. B‐cell lymphoid proliferations are a heterogenous group of non‐neoplastic cutaneous diseases that must be histopathologically distinguished from cutaneous B‐cell lymphomas. These proliferations can be observed as reactive phenomena to infections, medications, allergens, neoplasms, and more. Furthermore, there are many inflammatory conditions that present with reactive B‐cell infiltrates, including actinic prurigo, Zoon balanitis, Rosai‐Dorfman disease, and cutaneous plasmacytosis. This review summarizes multiple cutaneous B‐cell lymphoid proliferations within the major categories of reactive and disease‐associated CLH. Further we discuss major discriminating features of atypical CLH and malignancy. Understanding the specific patterns of B‐cell CLH is essential for the proper diagnosis and treatment of patients presenting with such lesions.

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Section: Non‐neoplastic Inflammatory Conditions With Clhmentioning

confidence: 99%

Cutaneous reactive B‐cell lymphoid proliferations

Khalil

Donthi²,

Gru

2022

J Cutan Pathol

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“…Pruritus may have been caused by AITL with hyperplasia of cytokine-producing FDCs. Malignant lymphoma-associated prurigo has been reported in cases of Hodgkin’s lymphoma,39 cutaneous B-cell lymphoma,40 adult T-cell lymphoma41 42 and mycosis fungoides 43. Kabashima and Irie44 described the importance of IL-31 in the process of pruritic diseases and as the therapeutic target against intractable pruritus.…”

Section: Discussionmentioning

confidence: 99%

Epstein-Barr virus-positive mucocutaneous ulcer, plasmablastic type, associated with nodal CD4+ angioimmunoblastic T-cell lymphoma and generalised pruritus: a self-limiting lymphoproliferative disorder resembling cutaneous plasmablastic lymphoma

et al. 2022

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A woman in her 80s reported of generalised pruritus, which was treated with phototherapy and steroid administration. Two months after onset, lymph node biopsy revealed CD4+ angioimmunoblastic T-cell lymphoma with systemic superficial nodal involvement. Intractable prurigo was judged as T-cell lymphoma related. After effective chemotherapy (7 months later), skin nodules appeared multifocally, including on the lip, thumb and lower leg. The biopsied infiltrative lesion on the right lower leg microscopically revealed subcutaneous growth of atypical plasmablasts with nearly 100% Ki-67 labelling and Epstein-Barr virus (EBV)-encoded small nuclear RNA positivity. Plasmablastic lymphoma (CD45/CD19/CD38/CD138/MUM1+, CD20/CD79a/PAX5-) was suspected. Immunoglobulin light-chain restriction and nuclear expression of c-myc protein were undetectable, and the ulcers were spontaneously epithelialised by the cessation of steroid administration. After 10 months, non-progressive prurigos persisted on the extremities, but without regrowth of nodal T-cell lymphoma and cutaneous lymphoproliferative lesion. Reactive nature of the EBV-induced mucocutaneous plasmablastic growth (EBV-positive mucocutaneous ulcer, plasmablastic type) is discussed.

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“…In general, these lesions are repaired by the MMR system or by translesional synthesis (56). However, this azathioprine‐induced DNA damage might not greatly add to the skin cancer risk in OTRs as defective MMR does not correlate with the skin cancer risk in OTRs treated with azathioprine (57). Furthermore, transcription blockage by azathioprine‐induced DNA lesions leads to enhanced apoptosis, which prevents tumorigenesis.…”

Section: Effects Of Immunosuppressive Medications On Skin Cancer Riskmentioning

confidence: 99%

Skin cancer in organ transplant recipients: effects of immunosuppressive medications on DNA repair

Kuschal

Thoms

Schubert

et al. 2011

Experimental Dermatology

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UV-induced skin cancers comprise a major problem in organ transplant recipients (OTRs). Cyclosporin A, a calcineurin inhibitor, is used as a standard immunosuppressant and clearly increases the skin cancer risk. Azathioprine does not appear to result in such an increase in skin cancer risk, and mTOR inhibitors are associated with an even lesser skin cancer risk. The underlying molecular mechanisms of these clinically important differences among immunosuppressants are still unclear and may relate to other than immunological effects. Insights may be gained by the multistep skin cancer theory and xeroderma pigmentosum, where defective nucleotide excision repair (NER) results in a cellular mutator phenotype and cutaneous carcinogenesis. This viewpoint assay summarizes current knowledge about the influence of the most commonly used immunosuppressive drugs in OTRs on DNA repair. Calcineurin inhibition results in a 200-fold increased skin cancer risk compared with the normal population and inhibits NER. The skin cancer risk under azathioprine is threefold less compared with calcineurin inhibitors, which may relate to inhibition of only the last step of NER, i.e. gap filling. mTOR inhibitors do not reduce NER in the global genome and can inhibit the growth of already initiated tumors, which may account for the markedly reduced skin cancer risk compared with calcineurin inhibitors. We conclude that OTRs may benefit from treatment regimens other than calcineurin inhibitors and speculate that a targeted modulation of calcineurindependent signalling may prevent UV-induced tumor formation by enhancing NER not only in OTRs but also in the general population, at least in part.

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Primary cutaneous B-cell lymphoma associated with actinic prurigo

Cited by 11 publications

References 19 publications

Cutaneous reactive B‐cell lymphoid proliferations

Cutaneous reactive B‐cell lymphoid proliferations

Epstein-Barr virus-positive mucocutaneous ulcer, plasmablastic type, associated with nodal CD4+ angioimmunoblastic T-cell lymphoma and generalised pruritus: a self-limiting lymphoproliferative disorder resembling cutaneous plasmablastic lymphoma

Skin cancer in organ transplant recipients: effects of immunosuppressive medications on DNA repair

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