Drug-induced reversible lymphoid dyscrasia: a clonal lymphomatoid dermatitis of memory and activated T cells.

Drug-induced reversible lymphoid dyscrasia: a clonal lymphomatoid dermatitis of memory and activated T cells.
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药物引起的可逆性淋巴恶液质:记忆和活化 T 细胞的克隆性淋巴瘤样皮炎。

DOI:
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发表时间:
2003
期刊:
影响因子:
3.3
通讯作者:
F. Burns
F. Burns
中科院分区:
医学3区
文献类型:
--
作者:
C. Magro;A. Crowson;A. Kovatich;F. Burns

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某些全身性疾病使患者容易对免疫干扰药物产生过度的淋巴细胞反应,这可能会进展为恶性淋巴瘤。许多病理学家和临床医生认为,通过表型和分子分析可以可靠地区分假性淋巴瘤和皮肤 T 细胞淋巴瘤 (CTCL)。我们在药物治疗中遇到了 15 例非典型皮肤 T 细胞淋巴样增生的病例。我们使用 CD2、3、4、7、8、20、30 和 CD62 K 抗体探索表型异常,并通过聚合酶链式反应方法寻找 T 细胞受体基因重排。淋巴浸润显示出可重复的 CD7 和/或 CD62 K 缺失,与 T 细胞克隆性和可变的 CD30 阳性结果一致(与 CTCL 相似),但在药物调节后皮疹得到缓解或显着改善。我们假设这些浸润代表了 CD7 和 CD62 K 阴性激活记忆 T 淋巴细胞响应抗原触发而不受抑制的扩张。我们提出术语“药物引起的可逆性淋巴样恶液质”来描述这一实体。
Certain systemic conditions predispose patients to excessive lymphocyte responses to immune-perturbing drugs, which may progress to malignant lymphoma. Many pathologists and clinicians believe that differentiation of pseudolymphoma from cutaneous T cell lymphoma (CTCL) can be reliably made through phenotypic and molecular analysis. We encountered 15 cases of atypical cutaneous T-cell lymphoid hyperplasia in the setting of drug therapy. We explored phenotypic anomalies using antibodies to CD2, 3, 4, 7, 8, 20, 30 and CD62 K and sought T-cell receptor gene rearrangements by a polymerase chain reaction methodology. The lymphoid infiltrates showed reproducible CD7 and/or CD62 K deletion in concert with T cell clonality and variable CD30 positivity-findings similar to those of CTCL-but the rashes resolved or improved substantially after drug modulation. We hypothesize that the infiltrates represent an unrepressed expansion of CD7- and CD62 K-negative activated memory T lymphocytes in response to antigenic triggers. We propose the term "drug-induced reversible lymphoid dyscrasia" to describe this entity.
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