Complete remission of refractory, ulcerated, primary cutaneous CD30+ anaplastic large cell lymphoma following brentuximab vedotin therapy.
Complete remission of refractory, ulcerated, primary cutaneous CD30+ anaplastic large cell lymphoma following brentuximab vedotin therapy.
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brentuximab vedotin 治疗后难治性溃疡性原发性皮肤 CD30 间变性大细胞淋巴瘤完全缓解。
DOI：
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发表时间：
2015
影响因子：
3.6
通讯作者：
K. Möllenhoff
中科院分区：
文献类型：
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作者：
N. Patsinakidis;A. Kreuter;R. Moritz;M. Stücker;P. Altmeyer;K. Möllenhoff
原发性皮肤CD 30+间变性大细胞淋巴瘤（pc-ALCL）属于罕见的非蕈样真菌病T细胞淋巴瘤（1）。与淋巴瘤样丘疹病相似，pc-ALCL的特征性免疫组织化学发现是浸润肿瘤性T细胞的CD 30阳性。迄今为止，有关pc-ALCL治疗的数据有限，目前的建议主要基于病例报告和小型队列研究（2）。手术切除和/或放射治疗通常在有限的疾病中进行。在播散性疾病的病例中，多药化疗显示出良好的效果，但伴随着高毒性和高复发率。在本文中，我们报告了一例使用维布妥昔单抗成功治疗的难治性、广泛性pc-ALCL病例。一位56岁的白人男性，最初被转诊到我们的部门与一个坚实的结节，直径4厘米，位于左侧腘区。患者的进一步病史包括冠心病、外周动脉疾病和高尿酸血症。皮损活检的组织学评价显示，在整个真皮内弥漫性淋巴细胞浸润，主要是大的间变性细胞。免疫组织化学分析显示，70%以上的浸润细胞中CD 4-、CD 5-和CD 30-阳性，50%以上的浸润细胞中Ki-67表达（图1）。淋巴细胞显示CD 3表达缺失，间变性淋巴瘤激酶-1（ALK-1）和T细胞β链抗原受体F1（β F-1）阴性。小核淋巴细胞点状表达CD 8。此时，无皮外疾病的证据。根据临床和组织病理学结果，诊断为CD 30 + pc-ALCL，并完全切除肿瘤。7个月后，患者在先前存在的瘢痕处出现一个新的结节，左侧腹股沟区可触及肿大的淋巴结。病变的组织学分析显示CD 30 + pc-ALCL的继发性浸润（8个切除淋巴结中5个的组织学评价显示正常淋巴结结构丧失以及大量肿瘤浸润，包括大型间变性增殖性CD 30+淋巴细胞）。完整的计算机断层扫描（CT）和骨髓活检无异常。我们决定对腘动脉和腹股沟区进行放射治疗，并采用低剂量甲氨蝶呤（15 mg/周）治疗。然而，新的皮肤病变和淋巴结转移在几周内发展。随后的腹股沟淋巴结切除术，第二个疗程的放射治疗，低剂量干扰素α，贝沙罗汀，和6个周期的吉西他滨单药化疗没有结果。
Primary cutaneous CD30 + anaplastic large cell lympho-mas (pc-ALCL) belong to the group of rare, non-mycosis fungoides T-cell lymphomas (1). Similar to lymphomatoid papulosis the characteristic immunohistochemical finding of pc-ALCL is CD30-positivity of infiltrating neoplastic T cells. To date, only limited data is available on the treatment of pc-ALCL and current recommendations are largely based on case reports and small cohort studies (2). Surgical excision and/or radiotherapy are usually performed in limited disease. In cases of disseminated disease, multi-agent chemotherapy has shown good effects, but is accompanied with high toxicity and high recurrence rates. Herein, we report a case of refractory, widespread pc-ALCL that was successfully treated with brentuximab vedotin. A 56-year-old Caucasian man was initially referred to our department with a solid erythematous nodule 4 cm in diameter located in the left popliteal region. The patient's further medical history included coronary heart disease, peripheral arterial disease, and hyperuricemia. Histopathological evaluation of a lesional biopsy showed diffuse lymphocytic infiltrations of primarily large anaplastic cells within the entire dermis. Immunohistochemical analysis revealed CD4-, CD5-, and CD30-positivity in more than 70% and expression of Ki-67 in more than 50% of infiltrating cells (Fig. 1). The lymphocytes showed a loss of CD3 expression and were negative for anaplastic lymphoma kinase-1 (ALK-1) and T-cell beta chain antigen receptor F1 (beta F-1). CD8 was punctually expressed by small nuclei lymphocytic cells. At this time, there was no evidence for extracutaneous disease. Based on the clinical and histopathological findings, a diagnosis of CD30 + pc-ALCL was made and the tumour was completely excised. Seven months later the patient presented with a new nodule located at the preexisting scar as well as palpable, enlarged lymph nodes in the left inguinal region. Histological analysis of the lesions showed secondary infiltration of the CD30 + pc-ALCL (the histological evaluation of 5 out of 8 removed lymph nodes showed loss of normal lymph node architecture as well as large amounts of tumour infiltrates consisting of large, anaplastic, proliferating, CD30 + lymphoid cells). Complete computed tomography (CT) scan and bone marrow biopsy were unremarkable. We decided to initiate radiation therapy of the popliteal and inguinal area as well as low-dose therapy with methotrexate (15 mg/week). However, new skin lesions and lymph node metastases developed within a few weeks. Subsequent inguinal lymphadenectomy, a second course of radiation therapy, low-dose interferon alpha, bexarotene, and 6 cycles of mono-chemotherapy with gemcitabine did not result …
肝细胞生长因子可降低 EGFR-T790M 突变型肺癌对不可逆表皮生长因子受体抑制剂的敏感性。
影响因子：
11.5
作者：
Yamada T;Yano S;et al.
通讯作者：
et al.