重组干扰素α -2b治疗ph1阳性慢性髓性白血病:完全细胞遗传学应答一例报告

Shigeru Shirakawa , Tohru Kobayashi , Kazuhiro Nishii , Kenkichi Kita
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引用次数: 0

摘要

在一项研究中,8例22至80岁的ph1阳性慢性髓性白血病(CML)患者接受干扰素α -2b治疗,初始剂量为每天400万单位(MU)/m2。1例加速期患者用长春地西和强的松进行预处理,在干扰素治疗期间白细胞计数增加。此外,7名慢性患者中有1名患者此前未接受治疗,但因皮肤出疹而退出治疗。根据Alimena等[1]的应答标准,其余6例慢性期患者中有3例血液学应答(2例完全,1例部分),2例细胞遗传学改善(1例完全,1例轻微)。不良反应包括发热(6例)、不适(2例)、厌食(1例)、谵妄(1例)、肝功能障碍(2例)、皮肤出疹(1例)。我们在这里提出的治疗前的特点和临床过程的病人谁达到完全细胞遗传学反应(CCR)。32岁女性患者,因明显肝脾肿大(脾在肚脐下11cm)和贫血入院,诊断为ph1阳性CML,每日6 MU/体干扰素α -2b治疗4个月,此后每周2次。预处理血细胞计数:红细胞2.17 × 106/μL;血红蛋白6.6 g/dL;白细胞(WBC) 206,700/μL;血小板610 × 103/μL。患者在干扰素治疗第32周获得完全血液学缓解[1],肝脾肿大消退。细胞遗传学和分子生物学分析显示,在第38周时Ph1染色体部分抑制(75%的Ph1阳性),在第140周时完全细胞遗传学应答(CCR, 0%的Ph1阳性)。综上所述,在1例Ph1阳性CML患者中,长期单独使用干扰素α -2b可诱导Ph1染色体完全抑制,且CCR持续时间超过4个月。为了提高细胞遗传学的改善,应研究干扰素与其他治疗的联合应用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Treatment of Ph1-positive chronic myelogenous leukaemia with recombinant interferon alfa-2b: A case report of complete cytogenetic response

A STUDY was undertaken in which eight patients aged 22 to 80 years with Ph1-positive chronic myelogenous leukaemia (CML) were treated with interferon alfa-2b at an initial dose of 4 million units (MU)/m2 per day.

One patient in accelerated phase was pretreated with vindesine and prednisone, and showed an increase in white blood cell count during interferon treatment. In addition, one of the seven patients in chronic phase, who was previously untreated, dropped out because of skin eruption. According to the response criteria of Alimena et al. [1], three of the other six patients in chronic phase achieved haematological response (two complete, one partial) and two had cytogenetic improvements (one complete, one minor).

Adverse effects included fever (six patients), malaise (two), anorexia (one), delirium (one), liver disorder (two) and skin eruption (one).

We present here the pre-treatment features and clinical course of a patient who achieved complete cytogenetic response (CCR). A 32-year-old female patient, admitted to hospital because of marked hepatosplenomegaly (spleen 11 cm under the navel) and anaemia, was diagnosed as having Ph1-positive CML and treated with interferon alfa-2b 6 MU/body daily for 4 months and twice weekly thereafter. Her pretreatment blood cell counts were as follows: red blood cells 2.17 × 106/μL; haemoglobin 6.6 g/dL; white blood cells (WBC) 206,700/μL; and platelets 610 × 103/μL.

The patient achieved complete haematological response [1] at the 32nd week of interferon administration, together with resolution of hepatosplenomegaly.

Cytogenetic and molecular biological analyses revealed partial suppression of the Ph1 chromosome at the 38th week (75% Ph1-positive) and complete cytogenetic response (CCR, 0% Ph1-positive) at the 140th week of interferon treatment.

In conclusion, long-term administration of interferon alfa-2b alone induced complete suppression of the Ph1 chromosome in one patient with Ph1-positive CML, and the duration of this CCR is more than 4 months. The combination of alpha interferon with other treatments in order to enhance cytogenetic improvement should be investigated.

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