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首页> 外文期刊>Haematologica >Chronic myeloid leukemia patients resistant to or intolerant of interferon alpha and subsequently treated with imatinib show reduced immunoglobulin levels and hypogammaglobulinemia | Haematologica
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Chronic myeloid leukemia patients resistant to or intolerant of interferon alpha and subsequently treated with imatinib show reduced immunoglobulin levels and hypogammaglobulinemia | Haematologica

机译：抵抗或不耐受干扰素α的慢性骨髓性白血病患者，随后接受伊马替尼治疗，显示免疫球蛋白水平降低和低血球蛋白血症血液学

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BACKGROUND AND OBJECTIVES: Imatinib mesylate inhibits ABL tyrosine kinase. This protein serves a complex role in cell cycling and is important in lymphopoiesis. We describe the immunologic findings in patients with chronic myeloid leukemia resistant to or intolerant of interferon (IFN) a who were treated with imatinib. This aspect could be of interest since patients with these characteristics may be exposed to this treatment for long periods. DESIGN AND METHODS: Immunologic and hematologic evaluation (including immunoglobulin levels and parameters of autoimmunity), immunophenotyping analysis of peripheral blood and bone marrow, and cytogenetic bone marrow analysis were performed at sequential time points of the treatment (0, 3, 6, and 9 and 12 months). The relationships among immunologic variables, and between the immunologic findings and response, were investigated. RESULTS: Hypogammaglobulinemia IgG, IgA and IgM developed in 28%, 14% and 22% of the patients, respectively. Lymphocyte counts decreased significantly along the treatment. No correlation was found between Ig levels and lymphocyte counts or CD4, CD8 or CD19 subpopulations in peripheral blood, nor between Ig levels and bone marrow B-lineage precursors. No autoimmune phenomena were detected. Hypogammaglobulinemia had no clinical repercussions in patients who developed it. The percentage reductions of IgG, IgA and IgM levels were higher in patients with major genetic response to imatinib. INTERPRETATION AND CONCLUSIONS: Hypogammaglobulinemia can develop in as many as 20-25% of patients with chronic myeloid leukemia previously exposed to IFN a and who are then treated with imatinib. The reduction of Ig is greater in patients with a better cytogenetic response, perhaps reflecting that the efficacy of imatinib in blocking BCR-ABL kinase activity runs in parallel with ABL inhibition, leading to a dysregulation of B-lymphocyte function. Close immunologic evaluation is recommended in these patients.
机译：背景与目的：甲磺酸伊马替尼抑制ABL酪氨酸激酶。该蛋白在细胞周期中起着复杂的作用，在淋巴细胞生成中很重要。我们描述了用伊马替尼治疗的对干扰素（IFN）a耐药或不耐受的慢性粒细胞白血病患者的免疫学发现。这方面可能是令人感兴趣的，因为具有这些特征的患者可能会长期接受这种治疗。设计与方法：在治疗的连续时间点（0、3、6和9）进行了免疫学和血液学评估（包括免疫球蛋白水平和自身免疫性参数），外周血和骨髓的免疫表型分析以及细胞遗传学骨髓分析和12个月）。研究了免疫学变量之间以及免疫学发现与反应之间的关系。结果：分别有28％，14％和22％的患者发生了球蛋白血症IgG，IgA和IgM。在治疗过程中，淋巴细胞计数显着下降。在外周血中Ig水平与淋巴细胞计数或CD4，CD8或CD19亚群之间，Ig水平与骨髓B谱系前体之间均未发现相关性。没有检测到自身免疫现象。发生低球蛋白血症的患者没有临床影响。对伊马替尼有重大遗传反应的患者中IgG，IgA和IgM水平的降低百分比更高。解释和结论：早先暴露于IFN a并随后接受伊马替尼治疗的慢性髓样白血病患者中，多达20％至25％的患者发生了球蛋白球蛋白血症。在具有更好的细胞遗传学反应的患者中，Ig的降低更大，这可能反映了伊马替尼在阻断BCR-ABL激酶活性方面的功效与ABL抑制同时发生，从而导致B淋巴细胞功能失调。建议对这些患者进行严格的免疫学评估。

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