非霍奇金淋巴瘤MACOP-B化疗期间乳酸脱氢酶水平。

B McAdam, T Smith, W C Love, M Murphy, P A Daly
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引用次数: 5

摘要

乳酸脱氢酶(LD)水平在中重度非霍奇金淋巴瘤(NHL)的MACOP-B化疗期间持续升高。水平在第9周达到顶峰,并在治疗完成后的6周内降至正常水平。对7名患者进行的同工酶模式前瞻性研究显示,LD1和LD2平行升高,表明总LD升高有肿瘤组织以外的来源。在没有心肌或肾脏损害证据的情况下,造血组织是最可能的来源。由于没有溶血的证据,血清中维生素B12和叶酸水平正常,红细胞叶酸水平正常,红细胞生成被认为是潜在的机制。平均红细胞体积的上升进一步强化了这一观点。强化使用甲氨蝶呤和复方新诺明作为预防卡氏肺囊虫被认为是骨髓功能障碍的最可能原因。未能认识到在这种治疗过程中LD水平的上升与治疗有关,而不是肿瘤起源,可能导致不适当的改变或放弃治疗。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Lactate dehydrogenase levels during MACOP-B chemotherapy for non-Hodgkin's lymphoma.

Lactate dehydrogenase (LD) levels rose consistently during MACOP-B chemotherapy for intermediate and high-grade non-Hodgkin's lymphoma (NHL). Levels peaked at week nine and fell to normal within six weeks of completion of therapy. Isoenzyme patterns, studied prospectively in seven patients, showed a parallel rise in LD1 and LD2 suggesting a source other than tumour tissue for the rise in total LD. In the absence of evidence of myocardial or renal damage, haematopoietic tissue was the most likely source. With no evidence of haemolysis, normal serum levels of vitamin B12 and folate and normal red cell folate, dyserythropoiesis was considered to be the underlying mechanism. A rising mean corpuscular volume further reinforced this suggestion. Intensive use of methotrexate along with co-trimoxazole as prophylaxis against pneumoycystis carinii is considered the most likely cause of marrow dysfunction. Failure to recognise that rising LD levels during such therapy is treatment-related, rather than of tumour origin, may lead to inappropriate change or abandonment of therapy.

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