Paradoxical response to disseminated non-tuberculosis mycobacteriosis treatment in a patient receiving tumor necrosis factor-α inhibitor: a case report.
Paradoxical response to disseminated non-tuberculosis mycobacteriosis treatment in a patient receiving tumor necrosis factor-α inhibitor: a case report.
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DOI：
10.1186/1471-2334-14-114
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发表时间：
2014-02-28
影响因子：
3.7
通讯作者：
Kohno S
中科院分区：
文献类型：
--
作者：
Takazono T;Nakamura S;Imamura Y;Miyazaki T;Izumikawa K;Kakeya H;Yanagihara K;Kohno S
已知的生物制剂，如肿瘤坏死因子-α抑制剂，可引起分枝杆菌感染。在这里，我们报告了一例由肿瘤坏死因子-α抑制剂治疗引起的播散性非结核病例，以及对抗分枝杆菌治疗可能出现的矛盾反应。1例68岁男性复发性多软骨炎患者对糖皮质激素治疗无效，因此阿达莫单抗联合口服糖皮质激素。用40 mg阿达利玛单抗治疗后，他的临床表现迅速改善。随着口服糖皮质激素剂量的逐渐减少，开始使用他克莫司(1 Mg)。然而，患者在开始阿达利单抗治疗15个月后出现间歇性高烧和生产性咳嗽。胸部计算机断层扫描发现纵隔淋巴结病变的两个肺野出现新的颗粒状阴影和多发结节，并从2份痰标本中分离出细胞内分枝杆菌，根据这些发现，患者被诊断为非结核分枝杆菌病。停止他克莫司治疗，开始口服克拉霉素(800 mg/d)、利福平(450 mg/d)和乙胺丁醇(750 mg/d)治疗。然而，尽管接受了4个月的治疗，他的病情继续恶化；此外，椎旁和皮下脓肿发展并增大了纵隔淋巴结病的大小。纵隔淋巴结病和右大腿后皮下脓肿的活检表明存在禽型分枝杆菌复合体(MAC)，诊断为播散性非结核分枝杆菌病。尽管接受了9个月的抗分枝杆菌治疗，纵隔淋巴结病和椎旁和皮下脓肿已经扩大，并出现了更多的皮下脓肿，尽管显微镜检查和痰和皮下脓肿样本的培养结果为阴性。我们认为这是一种自相矛盾的反应，类似于其他报告中停止生物制剂治疗并增加口服糖皮质激素剂量的结核病患者。随着剂量的增加，患者的症状逐渐改善，他的淋巴结和脓肿开始缩小。临床医生应该考虑当非结核分枝杆菌病的临床表现恶化时，尽管进行了抗分枝杆菌治疗，或者在停用肿瘤坏死因子-α抑制剂后，可能会出现矛盾的反应。然而，需要更多的证据来验证我们的发现，并确定针对此类情况的最佳管理策略。
Biological agents such as tumor necrosis factor-α inhibitors are known to cause mycobacterium infections. Here, we report a disseminated non-tuberculosis case caused by TNF-α inhibitor therapy and a probable paradoxical response to antimycobacterial therapy. A 68-year-old man with relapsing polychondritis was refractory to glucocorticoid therapy; adalimumab was therefore administered in combination with oral glucocorticoids. Treatment with 40 mg of adalimumab led to rapid improvement of his clinical manifestations. The administration of tacrolimus (1 mg) was started as the dosage of oral glucocorticoids was tapered. However, the patient developed an intermittent high fever and productive cough 15 months after starting adalimumab treatment. A chest computed tomography scan revealed new granular shadows and multiple nodules in both lung fields with mediastinal lymphadenopathy, and Mycobacterium intracellulare was isolated from 2 sputum samples; based on these findings, the patient was diagnosed with non-tuberculosis mycobacteriosis. Tacrolimus treatment was discontinued and oral clarithromycin (800 mg/day), rifampicin (450 mg/day), and ethambutol (750 mg/day) treatment was initiated. However, his condition continued to deteriorate despite 4 months of treatment; moreover, paravertebral and subcutaneous abscesses developed and increased the size of the mediastinal lymphadenopathy. Biopsy of the mediastinal lymphadenopathy and a subcutaneous abscess of the right posterior thigh indicated the presence of Mycobacterium avium complex (MAC), and the diagnosis of disseminated non-tuberculosis mycobacteriosis was confirmed. Despite 9 months of antimycobacterial therapy, the mediastinal lymphadenopathy and paravertebral and subcutaneous abscesses had enlarged and additional subcutaneous abscesses had developed, although microscopic examinations and cultures of sputum and subcutaneous abscess samples yielded negative results. We considered this a paradoxical reaction similar to other reports in tuberculosis patients who had discontinued biological agent treatments, and increased the dose of oral glucocorticoids. The patient’s symptoms gradually improved with this increased dose and his lymph nodes and abscesses began to decrease in size. Clinicians should consider the possibility of a paradoxical response when the clinical manifestations of non-tuberculosis mycobacteriosis worsen in spite of antimycobacterial therapy or after discontinuation of tumor necrosis factor-α inhibitors. However, additional evidence is needed to verify our findings and to determine the optimal management strategies for such cases.
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5.2
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10
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影响因子：
11.8
作者：
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