Milenković Branislava, Dudvarski-Ilić Aleksandra, Janković Goran, Martinović Lena, Mijac Dragana
Faculty of Medicine, University of Belgrade, Belgrade, Serbia.
Srp Arh Celok Lek. 2011 Jul-Aug;139(7-8):514-7.
Tumour necrosis factor alpha (TNFalpha) has a central role in the host immune response to mycobacterial infection.TNFalpha blockade may therefore result in reactivation of recent or remotely acquired infection. In reported mycobacterium tuberculosis infections, extra-pulmonary and disseminated tuberculosis (TB) was common, appeared rapidly, and if unrecognized, with fatal outcome. We present a female patient with miliary TB following treatment with infliximab for fistulizing Crohn's disease.
Five years before admission, the patient was diagnosed with Crohn's disease, with inflammation limited to the terminal ileum and sigmoid colon and has been on azathioprine 100 mg/day for the last 10 months. Three months before admission to the hospital she developed an enterocutaneous fistula for which therapy with infliximab was started in addition to azathioprine therapy. A tuberculin skin test and a chest x-ray were performed prior to the first infusion with normal findings. She presented with a 6-week history of fever, weakness, weight-loss and a 2-week dry cough. Chest x-ray and computed tomography displayed remarkable bilateral hilar and mediastinal lymphadenopathy and uniformly distributed fine nodules throughout both lung fields varying in size from 2 to 3 mm, without any signs of cavitation. Since there were clinical and morphological signs that indicated miliary TB, the treatment with antituberculous therapy was started and six weeks later all of the symptoms completely resolved and the lesions visible on x-ray diminished.
The clinical use of TNF-inhibitors is associated with increased risk of developing tuberculosis. Physicians should be aware of the increased risk of reactivation of TB among patients treated with anti-TNF agents and regularly look for usual and unusual symptoms of TB.
肿瘤坏死因子α(TNFα)在宿主对分枝杆菌感染的免疫反应中起核心作用。因此,TNFα阻断可能导致近期或既往获得性感染的重新激活。在已报道的结核分枝杆菌感染中,肺外和播散性结核病很常见,出现迅速,若未被识别则会导致致命后果。我们报告一例在用英夫利昔单抗治疗瘘管性克罗恩病后发生粟粒性结核病的女性患者。
入院前五年,患者被诊断为克罗恩病,炎症局限于回肠末端和乙状结肠,在过去10个月中一直服用硫唑嘌呤,剂量为每日100毫克。入院前三个月,她出现了肠皮肤瘘,除硫唑嘌呤治疗外,开始使用英夫利昔单抗治疗。首次输注前进行了结核菌素皮肤试验和胸部X光检查,结果正常。她有6周的发热、虚弱、体重减轻病史以及2周的干咳。胸部X光和计算机断层扫描显示双侧肺门和纵隔淋巴结明显肿大,双肺野均匀分布着大小从2至3毫米不等的细小结节,无任何空洞迹象。由于有临床和形态学迹象表明为粟粒性结核病,开始进行抗结核治疗,六周后所有症状完全缓解,X光片上可见的病变缩小。
TNF抑制剂的临床使用与发生结核病的风险增加有关。医生应意识到接受抗TNF药物治疗的患者中结核病重新激活的风险增加,并定期寻找结核病的常见和不寻常症状。