背景:结核性胸腔积液(TPE)是一种小细菌,仅靠实验室调查使其诊断变得困难。我们介绍了一例TPE患者,最初被误诊为硫唑嘌呤引起的肺损伤。TPE的诊断是在临床评估的帮助下得出的。实验室和放射学调查。
方法:一名25岁的慢性吸烟者患有交感性眼炎,长期免疫抑制,潜伏性结核感染和明显的结核病家族史,并伴有三周的咳嗽病史,低烧,夜间出汗和减肥。肺部检查显示右下区域的呼吸音减少。胸部X线显示右侧胸腔积液轻微,右上叶小面积实变。胸膜液渗出性以单核白细胞为主。痰液和胸膜液的直接涂片;胸膜液的聚合酶链反应;和痰,胸水和血培养对结核分枝杆菌(MTB)和其他生物体均为阴性.由于他对广谱抗生素的疗程没有反应,然后他被治疗为硫唑嘌呤引起的肺损伤。然而,尽管停止了硫唑嘌呤,但他的病情没有改善。胸部的对比增强计算机断层扫描显示右上叶巩固,有树在芽中的变化,双侧肺不张,胸膜下结节,轻度右侧胸腔积液和纵隔淋巴结肿大。支气管肺泡灌洗对恶性细胞和微生物呈阴性,包括,MTB。然而,没有做胸膜活检。他根据经验接受抗结核治疗9个月,并显示完全康复。
结论:生活在结核病流行地区的免疫抑制个体需要高度怀疑TPE。有针对性的调查和合理的临床判断允许早期诊断和迅速开始治疗,以防止发病率和死亡率。
BACKGROUND: Tuberculous pleural effusion (TPE) is paucibacillary, making its diagnosis difficult based on laboratory investigations alone. We present a
case of a patient with a TPE who was initially misdiagnosed to have azathioprine-induced lung injury. The diagnosis of TPE was arrived at with the help of clinical assessment, laboratory and radiological investigations.
METHODS: A 25-year-old chronic smoker with sympathetic ophthalmia on long-term immunosuppression, latent tuberculosis infection and a significant family history of tuberculosis presented with a three-week history of productive cough, low-grade fever, night sweats and weight loss. Examination of the lungs showed reduced breath sounds at the right lower zone. Chest x-ray showed minimal right pleural effusion with a small area of right upper lobe consolidation. The pleural fluid was exudative with predominant mononuclear leukocytes. Direct smears of sputum and pleural fluid; polymerase chain reaction of pleural fluid; and sputum, pleural fluid and blood cultures were negative for M. tuberculosis (MTB) and other organisms. As he did not respond to a course of broad-spectrum antibiotics, he was then treated as a
case of azathioprine-induced lung injury. However, his condition did not improve despite the cessation of azathioprine. A contrast-enhanced computed tomography of the thorax showed right upper lobe consolidation with tree-in-bud changes, bilateral lung atelectasis, subpleural nodule, mild right pleural effusion and mediastinal lymphadenopathy. Bronchoalveolar lavage was negative for malignant cells and microorganisms including, MTB. However, no pleural biopsy was done. He was empirically treated with anti-tubercular therapy for 9 months duration and showed complete recovery.
CONCLUSIONS: A high index of suspicion for TPE is required in individuals with immunosuppression living in regions endemic to tuberculosis. Targeted investigations and sound clinical judgement allow early diagnosis and prompt treatment initiation to prevent morbidity and mortality.