A 77-year-old woman presented to our hospital with complaints of persistent cough and low-grade fever for two months. Her medical history revealed glaucoma and osteoporosis seven years previously. Her vital signs were normal except for mild tachypnoea (respiratory rate, 24 breaths/min) and fever at 38.2°C. Physical examination showed decreased breath sounds at the right middle to lower lung fields. Chest X-ray taken at the first visit showed moderate right-sided pleural effusion and right hilar lymphadenopathies (Fig. ) confirmed by enhanced thoracic computed tomography (CT), which revealed a homogeneous enhanced mass as large as 3 cm in diameter (Fig. , arrow) with subcarinal lymphadenopathies (Fig. , arrow head). There was no calcification both in right hilar/mediastinal lymphadenopathies and in lung parenchyma.\nSerum laboratory data were normal except for mild elevation in white blood cell count at 17,000/μL (cell differential of neutrophil 63.3%, eosinophil 1.1%, basophil 0.8%, monocyte 13.3%, and lymphocyte 21.5%) and C-reactive protein at 1.19 mg/dL. Other data were normal; total protein (TP) of 7.1 g/dL, lactate dehydrogenase (LDH) of 217 IU/L, total cholesterol (T-cho) of 202 mg/dL, and triglyceride of 71 mg/dL. An interferon-gamma release assay was positive.\nAlthough thoracentesis of the right side was milky yellow in appearance (Fig. ), no pathogens were isolated including Mycobacterium, and polymerase chain reaction (PCR) for TB or Mycobacterium avium-complex (MAC) was also negative. No malignant cells were identified (class II). Chemical analysis revealed exudative pleural effusion (LDH 126 IU/L and TP 4.2 g/dL) as well as mild elevation of total cell count (1500/μL), predominantly lymphocytes (89%) followed by neutrophils (3%). Interestingly, the level of triglyceride (TG) in pleural fluid was markedly elevated (713 mg/dL), while the values of adenosine deaminase (ADA) (31.7 IU/L) and glucose (107 mg/dL) were normal. She thus met the criteria of chylothorax of TG greater than 110 mg/dL and a pleural to serum T-cho ratio less than 1 (0.48).\nOn the basis of the suspicion of a malignant disease-induced chylothorax, fluorodeoxyglucose–positron emission tomography–CT (FDG–PET–CT) was performed. The FDG–PET–CT demonstrated high FDG uptake in the right hilum, with a maximum standardized uptake value (SUV) of 7.04, and in the subcarinal lymphadenopathies, with a value of 9.65 (Fig. ).\nTwo weeks after the first visit, bronchoscopy was performed. Endobronchial ultrasound-guided transbronchial needle aspiration taken from the subcarinal lymph node showed necrotic tissue with abundant neutrophils or monocytes, which was of no diagnostic value. All retrieved respiratory samples were negative for bacterial or acid-fast culture or PCR methods on TB and MAC.\nOne month later, her symptoms and moderate right-sided pleural effusion persisted; thus, thoracoscopic surgery was performed. Curiously, a noticeable enlarged milky yellow lymphatic duct was found (Fig. , arrow) with its proximal portion seemingly compressed by the adjacent enlarged subcarinal lymphadenopathies (asterisk). Biopsied specimens obtained from the subcarinal lymph node showed epithelioid cell granulomas containing Langhans giant cells (Fig. , arrows) along with necrosis, fibrosis, fibrous venous occlusion, and lymphoid hyperplasia. Although no acid-fast organisms were detected by the Ziehl–Neelsen stain, these findings suggested mycobacterial lymphadenitis associated with TB, she was thus diagnosed with TB lymphadenitis-associated chylothorax. During the thoracoscopic surgery, cauterization of the lymphatic duct was performed, which resulted in a partial resolution of the pleural effusion. The patient rejected treatment for tuberculous lymphadenitis, and four months later (six months after the first visit), the amount of right pleural effusion had rapidly increased again. Thoracentesis found that the colour of the pleural fluid had changed from milky yellow to red (Fig. ) together with an elevation of ADA 77 IU/L and LDH 472 IU/L, suggestive of tuberculous pleuritis. Finally, she was treated with anti-tuberculous drugs, which led to the complete resolution of symptoms, right-sided pleural effusion, and mediastinal lymphadenopathies.
An HIV-exposed uninfected 20-month-old boy presented to Chris\nHani Baragwanath Academic Hospital in Johannesburg, South Africa,\nwith a 2-day history of shortness of breath, cough and noisy breathing.\nHe had also experienced night sweats, fever and vomiting for a week.\nTwo weeks prior to this presentation, he had been diagnosed with\nbacteriologically unconfirmed PTB at a primary healthcare clinic and\nwas empirically started on a four-drug antituberculosis treatment\nregimen (rifampicin, isoniazid, pyrazinamide and ethambutol). The\ndiagnosis was based on a chest X-ray and a positive Mantoux\ntest. His father (a household contact) had been diagnosed with PTB,\nand had been on first-line antituberculosis treatment for 4 months. \nThe boy had had normal growth and development up to 1 year of age,\nbut had subsequently lost weight, and fallen from a weight-for-height\nz-score +2 to the median over the preceding 8 months.\nOn admission, he was apyrexial, tachycardic and in moderate\nrespiratory distress, with oxygen saturations of 97% in room air. He\nhad marked chest wall indrawing and bilateral posterior cervical\nand axillary lymph nodes (<0.5 cm in diameter). He was clinically\nhyperinflated, with bilateral wheezing. The rest of his clinical\nexamination was normal.\nHe was diagnosed with viral bronchiolitis, and therefore a chest\nX-ray was not performed. He was started on oxygen and hypertonic\nsaline nebulisation. He responded poorly to this initial treatment\nand was therefore started on oral corticosteroids and amoxicillin on\nday 2 of hospitalisation, and his first-line antituberculosis treatment\nwas continued. Gastric aspirate samples for microscopy for acid-fast\nbacilli, Xpert MTB/RIF (Cepheid, USA) and culture for mycobacteria\nwere negative.\nDuring his hospital admission period his wheezing persisted,\nand he remained in moderate respiratory distress. On the fifth day\nof admission, he developed percussion dullness and absent breath\nsounds over the right hemithorax.\nA chest X-ray at this point revealed a large right-sided pleural\neffusion . A computed tomography scan of the chest revealed\nhilar lymphadenopathy and a large right-sided pleural effusion. The\nthoracic duct could not be visualised. Diagnostic pleurocentesis\nconfirmed a chylothorax. It was suspected that tuberculous lymph\nnodes had eroded the thoracic duct causing the chylothorax, and\ntherefore a bronchoscopy was performed, which revealed caseating\nlymph nodes in the right main bronchus suggestive of TB, and 90%\nobstruction of the left main bronchus. The Xpert MTB/RIF (Cephaid,\nUSA) test on a bronchoalveolar lavage specimen identified rifampicinresistant Mycobacterium tuberculosis. Gastric aspirates, pleural fluid\nand bronchoalveolar lavage samples were all smear-negative for acidfast bacilli and mycobacterial culture-negative.\nThe chylothorax was managed with a low-fat diet (with additional\nmedium-chain triglycerides), therapeutic taps for worsening\nrespiratory distress and an octreotide infusion. The boy was\ncommenced on multidrug-resistant TB (MDR-TB) treatment\n(amikacin, levofloxicin, ethionamide, terizidone, pyrazinamide,\nethambutol and high-dose isoniazid) and oral steroids.\nFor further management, he was transferred to a hospital dedicated\nto the care of MDR-TB patients. One month later, he showed marked\nclinical improvement, with almost complete radiological resolution of\nthe chylothorax, and reduced hilar lymphadenopathy . The\nfull case overview is shown in .