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.
A 17-year-old girl was admitted to the Korean University Ansan Hospital with a one-month history of fever, abdominal distention and dyspnea. The patient had been treated in another hospital for 10 days but the cause of ascites and pleural effusion had not been discovered. She was transferred to our hospital for further care. On admission, body temperature was 38.6℃, heart rate was 146/min and body weight was 56 kg. On chest auscultation, breathing sound was decreased on both lower lung fields. Abdominal examination revealed shifting dullness and the lower extremities were severely edematous. A chest radiograph taken on admission showed diffuse fine nodular opacities in both lungs and bilateral pleural effusion. Chest computed tomography (CT) showed pleural effusion of both sides, more serious on the left side, and pericardial effusion and multifocal nodular consolidation on both lung fields (). Abdominal CT showed a large amount of ascites with diffuse peritoneal thickening and multiple necrotic lymphadenopathy in the abdominal cavity, and enhanced wall thickening in the distal ileum and ascending colon (). Initial laboratory results were as follows: white blood cell count 6,670/mm3, hemoglobin 6.7 g/dL, serum total protein 4.6 g/dL and albumin 2.2 g/dL. Thoracentesis and paracentesis were performed to verify the nature of fluid apparent in the chest and abdominal CT images.\nPleural fluid () was turbid and whitish-colored, with pH 8.0, protein level 3.1 g/dL, lactate dehydrogenase of 5,855 IU/L, triglyceride 133 mg/dL and adenosine deaminase 121.6 IU/L. The lactate dehydrogenase ratio of pleural fluid versus serum was 15, consistent with exudate. Ascites () was milk-like and turbid in appearance, pH 8.0, albumin level 0.5 g/dL, triglyceride 864 mg/dL and adenosine deaminase 14.8 IU/L. We diagnosed chylothorax and chylous ascites because the triglyceride level of pleural fluid and ascites were higher than 110 mg/dL and 200 mg/dL, respectively. Direct smear of pleural fluid and ascites for acid fast bacilli (AFB) was positive only in pleural fluid. So, finally we diagnosed the patient as having TB associated with chylothrax and chylous ascites on the basis of positive AFB stain and abdomen CT. Initially, the patient received anti-TB treatment with quadritherapy including isoniazid 300 mg/day, rifampin 600 mg/day, pirazinamide 1,500 mg/day and etambutol 1,200 mg/day. The patient also was put on a high protein and low fat diet with medium chain triglyceride. Mycobacterium tuberculosis was cultured from sputum and pleural fluid on 28th day from admission and the isolate was susceptible to all anti-TB medications. The patient improved continuously after anti-tuberculosis medication, and pleural effusion and ascites were slightly decreased on follow-up chest and abdomen X-ray. The patient was discharged on day 60 of hospitalization with ongoing anti-tuberculosis treatment.