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.
Female patient aged 75 years who had no history of chronic disease apart from depression presented at outpatient clinic with complaints of lassitude, loss of appetite, exertional dyspnea for 4 months, and dry coughing for 2 months. Her examination revealed marked decrease in respiratory sounds at basal segments of the right lung. Hematological values, sedimentation, glucose, urea, creatinine, sodium, potassium, total protein, and albumin levels were within normal limits. Levels of alanine aminotransferase (189 U/L), aspartate aminotransferase (113 U/L), cholesterol (251 mg/ dL), and lactate dehydrogenase (LDH) (193 U/L) were also measured. X-ray graphy revealed a dark shadow, consistent with pleural fluid masking the demarcation line between mediastinum and pleura at the inferior zone of the right lung (). Thoracic computed tomography (CT) revealed multiple sites of lymphadenopathy, the largest containing dense calcification 22 mm in size, and marked pleural effusion on the right side (). Milky fluid with high density sampled from pleural effusion did not precipitate after centrifugation, and contained TG (1072 mg/dL), cholesterol (173 mg/dL), LDH (148 U/L), and albumin (2.7 g/ dL) at indicated concentrations. Sudan staining disclosed presence of fat globules. Lymphocyte dominancy was also detected in pleural fluid. Sputum ARB -negativity was detected 3 times, and bronchoscopy of the patient did not reveal any endobronchial pathology. Pleural biopsy was performed. Bronchial lavage and bronchoscopic biopsy results indicated benign condition of chronic pleuritis. Positron emission tomography-CT was obtained to rule out mediastinal tumor. During lymphatic scanning performed to detect etiology of chylothorax, images taken at second, fourth, and sixth hours demonstrated passage of radiographic contrast substance through bilateral inguinal, parailiac, paracaval, and paraaortic lymph nodes, and accumulation of radioactivity in these lymph nodes at popliteal, femoral, and pelvic regions, respectively. On delayed thoracic images, no uptake of radioactivity apart from background activity was observed. Images suggested possible thoracic duct obstruction. Mediastinal lymph node biopsy performed at external center revealed presence of granulomas demonstrating caseous necrosis. Abdominal ultrasound was normal. Antituberculosis treatment was initiated. Symptoms regressed with treatment, and level of liver enzymes decreased. At sixth month, marked regression in pleural effusion was observed ().