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Active pulmonary tuberculosis in a patient with Langerhans cell histiocytosis.

L cell histiocytosis (LCH) or pulmonary histiocytosis is an uncommon parenchymal lung disease of unknown origin. The lesions of LCH contain single of multifocal proliferation of histiocytes similar in phenotype to dendritic Langerhansʼcell.1 The natural history is extremely a variable. The disorder ranges in clinical severity from a solitary eosinophilic granuloma of bone to a generalized disease with multiple organ involvement. Rarely, LCH has been reported to be associated with some disorders such as pulmonary tuberculosis.2 Here, we report a cases of a 21-year-old male patient with LCH and active pulmonary tuberculosis. A 21-year-old male patient was hospitalized due to complaints of progressive dyspnea in the last 6 months, occasional cough and night sweats. There was nothing marked in the medical history of the patient who was working in tourism industry. He had 9 years smoking history. Physical examination of respiratory system and other systems were normal. Routine hematological studies were normal; there was no peripheral eosinophilia, the erythrocyte sedimentation rate was 35 mm/h. Other hematological and biochemical data on admission were within normal ranges. Postero-anterior (PA) chest x-ray revealed extended heterogeneous reticulonodular infiltration in both lung fields. Thorax high resolution computed tomography (HRCT) revealed a reticulonodular infiltration involving all lung areas in which there were thin walled cavitary lesions among those the biggest one was 10 mm in diameter (Figure 1). Nonspecific culture of sputum revealed normal oral flora. Tuberculin skin test was negative. Acid-fast bacilli (AFB) was not detected in the sputum, in gastric lavage, and in bronchial washing fluid under microscopic examination. A fiber optic bronchoscopy was performed. There was no endobronchial pathology. Brochoalveolar lavage fluid examination and cell distribution were nondiagnostic. Transbronchial biopsy specimens showed normal lung mucosa and parenchyma. Pulmonary function tests (PFT) revealed restrictive disease. The PFT presented the following values: Vital capacity (VC), 3.45 L (62% pred); forced vital capacity (FVC), 2.85 L (56% pred); FEV1, 2.79 (78% pred); and peak expiratory flow rate, 6.25 L/sec (71% pred). Diffusion capacity was lowered (4.9 mmol/min/kPa, 62% pred). The patient underwent a video assist thoracic surgery for definite diagnosis. Histopathological examination of the specimen of biopsy revealed many eosinophils, histiocytes and lymphocytes all of which showed centrilobular distribution pattern consisting of dense chronic inflammation, edema, and fibrosis. Muscular hyperplasia and dilatation were detected. Immunohistochemical study of S-100 protein of biopsy specimen showed S-100 protein positive histiocytes in granulomatous lesions. In addition, moderate interstitial fibrosis was seen with trichrome staining. Histological findings were compatible with LCH. There was no clinical or laboratory finding compatible with LCH in other organs. Abdominal ultrasound was normal. During laboratory evaluation Mycobacterium tuberculosis was isolated on culture media. The final diagnosis was LCH and pulmonary tuberculosis. Antituberculosis treatment with izoniazid, rifampicin, pyrazinamide and ethambutol was started. Corticosteroids were not used for the treatment. A repeat thorax HRCT examination after 6 months from the beginning of the treatment revealed marked improvement in nodular lesions, and thin walled cystic lesions in the upper lung fields. Marked regression was detected for micro nodular opacities in both lung fields. Our patient was diagnosed with pulmonary LCH proven through lung biopsy and AFB culture positive pulmonary tuberculosis. Antituberculosis treatment resulted in an objective radiological improvement and AFB culture negativity. The clinical course of LCH ranges from spontaneous resolution to a chronic and sometimes lethal disease. The etiology of LCH remains obscure, but the vast Clinical Notes