ObjectiveIt has recently been described that circulatory and BAL regulatory T-cells (Tregs), defined as CD4+CD25highCD127low are increased in patients with active sarcoidosis compared with other interstitial lung diseases.Materials and methodsWe studied prospectively 17 patients (10 women, 7 men) of median age 39 years (range 27-65) with active granulomatous lung diseases (GLD) (10 patients with sarcoidosis (BBS), and 7 with hypersensitivity pneumonitis (HP), and 9 healthy controls. Bronchoalveolar lavage fluid (BAL) and induced sputum Treg counts, CD4+, CD8+, CD25+ cells were quantified by flow cytometry. Disease activity was measured by ACE serum level. Pulmonary function tests were performed using an Elite DL Medgraphics body box.ResultsWe found Treg cells count significantly elevated in induced sputum from active GLD (38.3% vs. 7.1% and 5.3% in BBS, HP, and control, respectively). A significantly higher percentage of Treg cells characterized BAL cells from HP patients (2.27%; 9.5%; 2.1%, in BBS, HP and control, respectively). There was a strong correlation with ACE serum level and Treg cell count in BAL fluid of BBS patients, with no such correlation within HP patient group, nor Treg cell count and pulmonary function tests.ConclusionsOur data suggest a potential role of CD4+CD25 high CD127 low induced sputum and BAL lymphocytes from patients with active granulomatous lung diseases and hypersensitivity pneumonitis. An increased number of Treg cells in active GLD may be involved in immune regulation in active granulomatous lung diseases. The results indicate that analysis of these cells could be useful as markers of disease activity in granulomatous lung diseases.
A twenty eight-year-old male presented with a two week history of dyspnea, cough, hemoptysis, chest pain, and fever 38-39°C. He also complained of loss of appetite, general weakness and left leg pain for two months preceding admission. He was referred with suspicion of lung tumor to our institution. Chest X-ray showed almost total atelectasis of the right lung with compensatory overinflation of the contralateral lung. Using computed tomography (CT), a lesion of diameter of 19.3 × 14.1 × 19.1 cm in the right lung, pleuritis, TH3 osteolysis, and compensatory overinflation of the left lung was seen. Bronchoscopy revealed a total obstruction of the right main bronchus due to submucosal infiltration and compression of the right main bronchus with negative histology of bronchial biopsy specimens. transthoracic fine needle aspiration revealed celullae suspectae probabiliter neoplasmaticae suggesting tumor fusocellularis. USG of the abdomen revealed liver with numerous heterogeneous, solid areas hypo- and hyperechogenic, some of them with features of liquid or the disintegration up to diameter of 74 mm. Subsequent fine needle aspirations of the thorax and liver revealed fibrolamellar hepatocarcinoma and carcinoma adenoides of the lung. Patient underwent chemotherapy with 5-FU/DDP/VCR with no response. This report presents a case of a rare lung metastasis from FL-HCC.
A fifty-year-old female presented with a one month history of progressive dyspnea, productive cough, pain of elbows and knees, and 40°C fever despite antibiotic treatment. She has been diagnosed of bronchial asthma over 25 years before admission and oral and depot glucocorticosteroids as a long-term therapy was applied. Recently, an attempt of inhaled corticosteroids and LABA treatment was introduced with no success. Four years before admission she also developed peripheral neuropathy. Physical examination revealed tachypnea, wheezes, rhonchi and wet cracles on auscultation, tachycardia, skin nodules, urticarial rash and necrotic bullae all over the body. Chest X-ray showed transient, patchy, nonsegmental areas of consolidation with predilection for lower zones with the area of consolidation in lower left zone. Obstruction was found on spirometry. Tachycardia on ECG and myocardial fluid on ECHO were also detected. Lab exams revealed elevated CRP, WBC, eosinophils, and IgE levels. ANA and ANCA antibodies were not found. Patient was diagnosed of Churg Strauss Syndrome and initial treatment of prednisone was introduced. After four days of treatment, temperature normalized, and dyspnea diminished. After one month of therapy skin lesions regressed. After 18 months of the treatment patient reports no signs, nor symptoms of the disease. Patient continues oral corticosteroid therapy.
A 61-year-old Caucasian was admitted to Department of Chest Diseases and Tuberculosis, Medical University of Bialystok, Poland for progressive muscle weakness and weight loss. Eighteen months prior to admission, the patient had been diagnosed with pulmonary embolism. At that point he was started on Enoxaparin QD. Past medical history was unremarkable. In the interim, the patient developed fever, myalgia and progressive dyspnea. Physical examination on admission revealed a rash on his upper torso and back, and the extensor surfaces of all four extremities. Laboratory values included CPK 8229, MB fraction 219, LDH 981. Chest X-ray and CT scan revealed bilateral patchy consolidations and ground-glass opacities. EMG was consistent with myositis. The patient was started on solumedrol 40 mg i.v., b.i.d., and then switched to prednisone 40 mg b.i.d. His symptoms and muscle strength improved remarkably. The patient was discharged with prednisone with an outpatient follow up.
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