Istory and was not a smoker. He had suffered, since 1999, from : Différence entre versions

Version du 1 mars 2018 à 14:35

The HRCT showed bilateral confluent hyperdensities consistent with BAPTA msds peribronchovascular micronodules, ground-glass hyperdensities, and alveolar condensation, together with 2 excavated lesions in the left lower lobe. The PFT showed the following: vital capacity (VC)--2.71 L (71 ); forced expiratory volume in 1 second/VC--78 ; and diffusing capacity of the lung for carbon monoxide (DLCO)-- 85 . Bronchoscopy showed an erosive bronchitis and bronchial biopsies revealed a nongranulomatous ulcerated bronchitis. The BAL content was 486 cells/mm3 with 95 neutrophils. An empirical antibiotic therapy (ceftriaxone and spiramycin) was not beneficial. Because AOSD was suspected, a 1 mg/kg/d prednisone treatment was started. This treatment proved highly efficient; all the above-described symptoms regressed. Chest computed tomography (CT) reversed to normal after 2 months of treatment. However, the patient developed a steroid dependence at 15 mg/d prednisone. Colchicine and then hydroxychloroquine was added as steroid-sparing treatment. During the following 3 years, 5 relapses of subacute interstitial lung disease occurred when corticosteroids were tapered below 10 mg/d but resolved with higher dosage. Three years later, the pulmonary functional tests were recovered: VC--2.71 L (71 ); forced expiratory volume in 1 second/VC--78 ; and DLCO/alveolar volume: 82 . During the following years, the lung involvement did not relapse but the patient developed a chronic reHLH. He was started on intravenous immunoglobulins and azathioprine. Infliximab 5 mg/kg was also introduced in 2007 but did not allow controlling the disease; the patient remained steroid-dependent at 20 mg/d prednisone. In 2011, the patient died from myocardial infarction.3.1.3. Case 3. In April 2006, a 42-year-old man with a history of heroin abuse and ongoing substitution treatment, cured hepatitis C, and left ulnar osteitis presented with cough and dyspnea. A 5day treatment with amoxicillin lavulanate and prednisone was inefficient. Two days later, he exhibited fever (39 ), polyarthralgia, and myalgia. A CT showed bilateral axillary and mediastinal lymphadenopathy together with a right segmental atelectasis. Finally, the progression was favorable after switching for pristinamycin. In June 2006, the patient was referred to our center after a 7-kg weight loss during the last 2 months, recurrent fever, cough, and New York Heart Association-IV dyspnea. The clinical examination revea.Istory and was not a smoker. He had suffered, since 1999, from an intermittent biopsy-proven neutrophilic dermatitis considered as an atypical Sweet syndrome. He had during the last few months a transient rash, an intermittent fever (38?9 ), sweats, a 6-kg weight loss, sore throat, dysphonia, cough with mucopurulent sputum, arthralgia, and lymphadenopathy. He has been successfully treated with antibiotics and corticosteroids. The HRCT showed bilateral confluent hyperdensities consistent with peribronchovascular micronodules, ground-glass hyperdensities, and alveolar condensation, together with 2 excavated lesions in the left lower lobe. This was associated with a mild bilateral pleural effusion and mediastinal lymphadenopathy. The laboratory data were the following: CRP--158 mg/L; high ESR; procalcitonin--