Serpil C Erzurum MD; Gregory A. und...

Serpil C Erzurum MD; Gregory A. underbrush M.D.; Daniel L. Hamilos, MD; and James A. Waldron, MD

A 33-year-old man with a two-year history of asthma and sinusitis existinged with wheezing, pleuritis, bilateral pleural effusions, and patchy basilar infiltrates onward chest roentgenogram. Laboratory studies revealed peripheral line eosinophilia, and pulmonary function studies showed an obstructive pattern which was bronchodilator responsive. Thoracocentesis yielded an acidotic exudative effusion with depressed glucose, low [C.sub.3], eosinophilia, and a markedly increased rheumatoid factor. render free of access lung biopsy revealed extensive eosinophilic interstitial pneumonitis with necrotizing eosinophilic vasculitis. Although pleural effusions are not away in 29 percent of Churg-Strauss patients, these effusions have not been well described. This report describes the pleural fluid findings in a case of Churg-Strauss syndrome

Churg-Strauss syndrome is a disorder of hypereosinophilia and systemic vasculitis in subdues with asthma and allergic rhinitis. Pleural effusions are commonly reported as a manifestation of this syndrome; however, the cellular and biochemical characteristics have not been well described.[1-3] In this case of Churg-Strauss syndrome the patient's pleural effusion is completely described, and the differential diagnosis of acidotic eosinophilic pleural effusions is reviewed.

CASE REPORT

A 33-year-old nonsmoking man at handed with a two-year history of sinusitis and progressively worsening asthma. brace weeks before admission, he cause to growed pleurisy, first on the right and then in succession the left side of his chest, and a chest roentgenogram showed bilateral pleural effusions. His peripheral WBC was 34000 cells/cu mm with 66 percent eosinophils. A thoracocentesis upon the right yielded cloudy fluid with the following findings: LDH 2856 IU/L; protein, 42 g/dL; pH 708; starch-sugar less than 10 mg/dL; amylase, les than 30 U/L; RBC 600 cells/cu mm and WBC 10400 cells/cu mm with a 95 percent eosinophils. agricultures for bacteria and mycobacteria were negative, and cytology was negative for malignancy. The patient was referr to National Jewish Center for Immunology and Respiratory Medicine for further evaluation.

Physical examination was unremarkable with the exception of for the lung exam, which revealed dullnes at the two bases and diffuse expiratory wheezing. The patient was afebrile. life-blood studies revealed WBC 22,500 cells/cu mm with 628 percent eosinophils. Total eosinophil calculate was 14, 130 cells/cu mm Serum rheumatoid factor was 1:5120 serum antinuclear antibody was positive at 1:40 CH50 was 34 U/ml (normal 22-43) and [Csub3] 113 mg/dl (normal 83 to 77) Immediate and delayed Aspergillus skin touchstones were negative. The PPD was negative. Examination of stool for ova and parasites was negative, and filaria and paragonia serologies were negative. Pulmonary function examples revealed airflow limitation which improved after inhaled bronchodilator therapy. The chest x-ray film revealed bilateral pleural effusions with patchy basilar infiltrates (Fig 1) Comput tomography of the chest revealed an interstitial proces in the right upper lung right lower lung and left lower lung as well as bilateral effusions.

A left thoracocentesis with Cope needle pleural biopsy revealed the following: clear golden fluid; pH, 7.28; LDH 1714 IU/L; protein, 65 g/dL grape-sugar 6 mg/dL; cholesterol, 98 mg/dL; ANA, negative; rheumatoid factor, 1:10240; [Csub3] 255 mg/dL; WBC 4290 cells/?l; eosinophils, 2394 cells/cu mm; and RBC 5250 cells/cu mm Pleural fluid cytology was negative for malignant confined apartments Pleural biopsy showed chronic pleuritis with eosinophilic inflitration. Bronchoalveolar lavage yielded 128 x [10sup6] WBC/ml with 89 percent eosinophils, 3 percent lymphocyte and 7 percent macrophages. lay open lung biospy of the right lower lung revealed patchy interstitial and intraalveolar inflammatory infiltrates rich in eosinophilis, with prominent strokes of inflammatory cells about small pulmonary sailing crafts (Fig 2). Subpleural and interlobular connective tissue was heavily involved with an eosinophil-rich inflammatory infiltrate, and dilated lymphatic channels were at hand in these structures (Fig 3) There was hypertrophy of bronchiolar musculature, bronchial basement membrane thickening, and reduplication of bronchiolar mucosa with goblet lonely dwelling hyperplasia. Occasional arteries contained segmental or circumferential transmural inflammatory infiltrates with associated necrosis of a composing of the vessel wall; mural macrophage giant small cavitys were often present in these lesions (Fig 4) These histologic findings confirmed the clinical diagnosis of Churg-Strauss syndrome Prednisone, 60 mg/day was started, and within sum of two units weeks, the asthma symptoms, eosinophilia, and roentgenographic abnormalities resolv The patient has been followed for ten month onward tapering doses of prednisone without return of his symptoms.