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Chronic Eosinophilic Pneumonia As a Presenting Feature of Churg-Strauss Syndrome

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Chronic Eosinophilic Pneumonia As a Presenting Feature of Churg-Strauss Syndrome Copydght OERS Journals Ltd 1994 Eur Respir J, 1994, 7, 1006-1008 European Respiratory Journal Printed in UK - all rights resewed ISSN 0903 - 1936 CASE REPORT Chronic eosinophilic pneumonia as a presenting feature of Churg-Strauss syndrome J-J. Hueto-Perez-de-Heredia*, F-J. Dominguez-del-Valle*, E. Garcia*, M-L. Gomez**, J. Gallego*** Chronic eosinophilic pneumonia as a presenting feature of Churg-Strauss syndrome. J- *Section of Pneumology, **Service of J. Hueto-Perez-de Heredia, F-J. Dominguez-del-Valle,E. Garcia, M-LGomez, J. Gallego. Pathology, and ***Service of Neurology, OERS Journals hd 1994. Hospital de Navarra. Pamplona, Spain. ABSTRACT: We report on a case of Churg-Strauss syndrome in a 30 year old Correspondence: J-J. Hueto, Seccion de male with a history of perennial rhinitis. The syndrome began nine month ear- Neumologia, Hospital de Navarra, c./ lier with clinico-radiological features typical of chronic eosinophilic pneumonia. Irunlarrea. 3. 31008 Pamplona, Spain Diagnosis of vasculitis was made by skin biopsy, and at that time there was multi- Keywords: Chronic eosinophilic pneu- systemic involvement with pulmonary, cardiac, renal, cutaneous and muscular dii monia ease, and right vocal chord paralysis, which improved with corticosteroids and Churg-Straws syndrome cyclophosphamide. Received: April 20 1993 This case report illustrates the possible overlap of chronic eosinophilic pneume Accepted after revision December 5 1993 nia and the Churg-Strauss syndrome. Eur Respir J., 1994, 7, 10061008. Churg-Strauss syndrome (CSS) is a relatively unusual blood-stained sputum and constitutional symptoms, with disease, characterized by hypereosinophilia and systemic 10 kg weight-loss. In the days preceding admission, vasculitis, that develops in people with asthma and aller- fever, pleural pain and purulent expectoration were also gic rhinitis. The clinico-pathological parameters initi- present. Physical examination revealed a temperature of ally established by CHURG and Smuss [I] were subsequently 39"C, a slight redness of the pharynx and global dec- modified [2, 33. rease of vesicular breathing, with disseminated rhonchi Chronic eosinophilic pneumonia (CEP) was described at pulmonary auscultation. The physical examination as a single entity by CARRINGTONand co-workers [4, 51. was otherwise normal. It is characterized by fever, dyspnoea, cough and weight- Laboratory analyses performed produced the follow- loss. In a typical manifestation, pulmonary infiltrates ing observations: white blood cell (WBC) count appear as negatives of acute pulmonary oedema. Pulmonary, 15.17x109.1-1(eosinophils 7.8%), erythrocyte sedimenta- and usually blood, eosinophilia dramatically responds tion rate (ESR) 80 rnm in the first hour, total immuno- to corticosteroid treatment, but there is a tendency to globulin E (IgE) 467 IUmml-I. Data for basal arterial relapse, with reappearance of radiological infiltrates. Both blood gases were pH 7.51, arterial oxygen tension (Pao,) diseases belong to the group of eosinophilic pneumonias, 7.8 kPa, arterial carbon dioxide tension (Paco,) 4.3 kPa. and the presence or absence of systemic vasculitis dif- Two sputum cultures for fungi, Aspergillus precipitins ferentiates them. Reports of vasculitis initiating as CEP and a study of parasites in faeces were negative. The [68] are scarce. We present a case of CSS that had lung function tests (LFT) showed: forced vital capa- started nine months before as a pulmonary eosinophilia city (FVC) 3.46 1 (69% predicted), forced expiratory with a clinico-radiological picture compatible with CEP, volume in one second (FEV,) 2.40 1 (57% pred), FEV,/ and which in its vasculitis phase involved a paralysis of FVC (69%) with positive bronchodilator test. Lung dif- a vocal chord. fusion capacity was not measured. On the chest X-ray film (fig. 1) bilateral peripheral pulmonary infiltrates were present in axillar regions. Case report Fibreoptic bronchoscopy revealed an inflamed bronchial mucosa, and bronchoalveolar lavage (BAL) cell count A male aged 29 yrs, with a 10 yr history of rhinitis, comprised 48% eosinophils, and no fungi. Bronchial was admitted to our hospital in July 1990. He had not biopsy revealed a submucosal infiltrate of leucocytes, had hyposensitization treatment at any time, or drugs with polymorphonuclear cells and eosinophils predo- before admission, except for some sporadic treatment minating. A diagnosis of chronic eosinophilic pneume with ampicillin. For the past 5 months he had presen- nia was made, and tneatment was initiated with 60 mg-day' ted dyspnoea, respiratory noises, dry cough with some of prednisone, resulting in rapid clinical improvement, CHURG-STRAUSS SYNDROME 1007 The echocardiogram showed an aortic valve regurgita- tion grade II/IV, moderate rnitral regurgitation and vol- ume left ventricular overload with normal ejection hction. On skin biopsy (fig. 2a and b) the most remarkable finding was a central ulceration with a granulomatous Fig. 1. - Chest X-ray showing bilateral peripheral pulmonary infil- trates in axillar regions. disappearance of pulmonary infiltrations and blood hyper- eosinophilia, as well as normalization of LFT and ERS after 8 days. In September 1990, coinciding with a reduction in the corticosteroid dose, the patient began to experience a recurrence of coughing, expectoration, and respiratory sounds, without pulmonary infiltrates, blood hyper- eosinophilia or alterations in respiratory function. Later, on his own initiative, he reduced the dose of prednisone to 5 mg-day-', which led to progressive physical deterio- ration for four months. He was readmitted to hospital in March 1991, with an increase of respiratory symp- tomatology, coughing, expectoration (sometimes blood- stained), dyspnoea, loss of weight (about 19 kg), slight fever, widespread myalgias, skin lesions and voice dys- function. On physical examination the patient was in a generally poor condition, with pale skin, and semispherical papules with whitish adherent scales and ecchymoses, especially on the elbows, palmar zone of the fingers, ear lobes and the outer part of both ankles. Cardiac auscul- tation revealed a systolic murmur audible at each heart valve focus. Pulmonary auscultation revealed bilateral basal crepitations. WBC count was 23.72~109.1-1(eosi- nophils 47%). haemoglobin 91 gel-1, haematocrit 29%, ESR 128 mm in the first hour, immunoglobulin G (IgG) 38.6 gal-', and total IgE 1,251 IUml-1. In the urine, pro- teins were 2.1 g.24 h-', and blood 0.6 mg.1-' with 50-80 red cells-field-' in the sediment. Serum viral hepatitis B markers were negative, as were the Aspergillus precipi- tins. Data for basal arterial blood gases were pH 7.46, Paco, 4.83 kPa, Pao, 9.97 kPa. On chest X-ray, the cardiac silhouette was normal, with a slight right basal pulmonary interstitial pattern. Lung function tests showed: FVC 2.48 1 (49% pred); FEV, 1.92 1 (45% pred); FEV,/FVC 77%; total lung capacity (TLC) 5.46 1 (78% ired); single-breath dif- fusing capacity for carbon monoxide (sB-T~~~)8.34 Fig. 2. - a) Skin lesion with central ulceration and granulomatous % infiltrate at the bottom. (Haematoxylin and eosin; magnification x38). mmol'min-"kPa-' (7 pred)* SB-TLco'alveolar b) Detail of extravascular granulomatous foci with central fibrin, col- lation (SB-~NA)1.91 mm~l'fin-'.Wa-''l.' (90 % red). lagen degeneration, necrotic neutrophils and eosinophils, histiocytes We discovered a right band paralysis by laryngoscopy. and fibroblasts. (Haematoxylin-eosin; magnification x146). 1008 J-1. HUETO-PEREZ-DE-HEREDIA ET AL. infiltrate. The granulomatous lesions were extravascular, entities could favour idiopathic CEP being a part of the with a central zone of fibrinoid necrosis, collagen degene- CSS complex. ration, and necrotic neutrophils and eosinophils. There Mononeuritis multiplex is the most usual neurological were no recognized vascular structures within the necro- manifestation in CSS, but cranial nerves can also be sis. The vessels located in this area also showed fibri- affected, especially the optic nerve. Lesions of the 11, noid necrosis. IlI, VII and VIII nerves [10-131 have less frequently The patient was treated with prednisone and cyclophos- been described. We found no previous reports of vocal phamide, with a good response including rapid disap chord p,aralysis like that observed in our patient, which pearance of respiratory symptoms, fever and myalgias reverted after two months of treatment with cyclophos- during the first week, total normalization of eosinophil pharnide and corticosteroid. count and ESR after two weeks and of IgE after five In agreement with other authors [3, 101, we think that weeks, progressive disappearance of the dermal lesions several disorders associated with asthma and eosinophi- and vocal chord dysfunction with total recovery after two lia may be included in a spectrum of diseases, in which months, and normalization of the respiratory function the eosinophil could determine the development of the (volumes and TLCo) after one month. A slight TLCONA lesions. deficit (average 72 % pred) persisted after total normali- zation of lung volumes. The echocardiogram, repeated References 11 months later, was unchanged. Chwg J, Strauss L. Allergic granulomatosis, allergic angiitis and periarteritis nodosa. Am J Path01 1951; 27: Discussion 277-301. Chumbley LC, Harrison EG, De Remee RA. Allergic CSS and CEP are two infrequent disorders, probably granulomatosis and angiitis (Churg-Strauss syndrome): of immunological aetiology, in which the eosinophil,
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