Thrombocytosis in Chronic Eosinophilic Pneumonia

Brezis, M; Lafair, Joel

doi:10.1378/chest.76.2.231

Cited by 13 publications

(6 citation statements)

References 6 publications

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“…Increased serum IgE levels are seen in two-thirds of patients (28). The erythrocyte sedimentation rate is usually elevated (26), and peripheral blood thrombocytosis has also been reported (29). The percentage of eosinophils in the BAL fluid is very high (30).…”

Section: Chronic Eosinophilic Pneumoniamentioning

confidence: 99%

Eosinophilic Lung Diseases: A Clinical, Radiologic, and Pathologic Overview

Jeong¹,

Kim²,

Seo³

et al. 2007

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Eosinophilic lung diseases are a diverse group of pulmonary disorders associated with peripheral or tissue eosinophilia. They are classified as eosinophilic lung diseases of unknown cause (simple pulmonary eosinophilia [SPE], acute eosinophilic pneumonia [AEP], chronic eosinophilic pneumonia [CEP], idiopathic hypereosinophilic syndrome [IHS]), eosinophilic lung diseases of known cause (allergic bronchopulmonary aspergillosis [ABPA], bronchocentric granulomatosis [BG], parasitic infections, drug reactions), and eosinophilic vasculitis (allergic angiitis, granulomatosis [Churg-Strauss syndrome]). The percentages of eosinophils in peripheral blood and bronchoalveolar lavage fluid are essential parts of the evaluation. Chest computed tomography (CT) demonstrates a more characteristic pattern and distribution of parenchymal opacities than does conventional chest radiography. At CT, SPE and IHS are characterized by single or multiple nodules with a surrounding ground-glass-opacity halo, AEP mimics radiologically hydrostatic pulmonary edema, and CEP is characterized by nonsegmental airspace consolidations with peripheral predominance. ABPA manifests with bilateral central bronchiectasis with or without mucoid impaction. The CT manifestations of BG are nonspecific and consist of a focal mass or lobar consolidation with atelectasis. The most common CT findings in Churg-Strauss syndrome include sub-pleural consolidation with lobular distribution, centrilobular nodules, bronchial wall thickening, and interlobular septal thickening. The integration of clinical, radiologic, and pathologic findings facilitates the initial and differential diagnoses of various eosinophilic lung diseases.

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Section: Chronic Eosinophilic Pneumoniamentioning

confidence: 99%

Eosinophilic Lung Diseases: A Clinical, Radiologic, and Pathologic Overview

Jeong¹,

Kim²,

Seo³

et al. 2007

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275

164

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“…The IgE level may be elevated, a test for rheumatoid factor may be positive, and thrombocytosis may occur. 10 Spirometry usually reveals a restrictive defect, with a reduced carbon monoxide diffusing constant; airflow obstruction reflects coexisting asthma. Radiographic studies typically show peripheral infiltrates, the so-called photographic negative of pulmonary edema.…”

Section: T Able 4 a Rterial -B Lood G As V Alues And R Esultsmentioning

confidence: 99%

Case 30-2000

Jonathan¹,

Mark²

2000

N Engl J Med

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A 25-year-old man was admitted to the hospital because of asthma, cardiac failure, diarrhea, and weakness of the right hand.He had been well until two years earlier, when asthma developed. It was managed with bronchodilator medications and intermittent pulsed doses of corticosteroids, including prednisone. Seven months before admission, treatment with montelukast sodium was begun. The wheezing worsened, and repeated doses of corticosteroids were administered. Four months before admission, laboratory tests were performed (Tables 1 and 2). Several weeks before admission, the dose of prednisone was tapered, but information on the specific regimen was not available.One month before admission, a dry cough developed, with orthopnea, paroxysmal nocturnal dyspnea, and night sweats, without documented fever. At about the same time, the patient had a mildly pruritic rash on the dorsum of both hands that disappeared after a few days. Ciprofloxacin, clarithromycin, albuterol, salmeterol, fluticasone proprionate, fluvoxamine, lorazepam, and lithium were prescribed. Two weeks before admission, the patient awoke during the night with severe pain in the right shoulder that radiated to the arm and wrist, with paresthesias and weakness of the right hand. The pain soon resolved, but there was persistent numbness and weakness in the first three digits of the right hand, and the patient was unable to extend the second and third digits fully. At the same time, diarrhea developed.Four days before admission, the patient entered another hospital, where examination revealed crackles at both lung bases. His temperature was normal. A stool specimen was positive (+) for occult blood. Labo-ratory tests were performed (Tables 1 and 3). The results of liver-function tests were normal. Arterialblood gases were measured (Table 4). Radiographs of the chest showed cardiomegaly and pulmonary vascular congestion. A cardiac ultrasonographic study, performed at the bedside, revealed global left ventricular hypokinesis, with an ejection fraction of 30 percent.Furosemide, digoxin, methylprednisolone, and omeprazole were administered. Montelukast and fluvoxamine were withdrawn. On the second hospital day, two units of packed red cells were transfused, and the hemoglobin level rose from 7.7 to 11.7 g per deciliter. On the fourth day, the patient was transferred to this hospital.The patient resided with his parents and was unemployed because of severe obsessive-compulsive disorder. He was allergic to birch, oak, and dust mites. He had lost 5 kg in weight in recent weeks. The temperature was 36.6°C, the pulse was 82, and the respirations were 20. The blood pressure was 110/80 mm Hg. The oxygen saturation was 98 percent while the patient was breathing oxygen at a rate of 3 liters per minute.Physical examination showed palmar erythema. The lungs were clear except for bilateral wheezes. A stool specimen was negative for occult blood. Neurologic examination showed wasting of the first dorsal interosseous muscle of the right hand; muscle strength was 4/5 in the w...

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“…The patients' thrombocyte count returned to normal under steroid therapy as in our cases. 13,14 Tissue infiltration by eosinophils and release of some cytokines and humoral factors from the eosinophilic granules leads to tissue damage in multiple organs involving skin, lungs, heart, and CNS. 3 In our patients group, pulmonary (50%) and cardiac (50%) involvements were the most common clinical manifestations of idiopathic HES.…”

Section: Discussionmentioning

confidence: 99%

Hypereosinophilic Syndrome: Hacettepe Experience

Tavil

Aytaç²,

Ünal³

et al. 2016

Journal of Pediatric Hematology/Oncology

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The aim was to evaluate baseline demographic, clinical, and laboratory characteristics, treatment modalities, and outcome of children with idiopathic hypereosinophilic syndrome (HES) followed up in our center. Children who fulfilled the criteria of idiopathic HES followed up at Hacettepe University Faculty of Medicine, Pediatric Hematology Department between June 2004 and October 2013 were included in this study. Medical records of all children with idiopathic HES were reviewed to obtain regarding data. The mean age of 6 children with idiopathic HES was 52.8±44.3 months (13 to 132 mo) at diagnosis. Among 6 children with idiopathic HES; 2 had pulmonary involvement; 1 had cardiac and pulmonary involvement and splenomegaly; 1 had cardiac involvement and hepatosplenomegaly; 1 had cardiac and central nervous system involvement; and 1 had skin involvement. The mean follow-up duration was 36.5±31.4 months. Methyl prednisolone (MP) was used for the first-line therapy. Complete response was achieved with MP in 3 children. All steroid responsive children are alive; whereas 3 children who did not respond to MP had expired. In conclusion, cardiac and pulmonary involvement is the major causes of mortality in HES. Resistance to steroid therapy indicates poor prognosis.

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Thrombocytosis in Chronic Eosinophilic Pneumonia

Cited by 13 publications

References 6 publications

Eosinophilic Lung Diseases: A Clinical, Radiologic, and Pathologic Overview

Eosinophilic Lung Diseases: A Clinical, Radiologic, and Pathologic Overview

Case 30-2000

Hypereosinophilic Syndrome: Hacettepe Experience

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