Try these keywords: happy, success, awesome
 

از دکتر بپرسید!

در این بخش می توانید سوالات خود در رابطه با بیماری های ریوی را مطرح نمایید و دکتر در اسرع وقت پاسخگوی سوالات شما خواهد بود.

 

ساعت های کاری

  • شنبه - چهارشنبه............3.00 ب.ظ - 7.00 ب.ظ
  • شنبه.......................9.00 ب.ظ - 12.00 ب.ظ
  • یکشنبه.....................9.00 ب.ظ - 12.00 ب.ظ
 

رزرو وقت آنلاین

در این بخش شما کاربران عزیز می توانید قرار ملاقات خود با دکتر را رزرو نموده و هزینه را بصورت آنلاین پرداخت نمایید.

 

بیماری های ریه

در این قسمت از وب سایت مطالب مفیدی در رابطه با بیماری های ریه گنجانده شده است. ضمن اینکه نظرات کاربران هم زیر هر مطلب موجود می باشد.

دکتر علیرضا ثابت پور

فوق تخصص ریه و متخصص داخلی

عضو کالج سلطنتی متخصصان داخلی انگلیس

بهترین دکتر ریه ، فوق تخصص ریه و متخصص داخلی از انگلیس

فلوشیپ اعمال تهاجمی ریه و برونکسکوپی با تکنیک سنوگرافی

eosinophilia

 

Causes of pulmonary eosinophilia

Top of Form

INTRODUCTION — Eosinophilic lung diseases are a heterogeneous group of disorders that share the feature of abnormally increased numbers of eosinophils within the pulmonary parenchyma. The defining characteristics needed for the diagnosis of pulmonary eosinophilia include either [1-3]:

  • Peripheral blood eosinophilia with radiographically or tomographically identified pulmonary abnormalities
  • Lung tissue eosinophilia demonstrated in transbronchial or open lung biopsies
  • Increased eosinophils in bronchoalveolar lavage (BAL) fluid

Peripheral blood eosinophilia is, by no means, uniformly increased in many types of eosinophilic lung diseases [4,5], and routine chest radiographs may fail to detect infiltrates in some cases [6].

The major causes of pulmonary eosinophilia will be reviewed here (table 1 and table 2). The differential diagnosis of blood eosinophilia and eosinophilia of other tissues are discussed separately.

HELMINTHIC INFECTIONS — Helminthic infections elicit several pathophysiologically distinct forms of pulmonary eosinophilia based upon the characteristic behavior of the organisms in the lung and upon the associated host immune response.

Transpulmonary passage of helminth larvae (Löffler's syndrome) — Three types of helminths, Ascaris lumbricoides, hookworms, and Strongyloides stercoralis, have life cycles in which infecting larvae reach the lungs via the bloodstream, penetrate into alveoli, and ascend the airways before descending the alimentary tract into the small bowel [7].

The syndrome of transient pulmonary infiltrates and peripheral blood eosinophilia, a subset of the pulmonary eosinophilia syndromes, was originally described by Löffler; Ascaris infection acquired from the use of contaminated human nightsoil as fertilizer was determined to be the cause [8]. Subsequent investigations have confirmed that Ascaris is the most common cause of Löffler's syndrome worldwide. Hookworm larvae and Strongyloides less commonly elicit symptoms or pulmonary eosinophilia [7].

Symptomatic patients most often complain of an irritating, nonproductive cough and burning substernal discomfort that is aggravated by coughing or deep breathing. Dyspnea, wheezing, fever, and blood-tinged sputum containing eosinophil-derived Charcot-Leyden crystals may also be present.The chest radiograph may show round or oval infiltrates ranging in size from several millimeters to several centimeters in both lung fields; these lesions are more likely to be present when blood eosinophilia exceeds 10 percent. The infiltrates are migratory and may become confluent in perihilar areas but usually clear spontaneously and completely after several weeks.

Pulmonary parenchymal invasion — In contrast to the parasites mentioned above, several organisms can directly invade the pulmonary parenchyma and produce long-lasting pulmonary manifestations rather than briefly passing through the lungs en route to the gastrointestinal (GI) tract. These include Paragonimus lung flukes and cestodes causing echinococcosis and less commonly Taenia solium causing cysticercosis. As an example, Paragonimus lung flukes may invade the lungs and produce pleural effusions or eosinophil-enriched inflammatory infiltrates [7]. Recurrent hemoptysis can occur, and chocolate colored sputum may be observed, composed of a mixture of blood, inflammatory cells, and Paragonimus eggs. Blood eosinophilia tends to be prominent in the early stages of disease but minimal with established disease .

Leakage or rupture of pulmonary cysts in echinococcosis or cysticercosis can also cause pulmonary eosinophilia.

Heavy hematogenous seeding — This disease category describes eosinophilic pulmonary responses provoked by heavy deposition of helminthic larvae or eggs that are carried hematogenously into the lungs. This type of hematogenous spread is not essential for the parasite life cycle, in contrast to the "normal" transpulmonary migration noted above. Pulmonary symptoms such as cough, wheezing, and dyspnea may result, and blood eosinophilia is common. The syndrome can arise in several settings, including [7,9]:

  • Abnormal numbers of the hookworms or ascarids that cause cutaneous or visceral larva migrans with pulmonary involvement [10].
  • Abnormal numbers of hematogenous larvae in heavy trichinellosis infections.
  • Abnormal spread of schistosomal parasites to the lungs via collateral vessels following anthelminthic therapy. In addition, eosinophilic pneumonia may occur in the early phase (three to six weeks) after infection with schistosomes; patients may experience cough and shortness of breath, chest computed tomographic (CT) scanning may detect multiple small nodules and, less commonly, infiltrates [11].
  • Hyperinfection and dissemination of strongyloidiasis may produce invasion of a number of organs (including the lungs) separate from the transpulmonary passage, which is required for the helminthic life cycle.

Tropical pulmonary eosinophilia — This form of eosinophilic pneumonia results from a distinct immune response to the bloodborne microfilarial stages of the lymphatic filariae, Wuchereria bancrofti and, less commonly, Brugia malayi [12,13]. Pulmonary symptoms and infiltrates in a traveler or immigrant from a filaria-endemic region accompanied by dramatic peripheral eosinophilia, markedly elevated serum IgE, and antifilarial antibody levels are pathognomonic for this diagnosis. An identical but nonfilarial syndrome of tropical pulmonary eosinophilia of uncertain etiology has also been recognized [14].

NONHELMINTHIC INFECTIONS — Coccidioidal infection can cause eosinophilic pneumonia [15]. Differentiation from idiopathic eosinophilic pneumonia may be difficult because organisms may be absent from cultures and open lung biopsy specimens [16]. Pulmonary eosinophilia rarely complicates pulmonary tuberculosis [17].

MEDICATIONS AND TOXINS — Pulmonary eosinophilia has been reported following the ingestion or inhalation of a variety of medications and toxins. The clinical presentation ranges from asymptomatic pulmonary infiltration with eosinophilia to chronic cough with or without dyspnea and fever to acute eosinophilic pneumonia [18].

Although nonsteroidal anti-inflammatory drugs (NSAIDs) and antimicrobials (eg, nitrofurantoin, minocycline, sulfonamides, ampicillin and daptomycin) are the most common classes of drugs associated with pulmonary eosinophilia, a number of other agents have been implicated in more than 20 published case reports (eg, anticonvulsants, antidepressants, ACE inhibitors, beta blockers, hydrochlorothiazide and other sulfa-containing compounds, radiographic contrast media, L-tryptophan, methotrexate, amiodarone, and bleomycin). The Groupes d'Etudes de la Pathologie Pulmonaire Iatrogène maintains a frequently updated website listing drugs that have been associated with pulmonary infiltrates and eosinophilia with literature references [19].

A number of toxin exposures have also been associated with pulmonary eosinophilia including [20-28]:

  • Aluminum silicate and particulate metals [20]
  • Sulfite-exposed grape workers [21]
  • Scorpion stings [22]
  • Inhalation of heroin or crack cocaine [23]
  • Inhalation of organic chemicals during rubber manufacture [24]
  • Inhalation of dust [25] or smoke [26,27,29]
  • Abuse of 1,1,1-trichloroethane (Scotchguard) [28]

Rare outbreaks of pulmonary eosinophilia have been described. The largest of these, the "toxic oil syndrome", affected >20,000 people in Spain in 1981, and was associated with ingestion of rapeseed oil contaminated with aniline derivatives [30]. A similar outbreak, "eosinophilia-myalgia syndrome" occurred in 1989, in association with L-tryptophan ingestion. Although the predominant complaints were neuromuscular, >50 percent of the affected individuals had cough or dyspnea and 17 percent had pulmonary infiltrates [31].

The importance of drug and toxin-induced pulmonary eosinophilia cannot be overemphasized as many cases will resolve with withdrawal of the offending agent.

ACUTE EOSINOPHILIC PNEUMONIA — Idiopathic acute eosinophilic pneumonia (AEP) may be a cause of acute respiratory failure in a previously healthy patient. Most patients present with an acute febrile illness of less than seven days' duration characterized by a nonproductive cough, dyspnea, and a variety of nonspecific radiographic changes [32] .

Peripheral eosinophilia is rare at presentation, but may develop during the course of the disease. Hypoxemic respiratory insufficiency is frequently identified at presentation and often requires mechanical ventilation. Histopathology is notable for diffuse alveolar damage, hyaline membranes, and marked numbers of interstitial and lesser numbers of alveolar eosinophils [33]

CHRONIC EOSINOPHILIC PNEUMONIA — Chronic eosinophilic pneumonia (CEP) is another idiopathic disorder characterized by an abnormal accumulation of eosinophils in the lung [4]. The syndrome often presents as a subacute illness with a constellation of symptoms including cough, fever, progressive breathlessness, weight loss, wheezing, and night sweats; asthma accompanies or precedes the illness in 50 percent of cases. Peripheral eosinophilia is common, but may be absent in 10 to 20 percent of patients [4,34]. CEP occurs predominantly in women and nonsmokers; cases have been reported following radiation therapy for breast cancer [34,35].

The chest radiographic finding of bilateral peripheral or pleural-based infiltrates described as the "photographic negative" of pulmonary edema is virtually pathognomonic for the disease (picture 3) but found in fewer than one-third of cases [4]. Pleural effusions have been described in a few cases [36], and cavitation occurs rarely [37]. Histopathologic findings are characterized by interstitial and alveolar eosinophils and histiocytes, including multinucleated giant cells (picture 4). Fibrosis is minimal, and bronchiolitis obliterans organizing pneumonia (BOOP) is a commonly associated finding [4].

CHURG-STRAUSS SYNDROME — The Churg-Strauss syndrome (allergic granulomatosis and angiitis [CSS]) is a vasculitic disorder often characterized by sinusitis, asthma, and prominent peripheral blood eosinophilia [38]. It is the sole form of vasculitis that is associated with both eosinophilia and frequent lung involvement. In addition to the lungs, the skin and the cardiovascular, GI, and nervous (especially mononeuritis multiplex) systems may also be involved.

Chest x-ray abnormalities in patients with CSS are quite diverse, but most commonly consist of transient and patchy opacities without lobar or segmental distribution. Lung biopsy reveals eosinophilic infiltrates, an eosinophilic vasculitis (especially of the small arteries and veins), interstitial and perivascular necrotizing granulomas, and areas of necrosis .However, tissues from patients presenting with new onset CSS may not exhibit all of the classic pathologic features of this syndrome, but rather may resemble the eosinophilic infiltration seen in CEP [39]. In some patients with CSS, CEP has occurred prior to the onset of the vasculitic syndrome.

ALLERGIC BRONCHOPULMONARY ASPERGILLOSIS — Allergic bronchopulmonary aspergillosis (ABPA) is a complex hypersensitivity reaction that occurs when airways become colonized by Aspergillus [1,40,41]. Repeated episodes of bronchial obstruction, inflammation, and mucoid impaction can lead to bronchiectasis, fibrosis, and respiratory compromise. Immunologic responses elicited by Aspergillus fumigatus are responsible for this syndrome.

The clinical picture of ABPA is dominated by asthma (or cystic fibrosis) complicated by recurrent episodes of bronchial obstruction, fever, malaise, expectoration of brownish mucous plugs, peripheral blood eosinophilia, and hemoptysis. Wheezing is not always evident, and some patients present with asymptomatic pulmonary consolidation. Imaging studies show central bronchiectasis, but this finding is neither sensitive nor specific for the disorder .

Histologic findings in patients with ABPA include asthmatic bronchiolitis, eosinophilic pneumonia, bronchocentric granulomatosis, and mucoid impaction of bronchi [42]. On occasion, bronchocentric granulomatosis in the absence of endobronchial fungi occurs with associated pulmonary eosinophilia [43].

MISCELLANEOUS CAUSES — A number of other conditions are less commonly associated with pulmonary eosinophilia. Examples include:

Hypereosinophilic syndromes — The hypereosinophilic syndromes (HES), some of known and some of idiopathic etiology, are associated with marked peripheral eosinophilia and potential involvement of diverse organs such as the heart, GI tract, lungs, brain, and kidneys [44,45]. Other idiopathic lung diseases — Modest degrees of BAL eosinophilia may be found in patients with idiopathic pulmonary fibrosis, sarcoidosis, hypersensitivity pneumonitis, and connective tissue disorders [46]. Less commonly, pulmonary eosinophilia occurs in association with BOOP, rheumatoid arthritis, Sjögren's syndrome, postradiation therapy, graft-versus-host disease, and usual interstitial pneumonia [1,47,48]. Pulmonary eosinophilia may also be associated with lung allograft rejection [49].

Neoplasms — Peripheral and/or localized pulmonary eosinophilic infiltration occasionally occurs in conjunction with undifferentiated lung carcinomas or lung metastases of cervical tumors; squamous carcinomas of the vagina, penis, skin, or nasopharynx; adenocarcinomas of the stomach, large bowel or uterine body; or transitional cell bladder carcinomas [50]. Pulmonary eosinophilia may also occur when lymphoma, acute eosinophilic leukemia, or the Sézary syndrome involves the lung.

GENERAL DIAGNOSTIC APPROACH — The diagnostic approach to patients with these disorders must be dictated by the specific clinical findings and the setting in which they occur. Every patient should undergo a thorough history and physical examination.

History — Attention should paid to:

  • Medication and chemical exposures, including common NSAIDs and antibiotics, as well as occupational exposures to dust, smoke, or chemicals
  • Travel and immigration histories, including residence in or travel to regions endemic for coccidioidomycosis and varied parasites (more frequently encountered outside of the United States)
  • Respiratory history and findings, including antecedent or concomitant asthma, as found in those with ABPA, CSS, some with CEP and some with the helminthic etiologies. Duration of any antecedent symptoms should be considered. AEP is characteristically abrupt in onset, whereas CEP may develop insidiously over months. Asthma in CSS may begin years before the development of vasculitic lung involvement.
  • Presence of symptoms or signs of extrapulmonary organ involvement, since these may be indicative of systemic diseases, including CSS, HES, and neoplasms

Blood eosinophilia — The presence of an elevated blood eosinophil count helps to support the diagnosis of a number of the entities discussed above. However, the absence of blood eosinophilia does not exclude these conditions.

A bacterial pneumonia is typically associated with an eosinopenic response, in part due to heightened endogenous glucocorticoid production. Thus, even mild or moderate blood eosinophilia in a patient with an acute or subacute pulmonary disease should suggest one of the disorders considered above.

However, not all of the conditions that have pulmonary eosinophilia will have blood eosinophilia, especially AEP and some CEP. Any concomitant glucocorticoid therapy will also suppress blood eosinophilia. The magnitude of blood eosinophilia is not a reliable means to distinguish the possible etiologies of pulmonary eosinophilia.

Imaging — Radiographic imaging of the chest, especially by high resolution CT, can provide valuable findings early in the investigation of the patient. The ability of high resolution CT scans to help differentiate among the causes of pulmonary eosinophilia has been evaluated [51]. The three eosinophilic lung diseases that could be diagnosed with greatest certainty were CEP, ABPA and AEP.

  • Characteristic CT findings of CEP include: bilateral airspace consolidation and areas of ground-glass attenuation, involving predominantly the peripheral regions of the middle or upper lung zones [34,51-53].
  • Common CT findings of ABPA consist of bronchiectasis, mucous plugging, bronchial wall thickening, atelectasis, airspace consolidation, areas of ground-glass attenuation, and upper and central lung predominance [51]. The first three of these findings are the most indicative of ABPA.
  • CT findings in AEP include ground-glass attenuation, airspace consolidation, poorly defined nodules, interlobular septal thickening and pleural effusions. The triad of interlobular septal thickening, bronchovascular bundle thickening, and pleural effusions are most suggestive of this diagnosis [51].
  • CT findings in CSS [54], drug-induced pulmonary eosinophilia [55], HES, and simple pulmonary eosinophilia are varied and diverse. Thus, a radiologic diagnosis of these entities is rarely possible [51].

With all of the eosinophilic lung diseases, radiographic findings need to be combined with clinical and other features to guide the approach to diagnosis [51].

Invasive diagnostics — Unless the history and associated findings identify a provocative agent, such as a medication, as a likely cause of an eosinophilic lung disease, BAL should be performed. Fluid should be evaluated for the total and differential leukocyte counts. Since mild to moderate airway eosinophilia can occur in a number of common conditions, including asthma, a cut-off of ≥25 percent for the diagnosis of AEP and ≥40 percent for the diagnosis of CEP has been suggested, although the specificities of these criteria have not been evaluated prospectively [56].

If there have been appropriate geographic exposures for coccidioidomycosis or clinical and radiographic findings suggestive of ABPA, fungal cultures should be obtained. Bacterial and mycobacterial cultures should also be considered.

If the BAL is unrevealing, consideration should be given to obtaining lung tissue via a transbronchial or open lung biopsy approach depending upon the clinical and radiographic findings. Video-assisted thoracoscopic surgery (VATS) can substitute for a thoracotomy to provide tissue. If disease is more parenchymal and peripheral, a transbronchial biopsy is less likely to be revealing, and VATS or a limited thoracotomy should be considered.

For any of the potential persisting causes of pulmonary eosinophilia, especially CSS, it is preferable to establish and document the nature of the disease. While those with CSS, CEP, and many with HES will respond to glucocorticoid therapy, establishing a firm pathologic diagnosis upfront is prudent given the side effects of long-term glucocorticoid treatment and the options for second-line therapy in glucocorticoid-refractory disease. Moreover, since CSS has the potential to involve and damage other organs, documenting this vasculitis has important implications for the future management of the patient.

Serologies — Serologic testing can be helpful with some etiologies of pulmonary eosinophilia. However, these test results are not usually rapidly available, obviating their utility in the evaluation of an acutely ill patient. Serologies for coccidioidomycosis, ABPA, and the chronic helminth infections (eg, TPE, flukes) can help to support these diagnoses.

Enzyme linked immunosorbent assay (ELISA) testing for strongyloidiasis is helpful in excluding unrecognized infections with this parasite. This is important because a patient with undiagnosed strongyloidiasis who is treated with glucocorticoids can develop disseminated bacterial infections, which can be fatal.

EMPIRIC GLUCOCORTICOIDS — With the exception of strongyloidiasis, most of the varied etiologies of pulmonary eosinophilia will improve on glucocorticoids. However, it remains a clinical question whether glucocorticoids should be administered empirically.

Recommendations — Glucocorticoid administration is medically indicated if:

  • A patient is acutely hypoxemic and in respiratory distress AND
  • If the etiology is either AEP or a medication or toxin-elicited acute pulmonary eosinophilia

It should be noted, though, that AEP can resolve spontaneously without requiring glucocorticoid therapy [32].

For other more chronic or potentially systemic causes of pulmonary eosinophilia, we suggest NOT giving empiric glucocorticoids, at least until a diagnostic biopsy has been performed. Following a biopsy, glucocorticoids may be given as clinically indicated pending biopsy results. In contrast, if glucocorticoids are given before a biopsy or empirically, glucocorticoid therapy typically alters histopathologic features and suppresses tissue eosinophilia, obscuring the chance to obtain a definitive diagnosis.

Use of UpToDate is subject to the Subscription and License Agreement.

REFERENCES

  1. Allen JN, Davis WB. Eosinophilic lung diseases. Am J Respir Crit Care Med 1994; 150:1423.
  2. Bain GA, Flower CD. Pulmonary eosinophilia. Eur J Radiol 1996; 23:3.
  3. Umeki S. Reevaluation of eosinophilic pneumonia and its diagnostic criteria. Arch Intern Med 1992; 152:1913.
  4. Jederlinic PJ, Sicilian L, Gaensler EA. Chronic eosinophilic pneumonia. A report of 19 cases and a review of the literature. Medicine (Baltimore) 1988; 67:154.
  5. Hayakawa H, Sato A, Toyoshima M, et al. A clinical study of idiopathic eosinophilic pneumonia. Chest 1994; 105:1462.
  6. Dejaegher P, Derveaux L, Dubois P, Demedts M. Eosinophilic pneumonia without radiographic pulmonary infiltrates. Chest 1983; 84:637.
  7. Wilson, ME, Weller, PF. Eosinophilia. In: Tropical Infectious Diseases: Principles, Pathogens and Practice. 2nd ed. Guerrant, RL, Walker, DH, Weller, PF, eds. Elsevier, Philadelphia, 2006. p. 1478.
  8. LOFFLER W. Transient lung infiltrations with blood eosinophilia. Int Arch Allergy Appl Immunol 1956; 8:54.
  9. Roig J, Romeu J, Riera C, et al. Acute eosinophilic pneumonia due to toxocariasis with bronchoalveolar lavage findings. Chest 1992; 102:294.
  10. Inoue K, Inoue Y, Arai T, et al. Chronic eosinophilic pneumonia due to visceral larva migrans. Intern Med 2002; 41:478.
  11. Schwartz E, Rozenman J, Perelman M. Pulmonary manifestations of early schistosome infection among nonimmune travelers. Am J Med 2000; 109:718.
  12. Boggild AK, Keystone JS, Kain KC. Tropical pulmonary eosinophilia: a case series in a setting of nonendemicity. Clin Infect Dis 2004; 39:1123.
  13. Ottesen EA, Nutman TB. Tropical pulmonary eosinophilia. Annu Rev Med 1992; 43:417.
  14. Rocha A, Dreyer G, Poindexter RW, Ottesen EA. Syndrome resembling tropical pulmonary eosinophilia but of non-filarial aetiology: serological findings with filarial antigens. Trans R Soc Trop Med Hyg 1995; 89:573.
  15. Fohlman J, Sjölin J, Bennich H, et al. Coccidioidomycosis as imported atypical pneumonia in Sweden. Scand J Infect Dis 2000; 32:440.
  16. Lombard CM, Tazelaar HD, Krasne DL. Pulmonary eosinophilia in coccidioidal infections. Chest 1987; 91:734.
  17. Vijayan VK, Reetha AM, Jawahar MS, et al. Pulmonary eosinophilia in pulmonary tuberculosis. Chest 1992; 101:1708.
  18. Solomon J, Schwarz M. Drug-, toxin-, and radiation therapy-induced eosinophilic pneumonia. Semin Respir Crit Care Med 2006; 27:192.
  19. Foucher, P, Camus, P. Pneumotox online: the drug-induced lung diseases. (Available online at: www.pneumotox.com) Accessed: August 22, 2006.
  20. Schwarz YA, Kivity S, Fischbein A, et al. Eosinophilic lung reaction to aluminium and hard metal. Chest 1994; 105:1261.
  21. Marguerie C, Drouet M. [Occupational eosinophilic lung in a grape grower: role of sulfites]. Allerg Immunol (Paris) 1995; 27:163.
  22. Shah PK, Lakhotia M, Chittora M, et al. Pulmonary infiltration with blood eosinophilia after scorpion sting. Chest 1989; 95:691.
  23. Nadeem S, Nasir N, Israel RH. Löffler's syndrome secondary to crack cocaine. Chest 1994; 105:1599.
  24. Bascom R, Fisher JF, Thomas RJ, et al. Eosinophilia, respiratory symptoms and pulmonary infiltrates in rubber workers. Chest 1988; 93:154.
  25. Rom WN, Weiden M, Garcia R, et al. Acute eosinophilic pneumonia in a New York City firefighter exposed to World Trade Center dust. Am J Respir Crit Care Med 2002; 166:797.
  26. Hirai K, Yamazaki Y, Okada K, et al. Acute eosinophilic pneumonia associated with smoke from fireworks. Intern Med 2000; 39:401.
  27. Shintani H, Fujimura M, Yasui M, et al. Acute eosinophilic pneumonia caused by cigarette smoking. Intern Med 2000; 39:66.
  28. Kelly KJ, Ruffing R. Acute eosinophilic pneumonia following intentional inhalation of Scotchguard. Ann Allergy 1993; 71:358.
  29. Shorr AF, Scoville SL, Cersovsky SB, et al. Acute eosinophilic pneumonia among US Military personnel deployed in or near Iraq. JAMA 2004; 292:2997.
  30. Alonso-Ruiz A, Calabozo M, Perez-Ruiz F, Mancebo L. Toxic oil syndrome. A long-term follow-up of a cohort of 332 patients. Medicine (Baltimore) 1993; 72:285.
  31. Swygert LA, Maes EF, Sewell LE, et al. Eosinophilia-myalgia syndrome. Results of national surveillance. JAMA 1990; 264:1698.
  32. Philit F, Etienne-Mastroïanni B, Parrot A, et al. Idiopathic acute eosinophilic pneumonia: a study of 22 patients. Am J Respir Crit Care Med 2002; 166:1235.
  33. Tazelaar HD, Linz LJ, Colby TV, et al. Acute eosinophilic pneumonia: histopathologic findings in nine patients. Am J Respir Crit Care Med 1997; 155:296.
  34. Marchand E, Reynaud-Gaubert M, Lauque D, et al. Idiopathic chronic eosinophilic pneumonia. A clinical and follow-up study of 62 cases. The Groupe d'Etudes et de Recherche sur les Maladies "Orphelines" Pulmonaires (GERM"O"P). Medicine (Baltimore) 1998; 77:299.
  35. Cottin V, Frognier R, Monnot H, et al. Chronic eosinophilic pneumonia after radiation therapy for breast cancer. Eur Respir J 2004; 23:9.
  36. Samman YS, Wali SO, Abdelaal MA, et al. Chronic eosinophilic pneumonia presenting with recurrent massive bilateral pleural effusion : case report. Chest 2001; 119:968.
  37. Laufs U, Schneider C, Wassermann K, Erdmann E. Chronic eosinophilic pneumonia with atypical radiographic presentation. Respiration 1998; 65:323.
  38. Guillevin L, Cohen P, Gayraud M, et al. Churg-Strauss syndrome. Clinical study and long-term follow-up of 96 patients. Medicine (Baltimore) 1999; 78:26.
  39. Weller PF, Plaut M, Taggart V, Trontell A. The relationship of asthma therapy and Churg-Strauss syndrome: NIH workshop summary report. J Allergy Clin Immunol 2001; 108:175.
  40. Patterson R, Greenberger PA, Halwig JM, et al. Allergic bronchopulmonary aspergillosis. Natural history and classification of early disease by serologic and roentgenographic studies. Arch Intern Med 1986; 146:916.
  41. Gibson PG. Allergic bronchopulmonary aspergillosis. Semin Respir Crit Care Med 2006; 27:185.
  42. Logan PM, Müller NL. High-resolution computed tomography and pathologic findings in pulmonary aspergillosis: a pictorial essay. Can Assoc Radiol J 1996; 47:444.
  43. Katzenstein AL, Liebow AA, Friedman PJ. Bronchocentric granulomatosis, mucoid impaction, and hypersensitivity reactions to fungi. Am Rev Respir Dis 1975; 111:497.
  44. Slabbynck H, Impens N, Naegels S, et al. Idiopathic hypereosinophilic syndrome-related pulmonary involvement diagnosed by bronchoalveolar lavage. Chest 1992; 101:1178.
  45. Weller PF, Bubley GJ. The idiopathic hypereosinophilic syndrome. Blood 1994; 83:2759.
  46. Allen JN, Davis WB, Pacht ER. Diagnostic significance of increased bronchoalveolar lavage fluid eosinophils. Am Rev Respir Dis 1990; 142:642.
  47. Yousem SA. Eosinophilic pneumonia-like areas in idiopathic usual interstitial pneumonia. Mod Pathol 2000; 13:1280.
  48. Norman D, Piecyk M, Roberts DH. Eosinophilic pneumonia as an initial manifestation of rheumatoid arthritis. Chest 2004; 126:993.
  49. Mogayzel PJ Jr, Yang SC, Wise BV, Colombani PM. Eosinophilic infiltrates in a pulmonary allograft: a case and review of the literature. J Heart Lung Transplant 2001; 20:692.
  50. Horie S, Okubo Y, Suzuki J, Isobe M. An emaciated man with eosinophilic pneumonia. Lancet 1996; 348:166.
  51. Johkoh T, Müller NL, Akira M, et al. Eosinophilic lung diseases: diagnostic accuracy of thin-section CT in 111 patients. Radiology 2000; 216:773.
  52. Mayo JR, Müller NL, Road J, et al. Chronic eosinophilic pneumonia: CT findings in six cases. AJR Am J Roentgenol 1989; 153:727.
  53. Ebara H, Ikezoe J, Johkoh T, et al. Chronic eosinophilic pneumonia: evolution of chest radiograms and CT features. J Comput Assist Tomogr 1994; 18:737.
  54. Silva CI, Müller NL, Fujimoto K, et al. Churg-Strauss syndrome: high resolution CT and pathologic findings. J Thorac Imaging 2005; 20:74.
  55. Erasmus JJ, McAdams HP, Rossi SE. High-resolution CT of drug-induced lung disease. Radiol Clin North Am 2002; 40:61.
  56. Cottin V, Cordier JF. Eosinophilic pneumonias. Allergy 2005; 60:841.

© 2011 UpToDate, Inc. All rights reserved. |Subscription and License Agreement|Support Tag: [ecapp1103p.utd.com-194.225.62.103-421D9C2D23-80336.14]
Licensed to: Ministry of Hlth of Iran

آخرین تصاویر

تازه ترین پرسش های شما

درمان و تشخیص صحیح
با سلام و احترام : شرح حال : من ۳۷ ساله هستم حدود ۱۵ سال هست که سیگار می کشم .ه...
642 Hits
Posted on دوشنبه, 21 می 2018
با سلام وخسته نباشید مادربنده 64 ساله دریک سی تی اسکن تصادفی از ریه فهمیدن که دو...
260 Hits
Posted on جمعه, 18 می 2018
Aila, Kalesch, Marius and Joey Turkmenistan
Password proctected content
191 Hits
Posted on شنبه, 12 می 2018

اطلاعات تماس

  • آدرس : تهران,میدان ونک؛ خیابان ملاصدرا؛ خیابان شیخ بهایی جنوبی، بن بست نصرتی، پلاک 4 طبقه سوم، واحد 12
  • پست الکترونیک : info @ dralirezasabetpour.com
  • تلفن تماس : 88050421
  • لطفا جهت وقت گرفتن سعی کنید بین ۳ تا ۶ بعد از ظهر تماس بگیرید. 
  • در صورت موارد اورژانس می توانید بین ساعت ۴ تا ۶ به مطب مراجعه کنید .