Eosinophilic pneumonia

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Pneumonia
ICD-10 J12, J13, J14, J15, J16, J17, J18, P23
ICD-9 480-486, 770.0
DiseasesDB 10166
MeSH C08.381.677

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Editor(s)-in-Chief: C. Michael Gibson, M.S., M.D. [1] Phone:617-632-7753; Associate Editor(s)-In-Chief: Priyamvada Singh, M.D. [2]; Philip Marcus, M.D., M.P.H.[3]

Overview

Historical Perspective

Pathophysiology

Causes

Differentiating Pneumonia from other Diseases

Epidemiology and Demographics

Risk factors

Natural History, Complications and Prognosis

Prognosis predictor scores: CURB-65 | Pneumonia severity index | Criteria for severe community acquired pneumonia

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Diagnosis

Eosinophilic pneumonia is diagnosed in one of three circumstances: when a complete blood count reveals increased eosinophils and a chest x-ray or computed tomography (CT) identifies abnormalities in the lung, when a biopsy identifies increased eosinophils in lung tissue, or when increased eosinophils are found in fluid obtained by a bronchoscopy (bronchoalveolar lavage (BAL) fluid). Association with medication or cancer is usually apparent after review of a person's medical history. Specific parasitic infections are diagnosed after examining a person's exposure to common parasites and performing laboratory tests to look for likely causes. If no underlying cause is found, a diagnosis of AEP or CEP is made based upon the following criteria. AEP is most likely with respiratory failure after an acute febrile illness of usually less than one week, changes in multiple areas and fluid in the area surrounding the lungs on a chest x-ray, and greater than 25% eosinophils on a BAL. Other typical laboratory abnormalities include an elevated white blood cell count, erythrocyte sedimentation rate, and immunoglobulin E level. Pulmonary function testing usually reveals a restrictive process with reduced diffusion capacity for carbon monoxide. CEP is most likely when the symptoms have been present for more than a month. Laboratory tests typical for CEP include increased blood eosinophils, a high erythrocyte sedimentation rate, iron deficiency anemia, and increased platelets. A chest x-ray can show abnormalities anywhere, but the most specific finding is increased shadow in the periphery of the lung, away from the heart.

Treatment

When eosinophilic pneumonia is related to an illness such as cancer or parasitic infection, treatment of the underlying cause is effective in resolving the lung disease. When due to AEP or CEP, however, treatment with corticosteroids results in a rapid, dramatic resolution of symptoms over the course of one or two days. Either intravenous methylprednisolone or oral prednisone are most commonly used. In AEP, treatment is usually continued for a month after symptoms disappear and the x-ray returns to normal (usually four weeks total). In CEP, treatment is usually continued for three months after symptoms disappear and the x-ray returns to normal (usually four months total). Inhaled steroids such as fluticasone have been used effectively when discontinuation of oral prednisone has resulted in relapse.[4]

Because EP affects the lungs, individuals with EP have difficulty breathing. If enough of the lung is involved, it may not be possible for a person to breathe enough to live without support. Non-invasive machines such as a bilevel positive airway pressure machine may be used. Otherwise, placement of a breathing tube into the mouth may be necessary and a ventilator may be used to help the person breathe.

Prognosis

Eosinophilic pneumonia due to cancer or parasitic infection carries a prognosis related to the underlying illness. AEP and CEP, however, have very little associated mortality as long as intensive care is available and treatment with corticosteroids is given. CEP often relapses when prednisone is discontinued; therefore, some people with CEP require lifelong therapy. Chronic prednisone is associated with many side effects, including increased infections, weakened bones, stomach ulcers, and changes in appearance.[5]

Epidemiology

Eosinophilic pneumonia is a rare disease. Parasitic causes are most common in geographic areas where each parasite is endemic. AEP can occur at any age, even in previously healthy children, though most patients are between 20 and 40 years of age. Men are affected approximately twice as frequently as women. AEP has been associated with smoking. CEP occurs more frequently in women than men does not appear to be related to smoking. An association with radiation for breast cancer has been described.[6]

History

Chronic eosinophilic pneumonia was first described by Carrington in 1969, and it is also known as Carrington syndrome. Prior to that, eosinophilic pneumonia was a well described pathologic entity usually associated with medication or parasite exposures. Acute eosinophilic pneumonia was first described in 1989[7][8].

References

  1. ^ Bain, GA, Flower, CD. Pulmonary eosinophilia. Eur J Radiol 1996; 23:3. PMID 8872069
  2. ^ 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. PMID 12231487
  3. ^ Weller, PF. Parasitic pneumonias. In: Respiratory infections: Diagnosis and management, 3rd ed, Pennington, JE (Ed), Raven Press, New York, 1994, p. 695.
  4. ^ Jantz, MA, Sahn, SA. Corticosteroids in acute respiratory failure. Am J Respir Crit Care Med 1999; 160:1079. PMID 10508792
  5. ^ Naughton, M, Fahy, J, FitzGerald, MX. Chronic eosinophilic pneumonia. A longterm followup of 12 patients. Chest 1993; 103:162. PMID 8031327
  6. ^ Cottin, V, Frognier, R, Monnot, H, et al. Chronic eosinophilic pneumonia after radiation therapy for breast cancer. Eur Respir J 2004; 23:9
  7. ^ Carrington CB, Addington WW, Goff AM, et al. Chronic eosinophilic pneumonia. N Engl J Med 1969;280:788 -798 PMID 5773637
  8. ^ Badesch, DB, King, TE Jr, Schwarz, MI. Acute eosinophilic pneumonia: a hypersensitivity phenomenon?. Am Rev Respir Dis 1989; 139:249.
  9. ^ Allen, JN, Pacht, ER, Gadek, JE, et al. Acute eosinophilic pneumonia as a reversible cause of noninfectious respiratory failure. N Engl J Med 1989; 321:569.

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References

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