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Pneumonia, eosinophilic

Eosinophilic pneumonia (EP) is a disease in which a certain type of white blood cell called an eosinophil accumulates in the lung. These cells cause disruption of the normal air spaces (alveoli) where oxygen is extracted from the atmosphere. Several different kinds of eosinophilic pneumonia exist and can occur in any age group. The most common symptoms include cough, fever, difficulty breathing, and sweating at night. EP is diagnosed by a combination of characteristic symptoms, findings on a physical examination by a health provider, and the results of blood tests and x-rays. Prognosis is excellent once most EP is recognized and treatment with corticosteroids is begun. more...

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Types of eosinophilic pneumonia

Eosinophilic pneumonia is divided into different categories depending upon whether a cause can be determined or not. Known causes include certain medications or environmental triggers, parasitic infections, and cancer. EP can also occur when the immune system attacks the lungs, a disease called Churg-Strauss syndrome. When a cause can not be found, the EP is labeled "idiopathic." Idiopathic EP can be divided into "acute eosinophilic pneumonia" (AEP) and "chronic eosinophilic pneumonia" (CEP) depending on the symptoms a person is experiencing.

Symptoms

Most causes of eosinophilic pneumonia have similar symptoms. Cough, fever, increasing breathlessness, and night sweats are prominent and almost universal. Acute eosinophilic pneumonia typically follows a rapid course. Fever and cough may develop only one or two weeks before difficulties breathing progress to the point of respiratory failure requiring mechanical ventilation. Chronic eosinophilic pneumonia usually follows a slower course. Symptoms accumulate over several months and include fevers, cough, breathlessness, wheezing, and weight loss. Individuals with CEP are often diagnosed with asthma before CEP is finally recognized.

EP due to medications or environmental exposures is similar and occurs after an exposure to a known offending agent. EP due to parasitic infections has a similar prodrome in addition to a host of different symptoms related to the variety of underlying parasites. EP in the setting of cancer often develops in the context of a known diagnosis of lung cancer, cervical cancer, etc.

Pathophysiology

Eosinophilic pneumonia can develop in several different ways depending on the underlying cause of the disease. Eosinophils are thought to play a central role in defending the body against infection by parasites. Many diseases, such as asthma and eczema, are caused when eosinophils overreact to environmental triggers and release an excess of chemicals (cytokines) such as histamine. The common characteristic among different causes of EP is eosinophil overreaction or dysfunction in the lung.

Medications and environmental exposures

Medications, drugs of abuse, and environmental exposures may all trigger eosinophil dysfunction. Medications such NSAIDs (ie ibuprofen), nitrofurantoin, phenytoin, L-tryptophan, and ampicillin and drugs of abuse such as inhaled heroin and cocaine may trigger an allergic response which results in EP. Chemicals such as sulfites, aluminum silicate, and cigarette smoke can cause EP when inhaled. A New York City firefighter developed EP after inhalation of dust from the World Trade Center on September 11, 2001.

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Too much of a good thing: acute eosinophilic pneumonia with a "new" anti-depressant
From CHEST, 10/1/05 by Antonio V. Salud, II

INTRODUCTION: The incidence of acute eosinophilic pneumonia (AEP) among patients admitted with presumed community acquired pneumonia is uncertain, but AEP associated with shock is rare. [1] Medications can cause AEP with the pathophysiology attributed to acute hypersensitivity. [2] We report AEP possibly caused by duloxetine.

CASE PRESENTATION: A 30 year old Caucasian woman was admitted with five day history of fever, chills, dyspnea, cough, and nausea. She was diagnosed with pneumonia by chest x-ray and prescribed antibiotics one day prior to admission. Past medical history was significant for depression and chronic prescription narcotic use secondary to back pain. She was recently institutionalized for depression, weaned off narcotics, and prescribed duloxetine. Medications on admission were azithromycin, duloxetine, vitamin B12, multivitamin, and Garlic. She denied tobacco use but drank alcohol heavily prior to hospitalization for depression. She had no history of IV drug abuse or HIV exposures. She denied occupational, chemical, dust, or asbestos exposures. She had a parrot for five years, but no recent travel. On admission, the patient was in "mild distress" with temperature of 39.5[degrees]C, blood pressure 95/55 mmHg, heart rate 144 bpm, and respiratory rate 20. Her SpO2 was 90% on room air. Lung exam revealed diffuse crackles. She had 20.4 [10.sup.3]/uL white blood cells with 86% segmented neutrophils. Comprehensive metabolic panel and lactate were within normal limits. Admission ABG showed pH 7.44, PaCO2 30 mmHg, PaO2 49 mmHg and SaO2 84%. Blood cultures were ordered. The admission chest x-ray showed worsening consolidation bilaterally. She was placed on 4 liters oxygen, and ad-ministered ceftriaxone combined with azithromycin. The following day, her clinical course deteriorated with development of respiratory failure and shock. She was intubated and treated with vasopressors. Bronchoalveolar lavage showed no pathogens by stain or culture but revealed 80% eosinophils. Duloxetine was discontinued and methylprednisolone started. Antibiotics and vasopressors were discontinued after two days; the patient was extubated in three. She developed peripheral eosinophilia while still receiving methylprednisolone. She was discharged after eight hospital days on prednisone, fluoxetine, and gabapentin. As an outpatient, eosinophilia resolved then recurred. Eosinophilia finally normalized after fluoxetine was discontinued. Three weeks after discharge, repeat chest x-ray was normal and she was doing Pilates.

DISCUSSIONS: Acute eosinophilic pneumonia was first described as "double pneumonia" with respiratory failure.[3] The AEP diagnostic criteria[4] are: (1) Acute febrile illness < 5 days duration, (2) Hypoxemic respiratory failure, (3) Diffuse alveolar or mixed alveolar-interstitial chest X-ray infiltrates, (4) BAL eosinophils > 25%, (5) Absence of parasitic, fungal, or other infection, (6) Prompt and complete response to corticosteroids, (7) Failure to relapse after discontinuation of corticosteroids. This case fulfills these criteria, with duloxetine and secondarily fluoxetine the inciting agents. Medications are well known causes of eosinophilic pneumonia.[5] Venlafaxine was reported as an inciting agent in 2000. [6] Duloxetine and venlafaxine are similar in mechanism and pharmacodynamics. [7].

CONCLUSION: This may be the first report linking duloxetine with AEP. Cessation of exposure and corticosteroid treatment produced prompt and complete resolution of severe respiratory failure. The diagnosis of AEP was made only by bronchoalveolar lavage, emphasizing the importance of bronchoscopy in selected patients despite the risk imposed by severe hypoxemia.

REFERENCES:

[1] Buddharaju VL et al, Acute eosinophilic pneumonia associated with shock, Crit Care Med 1999;27(9):2014-2016.

[2] Badesch DB et al, Acute eosinophilic pneumonia: a hypersensitivity phenomenon? Amer Rev Respir Dis 1989;139:249-52.

[3] Ibid.

[4] Allen JN and Davis WB, Eosinophilic Lung Diseases, Am J Respir Crit Care Med 1994;150:1423-1438.

[5] http://www.pneumotox.com/indexf.php?fich=clin0&lg=en

[6] Fleisch MC et al, Eosinophilic pneumonia and respiratory failure associated with venlafaxine treatment, Eur Respir J 2000;15:205-208.

[7] Sharma A et al, Pharmacokinetics and Safety of Duloxetine, a Dual-Serotonin and Norepinephrine Reuptake Inhibitor, J Clin Pharmacol 2000;40:161-167.

DISCLOSURE: Antonio Salud II, None.

Antonio V. Salud II MD * Nathan Dean MD University of Utah, Salt Lake City, UT

COPYRIGHT 2005 American College of Chest Physicians
COPYRIGHT 2005 Gale Group

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