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Iatrogenic Eosinophilia—Reply

Iatrogenic Eosinophilia—Reply In reply Koga and Aizawa pointed out in their letter that drugs can also induce hypereosinophilia, with a broad spectrum of clinical manifestations. Interestingly, the reactions to drugs causing peripheral eosinophilia are usually the most severe ones. Examples of severe drug reactions associated with increased eosinophil counts are drug rash with eosinophilia and systemic symptoms, toxic epidermal necrolysis, eosinophilic fasciitis (Shulman syndrome), and eosinophilic pneumonia. Eosinophilic fasciitis and eosinophilic pneumonia are often associated,1 but they are fortunately rare. They can be provoked by a wide variety of medications, most frequently antibiotics and tryptophan derivatives. Toxic epidermal necrolysis encompasses some different severe skin reactions (including the Stevens-Johnson syndrome) due to drugs (from which mortality can be as high as 30%2) that are usually associated with peripheral eosinophilia. It is well-known that patients with human immunodeficiency virus infection are at higher risk of developing toxic epidermal necrolysis, probably because of the increased drug exposure and the concomitant immunosuppression. Antimicrobial agents and drugs for epilepsy are frequently reported as the culprit drugs. Drug rash with eosinophilia and systemic symptoms3 is a complex clinical picture including skin rash, eosinophilia, fever, lymph node enlargement, and liver or renal impairment. In our previously published revision of 1862 cases,4 there was no drug-induced eosinophilia, as testified by the negative clinical history for suspected exposure to drugs. This can be due, in our opinion, to several factors. First, some of the drug-induced diseases in a chronic form are rare, and therefore our case series was not large enough to detect them. Second, the severe immediate reactions to drugs with eosinophilia require critical care management, and therefore they were not referred to our departments of internal medicine. Third, most drug reactions seen in common clinical practice are self-resolving and transient, and the eosinophilia, if present, cannot be detected. The comments made by Koga and Aizawa are anyway appropriate and correct, and when evaluating a patient with eosinophilia, the possible exposure to drugs should always be investigated. References 1. Campagna ACBlanc PDCriswell LA et al. Pulmonary manifestations of the eosinophilia-myalgia syndrome associated with tryptophan ingestion. Chest. 1992;1011274- 1281PubMedGoogle ScholarCrossref 2. Bachot NRoujeau JC Differential diagnosis of severe cutaneous drug eruptions. Am J Clin Dermatol. 2003;4561- 572PubMedGoogle ScholarCrossref 3. Tas SSimonart T Management of drug rash with eosinophilia and systemic symptoms (DRESS syndrome): an update. Dermatology. 2003;206353- 356PubMedGoogle ScholarCrossref 4. Lombardi CPassalacqua G Eosinophilia and diseases: clinical revision of 1862 cases. Arch Intern Med. 2003;1631371- 1373PubMedGoogle ScholarCrossref http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Internal Medicine American Medical Association

Iatrogenic Eosinophilia—Reply

Abstract

In reply Koga and Aizawa pointed out in their letter that drugs can also induce hypereosinophilia, with a broad spectrum of clinical manifestations. Interestingly, the reactions to drugs causing peripheral eosinophilia are usually the most severe ones. Examples of severe drug reactions associated with increased eosinophil counts are drug rash with eosinophilia and systemic symptoms, toxic epidermal necrolysis, eosinophilic fasciitis (Shulman syndrome), and eosinophilic pneumonia. Eosinophilic...
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References (4)

Publisher
American Medical Association
Copyright
Copyright © 2004 American Medical Association. All Rights Reserved.
ISSN
0003-9926
eISSN
1538-3679
DOI
10.1001/archinte.164.1.106-b
Publisher site
See Article on Publisher Site

Abstract

In reply Koga and Aizawa pointed out in their letter that drugs can also induce hypereosinophilia, with a broad spectrum of clinical manifestations. Interestingly, the reactions to drugs causing peripheral eosinophilia are usually the most severe ones. Examples of severe drug reactions associated with increased eosinophil counts are drug rash with eosinophilia and systemic symptoms, toxic epidermal necrolysis, eosinophilic fasciitis (Shulman syndrome), and eosinophilic pneumonia. Eosinophilic fasciitis and eosinophilic pneumonia are often associated,1 but they are fortunately rare. They can be provoked by a wide variety of medications, most frequently antibiotics and tryptophan derivatives. Toxic epidermal necrolysis encompasses some different severe skin reactions (including the Stevens-Johnson syndrome) due to drugs (from which mortality can be as high as 30%2) that are usually associated with peripheral eosinophilia. It is well-known that patients with human immunodeficiency virus infection are at higher risk of developing toxic epidermal necrolysis, probably because of the increased drug exposure and the concomitant immunosuppression. Antimicrobial agents and drugs for epilepsy are frequently reported as the culprit drugs. Drug rash with eosinophilia and systemic symptoms3 is a complex clinical picture including skin rash, eosinophilia, fever, lymph node enlargement, and liver or renal impairment. In our previously published revision of 1862 cases,4 there was no drug-induced eosinophilia, as testified by the negative clinical history for suspected exposure to drugs. This can be due, in our opinion, to several factors. First, some of the drug-induced diseases in a chronic form are rare, and therefore our case series was not large enough to detect them. Second, the severe immediate reactions to drugs with eosinophilia require critical care management, and therefore they were not referred to our departments of internal medicine. Third, most drug reactions seen in common clinical practice are self-resolving and transient, and the eosinophilia, if present, cannot be detected. The comments made by Koga and Aizawa are anyway appropriate and correct, and when evaluating a patient with eosinophilia, the possible exposure to drugs should always be investigated. References 1. Campagna ACBlanc PDCriswell LA et al. Pulmonary manifestations of the eosinophilia-myalgia syndrome associated with tryptophan ingestion. Chest. 1992;1011274- 1281PubMedGoogle ScholarCrossref 2. Bachot NRoujeau JC Differential diagnosis of severe cutaneous drug eruptions. Am J Clin Dermatol. 2003;4561- 572PubMedGoogle ScholarCrossref 3. Tas SSimonart T Management of drug rash with eosinophilia and systemic symptoms (DRESS syndrome): an update. Dermatology. 2003;206353- 356PubMedGoogle ScholarCrossref 4. Lombardi CPassalacqua G Eosinophilia and diseases: clinical revision of 1862 cases. Arch Intern Med. 2003;1631371- 1373PubMedGoogle ScholarCrossref

Journal

Archives of Internal MedicineAmerican Medical Association

Published: Jan 12, 2004

Keywords: eosinophilia

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