Tropical pulmonary eosinophilia.
Identifieur interne : 005A02 ( PubMed/Corpus ); précédent : 005A01; suivant : 005A03Tropical pulmonary eosinophilia.
Auteurs : E A Ottesen ; T B NutmanSource :
- Annual review of medicine [ 0066-4219 ] ; 1992.
English descriptors
- KwdEn :
- Animals, Brugia (drug effects), Brugia (immunology), Diagnosis, Differential, Diethylcarbamazine (therapeutic use), Elephantiasis, Filarial (diagnosis), Elephantiasis, Filarial (drug therapy), Elephantiasis, Filarial (immunology), Humans, Immunoglobulin E (analysis), Immunoglobulin G (analysis), Pulmonary Eosinophilia (diagnosis), Pulmonary Eosinophilia (drug therapy), Pulmonary Eosinophilia (immunology), Wuchereria bancrofti (drug effects), Wuchereria bancrofti (immunology).
- MESH :
- chemical , analysis : Immunoglobulin E, Immunoglobulin G.
- chemical , therapeutic use : Diethylcarbamazine.
- diagnosis : Elephantiasis, Filarial, Pulmonary Eosinophilia.
- drug effects : Brugia, Wuchereria bancrofti.
- drug therapy : Elephantiasis, Filarial, Pulmonary Eosinophilia.
- immunology : Brugia, Elephantiasis, Filarial, Pulmonary Eosinophilia, Wuchereria bancrofti.
- Animals, Diagnosis, Differential, Humans.
Abstract
Tropical pulmonary eosinophilia is one of the many PIE syndromes [pulmonary infiltrates with eosinophilia (of the peripheral blood)]. It is caused by immunologic hyperresponsiveness to the filarial parasites Wuchereria bancrofti or Brugia malayi. Its clinical presentation includes nocturnal cough, dyspnea, wheezing, fever, weight loss, fatigue, interstitial mottling on chest radiograph, predominantly restrictive but also obstructive lung function abnormalities, and peripheral blood eosinophilia of more than 3000 per microliter. It can be distinguished from other PIE syndromes by the patient's history of residence in the tropics, by the presence of extraordinarily high levels of both serum IgE and antifilarial antibodies, and by the dramatic clinical improvement after treatment with the antifilarial drug diethylcarbamazine. Recent studies indicate that the compromised lung diffusion capacity of patients with acute tropical pulmonary eosinophilia is a function of the degree of the eosinophilic alveolitis present and that, despite a 3-week course of diethylcarbamazine, low-grade alveolitis persists in almost half of such patients; this persistent alveolitis is likely to be the cause of the progressive interstitial fibrosis seen in many untreated or inadequately treated patients with tropical pulmonary eosinophilia.
DOI: 10.1146/annurev.me.43.020192.002221
PubMed: 1580599
Links to Exploration step
pubmed:1580599Le document en format XML
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It is caused by immunologic hyperresponsiveness to the filarial parasites Wuchereria bancrofti or Brugia malayi. Its clinical presentation includes nocturnal cough, dyspnea, wheezing, fever, weight loss, fatigue, interstitial mottling on chest radiograph, predominantly restrictive but also obstructive lung function abnormalities, and peripheral blood eosinophilia of more than 3000 per microliter. It can be distinguished from other PIE syndromes by the patient's history of residence in the tropics, by the presence of extraordinarily high levels of both serum IgE and antifilarial antibodies, and by the dramatic clinical improvement after treatment with the antifilarial drug diethylcarbamazine. Recent studies indicate that the compromised lung diffusion capacity of patients with acute tropical pulmonary eosinophilia is a function of the degree of the eosinophilic alveolitis present and that, despite a 3-week course of diethylcarbamazine, low-grade alveolitis persists in almost half of such patients; this persistent alveolitis is likely to be the cause of the progressive interstitial fibrosis seen in many untreated or inadequately treated patients with tropical pulmonary eosinophilia.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">1580599</PMID><DateCreated><Year>1992</Year><Month>06</Month><Day>11</Day></DateCreated><DateCompleted><Year>1992</Year><Month>06</Month><Day>11</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0066-4219</ISSN><JournalIssue CitedMedium="Print"><Volume>43</Volume><PubDate><Year>1992</Year></PubDate></JournalIssue><Title>Annual review of medicine</Title><ISOAbbreviation>Annu. Rev. Med.</ISOAbbreviation></Journal><ArticleTitle>Tropical pulmonary eosinophilia.</ArticleTitle><Pagination><MedlinePgn>417-24</MedlinePgn></Pagination><Abstract><AbstractText>Tropical pulmonary eosinophilia is one of the many PIE syndromes [pulmonary infiltrates with eosinophilia (of the peripheral blood)]. It is caused by immunologic hyperresponsiveness to the filarial parasites Wuchereria bancrofti or Brugia malayi. Its clinical presentation includes nocturnal cough, dyspnea, wheezing, fever, weight loss, fatigue, interstitial mottling on chest radiograph, predominantly restrictive but also obstructive lung function abnormalities, and peripheral blood eosinophilia of more than 3000 per microliter. It can be distinguished from other PIE syndromes by the patient's history of residence in the tropics, by the presence of extraordinarily high levels of both serum IgE and antifilarial antibodies, and by the dramatic clinical improvement after treatment with the antifilarial drug diethylcarbamazine. Recent studies indicate that the compromised lung diffusion capacity of patients with acute tropical pulmonary eosinophilia is a function of the degree of the eosinophilic alveolitis present and that, despite a 3-week course of diethylcarbamazine, low-grade alveolitis persists in almost half of such patients; this persistent alveolitis is likely to be the cause of the progressive interstitial fibrosis seen in many untreated or inadequately treated patients with tropical pulmonary eosinophilia.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ottesen</LastName><ForeName>E A</ForeName><Initials>EA</Initials><AffiliationInfo><Affiliation>Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nutman</LastName><ForeName>T B</ForeName><Initials>TB</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Annu Rev Med</MedlineTA><NlmUniqueID>2985151R</NlmUniqueID><ISSNLinking>0066-4219</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007074">Immunoglobulin G</NameOfSubstance></Chemical><Chemical><RegistryNumber>37341-29-0</RegistryNumber><NameOfSubstance UI="D007073">Immunoglobulin E</NameOfSubstance></Chemical><Chemical><RegistryNumber>V867Q8X3ZD</RegistryNumber><NameOfSubstance UI="D004049">Diethylcarbamazine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002009" MajorTopicYN="N">Brugia</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003937" MajorTopicYN="N">Diagnosis, Differential</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004049" MajorTopicYN="N">Diethylcarbamazine</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004605" MajorTopicYN="N">Elephantiasis, Filarial</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007073" MajorTopicYN="N">Immunoglobulin E</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007074" MajorTopicYN="N">Immunoglobulin G</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011657" MajorTopicYN="N">Pulmonary Eosinophilia</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="Y">diagnosis</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014958" MajorTopicYN="N">Wuchereria bancrofti</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>39</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1992</Year><Month>1</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1992</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1992</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">1580599</ArticleId><ArticleId IdType="doi">10.1146/annurev.me.43.020192.002221</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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