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Evaluation of the Association of Polymorphisms in the Innate Immune System With the Risk for Blastomycosis Dermatitidis Infection in Patients Not Infected With HIV and Complications Associated With Blastomycosis Dermatitidis Infection

This study has been completed.
Sponsor:
Information provided by:
National Institutes of Health Clinical Center (CC)
ClinicalTrials.gov Identifier:
NCT00001702
First received: November 3, 1999
Last updated: October 7, 2009
Last verified: October 2009

November 3, 1999
October 7, 2009
July 1998
June 2007   (final data collection date for primary outcome measure)
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Complete list of historical versions of study NCT00001702 on ClinicalTrials.gov Archive Site
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Evaluation of the Association of Polymorphisms in the Innate Immune System With the Risk for Blastomycosis Dermatitidis Infection in Patients Not Infected With HIV and Complications Associated With Blastomycosis Dermatitidis Infection
Evaluation of the Association of Polymorphisms in the Innate Immune System With the Risk for Blastomycosis Dermatitidis Infection in Patients Not Infected With HIV and Complications Associated With Blastomycosis Dermatitidis Infection

Innate immunity plays an important role for fungal recognition and initiation of fungicidal activity. We hypothesize that subtle differences in different molecules of innate immunity may contribute to either the predisposition or clinical course of infection with Blastomycosis dermatitidis. To test this hypothesis, we propose to analyze the allelic frequencies of 15 different genes (mannose binding lectin, Fc-gamma receptor IIa and IIb, Fc-gamma receptors IIIa and IIIb, myeloperoxidase, tumor necrosis factor-alpha and -beta, interleukin 1A and 1B, interleukin-1 receptor antagonist, interleukin-10, NRAMP-1, chitotriosidase, and chemokine receptor 5) and their intragenic polymorphic forms and to compare this data to the incidence and severity of Blastomycosis dermatitidis infection. With this study we hope to identify a group of molecules of innate immunity which influence the risk and severity of invasive Blastomycosis dermatitidis infection.

Innate immunity plays an important role for fungal recognition and initiation of fungicidal activity. We hypothesize that subtle differences in different molecules of innate immunity may contribute to either the predisposition or clinical course of infection with Blastomycosis Dermatitidis. To test this hypothesis, we propose to analyze the allelic frequencies of 15 different genes (mannose binding lectin, Fc-gamma receptor Ila and IIb, Fc-gamma receptors IIIa and IIIb, myeloperoxidase, tumor necrosis factor-alpha and -beta, interleukin 1A and 1B, interleukin-1 receptor antagonist, interleukin-10, NRAMP-1, chitotriosidase, and chemokine receptor 5) and their intragenic polymorphic forms and to compare this data to the incidence and severity of Blastomycosis Dermatitidis infection. With this study we hope to identify a group of molecules of innate immunity which influence the risk and severity of invasive Blastomycosis Dermatitidis infection.

Observational
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Blastomycosis
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*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Completed
400
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June 2007   (final data collection date for primary outcome measure)
  • INCLUSION CRITERIA:

Patients in the database have been confirmed with a diagnosis of Blastomycosis dermatitides infection by a combination of isolation of the yeast form in a diagnostic microbiology laboratory and/or an elevated cryptococcal antigen titer (which is commercially available).

Only patients diagnosed and treated in the United States and Canada will be included in this analysis.

Only patients who are not co-infected with HIV will be included in the study.

Patient samples will be collected and clinical data will be evaluated only after signed consent has been obtained.

Both
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Contact information is only displayed when the study is recruiting subjects
United States
 
NCT00001702
980138, 98-C-0138
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National Cancer Institute (NCI)
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National Institutes of Health Clinical Center (CC)
October 2009

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP