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

This study has been completed.

Sponsor:

Information provided by:

National Institutes of Health Clinical Center (CC)

ClinicalTrials.gov Identifier:

NCT00001701

First received: November 3, 1999

Last updated: October 7, 2009

Last verified: October 2009

History of Changes

Tracking Information
First Received Date ^ICMJE	November 3, 1999
Last Updated Date	October 7, 2009
Start Date ^ICMJE	July 1998
Primary Completion Date	June 2007 (final data collection date for primary outcome measure)
Current Primary Outcome Measures ^ICMJE	Not Provided
Original Primary Outcome Measures ^ICMJE	Not Provided
Change History	Complete list of historical versions of study NCT00001701 on ClinicalTrials.gov Archive Site
Current Secondary Outcome Measures ^ICMJE	Not Provided
Original Secondary Outcome Measures ^ICMJE	Not Provided
Current Other Outcome Measures ^ICMJE	Not Provided
Original Other Outcome Measures ^ICMJE	Not Provided

Descriptive Information
Brief Title ^ICMJE	Evaluation of the Association of Polymorphisms in the Innate Immune System With the Risk for Cryptococcus Neoformans Infection in Patients Not Infected With HIV and Complications Associated With Cryptococcus Neoformans Infection
Official Title ^ICMJE	Evaluation of the Association of Polymorphisms in the Innate Immune System With the Risk for Cryptococcus Neoformans Infection in Patients Not Infected With HIV and Complications Associated With Cryptococcus Neoformans Infection
Brief Summary	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 Cryptococcus neoformans. 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 C neoformans infection. With this study we hope to identify a group of molecules of innate immunity which influence the risk and severity of invasive C neoformans infection.
Detailed Description	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 Cryptococcus neoformans. 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 C neoformans infection. With this study we hope to identify a group of molecules of innate immunity which influence the risk and severity of invasive C neoformans infection.
Study Type ^ICMJE	Observational
Study Design ^ICMJE	Not Provided
Target Follow-Up Duration	Not Provided
Biospecimen	Not Provided
Sampling Method	Not Provided
Study Population	Not Provided
Condition ^ICMJE	Cryptococcosis
Intervention ^ICMJE	Not Provided
Study Group/Cohort (s)	Not Provided
Publications *	Bellamy R, Ruwende C, Corrah T, McAdam KP, Whittle HC, Hill AV. Variations in the NRAMP1 gene and susceptibility to tuberculosis in West Africans. N Engl J Med. 1998 Mar 5;338(10):640-4. Blakemore AI, Tarlow JK, Cork MJ, Gordon C, Emery P, Duff GW. Interleukin-1 receptor antagonist gene polymorphism as a disease severity factor in systemic lupus erythematosus. Arthritis Rheum. 1994 Sep;37(9):1380-5. Boot RG, Renkema GH, Strijland A, van Zonneveld AJ, Aerts JM. Cloning of a cDNA encoding chitotriosidase, a human chitinase produced by macrophages. J Biol Chem. 1995 Nov 3;270(44):26252-6.
* Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.

Recruitment Information
Recruitment Status ^ICMJE	Completed
Enrollment ^ICMJE	300
Completion Date	Not Provided
Primary Completion Date	June 2007 (final data collection date for primary outcome measure)
Eligibility Criteria ^ICMJE	INCLUSION CRITERIA: Patients diagnosed with Cryptococcus neoformans infection will be identified from a data base overseen by Dr. Peter Pappas. Only patients diagnosed and treated in the United States and Canada will be included in this analysis. Only patients who are not coinfected with HIV will be included in the study. Patient samples will be collected and clinical data will be evaluated only after signed informed consent has been obtained.
Gender	Both
Ages	Not Provided
Accepts Healthy Volunteers	No
Contacts ^ICMJE	Contact information is only displayed when the study is recruiting subjects
Location Countries ^ICMJE	United States

Administrative Information
NCT Number ^ICMJE	NCT00001701
Other Study ID Numbers ^ICMJE	980137, 98-C-0137
Has Data Monitoring Committee	Not Provided
Responsible Party	Not Provided
Study Sponsor ^ICMJE	National Cancer Institute (NCI)
Collaborators ^ICMJE	Not Provided
Investigators ^ICMJE	Not Provided
Information Provided By	National Institutes of Health Clinical Center (CC)
Verification Date	October 2009
^ICMJE Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP

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