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B7 Coreceptor Molecules in Hyper IgD Syndrome Form of Mevalonate Kinase Deficiency (HIDS-MKD)

The recruitment status of this study is unknown. The completion date has passed and the status has not been verified in more than two years.
Verified March 2012 by Kenneth Michael Gibson, Michigan Technological University.
Recruitment status was:  Recruiting
Sponsor:
ClinicalTrials.gov Identifier:
NCT01568736
First Posted: April 2, 2012
Last Update Posted: April 2, 2012
The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details.
Information provided by (Responsible Party):
Kenneth Michael Gibson, Michigan Technological University
March 29, 2012
April 2, 2012
April 2, 2012
March 2012
March 2016   (Final data collection date for primary outcome measure)
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No Changes Posted
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B7 Coreceptor Molecules in Hyper IgD Syndrome Form of Mevalonate Kinase Deficiency
B7 Coreceptor Molecules as Clinically-Relevant Surrogate Biomarkers in the Hyper IgD Syndrome (HIDS) Form of Mevalonate Kinase Deficiency (MKD)

The hyper IgD syndrome (HIDS) is an inflammatory disease caused by mevalonate kinase deficiency. There is no cure, and available treatments of HIDS febrile episodes have shown limited clinical efficacy. The development of effective interventions for HIDS is limited by our poor understanding of the disease. The goal of the study is to better characterize the inflammatory response during HIDS episodes and to determine the relationship between this response and blood and urine markers of mevalonate kinase deficiency. This knowledge will help us learn more about the cause of the disease and should lead to the identification of new disease biomarkers that can be used to evaluate clinical efficacy in future therapeutic trials.

The primary hypothesis is that the costimulatory B7 glycoprotein abnormalities identified in the murine MKD model will be recapitulated in sera obtained from human HIDS patients, either before, during or after febrile episodes. The secondary hypothesis is that B7 glycoprotein molecule levels will correlate with clinical symptomatic severity score, other known biomarkers of HIDS, markers of inflammation and or markers of isoprenoid metabolism.

Not Provided
Observational
Observational Model: Case-Only
Time Perspective: Prospective
Not Provided
Retention:   Samples With DNA
Description:
Blood Urine
Non-Probability Sample
Subjects with Hyper IgD Syndrome (HIDS)
  • Hyper IgD Syndrome
  • Mevalonate Kinase Deficiency
Not Provided
Not Provided
Not Provided

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Unknown status
10
March 2016
March 2016   (Final data collection date for primary outcome measure)

Inclusion Criteria:

  • any race or ethnicity
  • diagnosed with HIDS

Exclusion Criteria:

  • parents' inability to donate blood
  • currently having cancer, renal failure, diabetes, liver disease, thyroid diseases, major infectious diseases or immunodeficiency
  • pregnancy
  • inability to provide consent
Sexes Eligible for Study: All
18 Years to 89 Years   (Adult, Senior)
No
Contact information is only displayed when the study is recruiting subjects
Netherlands,   United States
 
 
NCT01568736
STAIR 7003
Yes
Not Provided
Not Provided
Kenneth Michael Gibson, Michigan Technological University
Michigan Technological University
Not Provided
Not Provided
Michigan Technological University
March 2012