Psoriasis Inflammation and Systemic Co Morbidities
|ClinicalTrials.gov Identifier: NCT01170715|
Recruitment Status : Completed
First Posted : July 27, 2010
Last Update Posted : February 9, 2018
Psoriasis is a chronic relapsing prevalent inflammatory disease affecting 2-4% of the world's population. Severe psoriasis is a disabling disease affecting the physical and emotional well being of patients, and its effect on quality of life is similar to that seen with other major medical diseases such as diabetes, rheumatoid arthritis, and cancer. Lately, it is increasingly being recognized that psoriasis is not merely a skin disease but is probably associated with other co-morbidities such as psoriatic arthritis, Crohn's disease, the metabolic syndrome and cardio-vascular diseases (CVD). The metabolic syndrome is a combination of diabetes mellitus type II (or insulin resistance), hypertension, central obesity, and combined hyperlipidemia (elevated LDL; decreased HDL; elevated triglycerides). As the literature linking psoriasis and the metabolic syndrome expands, also reports of an increased rate of CVD mortality in psoriasis patients accumulates. These data emphasize that metabolic dysregulations are the leading risk factors for occlusive vascular events and early death in patients with severe psoriasis. Progress in understanding the pathogenesis of these apparently diverse diseases has discovered that low-grade systemic inflammation might be the common physiological pathway that may provide the biological plausibility of the associations discovered in the epidemiological studies. Since some of these co-morbidities often become clinically apparent years after the onset of psoriasis we assume that controlling systemic inflammation might prevent or reverse some of these co-morbidities.
Presently there is no study in psoriasis that shows that a "systemic" co-morbidity can be prevented or treated by reversing skin inflammation.
|Condition or disease||Intervention/treatment||Phase|
|Psoriasis||Drug: Etanercept||Not Applicable|
Show Detailed Description
|Study Type :||Interventional (Clinical Trial)|
|Estimated Enrollment :||30 participants|
|Intervention Model:||Single Group Assignment|
|Intervention Model Description:||Participants will be screened and enrolled based on inclusion/exclusion criteria. Those enrolled will have intervention for 52 weeks and assessed for outcome measures along the way.|
|Masking:||None (Open Label)|
|Primary Purpose:||Basic Science|
|Official Title:||Psoriasis Inflammation and Systemic Co-Morbidities: Is it Preventable or Reversible?|
|Actual Study Start Date :||July 13, 2010|
|Actual Primary Completion Date :||September 9, 2013|
|Actual Study Completion Date :||September 9, 2013|
Experimental: Experimental Group
Enbrel (etanercept): started with self-injection of 50 mg subcutaneous twice weekly for 12 weeks, followed by self-injection of 50 mg subcutaneous weekly for 40 weeks.
self-administered for 52 weeks
Other Name: Enbrel
- Change in histology [ Time Frame: From baseline, every 3 months, up to one year (52 weeks). ]To analyze specimens using histology and gene expression before, during, and after treatment.
- Change in gene expression [ Time Frame: From baseline, every 3 months, up to one year (52 weeks). ]To analyze specimens using histology and gene expression before, during, and after treatment.
- To analyze immunological biomarkers of inflammation in the blood using electrochemiluminescence of the MSD systems approach [ Time Frame: From baseline, every 3 months, up to one year (52 weeks). ]hs-CRP, IL-2 Receptor, Plasminogen activator inhibitor complex (PAI), tissue plasminogen activator (TPA), anti pro BNP, E-selectin, inflammatory cytokines and markers, metabolic markers, vascular markers [IL= interleukin; MMP =Matrix metallopeptidase; ICAM=Inter-Cellular Adhesion Molecule; VCAM= vascular cell adhesion molecule; SAA=Serum amyloid A;GLP-1= Glucagon-like peptide-1;CRP C-Reactive protein. The markers list: IFN-γ, IL-2, IL-4, IL-5, IL-10, IL-12p70, IL-13, IFN-γ, IL-2, IL-4, IL-5, IL-10, IL-12p70, IL-13, MMP- 1, MMP-3 and MMP-9, CRP, sICAM-1, sVCAM-1, SAA, adiponectin, GLP-1,insulin, resistin and other future markers not known at this time.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT01170715
|United States, New York|
|The Rockefeller University|
|New York, New York, United States, 10065|
|Principal Investigator:||James Krueger, MD, PhD||The Rockefeller University|