Effective continuous systemic therapy of severe plaque-type psoriasis is accompanied by amelioration of biomarkers of cardiovascular risk: results of a prospective longitudinal observational study.
BACKGROUND
Severe psoriasis is associated with significant cardiovascular mortality.


OBJECTIVE
We investigated the effects of continuous systemic therapy on the cardiovascular risk of patients with severe plaque-type psoriasis.


METHODS
A total of 42 consecutive patients receiving systemic treatment for their severe plaque-type psoriasis were included. The clinical course was monitored over 24 weeks. Initially as well as after 12 and 24 weeks, oral glucose tolerance tests were performed along with comprehensive laboratory monitoring.


RESULTS
Responding patients, defined as a Psoriasis Area and Severity Index (PASI)-50 response, showed correlations between the PASI and high-sensitive C-reactive protein (r = 0.45, P = 0.03) as well as with vascular endothelial growth factor (r = 0.76, P = 0.007). The adipokine resistin was positively and the potentially cardio-protective adiponectin was negatively correlated with the PASI (r = 0.50, P = 0.02 and r = -0.56, P = 0.007, respectively). Oral glucose tolerance tests yielded a correlation between the PASI and plasma levels for C-peptide (r = 0.73, P = 0.02) at t = 120 min in patients with a pathological Homeostasis Model Assessment (>2.5), indicating that the state of peripheral insulin resistance is driven at least in part by the severity of the psoriatic inflammation. Correlations between the change of adipokine levels and change in PASI were more pronounced among patients with better clinical improvement (PASI-75 vs. PASI-50).


CONCLUSIONS
We document an amelioration of biomarkers of cardiovascular risk in patients with severe plaque-type psoriasis responding to continuous systemic therapy. The impact on the patients'metabolic state was found to be better if the psoriatic inflammation was controlled for longer. Future studies need to compare the cardioprotective effects of different treatment modalities, based on hard clinical endpoints.
Department of Internal Medicine, Section for Diabetes, University Hospital of the Johann Wolfgang Goethe-University, Frankfurt am Main, Germany. boehncke@em.uni-frankfurt.de
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S
Boehncke
R
R
Salgo
J
J
Garbaraviciene
H
H
Beschmann
K
K
Hardt
S
S
Diehl
S
S
Fichtlscherer
D
D
Thaçi
W-H
WH
Boehncke
D000068879:Adalimumab; D054392:Adipokines / Q000097:blood; D000328:Adult; D000368:Aged; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism*; D002318:Cardiovascular Diseases / Q000097:blood / Q000453:epidemiology*; D016572:Cyclosporine / Q000627:therapeutic use; D000068800:Etanercept; D005260:Female; D005650:Fumarates / Q000627:therapeutic use; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use; D008137:Longitudinal Studies; D008297:Male; D008727:Methotrexate / Q000627:therapeutic use; D008875:Middle Aged; D011446:Prospective Studies; D011565:Psoriasis / Q000097:blood* / Q000188:drug therapy*; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D052243:Resistin / Q000097:blood*; D012307:Risk Factors; D012720:Severity of Illness Index; D016896:Treatment Outcome; D042461:Vascular Endothelial Growth Factor A / Q000097:blood*
D054392:Adipokines; D061067:Antibodies, Monoclonal, Humanized; D015415:Biomarkers; D005650:Fumarates; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D052243:Resistin; D042461:Vascular Endothelial Growth Factor A; D016572:Cyclosporine; D002097:C-Reactive Protein; D000068879:Adalimumab; D000068800:Etanercept; D008727:Methotrexate