title: Psoriasis therapy and cardiovascular risk factors: a 12-week follow-up study.
abstract: BACKGROUND
  Psoriatic patients present with an increased frequency of cardiovascular events.
  
  
  OBJECTIVE
  To study the impact of psoriasis duration and therapy on traditional and new cardiovascular risk factors.
  
  
  METHODS
  A longitudinal study performed between 2005 and the first trimester of 2008. Each patient was followed up for 12 weeks, and was observed before and 3, 6, and 12 weeks after starting therapy.
  
  
  METHODS
  Patients attending the Dermatology Service, University Hospital of Coimbra, Coimbra, Portugal were enrolled.
  
  
  METHODS
  Thirty-four patients with psoriasis vulgaris and 37 healthy volunteers as controls.
  
  
  METHODS
  Psoriasis Area and Severity Index (PASI); lipid profile, oxidized low-density lipoprotein (oxLDL), oxLDL/low-density lipoprotein (LDL), total antioxidant status, lipid peroxidation, C-reactive protein (CRP), and circulating levels of adiponectin.
  
  
  METHODS
  Ten patients started therapy with topical treatment, 11 with narrow-band UVB radiation (NB-UVB), and 13 with psolaren plus UVA (PUVA).
  
  
  RESULTS
  Before starting therapy, psoriatic patients presented with several risk changes in their lipid profiles, and significantly higher CRP, oxLDL, and oxLDL/LDL, and lower adiponectin levels (vs control subjects), which may further contribute to inflammation and atherogenesis. After treatment of the patients, although no significant differences were observed in the lipid profile compared with baseline, some changes suggested that the treatment could somehow alter lipid metabolism, as the reduction in high-density lipoprotein cholesterol (HDL-C) and apolipoprotein A and the increase in the atherogenic index cholesterol/HDL-C maintained an even higher significance (as shown by p-values) when compared with the control group. After topical therapy, there was a significant reduction in thiobarbituric acid reactivity only, suggesting that the reduction in the hyperproliferative process within the lesions is important for lipid peroxidation. After NB-UVB therapy, oxLDL/LDL, cholesterol/HDL-C, lipoprotein (a) [Lp(a)], and CRP remained higher than in the control subjects, reflecting persistent inflammation and atherogenic risk. After PUVA treatment, there was a significant reduction in Lp(a), associated with an almost significant increase in apolipoprotein-B (p = 0.054); these changes were not observed after NB-UVB treatment. However, after PUVA and NB-UVB treatment, CRP and, in the NB-UVB group, oxLDL/LDL were persistently higher than controls.
  
  
  CONCLUSIONS
  Our data show that psoriatic patients present with several lipid profile changes that seem to be related to the severity of the disease and/or the treatment used. Mild psoriasis patients receiving topical treatment presented before starting therapy with a lipid profile similar to controls, whereas those undergoing NB-UVB and PUVA, who had higher PASI scores, presented with several risk factors. Moreover, PUVA therapy seems to interact in a different way with lipids that might result from an interaction of psoralen with plasma lipids, namely Lp(a). Inflammation, a hallmark of psoriasis, also seems to be related to psoriasis severity. Both NB-UVB and PUVA were effective, as shown by the reduction in PASI score, as well as in the oxidative and inflammatory stress markers. However, after NB-UVB and PUVA, a low-grade inflammatory process still persisted, which might be related to the duration of remission of the disease.
authors.affiliation: Serviço de Bioquímica, Faculdade de Farmácia, Universidade do Porto, Porto, Portugal. ssn.coimbra@gmail.com
authors.forename: Susana
authors.initials: S
authors.lastname: Coimbra
authors.forename: Hugo
authors.initials: H
authors.lastname: Oliveira
authors.forename: Flávio
authors.initials: F
authors.lastname: Reis
authors.forename: Luís
authors.initials: L
authors.lastname: Belo
authors.forename: Susana
authors.initials: S
authors.lastname: Rocha
authors.forename: Alexandre
authors.initials: A
authors.lastname: Quintanilha
authors.forename: Américo
authors.initials: A
authors.lastname: Figueiredo
authors.forename: Frederico
authors.initials: F
authors.lastname: Teixeira
authors.forename: Elisabeth
authors.initials: E
authors.lastname: Castro
authors.forename: Petronila
authors.initials: P
authors.lastname: Rocha-Pereira
authors.forename: Alice
authors.initials: A
authors.lastname: Santos-Silva
mesh_terms: D052242:Adiponectin / Q000097:blood; D000328:Adult; D001623:Betamethasone / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D002117:Calcitriol / Q000031:analogs & derivatives / Q000627:therapeutic use; D002318:Cardiovascular Diseases / Q000097:blood / Q000209:etiology*; D003131:Combined Modality Therapy; D003879:Dermatologic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D005500:Follow-Up Studies; D005938:Glucocorticoids / Q000494:pharmacology / Q000627:therapeutic use*; D006801:Humans; D050356:Lipid Metabolism / Q000187:drug effects / Q000528:radiation effects; D008055:Lipids / Q000097:blood*; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000187:drug effects / Q000528:radiation effects; D011701:PUVA Therapy; D011565:Psoriasis / Q000097:blood / Q000150:complications* / Q000188:drug therapy* / Q000532:radiotherapy*; D012307:Risk Factors; D012720:Severity of Illness Index; D014467:Ultraviolet Therapy
chemical_list: D052242:Adiponectin; D015415:Biomarkers; D003879:Dermatologic Agents; D005938:Glucocorticoids; D008055:Lipids; C055085:calcipotriene; D002097:C-Reactive Protein; D001623:Betamethasone; D002117:Calcitriol