Further analyses of psoriasis patients showed that ACE I/D polymorphism was not associated with age at onset of disease, clinical type of psoriasis or gender.
A marginally significant difference (P=0 x 035) was found in the distribution of ACE I/D genotype frequencies between patients with psoriasis and controls.
Before therapy, tissue ACE activity was significantly increased in patients with psoriasis (4,14+/-0,34; X+/-SEM) in comparison to healthy individuals (1,86+/-0,16).
A marginally significant difference (P=0 x 035) was found in the distribution of ACE I/D genotype frequencies between patients with psoriasis and controls.
This study for the first time demonstrated that the ACE I/D and AT1R A <sub>1166</sub> C genes polymorphisms robustly increases the risk of developing psoriasis in population from west of Iran.
Skin infections, dermatitis/eczema, hyperlipidemia, and medications associated with psoriasis (beta blockers, angiotensin-converting enzyme (ACE) inhibitors, lithium, antimalarials, nonsteroidal anti-inflammatory drugs, and benzodiazepines) were included as potential confounders.
The prevalence of the homozygous ACE II genotype was significantly higher in patients with early-onset psoriasis than among control subjects (30.9% vs 19.2%, P = 0.016), yielding an odds ratio of 1.88 [95% confidence interval (CI): 1.12-3.15] for early-onset disease.
Atypical chemokine receptor 2 (ACKR2) binds and scavenges proinflammatory CC-chemokines, regulates cutaneous T-cell positioning, and limits the spread of inflammation <i>in vivo</i> Altered ACKR2 function has been implicated in several inflammatory disorders, including psoriasis, a common and debilitating T-cell-driven disorder characterized by thick erythematous skin plaques.
Our results have important implications for our understanding of how spatial restriction is imposed on the spread of inflammatory lesions and highlight systemic ACKR2 induction as a therapeutic strategy in the treatment and prevention of psoriasis and potentially a broad range of other immune-mediated diseases.
To conclude, the associated GGCCTT genotype in the promoter of MMP-2 gene was less frequent in patients with positive family history of psoriasis, diabetes and personal history of allergy compared with psoriatic patients without them (2/11 vs. 68/57, P = 0.007, Pcorr = 0.04; OR = 0.15, 95% CI = 0.03-0.72 for psoriatic patients with family history of psoriasis and diabetes and with allergy).
Efficacy through week52 was assessed by ≥20%/50%/70% improvement in ACR criteria (ACR20/50/70), Health Assessment Questionnaire-Disability Index (HAQ-DI), and ≥75% improvement in Psoriasis Area and Severity Index (PASI75); radiographic progression was measured using the PsA-modified van der Heijde-Sharp (vdH-S) score.
Exploratory endpoints at week 104 included 20, 50 and 70% improvement in ACR criteria (ACR20, 50, 70); 75 and 90% improvement in the Psoriasis Area Severity Index, 28-joint DAS with CRP, presence of dactylitis and enthesitis and other patient-reported outcomes.
Preferences for outcome (probability of 50 % and 90 % improvement, time until response, sustainability of success, probability of mild and severe adverse events, probability of ACR 20 response) and process attributes (treatment location, frequency, duration, and delivery method) were analyzed in 200 participants with moderate-to-severe psoriasis using conjoint analysis.