**Background:** Psoriasis is a chronic, immune-mediated inflammatory disease affecting the skin and joints. Vitamin D is a key modulator of immune response with antiproliferative effects on keratinocytes, and vitamin D deficiency is increasingly recognized as a global health issue. While vitamin D analogs are used therapeutically in psoriasis, the relationship between vitamin D status and disease severity—particularly in patients with and without psoriatic arthritis (PsA)—remains incompletely understood, with conflicting results across studies.
**Methods:** This retrospective cross-sectional study was conducted at a university hospital dermatology outpatient clinic in Juiz de Fora, Minas Gerais, Brazil (latitude 21°S, 43°W). Medical records of 350 patients treated between January and December 2016 were reviewed; 300 patients met inclusion criteria (plaque psoriasis, age 18–60 years, no vitamin D supplementation, no phototherapy or topical vitamin D analog use, no severe systemic diseases). Patients were divided into two groups: psoriasis without PsA (n=227, 75.67%) and psoriasis with PsA (n=73, 24.33%), the latter diagnosed according to CASPAR criteria. Data collected included demographics, family history, age at onset, disease duration, PASI score (stratified as mild <10 or moderate-to-severe ≥10), Fitzpatrick skin phototype, season of blood draw, and serum 25(OH)D levels measured by chemiluminescence. Vitamin D status was categorized as deficient (<20 ng/mL), insufficient (20–<30 ng/mL), or sufficient (≥30 ng/mL). Statistical analyses included Student's t-test, chi-square test, Pearson correlation, multiple linear regression, and binary logistic regression.
**Key Results:** Hypovitaminosis D (<30 ng/mL) was highly prevalent: 82.2% in patients with PsA and 74.9% in those without PsA. Mean serum 25(OH)D was significantly lower in the PsA group (23.43 ± 6.55 ng/mL) compared to the non-PsA group (25.39 ± 7.30 ng/mL, P=0.033). Vitamin D deficiency (<20 ng/mL) was present in 31.5% of PsA patients vs. 23.8% of non-PsA patients. An inverse correlation between PASI and vitamin D levels was found in both groups (without PsA: r=−0.59, P<0.001; with PsA: r=−0.52, P<0.001). Multiple linear regression (adjusted R²=0.31, P<0.001) identified moderate-to-severe psoriasis as a strong negative predictor of 25(OH)D levels (β=−6.712, 95% CI: −8.51 to −4.91, P<0.0001). Season was also a significant predictor: compared to winter, summer was associated with higher vitamin D levels (β=8.708, 95% CI: 6.07–11.33, P<0.0001), as were spring (β=4.512, P=0.002) and autumn (β=3.525, P=0.017). Skin phototype V was inversely associated with vitamin D levels (β=−3.783, 95% CI: −6.89 to −0.95, P=0.014). Binary logistic regression confirmed a strong association between PASI and vitamin D deficiency (<30 ng/mL) (OR 1.78, 95% CI: −0.20 to 0.53, P<0.001). The presence of arthritis, family history, age at diagnosis, and disease duration were not significant independent predictors in the multivariate model.
**Clinical Implications:** This study demonstrates that hypovitaminosis D is highly prevalent among patients with plaque psoriasis, particularly those with concomitant PsA, and is inversely correlated with disease severity as measured by PASI. Season and skin phototype are important modifiable/non-modifiable factors influencing vitamin D status. These findings support the routine monitoring of serum 25(OH)D in psoriatic patients, especially those with moderate-to-severe disease, higher phototypes, and during seasons with lower sun exposure. Vitamin D supplementation may be a beneficial adjunctive strategy in this population, though interventional studies are needed to confirm therapeutic benefit. Limitations include the retrospective design, absence of dietary and sun exposure data, and lack of representation of phototypes I, II, and VI.