Psoriasis is a chronic immune-mediated inflammatory skin disease, with a prevalence of about 2%–3% in the general population.1 The primary manifestation of psoriasis most commonly manifests on the skin, although inflammatory processes can occur also in other organs.2 Indeed, nowadays psoriasis is considered a systemic pathology, including also other conditions, from psoriatic arthritis to obesity and metabolic disease (MetS), which increased cardiovascular risk in psoriatic patients.3 Histologically, the dermatosis is characterized by hyperproliferation of keratinocytes, impaired epidermal barrier function at the sites of skin lesions, and skin infiltration by activated inflammatory cells8. The aetiology of psoriasis is not fully understood. Several factors contribute to its development, such as auto-immunological, genetic, hormonal and psychosomatic issues.4

Vitamin D, also known as the sunshine vitamin, has long been known to be a hormone that regulates calcium-phosphorous homeostasis and safeguards the integrity of the skeletal system.1 The epidermis is the natural source of vitamin D synthesis by the action of ultraviolet light (UV) B of the sun or other UVB source.2 On the other hand, evidence is accumulating that vitamin D might represent a key modulator of immune and inflammation mechanisms.5

Present study aimed to evaluate the effect of vitamin D supplementation as an adjunct to standard therapy on clinical outcomes and disease severity (PASI score) in patients with psoriasis.

The present study was conducted in the Departments of Pharmacology and Dermatology at MNR Medical College, Hyderabad, a tertiary care teaching hospital, over a period extending from December 2020 to June 2022. This was a prospective, randomized, comparative study designed to evaluate the role of vitamin D in patients with psoriasis. A total of 70 patients diagnosed with psoriasis, attending either the outpatient or inpatient services of the Dermatology department, were enrolled after satisfying the inclusion criteria. Adults aged above 18 years, of either gender, and willing to provide informed written consent were included in the study. Patients were excluded if they had significant comorbid conditions such as renal dysfunction or arrhythmias, hypercalcemia, were pregnant or lactating, severely ill or mentally unfit to participate, or unwilling to provide consent. Ethical clearance was obtained from the Institutional Ethical Committee prior to the commencement of the study. A predesigned, pretested, semi-structured, and pre-coded proforma was used to systematically record demographic details, clinical history, examination findings, and laboratory parameters. After enrollment, all patients underwent baseline biochemical investigations including random blood sugar (GOD-POD method), serum calcium (Arsenazo method), serum vitamin D levels (chemiluminescence assay), and serum creatinine (Jaffe’s method). Only patients with serum vitamin D levels less than 20 ng/mL were considered for randomization. Participants were then randomly allocated into two equal groups of 35 each. Group A received standard psoriasis treatment, which included topical therapy, phototherapy, and/or systemic oral or injectable medications as per clinical indication, without vitamin D supplementation. Group B received the same standard treatment protocol along with vitamin D supplementation in the form of Calshine 60,000 IU sachets administered orally once weekly for six weeks. Compliance with treatment was monitored during follow-up visits. All patients were followed up for a duration of eight weeks. Clinical assessment of disease severity and response to treatment was performed using the Psoriasis Area and Severity Index (PASI) score at baseline and at the end of the study period. Repeat estimation of serum vitamin D and calcium levels was carried out at the end of follow-up to evaluate biochemical improvement and to correlate with clinical outcomes. Patients were also monitored for any adverse drug reactions or complications during the study period. Data collected were entered into Microsoft Excel 2010 and analyzed using Microsoft Excel and Epi Info version 7.2.0. Descriptive statistics were used to summarize the data, with continuous variables expressed as mean ± standard deviation (SD) and categorical variables as frequencies and percentages. Inferential statistical analysis was performed using Student’s t-test to compare intergroup differences for continuous variables. Pearson’s correlation coefficient was applied to assess the relationship between serum vitamin D levels and PASI scores. A p-value of less than 0.05 was considered statistically significant.

Study include total of 70 cases of psoriasis, with 35 cases in each group.

The comparison of socio-demographic and lifestyle characteristics between Group A and Group B shows that both groups were largely comparable, with no statistically significant differences observed across the variables studied. The age distribution was similar between the two groups (p = 0.67), with the majority of participants falling in the 51–60 years category in Group A and 20–30 years in Group B, though the variation was not significant. Gender distribution was identical in both groups, with males constituting 57.1% and females 42.9% (p = 1.0). Similarly, place of residence showed no difference, as the majority of participants in both groups belonged to rural areas (77.1%) (p = 1.0). Regarding lifestyle factors, dietary habits did not differ significantly (p = 0.2), although a higher proportion of mixed diet was observed in Group B. Physical activity levels were comparable (p = 0.23), with most participants in both groups reporting no regular exercise. The prevalence of smoking was slightly higher in Group B (31.4%) compared to Group A (20.0%), but this difference was not statistically significant (p = 0.27). Similarly, alcohol consumption was more common in Group B (40.0%) than in Group A (20.0%), approaching but not reaching statistical significance (p = 0.068).

The comparison of clinical and biochemical parameters between Group A and Group B demonstrates that both groups were largely comparable, with no statistically significant differences observed across the variables assessed. Systolic blood pressure (SBP) distribution was identical in both groups, with 60% of participants having normal SBP and 40% having elevated levels (p = 1.0), indicating perfect matching. Diastolic blood pressure (DBP) showed a higher proportion of elevated values in Group B (82.9%) compared to Group A (62.9%), while normal DBP was more common in Group A (37.1% vs. 17.1%); however, this difference approached but did not reach statistical significance (p = 0.06). Fasting blood sugar (FBS) levels were comparable between the groups (p = 0.27), although a slightly higher proportion of elevated FBS was observed in Group B (31.4%) than in Group A (20.0%). Similarly, triglyceride (TG) levels did not differ significantly (p = 0.2), with elevated levels more frequent in Group B (40.0%) compared to Group A (25.7%). High-density lipoprotein (HDL) levels were also comparable (p = 0.71), with a slightly higher proportion of reduced HDL in Group A. Serum calcium levels showed no significant difference (p = 0.2), although low calcium levels were somewhat more common in Group B (40.0%) than in Group A (25.7%).

The comparison of severity levels between Group A and Group B at baseline and at 8 weeks reveals important changes over time. At baseline, both groups were comparable, with no statistically significant difference in severity distribution (p = 0.86). The majority of patients in both groups had moderate disease (Group A: 54.3%, Group B: 60.0%), followed by mild and severe categories, indicating a similar starting point for both groups. However, at 8 weeks, a statistically significant difference was observed between the groups (p = 0.02). Group B showed a marked improvement, with the majority of patients shifting to the mild category (54.3%), compared to only 14.3% in Group A. Conversely, Group A had a higher proportion of patients in the severe category (51.4%) compared to Group B (14.3%). Moderate severity was observed in 42.9% of Group A and 31.4% of Group B.

Figure 1: Comparison of Mean PASI Scores at Baseline and at 8 Weeks

The comparison of mean PASI scores between Group A and Group B at baseline and at 8 weeks shows notable differences in treatment response. At baseline, both groups were comparable, with mean PASI scores of 7.15 ± 2.81 in Group A and 7.70 ± 3.54 in Group B, and the difference was not statistically significant (p = 0.47). This indicates that the initial severity of disease was similar in both groups. However, at 8 weeks, a statistically significant difference was observed (p = 0.03). Group B demonstrated a greater reduction in PASI score, with a mean of 3.24 ± 2.92, compared to 5.79 ± 2.56 in Group A. This suggests that patients in Group B experienced a more pronounced improvement in disease severity over the study period.

Vitamin D is an essential nutrient in humans; it is produced by the body through exposure to the sun (the primary source of vitamin D), or more precisely, to mild ultraviolet B (UVB) light. Other sources of vitamin D include food and dietary supplements. In 1928, the chemist and medical doctor Adolf Otto Reinhold Windaus was awarded the Nobel Prize for chemistry for the discovery of vitamin D. Chemically, vitamin D2 was first characterized in 1932, and vitamin D3 was characterized in 1936. Currently, vitamin D is known as a hormone that regulates calcium-phosphorus homeostasis and protects the integrity of the skeletal system. Vitamin D levels are influenced by many factors, including the season, period of sun exposure, time of the day, latitude, use of sunscreen, clothing, skin color, body weight, and medical conditions.57 When epidermal cells are exposed to UVB, 7-dehydrocholesterol can be transformed into pre-vitamin D, which isomerizes to vitamin D3. Next, vitamin D3 undergoes 25-hydroxylation, through an enzymatic conversion in the liver, to form 25(OH) vitamin D (calcidiol), the primary circulating form of vitamin D. The plasma half-life of 25(OH) vitamin D is 2–3 weeks. Calcidiol is converted in the kidneys by 1-alpha-hydroxylation to the most active form, 1,25(OH)2D (calcitriol), which has a plasma half-life of 4–6 h. This entire process is modulated by parathyroid hormone, hypophosphatemia, growth hormone, and other mediators.6 Psoriasis is a chronic autoimmune skin disease with a strong genetic predisposition, characterized by sustained inflammation and followed by uncontrolled proliferation of keratinocytes and dysfunctional differentiation. The first-line therapy for mild-to-moderate psoriasis is topical administration of corticosteroids and vitamin D analogues. Keratinocytes and lymphocytes that infiltrate the lesions express the vitamin D receptor, which explains the effectiveness of this therapy in psoriasis. The pathogenesis of psoriasis is not fully elucidated. The development of psoriasis plaques is mediated by Th1 cells and connected to keratinocyte hyperproliferation. This connection could explain the efficacy of immunosuppressive and antiproliferative vitamin D-like compounds, such as calcipotriol, in psoriasis. Ligands for vitamin D receptor inhibit the expression of pro-inflammatory cytokines produced by T lymphocytes (i.e., IL-2, IFN-γ, IL-6, and IL-8). Thus, the biological activity of vitamin D3 analogues leads to suppression of the T cell-mediated immune response. Moreover, dendritic antigen-presenting cells are modulated by 1a,25(OH)2D3 and its analogues, which inhibit the differentiation, maturation, activation, and survival of these cells. Given current knowledge, it is reasonable to assume that epidermal production of vitamin D could be at least partially affected in skin psoriatic lesions, which may contribute to worsening symptoms. A total of 70 psoriasis patients were included, with 35 patients in each group. In Group A, the majority belonged to the 51–60 years age group (28.6%), followed by 31–40 and 41–50 years (22.9% each). In Group B, most patients were aged 20–30 years (34.3%), followed by 51–60 years (22.9%) and 31–40 and 41–50 years (17.1% each). Both groups had a similar gender distribution, with 57.1% males and 42.9% females. The overall mean age of participants was 42.78 ± 12.2 years, with a median age of 43.12 years. Comparable findings were reported by Pokharel R et al, who observed a mean age of 42.93 ± 14.28 years among 120 psoriasis patients,7 and by Bhat GH et al, who reported a mean age of 44.6 ± 13.5 years with a male predominance (61.8%), supporting the consistency of demographic patterns across studies.8 At baseline, 31.4% of patients in Group A and 25.7% in Group B had mild disease, while the majority presented with moderate disease (54.3% in Group A and 60% in Group B), and 14.3% in both groups had severe disease. There was no statistically significant difference between the two groups with respect to baseline disease severity (p>0.05). However, after 8 weeks of treatment, a marked shift in severity distribution was observed. In Group B, 54.3% of patients improved to mild disease compared to only 14.3% in Group A. Moderate disease was seen in 42.9% of Group A and 31.4% of Group B, while severe disease persisted in 51.4% of Group A compared to only 14.3% in Group B. This difference was statistically significant (p<0.05), indicating better clinical improvement in the vitamin D supplemented group. These findings are consistent with previous studies. Pokharel R et al., reported that most patients had moderate disease (50%), with 29.2% mild and 20.8% severe disease.7 Similarly, Bhat GH et al., observed that 43.9% of patients had moderate disease, though only 4.2% had mild disease. They also demonstrated a significant association between disease severity and vitamin D levels, with severe psoriasis patients showing markedly lower 25-hydroxy vitamin D levels (OR = 6.3; p=0.004).8 This supports the present study’s observation that vitamin D supplementation is associated with improved disease severity outcomes. In the present study, 25.7% of patients in Group A and 40% in Group B had low serum calcium levels, with no statistically significant difference between the groups (p>0.05). The mean serum calcium levels were 8.91 ± 0.89 mg/dL in Group A and 8.76 ± 0.85 mg/dL in Group B, again showing no significant difference (p>0.05), indicating that both groups were comparable with respect to baseline calcium status. In contrast, Bhat GH et al., reported significantly lower mean 25-hydroxy vitamin D levels in psoriasis patients (28.3 ± 15.0 ng/mL) compared to controls (37.8 ± 9.8 ng/mL), with a statistically significant difference (P < 0.0001).8 While their study highlights the association between vitamin D deficiency and psoriasis, the present study demonstrates that serum calcium levels did not differ significantly between groups, suggesting that calcium may not directly influence disease severity or treatment response in comparison to vitamin D. The mean baseline PASI score in Group A and Group B was 7.15 ± 2.81 and 7.70 ± 3.54 respectively, with no statistically significant difference between the groups (p>0.05), indicating comparability at baseline. After 8 weeks of treatment, the mean PASI score decreased to 5.79 ± 2.56 in Group A and 3.24 ± 2.92 in Group B. Although a greater reduction was observed in Group B, the difference between the groups was not statistically significant (p>0.05). The PASI score, a widely accepted tool since 1978, reflects both severity and extent of psoriasis and is commonly used to monitor treatment response. These findings are supported by previous studies. Pokharel R et al., reported a lower mean PASI score of 1.92 ± 0.705,7 while Perez et al., demonstrated a significant reduction in PASI from 18.4 ± 1.0 at baseline to 9.7 ± 0.8 and 7.0 ± 1.3 during follow-up.9 Several interventional studies have shown variable degrees of improvement with vitamin D therapy: Morimoto et al., reported >76% moderate improvement,10 Takamoto et al., observed moderate improvement in 25% of patients,11 and Smith et al., noted marked improvement in 50% of cases.12 Similarly, Holland et al., reported complete resolution in 46.67% of patients,13 while Huckins et al., found 44.44% had marked improvement.14 Siddiqui et al., observed slight improvement in 45% of cases.15 Gaal et al., reported modest changes in PASI scores,16 whereas Finamore et al.,17 and Disphanurat et al., demonstrated significant clinical improvement over time.18 Lourencetti M et al., in their review, concluded that vitamin D therapy is generally safe and effective, with good clinical outcomes across multiple studies.19 These observations align with the present study, where a greater reduction in PASI scores was seen in the vitamin D supplemented group, suggesting a beneficial role in improving disease severity. Studies evaluating high-dose vitamin D₃ supplementation (greater than 60,000 IU) have reported clinical benefits, including resolution of anti-TNF-α–induced psoriasiform lesions in patients with rheumatoid arthritis and concurrent vitamin D deficiency. Most earlier studies used empirical dosing, with a shift toward higher doses after 2014. Serum 25(OH)D levels were primarily monitored for safety rather than correlation with clinical improvement. However, doses of vitamin D₂ exceeding 40,000 IU have been associated with hypercalcemia toxicity. Millsop et al., in their analysis of six prospective trials, highlighted potential adverse effects of oral vitamin D supplementation, including hypercalcemia, hypercalciuria, nephrolithiasis, and, with prolonged overdose, bone demineralization.20 Nevertheless, some studies reported biochemical increases in serum and urinary calcium without clinically significant adverse effects.21 Zuccotti et al., emphasized that although vitamin D supplementation may not consistently produce significant clinical improvement, it may help prevent psoriasis-related comorbidities through modulation of immune and inflammatory pathways.22 Similarly, Barrea et al., suggested that oral vitamin D intake up to 10,000 IU daily is generally safe and may contribute to clinical improvement, with some studies reporting PASI score improvement in up to 88% of patients and moderate improvement in 25–50% of cases.23 However, conflicting evidence exists, as another study concluded that available data are insufficient to definitively establish the efficacy of oral vitamin D in psoriasis.24 Marino et al., reported that administration of 60,000 IU oral vitamin D for six months resulted in increased serum vitamin D levels along with a reduction in PASI scores, supporting its potential therapeutic role.25 Limitation: The present study has certain limitations. The relatively small sample size (n=70) and short follow-up period (8 weeks) may limit the generalizability of findings and the ability to assess long-term efficacy and safety of vitamin D supplementation. Lack of blinding may introduce observer bias, particularly in PASI scoring, and variability in standard treatment modalities could act as a confounding factor. Additionally, inclusion of only vitamin D–deficient patients and the single-center design further restrict the applicability of results to the broader population. Future studies should involve larger, multicentric cohorts with longer follow-up periods to better evaluate sustained clinical outcomes and safety. Standardization of treatment protocols, incorporation of blinding, and inclusion of patients with varying vitamin D levels would help provide more robust evidence regarding the role of vitamin D in psoriasis management.

In the present prospective randomized comparative study, both groups were found to be comparable at baseline with respect to demographic profile, clinical characteristics, comorbid conditions, biochemical parameters, and initial PASI scores, with no statistically significant differences observed. After 8 weeks of follow-up, although both groups showed improvement in disease severity, the vitamin D supplemented group (Group B) demonstrated a significantly greater reduction in psoriasis severity compared to the standard treatment group (Group A), as evidenced by improved PASI scores and a shift towards milder disease categories (p<0.05). Other clinical and metabolic parameters, including serum calcium and lipid profile, remained comparable between the two groups, indicating that the observed clinical benefit was primarily associated with vitamin D supplementation rather than baseline differences. Overall, the study suggests that vitamin D supplementation as an adjunct to standard therapy may have a beneficial role in improving clinical outcomes in psoriasis patients, particularly in reducing disease severity over short-term follow-up. These findings support the potential immunomodulatory and therapeutic role of vitamin D in psoriasis management. However, further large-scale, long-term studies are warranted to confirm its sustained efficacy and to better understand its impact on metabolic and inflammatory parameters in psoriasis.

Funding: Nil

Conflict of interest: Nil

1. Flatz L, Conrad C. Role of T-cell-mediated inflammation in psoriasis: pathogenesis and targeted therapy. Psoriasis Targets Ther. 2013;1–10.
2. Chong L. Is Psoriasis a Cutaneous Disease or Systemic Disease. Med Bull. 2010;15(11).
3. Johnson-Huang LM, Lowes MA, Krueger JG. Putting together the psoriasis puzzle: an update on developing targeted therapies. Dis Model Mech. 2012;5(4):423–33.
4. Raharja A, Mahil SK, Barker JN. Psoriasis: a brief overview. Clin Med (Northfield Il). 2021;21(3):170–3.
5. Kongsbak M, Levring TB, Geisler C, Von Essen MR. The vitamin d receptor and T cell function. Front Immunol. 2013;4:51253.
6. Stanescu AMA, Simionescu AA, Diaconu CC. Oral vitamin D therapy in patients with psoriasis. Nutrients. 2021;13(1):163.
7. Pokharel R, Agrawal S, Pandey P, Lamsal M. Assessment of Vitamin D Level in Patients with Psoriasis and Its Correlation with Disease Severity: A Case-Control Study. Psoriasis (Auckland, NZ). 2022;12:251–8.
8. Bhat GH, Guldin S, Khan MS, Yasir M, Prasad G. Vitamin D status in Psoriasis: impact and clinical correlations. BMC Nutr. 2022;8(1):115.
9. Perez A, Raab R, Chen TC, Turner A, Hollck MF. Safety and efficacy of oral calcitriol (1, 25‐dihydroxyvitamin D3) for the treatment of psoriasis. Br J Dermatol. 1996;134(6):1070–8.
10. Morimoto S, Yoshikawa K, Kozuka T, Kitano Y, Imanaka S, Fukuo K, et al. An open study of vitamin D3 treatment in psoriasis vulgaris. Br J Dermatol. 1986;115(4):421–9.
11. Takamoto S, Onishi T, Morimoto S, Imanaka S, Yukawa S, Kozuka T, et al. Effect of 1α-hydroxycholecalciferol on psoriasis vulgaris: A pilot study. Calcif Tissue Int. 1986;39(6):360–4.
12. Smith EL, Pincus SH, Donovan L, Holick MF. A novel approach for the evaluation and treatment of psoriasis: oral or topical use of 1, 25-dihydroxyvitamin D3 can be a safe and effective therapy for psoriasis. J Am Acad Dermatol. 1988;19(3):516–28.
13. Holland DB, Wood EJ, Roberts SG, West MR, Cunliffe WJ. Epidermal keratin levels during oral 1-alpha-hydroxyvitamin D3 treatment for psoriasis. Skin Pharmacol Physiol. 1989;2(2):68–76.
14. Huckins D, Felson DT, Holick M. Treatment of psoriatic arthritis with oral 1, 25‐dihydroxyvitamin D3: a pilot study. Arthritis Rheum Off J Am Coll Rheumatol. 1990;33(11):1723–7.
15. Siddiqui MA, Al-Khawajah MM. Vitamin D3 and psoriasis: a randomized double-blind placebo-controlled study. J Dermatolog Treat. 1990;1(5):243–5.
16. GAáL J, Lakos G, Szodoray P, Kiss J, HORVáTH I, Horkay E, et al. Immunological and clinical effects of alphacalcidol in patients with psoriatic arthropathy: results of an open, follow-up pilot study. Acta Derm Venereol. 2009;89(2):140–4.
17. Finamor DC, Sinigaglia-Coimbra R, Neves LCM, Gutierrez M, Silva JJ, Torres LD, et al. A pilot study assessing the effect of prolonged administration of high daily doses of vitamin D on the clinical course of vitiligo and psoriasis. Dermatoendocrinol. 2013;5(1):222–34.
18. Disphanurat W, Viarasilpa W, Chakkavittumrong P, Pongcharoen P. The clinical effect of oral vitamin D2 supplementation on psoriasis: a double‐blind, randomized, placebo‐controlled study. Dermatol Res Pract. 2019;2019(1):5237642.
19. Lourencetti M, Abreu MM de. Use of active metabolites of vitamin D orally for the treatment of psoriasis. Rev Assoc Med Bras. 2018;64(7):643–8.
20. Millsop JW, Bhatia BK, Debbaneh M, Koo J, Liao W. Diet and psoriasis, part III: role of nutritional supplements. J Am Acad Dermatol. 2014;71(3):561–9.
21. El-Azhary RA, Peters MS, Pittelkow MR, Kao PAIC, Muller SA. Efficacy of vitamin D3 derivatives in the treatment of psoriasis vulgaris: a preliminary report. In: Mayo Clinic Proceedings. Elsevier; 1993. p. 835–41.
22. Zuccotti E, Oliveri M, Ratto D, Di Iorio C, Occhinegro A, Rossi P, et al. Nutritional strategies for psoriasis: current scientific evidence in clinical trials. Eur Rev Med Pharmacol Sci. 2018;22(23).
23. Barrea L, Savanelli MC, Di Somma C, Napolitano M, Megna M, Colao A, et al. Vitamin D and its role in psoriasis: An overview of the dermatologist and nutritionist. Rev Endocr Metab Disord. 2017;18(2):195–205.
24. Thompson KG, Kim N. Dietary supplements in dermatology: A review of the evidence for zinc, biotin, vitamin D, nicotinamide, and Polypodium. J Am Acad Dermatol. 2021;84(4):1042–50.
25. Marino R, Misra M. Extra-skeletal effects of vitamin D. Nutrients. 2019;11(7):1460.