Next Article in Journal
Body Composition Changes after a Weight Loss Intervention: A 3-Year Follow-Up Study
Next Article in Special Issue
Vitamin D Supplementation to Prevent COVID-19 Infections and Deaths—Accumulating Evidence from Epidemiological and Intervention Studies Calls for Immediate Action
Previous Article in Journal
Promising Potential of Crude Polysaccharides from Sparassis crispa against Colon Cancer: An In Vitro Study
Previous Article in Special Issue
The Health Effects of Vitamin D and Probiotic Co-Supplementation: A Systematic Review of Randomized Controlled Trials
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:

Oral Vitamin D Therapy in Patients with Psoriasis

Ana Maria Alexandra Stanescu
Anca Angela Simionescu
2,* and
Camelia Cristina Diaconu
Department of Family Medicine, “Carol Davila” University of Medicine and Pharmacy, 050474 Bucharest, Romania
Department of Obstetrics and Gynecology, Filantropia Clinical Hospital, “Carol Davila” University of Medicine and Pharmacy, 050474 Bucharest, Romania
Department of Internal Medicine, Clinical Emergency Hospital of Bucharest, “Carol Davila” University of Medicine and Pharmacy, 050474 Bucharest, Romania
Author to whom correspondence should be addressed.
Nutrients 2021, 13(1), 163;
Submission received: 10 December 2020 / Revised: 2 January 2021 / Accepted: 4 January 2021 / Published: 6 January 2021


Vitamin D treatment is effective when applied topically to the skin for plaque-type psoriasis. Oral vitamin D supplementation might be effective as an adjuvant treatment option in psoriasis. This umbrella review aimed to highlight the current knowledge regarding the use of oral vitamin D for treatment of patients with psoriasis. We performed a literature search and identified 107 eligible full-text articles that were relevant to the research interest. Among these, 10 review articles were selected, and data were extracted. A data synthesis showed that only a few studies monitored oral vitamin D efficacy in patients with psoriasis. No studies investigated the optimal dose of systemic vitamin D in psoriasis. However, most studies did not observe side effects for doses within a relatively narrow range (0.25 to 2 μg/day). These results suggest that more large-scale studies are needed to determine the efficacy, optimal dose, and adverse effects of vitamin D administration in patients with psoriasis.

1. Introduction

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 [1]. In 1928, the chemist and medical doctor Adolf Otto Reinhold Windaus was awarded the Nobel Prize for chemistry for the discovery of vitamin D [1,2,3]. 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 [4]. 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 [5,6].
When epidermal cells are exposed to UVB, 7-dehydrocholesterol can be transformed into pre-vitamin D, which isomerizes to vitamin D3 [7]. 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 [8]. This entire process is modulated by parathyroid hormone, hypophosphatemia, growth hormone, and other mediators.
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 [9]. The first-line therapy for mild-to-moderate psoriasis is topical administration of corticosteroids and vitamin D analogues [10,11]. Keratinocytes and lymphocytes that infiltrate the lesions express the vitamin D receptor, which explains the effectiveness of this therapy in psoriasis [12].
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 [13]. 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) [14]. 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 [15]. 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.
Current knowledge, which holds that vitamin D treatment applied to the skin is effective, has given rise to the possibility that oral vitamin D supplementation might be an effective adjuvant treatment option in psoriasis. Due to the controversial and understudied nature of this topic, this umbrella review aimed to summarize current evidence, with an emphasis on clinical outcomes, on oral vitamin D treatment in patients with psoriasis. The need for this umbrella review derives from the controversies on this subject and the lack of systematic investigations.

2. Materials and Methods

2.1. Search Strategy

Our review strategy was based on the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) checklist [16]. We performed a literature search in August 2020 in PubMed and Scopus. The search included the period 2010–2020, and we used the following search terms: “oral vitamin D” AND “psoriasis” AND “treatment” [all text].

2.2. Inclusion and Exclusion Criteria

We scanned the full text of each identified article for relevance to the research interest. All articles written in the English language that addressed oral vitamin D and its analogue treatment in patients with psoriasis and a posttreatment score evaluation (PASI score—Psoriasis Area Severity Index and patient global assessment) were included. Based on the umbrella review typology, we only selected review-type articles, including clinical cases. We excluded articles that did not have a main focus on oral vitamin D administration in psoriasis as a monotherapy, those that only mentioned a phrase regarding this type of administration, studies having less than 2 patients included or psoriasis-associated diseases, studies that compared vitamin D effects and corticosteroids, and reports from meeting abstracts. We did not apply restrictions on the age of inclusion or the type or severity of psoriasis.

2.3. Data Extraction

The data were extracted and summarized in a table (Table 1). The characteristics of individual studies included in the review articles were the number of patients, type of study, and study location.

3. Results

We followed the PRISMA principles in developing this review (Figure 1). In total, after searching for keywords, we identified 395 records. Duplicates were removed, and after applying the other search criteria, we screened 107 eligible full-text articles. According to the established criteria, 10 review articles were included in the final analysis.
A relatively small number of studies have investigated the effectiveness of oral vitamin D in patients with psoriasis. Accordingly, we identified a fairly small number of systemic reviews and meta-analyses. Some reviews discussed transient oral administration of vitamin D in other contexts or as a subset of cutaneous vitamin D therapy. The characteristics of the included original studies are shown in Table 1.
To our knowledge, the first case of psoriasis treated with 1-alpha hydroxyvitamin D3 for osteoporosis was reported in 1985, and the treatment resulted in psoriasis remission [29]. This case led to further research on the effects of systemic vitamin D administration on psoriasis. In 2013, Kamangar et al. studied oral vitamin D in patients with psoriasis and in patients with psoriatic arthritis. In most cases, psoriasis improved visibly after treatment with 0.25 μg to 1 μg/day of 1,25-(OH)2D3, with no adverse effects. The authors concluded that oral vitamin D was a safe and effective therapeutic option for treating psoriasis vulgaris [18]. Treatment effectiveness after oral administration of vitamin D3 and D2 in patients with psoriasis, based on the original studies, is shown in Table 2 and Table 3.
The patients were monitored clinically in the included studies, with one of the most commonly used scores being the PASI score, which takes into account the overall severity score and the percentage of body surface area affected by psoriasis. The PASI score has been used to monitor the effectiveness of antipsoriatic medication since 1978 [42].
Table 4 details the scores and clinical modalities used to determine the clinical efficacy of orally administered vitamin D in psoriasis.
Lourencetti and Morgado de Abreu analyzed 10 clinical studies published between 1986 and 2013 from the perspective of vitamin D administration in patients with several forms of psoriasis of varying degrees of severity. The dose ranged from 0.25 to 4 μg/day. These authors observed predominantly good efficacy and tolerance, with side effects noted only at high doses. They concluded that this therapeutic alternative was safe and effective for treating psoriasis [19]. In the context of psoriasis, Soleymani et al. also addressed some concerns about oral vitamin D effects on calcium absorption in the gut, and subsequent systemic calcium homeostasis [20].
The diagnostic marker used for vitamin D deficiency is serum 25(OH)D, its cut-off level varying over the years. The normal serum 25(OH)D levels are estimated to extend from about 25 to 225 nmol/L (10 to 90 ng/mL) and there seems to be a correlation between the low-level of 25(OH)D and the risk of chronic diseases. UVA/UVB phototherapy significantly increased the 25(OH)D serum level in patients with psoriasis and atopic dermatitis and reduced serum parathormone concentrations. There is no study demonstrating the correlation between serum 25(OH)D levels and severity of psoriasis [43,44]
Dietary calcium absorption enhancement could be avoided by taking vitamin D orally in the evening [32,45]. Serum vitamin D levels in patients with psoriasis were correlated with seasonal variations and disease severity [46]. A linear correlation could not be demonstrated, but numerous studies have shown low serum vitamin D levels in patients with psoriasis [20]. There is limited data on the dose-dependence of vitamin D deficiency in the pathogenesis of psoriasis and on the role of vitamin D deficiency in the therapeutic response. Vitamin D 1,25(OH) may act in psoriasis as an inhibitor of T-cell proliferation and Th1 development. Vitamin D 1,25(OH) modulates antigen-presenting cell function; induces hyporesponsiveness to antigens; inhibits the production of IL2, IL-17, IL-8, and interferon-gamma; increases the production of IL-10; and increases regulatory T cells [47]. A study using high doses of vitamin D3 (more than 60,000 IU) reported the resolution of anti-TNFα-induced psoriasiform lesions in a patient with rheumatoid arthritis and vitamin D deficiency [48].
The doses of vitamin D administered in the reviewed studies were mostly empirical; high doses of D3 were used after the year 2014. The changes in serum concentrations of vitamin D metabolite 25(OH)D were used to monitor the side effects and were not related to the degree of improvement or worsening in psoriasis lesions. A vitamin D2 dose higher than 40,000 IU was associated with hypercalcemia toxicity [40].
Millsop et al. analyzed six prospective trials on oral vitamin D treatment for psoriasis. In addition to describing the overall results, they pointed out that the possible side effects of oral vitamin D supplementation included hypercalcemia, hypercalciuria, and kidney stones, and long-term vitamin D overdoses could lead to bone demineralization [21]. Some studies reported increases in blood calcium and vitamin D levels or an increase in urinary calcium after starting oral supplementation, but no patient experienced adverse clinical side effects [31].
Zuccotti et al. addressed nutritional strategies for psoriasis. They also discussed oral vitamin D administration in psoriasis; although the patients did not show significant improvements, the authors concluded that vitamin D supplementation might aid in preventing psoriasis-related comorbidities. The proposed mechanism was that vitamin D might represent a key modulator of immune and inflammatory pathways. They hypothesized that, in psoriasis, an interruption of the immunological homeostasis and a reduction of the inflammation process might be due to low vitamin D levels, which can reduce the number of circulating regulatory T cells [29].
Barrea et al. addressed several aspects of the role of vitamin D in psoriasis, including oral vitamin D supplementation. They suggested that intakes of oral vitamin D up to 10,000 IU daily were not associated with harmful effects; this dose was comparable to the maximum cutaneous vitamin D production, and no study has reported vitamin D intoxication from cutaneous synthesis alone. Although the doses and durations of vitamin D administration were not mentioned, they highlighted results from two studies: One found a clinical improvement of the PASI score in 88% of the patients, and the other reported moderate or better improvements in 25–50% of patients with psoriasis [33].
Another study that did not highlight the dosage or duration of vitamin D administration suggested that the results were somewhat contradictory, concluding that the data were insufficient to determine the effectiveness of oral vitamin D administration in psoriasis [49].
Marino et al. mentioned a single study that compared the effects of 60,000 IU oral vitamin D in 45 patients vs. a placebo for six months. The results showed an increase in serum vitamin D and reductions in the PASI [41].
Bouillon et al. referred to a study that did not find any association between vitamin D supplementation and the induction of psoriasis in over 70,000 women [22,50]. In contrast, Hambly et al. reviewed several studies that administered systemic vitamin D to patients with psoriasis. Improvements were reported in many cases, and no adverse effects were reported. However, they concluded that further studies are needed [25].
Analyzing the dose-dependence relationship for the outcomes of using oral vitamin D in psoriasis, we noticed several differences and ambiguities in what could influence this relationship. Starting with 1986 and until 2013, the doses administered had a uniform character, between 0.25 μg/day and 2.0 μg/day (10–80 IU/day), very low compared to the doses of vitamin D used at the current time, even in other diseases. The outcome of the administered doses could be influenced by several factors not sufficiently documented, for example, the degree of sun exposure, which is quite challenging to monitor, considering that sun exposure of the whole body at a peak time for 1–2 h causes up to 20,000 IU vitamin D3 to enter the circulation [51]. Other variables are represented by the patient’s weight, skin tone, the circulating serum level of vitamin D, and the vitamin D deposits. The number of patients enrolled in existing studies is small, and studies are still very few. Given all this, it is not easy to achieve a dose-dependence relationship for the outcomes. More well-documented studies are needed.
From another perspective, namely, that of vitamin D toxicity, the reviewed studies showed no signs of toxicity in the patients followed, most likely due to the low doses used. McCullough et al. showed remarkable clinical benefit at doses ranging from 25,000 IU/day to 60,000 IU/day in psoriasis, cancer, and asthma, without the development of toxicity or hypercalcemia [52]. In another publication, the same authors argued that the administration of 10,000 IU/day to 25,000 IU/day of oral vitamin D is safe for the population [53].
Vitamin D is biologically inactive and treatment with vitamin D refers to its active metabolites: cholecalciferol (vitamin D3) and ergocalciferol (vitamin D2). Vitamin D3 is more frequently administered than calcitriol or alpha-calcidol, since it is safer and less expensive. Keratinocytes and immune lymphocyte T cells express vitamin D receptor (VDR) and contain enzymes able to convert active metabolites of vitamin D, 25(OH)D-calcidiol to active 1,25(OH)2D-calcitriol. Alterations in calcitriol levels and polymorphisms of the VDR gene have been shown to be associated with several malignant and autoimmune diseases, including psoriasis vulgaris [52,53].
Since the body has been shown to make up to 10,000 to 25,000 IU of vitamin D3 a day in response to adequate ultraviolet-B (UVB) exposure, it could be presumed that taking daily supplements of vitamin D3 in doses up to this amount may prevent or treat chronic diseases associated with vitamin D deficiency. Vitamin D level as a risk factor and also as a treatment option is studied in cancer, cardiovascular diseases, osteoporosis, autoimmune diseases, influenza, type 2 diabetes mellitus, Alzheimer disease, and depression in the postpartum and non-postpartum periods [54,55,56,57,58,59,60,61]. Vitamin D3 exerts significant control over normal cellular metabolism via plasma membranes ion channels and via VDR genes located near autoimmune and cancer-associated genes [53].
Compared to existing studies regarding the administration of vitamin D in psoriasis, vitamin D administration in cancer has been much more studied. Several studies have looked at the effectiveness of various doses, various frequencies of administration, and types of vitamin D such as cholecalciferol: 400–4800 IU/day, 20,000 IU/week, 30,000–100,000 IU/month, 120,000 IU every two months, 100,000 IU every three months, 100,000 IU every four months, or 500,000 IU once/year; ergocalciferol: 1000 IU daily; calcitriol 0.25–0.50 μg daily or 0.25 μg twice daily; alfacalcidol: 1.0 μg daily [62,63]. One very recent study evaluated vitamin D supplementation, which has been associated with a reduced mortality in patients with psoriasis [64]. We want to draw attention to a broad plan for the administration of vitamin D that has not yet been studied to treat psoriasis.

4. Conclusions

Although vitamin D has been used successfully for many years as a topical therapy in the fight against psoriasis, only recently have studies examined systemic vitamin D administration in psoriasis. We examined the pros and cons of this treatment, with the aim of determining whether systemic vitamin D would be a feasible therapeutic option for these patients. Among the existing reviews, very few were systematic in design. Indeed, from 1985 to the present, only a few studies have monitored the effectiveness of oral vitamin D in patients with psoriasis; consequently, the reviews were insufficient and inconclusive. Most studies did not observe side effects for doses within a relatively narrow range (0.25 to 2 μg/day). No evidence has been reported about the efficacy of the highest doses of systemic vitamin D in psoriasis. However, most studies did not observe side effects. Based on these results, we can conclude that more large-scale studies are needed to determine the efficacy, optimal dosing, and adverse effects of vitamin D administration in patients with psoriasis.

Author Contributions

Conceptualization, A.M.A.S., A.A.S., and C.C.D.; methodology, A.M.A.S. and A.A.S.; software, A.M.A.S., A.A.S., and C.C.D. validation, A.M.A.S., A.A.S., and C.C.D.; formal analysis, A.M.A.S. and A.A.S.; investigation A.M.A.S. and A.A.S.; resources, A.M.A.S., A.A.S., and C.C.D.; data curation, A.M.A.S. and A.A.S.; writing—original draft preparation, A.M.A.S.; writing—review and editing, A.M.A.S., A.A.S., and C.C.D.; visualization, A.M.A.S., A.A.S., and C.C.D.; supervision, A.M.A.S., A.A.S., and C.C.D.; project administration, A.M.A.S. All authors have read and agreed to the published version of the manuscript.


This research received no external funding.

Conflicts of Interest

The authors declare no conflict of interest.


  1. Martens, P.J.; Gysemans, C.; Verstuyf, A.; Mathieu, A.C. Vitamin D’s effect on immune function. Nutrients 2020, 12, 1248. [Google Scholar] [CrossRef]
  2. Windaus, A.; Linsert, O.; Luttringhaus, A.; Weidlich, G. Über das krystallisierte Vitamin D2. Ann. Chem. Liebigs 1932, 492, 226–241. [Google Scholar] [CrossRef]
  3. Windaus, A.; Schenck, F.; von Werder, F. Über das antirachitisch wirksame bestrahlungs-produkt aus 7-dehydrocholesterin. Z Physiol. Chem. Hoppe Seylers 1936, 241, 100–103. [Google Scholar] [CrossRef]
  4. Charoenngam, N.; Holick, M.F. Immunologic effects of vitamin D on human health and disease. Nutrients 2020, 12, 2097. [Google Scholar] [CrossRef] [PubMed]
  5. Brandão-Lima, P.N.; Santos, B.D.C.; Aguilera, C.M.; Freire, A.R.S.; Martins-Filho, P.R.S.; Pires, L.V. Vitamin D food fortification and nutritional status in children: A systematic review of randomized controlled trials. Nutrients 2019, 11, 2766. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  6. Holick, M.F. Vitamin D deficiency. N. Engl. J. Med. 2007, 357, 266–281. [Google Scholar] [CrossRef]
  7. Misra, M.; Pacaud, D.; Petryk, A.; Collett-Solberg, P.F.; Kappy, M. Drug and therapeutics committee of the Lawson Wilkins pediatric endocrine society. Vitamin D deficiency in children and its management: Review of current knowledge and recommendations. Pediatrics 2008, 122, 398–417. [Google Scholar] [CrossRef] [Green Version]
  8. Chang, S.W.; Lee, H.C. Vitamin u8h brD and health—The missing vitamin in humans. Pediatrics Neonatol. 2019, 60, 237–244. [Google Scholar] [CrossRef] [Green Version]
  9. Rendon, A.; Schäkel, K. Psoriasis pathogenesis and treatment. Int. J. Mol. Sci. 2019, 20, 1475. [Google Scholar] [CrossRef] [Green Version]
  10. Slominski, A.; Kim, T.K.; Zmijewski, M.A.; Janjetovic, Z.; Li, W.; Chen, J.; Kusniatsova, E.I.; Semak, I.; Postlethwaite, A.; Miller, D.D.; et al. Novel vitamin D photoproducts and their precursors in the skin. Dermatoendocrinology 2013, 5, 7–19. [Google Scholar] [CrossRef] [Green Version]
  11. Stanescu, A.M.A.; Grajdeanu, I.V.; Iancu, M.A.; Pantea Stoian, A.; Bratu, O.G.; Socea, B.; Socea, L.I.; Diaconu, C.C. Correlation of oral vitamin D administration with the severity of psoriasis and the presence of metabolic syndrome. Rev. Chim. 2018, 69, 1668–1672. [Google Scholar] [CrossRef]
  12. Burfield, L.; Burden, A.D. Psoriasis. J. R. Coll. Physicians Edinb. 2013, 43, 334–338. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  13. Brown, A.; Slatopolsky, E. Vitamin D analogs: Therapeutic applications and mechanisms for selectivity. Mol. Asp. Med. 2008, 29, 433–452. [Google Scholar] [CrossRef] [PubMed]
  14. Piotrowska, A.; Wierzbicka, J.; Żmijewski, M.A. Vitamin D in the skin physiology and pathology. Acta Biochim. Pol. 2016, 63, 17–29. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  15. Penna, G.; Adorini, L. 1 Alpha,25-dihydroxyvitamin D3 inhibits differentiation, maturation, activation, and survival of dendritic cells leading to impaired alloreactive T cell activation. J. Immunol. 2000, 164, 2405–2411. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  16. Moher, D.; Liberati, A.; Tetzlaff, J.; Altman, D.G. The PRISMA group. Preferred reporting items for systematic reviews and meta-analyses: The PRISMA statement. PLoS Med. 2009, 6, e1000097. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  17. Morimoto, S.; Yoshikawa, K.; Kozyka, T.; Kitano, Y.; Imanaka, S.; Fukuo, K.; Koh, E.; Kumahara, Y. An open study of vitamin D3 treatment in psoriasis vulgaris. Br. J. Dermatol. 1986, 115, 421–429. [Google Scholar] [CrossRef]
  18. Kamangar, F.; Koo, J.; Heller, M.; Lee, E.; Bhutani, T. Oral vitamin D, still a viable treatment option for psoriasis. J. Dermatolog. Treat. 2013, 24, 261–267. [Google Scholar] [CrossRef]
  19. Lourencetti, M.; Abreu, M.M. Use of active metabolites of vitamin D orally for the treatment of psoriasis. Rev. Assoc. Med. Bras. 2018, 64, 643–648. [Google Scholar] [CrossRef]
  20. Soleymani, T.; Hung, T.; Soung, J. The role of vitamin D in psoriasis: A review. Int. J. Dermatol. 2015, 54, 383–392. [Google Scholar] [CrossRef]
  21. Millsop, J.W.; Bhatia, B.K.; Debbaneh, M.; Koo, J.; Liao, W. Diet and psoriasis, part III: Role of nutritional supplements. J. Am. Acad. Dermatol. 2014, 71, 561–569. [Google Scholar] [CrossRef] [Green Version]
  22. Bouillon, R.; Marcocci, C.; Carmeliet, G.; Bikle, D.; White, J.H.; Dawson-Hughes, B.; Lips, P.; Munns, C.F.; Lazaretti-Castro, M.; Giustina, A.; et al. Skeletal and extraskeletal actions of vitamin D: Current evidence and outstanding questions. Endocr. Rev. 2019, 40, 1109–1151. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  23. Takamoto, S.; Onishi, T.; Morimoto, S.; Imanaka, S.; Yukawa, S.; Kozuka, T.; Kitano, Y.; Seino, Y.; Kumahara, Y. Effect of 1 alpha-hydroxycholecalciferol on psoriasis vulgaris: A pilot study. Calcif. Tissue Int. 1986, 39, 360–364. [Google Scholar] [CrossRef]
  24. Smith, E.L.; Pincus, S.H.; Donovan, L.; Holick, M.F. 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, 516–528. [Google Scholar] [CrossRef]
  25. Hambly, R.; Kirby, B. The relevance of serum vitamin D in psoriasis: A review. Arch. Dermatol. Res. 2017, 309, 499–517. [Google Scholar] [CrossRef] [PubMed]
  26. Holland, D.B.; Wood, E.J.; Roberts, S.G.; West, M.R.; Cunliffe, W.J. Epidermal keratin levels during oral 1-alpha-hydroxyvitamin D3 treatment for psoriasis. Skin Pharmacol. 1989, 2, 68–76. [Google Scholar] [CrossRef]
  27. Huckins, D.; Felson, D.T.; Holick, M. Treatment of psoriatic arthritis with oral 1,25-dihydroxyvitamin D3: A pilot study. Arthritis Rheum. 1990, 33, 1723–172715. [Google Scholar] [CrossRef]
  28. Siddiqui, M.A.; Al-Khawajah, M.M. Vitamin D3 and psoriasis: A randomized double-blind placebo-controlled study. J. Dermatol. Treat. 1990, 1, 243–245. [Google Scholar] [CrossRef]
  29. Zuccotti, E.; Oliveri, M.; Girometta, C.; Ratto, D.; Di Iorio, C.; Occhinegro, A.; Rossi, P. Nutritional strategies for psoriasis: Current scientific evidence in clinical trials. Eur. Rev. Med. Pharmacol. Sci. 2018, 22, 8537–8551. [Google Scholar] [CrossRef]
  30. Lugo-Somolinos, A.; Sanchez, J.L.; Haddock, L. Efficacy of 1, alpha 25-dihydroxyvitamin D (Calcitriol) in the treatment of psoriasis vulgaris: An open study. Bol. Asoc. Med. P R 1990, 82, 450–453. [Google Scholar]
  31. el-Azhary, R.A.; Peters, M.S.; Pittelkow, M.R.; Kao, P.C.; Muller, S.A. Efficacy of vitamin D3 derivatives in the treatment of psoriasis vulgaris: A preliminary report. Mayo Clin. Proc. 1993, 68, 835–841. [Google Scholar] [CrossRef]
  32. Perez, A.; Raab, R.; Chen, T.C.; Turner, A.; Holick, M.F. Safety and efficacy of oral calcitriol (1,25-dihydroxyvitamin D3) for the treatment of psoriasis. Br. J. Dermatol. 1996, 134, 1070–1078. [Google Scholar] [CrossRef]
  33. Barrea, L.; Savanelli, M.C.; Di Somma, C.; Napolitano, M.; Megna, M.; Colao, A.; Savastano, S. Vitamin D and its role in psoriasis: An overview of the dermatologist and nutritionist. Rev. Endocr. Metab. Disord. 2017, 18, 195–205. [Google Scholar] [CrossRef] [Green Version]
  34. Gaál, J.; Lakos, G.; Szodoray, P.; Kiss, J.; Horváth, I.; Horkay, E.; Nagy, G.; Szegedi, A. Immunological and clinical effects of alphacalcidol in patients with psoriatic arthropathy: Results of an open, follow-up pilot study. Acta Derm. Venereol. 2009, 89, 140–144. [Google Scholar]
  35. Finamor, D.C.; Sinigaglia-Coimbra, R.; Neves, L.C.; Gutierrez, M.; Silva, J.J.; Torres, L.D.; Surano, F.; Neto, D.J.; Novo, N.F.; Juliano, Y.; 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. Dermatoendocrinology 2013, 5, 222–234. [Google Scholar] [CrossRef] [Green Version]
  36. Umar, M.; Sastry, K.S.; Al Ali, F.; Al-Khulaifi, M.; Wang, E.; Chouchane, A. I: Vitamin D and the pathophysiology of inflammatory skin diseases. Skin Pharmacol. Physiol. 2018, 31, 74–86. [Google Scholar] [CrossRef]
  37. Hata, T.; Audish, D.; Kotol, P.; Coda, A.; Kabigting, F.; Miller, J.; Alexandrescu, D.; Boguniewicz, M.; Taylor, P.; Aertker, L.; et al. A randomized controlled double-blind investigation of the effects of vitamin D dietary supplementation in subjects with atopic dermatitis. J. Eur. Acad. Dermatol. Venereol. 2014, 28, 781–789. [Google Scholar] [CrossRef] [Green Version]
  38. Jarrett, P.; Camargo, C.A., Jr.; Coomarasamy, C.; Scragg, R. A randomized, double-blind, placebo-controlled trial of the effect of monthly vitamin D supplementation in mild psoriasis. J. Dermatolog. Treat. 2018, 29, 324–328. [Google Scholar] [CrossRef]
  39. Ingram, M.A.; Jones, M.B.; Stonehouse, W.; Jarrett, P.; Scragg, R.; Mugridge, O.; von Hurst, P.R. Oral vitamin D3 supplementation for chronic plaque psoriasis: A randomized, double-blind, placebo-controlled trial. J. Dermatolog. Treat. 2018, 29, 648–657. [Google Scholar] [CrossRef]
  40. 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, 5237642. [Google Scholar] [CrossRef]
  41. Marino, R.; Misra, M. Extra-sekeletal effects of vitamin D. Nutrients 2019, 11, 1460. [Google Scholar] [CrossRef] [Green Version]
  42. Fredriksson, T.; Pettersson, U. Severe psoriasis—Oral therapy with a new retinoid. Dermatologica 1978, 157, 238–244. [Google Scholar] [CrossRef]
  43. Heaney, R.P. Guidelines for optimizing design and analysis of clinical studies of nutrient effects. Nutr. Rev. 2014, 72, 48–54. [Google Scholar] [CrossRef]
  44. Le, P.; Tu, J.; Gebauer, K.; Brown, S. Serum 25-hydroxyvitamin D increases with UVB and UVA/UVB phototherapy (broadband UVB, narrowband UVB (NBUVB) and heliotherapy) in patients with psoriasis and atopic dermatitis. Australas J. Dermatol. 2016, 57, 115–121. [Google Scholar] [CrossRef]
  45. Tremezaygues, L.; Reichrath, J. Vitamin D analogs in the treatment of psoriasis: Where are we standing and where will we be going? Dermatoendocrinology 2011, 3, 180–186. [Google Scholar] [CrossRef]
  46. Orgaz-Molina, J.; Buenda-Eisman, A.; Arrabal-Polo, M.A.; Ruiz, J.C.; Arias-Santiago, S. Deficiency of serum concentration of 25-hydroxyvitamin D in psoriatic patients: A case-control study. J. Am. Acad. Dermatol. 2012, 67, 931–938. [Google Scholar] [CrossRef]
  47. Adams, J.S.; Hewison, M. Update in vitamin D. J. Clin. Endocrinol. Metab. 2010, 95, 471–478. [Google Scholar] [CrossRef] [Green Version]
  48. Werner de Castro, G.R.; Neves, F.S.; Pereira, I.A.; Fialho, S.C.; Ribeiro, G.; Zimmermann, A.F. Resolution of adalimumab-induced psoriasis after vitamin D deficiency treatment. Rheumatol. Int. 2011, 32, 1313–1316. [Google Scholar] [CrossRef]
  49. Thompson, K.G.; Kim, N. Dietary supplements in dermatology: A review of the evidence for zinc, biotin, vitamin D, nicotinamide, and Polypodium. J. Am. Acad. Dermatol. 2020. [Google Scholar] [CrossRef]
  50. Merola, J.F.; Han, J.; Li, T.; Qureshi, A.A. No association between vitamin D intake and incident psoriasis among US women. Arch. Dermatol. Res. 2014, 306, 305–307. [Google Scholar] [CrossRef]
  51. Nair, R.; Maseeh, A. Vitamin D: The “sunshine” vitamin. J. Pharmacol. Pharmacother. 2012, 3, 118–126. [Google Scholar] [CrossRef] [PubMed]
  52. McCullough, P.J.; Lehrer, D.S.; Amend, J.J. Daily oral dosing of vitamin D3 using 5000 TO 50,000 international units a day in long-term hospitalized patients: Insights from a seven year experience. J. Steroid Biochem. Mol. Biol. 2019, 189, 228–239. [Google Scholar] [CrossRef] [PubMed]
  53. McCullough, P.; Amend, J.J. Results of daily oral dosing with up to 60,000 international units (iu) of vitamin D3 for 2 to 6 years in 3 adult males. J. Steroid Biochem. Mol. Biol. 2017, 173, 308–312. [Google Scholar] [CrossRef] [PubMed]
  54. Garland, C.F.; French, C.B.; Baggerly, L.L.; Heaney, R.P. Vitamin D supplement doses and serum 25-hydroxyvitamin D in the range associated with cancer prevention. Anticancer Res. 2011, 31, 617–622. [Google Scholar]
  55. Dawson-Hughes, B.; Staten, M.A.; Knowler, W.C.; Nelson, J.; Vickery, E.M.; LeBlanc, E.S.; Neff, L.M.; Park, J.; Pittas, A.G.; D2d Research Group. Intratrial exposure to vitamin D and new-onset diabetes among adults with prediabetes: A secondary analysis from the vitamin D and type 2 diabetes (D2d) study. Diabetes Care 2020, 43, 2916–2922. [Google Scholar] [CrossRef]
  56. Danik, J.S.; Manson, J.E. Vitamin d and cardiovascular disease. Curr. Treat. Options Cardiovasc. Med. 2012, 14, 414–424. [Google Scholar] [CrossRef] [Green Version]
  57. Chai, B.; Gao, F.; Wu, R.; Dong, T.; Gu, C.; Lin, Q.; Zhang, Y. Vitamin D deficiency as a risk factor for dementia and Alzheimer’s disease: An updated meta-analysis. BMC Neurol. 2019, 19, 284. [Google Scholar] [CrossRef]
  58. Aghajafari, F.; Letourneau, N.; Mahinpey, N.; Cosic, N.; Giesbrecht, G. Vitamin D deficiency and antenatal and postpartum depression: A systematic review. Nutrients 2018, 10, 478. [Google Scholar] [CrossRef] [Green Version]
  59. Cuomo, A.; Giordano, N.; Goracci, A.; Fagiolini, A. Depression and vitamin D deficiency: Causality, assessment, and clinical practice implications. Neuropsyvchiatry 2017, 7, 606–614. [Google Scholar] [CrossRef] [Green Version]
  60. Gruber-Bzura, B.M. Vitamin D and influenza-prevention or therapy? Int. J. Mol. Sci. 2018, 19, 2419. [Google Scholar] [CrossRef] [Green Version]
  61. American Geriatrics Society Workgroup on Vitamin D Supplementation for Older Adult. Recommendations abstracted from the American geriatrics consensus statement on Vitamin D for prevention of falls and their consequences. J. Am. Geriatr. Soc. 2014, 62, 147–152. [Google Scholar] [CrossRef] [PubMed]
  62. Goulão, B.; Stewart, F.; Ford, J.A.; MacLennan, G.; Avenell, J.A. Cancer and vitamin D supplementation: A systematic review and meta-analysis. Am. J. Clin. Nutr. 2018, 107, 652–663. [Google Scholar] [CrossRef]
  63. Bittenbring, J.T.; Neumann, F.; Altmann, B.; Achenbach, M.; Reichrath, J.; Ziepert, M.; Geisel, J.; Regitz, E.; Held, G.; Pfreundschuh, M. Vitamin D deficiency impairs rituximab-mediated cellular cytotoxicity and outcome of patients with diffuse large B-cell lymphoma treated with but not without rituximab. J. Clin. Oncol. 2014, 32, 3242–3248. [Google Scholar] [CrossRef] [PubMed]
  64. Fu, H.; Tang, Z.; Wang, Y.; Ding, X.; Rinaldi, G.; Rahmani, J.; Xing, F. Relationship between vitamin D level and mortality in adults with psoriasis: A retrospective cohort study of NHANES data. Clin. Ther. 2020. [Google Scholar] [CrossRef]
Figure 1. PRISMA 2009 Flow Diagram. From Moher, D.; Liberati, A.; Tetzlaff, J.; Altman, D.G. The Prisma Group (2009). Preferred reporting items for systematic reviews and meta-analyses: The PRISMA statement. PLoS Med 6(7): e1000097. For more information, visit [16].
Figure 1. PRISMA 2009 Flow Diagram. From Moher, D.; Liberati, A.; Tetzlaff, J.; Altman, D.G. The Prisma Group (2009). Preferred reporting items for systematic reviews and meta-analyses: The PRISMA statement. PLoS Med 6(7): e1000097. For more information, visit [16].
Nutrients 13 00163 g001
Table 1. The characteristics of the original studies included in the analyzed reviews.
Table 1. The characteristics of the original studies included in the analyzed reviews.
Authors and YearType of StudyNumber of PatientsStudy LocationReviews Including the Original Study from the First Column
Morimoto et al., 1986 [17]Open-design study21JapanKamangar et al., 2013 [18]
Lourenceti et al., 2018 [19]
Soleymani et al., 2015 [20]
Millsop et al., 2014 [21]
Bouillon et al., 2018 [22]
Takamoto et al., 1986 [23]Descriptive study7JapanKamangar et al., 2013 [18]
Lourenceti et al., 2018 [19]
Smith et al., 1988 [24]Descriptive study14USAKamangar et al., 2013 [18]
Lourenceti et al., 2018 [19]
Millsop et al., 2014 [21]
Bouillon et al., 2018 [22]
Hambly et al., 2017 [25]
Holland et al., 1989 [26]Descriptive study15UKHambly et al., 2017 [25]
Huckins et al., 1990 [27]Open-label trial6USAKamangar et al., 1990 [18]
Lourenceti et al., 2018 [19]
Siddiqui et al., 1990 [28]Prospective randomized double-blind control study41Saudi ArabiaMillsop et al., 2014 [21]
Zuccotti et al., 2018 [29]
Lugo-Somolinos et al., 1990 [30]Descriptive study10Puerto RicoHambly et al., 2017 [25]
El-Alzhari et al., 1993 [31]Descriptive study8USALourenceti et al., 2018 [19]
Millsop et al., 2014 [21]
Perez et al., 1996 [32]Open trial85USAKamangar et al., 2013 [18]
Lourenceti et al., 2018 [19]
Soleymani et al., 2015 [20]
Millsop et al., 2014 [21]
Barrea et al., 2017 [33]
Bouillon et al., 2018 [22]
Hambly et al., 2017 [25]
Gaal et al., 2009 [34]Case-control10USAKamangar et al., 2013 [18]
Zuccotti et al., 2018 [29]
Finamor et al., 2013 [35]Open-label clinical trial9HungaryLourenceti et al., 2018 [19]
Millsop et al., 2014 [21]
Umar et al., 2018 [36]
Hambly et al., 2017 [25]
Hata et al., 2014 [37]Randomized placebo-controlled16BrazilHambly et al., 2017 [25]
Jarret et al., 2018 [38]Randomized double blind, placebo-controlled study65USAZuccotti et al., 2018 [29]
Ingram et al., 2018 [39]Randomized double blind, placebo-controlled study101New Zealand
Disphanurat et al., 2019 [40]Randomized double blind, placebo-controlled study45ThailandMarino et al., 2019 [41]
Table 2. Treatment effectiveness after oral administration of vitamin D3 in patients with psoriasis.
Table 2. Treatment effectiveness after oral administration of vitamin D3 in patients with psoriasis.
Studies, Year
DoseDuration of AdministrationEfficacyType/Severity of PsoriasisEffectivenessTreatment Side Effects
Morimoto et al., 1986 [17]1.0 μg/day
(40 IU/day)
6 months2.7 +/− 0.6 monthsPsoriasis vulgarisMore than moderate improvement (+2) in 76% of patientsNo
0.5 μg/day
(20 IU/day)
6 months3 monthsPsoriasis vulgarisModerate improvement (+2) in 25% of patientsNo
Takamoto et al., 1986 [23]1.0 μg/day
(40 IU/day)
12 monthsmore than 8 monthsPsoriasis vulgaris
Complete remission and marked improvement (+3 up to +4) in 28.57%
Minimal improvement (+1) in 15% of patients
Smith et al., 1988 [24]0.25 μg (10 IU) once or twice/day
increased by 0.25 to 0.5 μg/day every 2 weeks to a maximum of 2.0 μg (80 IU)/day
2 monthsless than 2 monthsmoderate to severe psoriasis
50% of patients +4
21.43% of patients +2/+3
21.43% of patients +1
7.14% of patients 0
Holland et al., 1989 [26]1.0 μg/day
(40 IU)
6 months6–8 weeksPlaque psoriasis46.67% of patients had complete resolution of lesions (+4), 2 within 6 weeks and the rest after 4–6 months of therapy.No
Huckins et al., 1990 [27]1.0 μg/day
0.5 μg/day increased by 0.25 μg/day every 2 weeks to a maximum of 2.0 μg (80 IU)/day
6 months2–3 monthsPsoriatic arthritis
44.44% of patients marked improvement (+3)
22.22% of patients presented worsening of their psoriasis during the trial
hypercalciuria in 20% of patients
Siddiqui et al., 1990 [28]1 μg/day
12 weeksNot specifiedPsoriasis vulgaris45% of patients showed slight improvement (+1).
Lugo-Somolinos et al., 1990 [30]0.5 μg/day
1α,25-(OH)2 -D3
(20 IU)
after 3 monthsModerate to severe psoriasis40% of patients showed moderate improvement.No
El-Alzhari et al., 1993 [31]0.5 μg/day increased by 0.5 μg biweekly to a maximal dosage of 2.0 μg daily.
6 months2 monthsPsoriasis vulgaris moderate to severe
12.5% of patients marked improvement (+3)
12.5% of patients had moderate improvement (+2)
75% of patients had mild improvement or no improvement (0 to +1)
Perez et al., 1996 [32]0.5 μg/day increments of 0.5 μg every 2 weeks
6 months–3 years6 monthsPsoriasisvulgarisGlobal severity score for the patients’ lesions had a mean value of 7.7 ± 1.2; the mean global severity score significantly decreased to 3.2 ± 1.9.
The mean baseline PASI score was 18.4 ± 1.0; at 6 and 36 months of treatment the mean PASI score was reduced to 9.7 ± 0.8 and 7.0 ± 1.3, respectively.
Gaal et al., 2009 [34]0.25 μg twice daily
6 monthsNot specifiedPsoriatic arthritisPASI scores were 12.8 +/− 14.3 vs. 11.9 +/− 14.4. on average.No
Finamor et al., 2013 [35]35,000 IU per day
vit. D3
6 monthsNot specifiedPsoriasis vulgaris moderate to severeThe clinical condition of all patients significantly improved (+3 to +4).-
Hata et al., 2014 [37]4000 IU/day
vit. D3
6 monthsNot specifiedMild psoriasisNo change in PASI score (0)No
Jarret et al., 2018 [38]100,000 IU/month
(3300 IU/day)
vit. D3
4 yearsNot specifiedMild psoriasisThe trial results do not support the use of monthly vitamin D3 supplementation (100,000 IU per month) as a treatment for mild psoriasis in patients over 50 years old.
Ingram et al., 2018 [39]200,000 IU at baseline, then 100,000 IU/month
vit. D3
11 months6 monthsChronic psoriasisNo benefitNot specified
Legend: PASI = psoriasis area severity index score; RCT = randomized clinical trial. 250 μg = 10,000 IU. The degree of improvement of psoriasis lesions was scored by the authors using a 5-point scale: 0, no effect; + 1, minimal improvement up to 25% improved; +2, moderate improvement, 26% to 50% improved; +3, marked improvement, 51% to 75% improved; +4, >75% improved to clear lesions; by PASI score; or by Global Severity Score.
Table 3. Treatment effectiveness of oral vitamin D2 administered in patients with psoriasis.
Table 3. Treatment effectiveness of oral vitamin D2 administered in patients with psoriasis.
DosePeriod of AdministrationEfficacy ObservedType/Severity of PsoriasisEffectivenessTreatment Side Effects
Disphanurat et al., 2019 [40]20,000 IU/every 2 weeks
vit. D2
6 months3–6 monthsChronic plaque-type psoriasis—mild psoriasisPASI score decreased at 3 and 6 months, moderate
Table 4. Psoriasis outcome measures used for treatment effectiveness.
Table 4. Psoriasis outcome measures used for treatment effectiveness.
Morimoto et al. [17]Clinical photographs taken at every examination
Clinical score: complete remission (+4), marked improvement (+3), moderate improvement (+2), slight improvement (+1), no change (o), deterioration (−1).
Smith et al. [24]Clinical examination
Clinical score: no change (0), minimal improvement up to 25% improved (+1), 26% to 50% improved (+2), 51% to 75% improved (+3), >75% improved to clear (+4).
Takamoto et al. [23]Clinical examination: complete remission (4) (complete flattering of plaques including borders, percentage of area improved: 95% or more); marked improvement (3) (nearly complete flattering of all plaques still palpable, area improved: 50–90%); definite improvement (2) (partial flattering of plaque, less scaling and less erythema, area improved: 20–50%), minimal improvement (1) (slightly less scaling and less erythema, area improved: 5–20%); no change (0); aggravation (−1) by the percentage of skin involvement was improved.
Huckins et al. [27]Clinical photographs taken at every examination
Clinical score of erythema: deterioration (−1), no change (0), mild improvement (1), moderate improvement (2), marked improvement (3)
Gaal et al. [34]
PASI score
Perez et al. [32]Clinical photographs taken at every examination
PASI score, global severity score
Global Improvement Scale: deterioration (−1), no change (0), mild improvement (1), moderate improvement (2), excellent improvement (3)
El-Azhary et al. [31]Clinical evaluation of the percentage of body surface involved
Grading the erythema, scale, and thickness of the lesions as worsening (−1), no improvement (0), mild improvement (+1), moderate improvement (+2), marked improvement (+3).
Finamor et al. [35]
PASI score
Siddiqui et al. [28]PASI score
Worsening PASI score (−1), no improvement (0), slight improvement (+1), moderate improvement (+2), marked improvement (+3).
Holland et al. [26]
Clinical photographs taken
Clinical criteria
Hata et al. [37]PASI score
Punch biopsies of psoriatic skin lesion and uninvolved skin
Jarret et al. [38]
PASI score
Physician‘s Global Assessment Score
Dermatology Life Quality Index
Psoriasis Disability Index
Ingram et al. [39]
PASI score
Disphanurat et al. [40]
PASI score
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Share and Cite

MDPI and ACS Style

Stanescu, A.M.A.; Simionescu, A.A.; Diaconu, C.C. Oral Vitamin D Therapy in Patients with Psoriasis. Nutrients 2021, 13, 163.

AMA Style

Stanescu AMA, Simionescu AA, Diaconu CC. Oral Vitamin D Therapy in Patients with Psoriasis. Nutrients. 2021; 13(1):163.

Chicago/Turabian Style

Stanescu, Ana Maria Alexandra, Anca Angela Simionescu, and Camelia Cristina Diaconu. 2021. "Oral Vitamin D Therapy in Patients with Psoriasis" Nutrients 13, no. 1: 163.

Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details here.

Article Metrics

Back to TopTop