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Exploration of Medicine Impact of vitamin D on ultraviolet-induced photoaging and skin diseases
Abstract
Excessive exposure to ultraviolet (UV) radiation causes premature aging of the skin, known as photoaging. UV radiation induces DNA damage, oxidative stress, inflammatory reactions, and degradation of extracellular matrix (ECM) proteins, contributing to the aged skin phenotype. The skin synthesizes vitamin D upon UVB exposure, which plays a pivotal role in the proper function of multiple body systems. Vitamin D protects skin from photo-damage by repairing cyclobutane pyrimidine dimers, reversing oxidative stress, and reducing chronic inflammation. Moreover, various epidemiological studies have identified vitamin D deficiency as a marker for common dermatological disorders. Improvement of clinical outcomes with vitamin D supplementation further suggests its protective role against skin pathologies. This review comprehensively covers the involvement of vitamin D in combating UV-induced photoaging and various skin disorders, highlighting the significance of maintaining vitamin D adequacy for healthy skin.
... All the biological phenomena regulated by VD agree with the current literature. For example, the downregulation of oxidative phosphorylation in the yellow module, except in the epidermis (basal and suprabasal 2 cells), determines the stress induced by UV light [72,73] and the inhibition of protein and mRNA synthesis in the brown and dark grey modules, suggesting the energy-conserving profile of vitamin D, which is particularly important in the context of an anti-inflammatory profile. ...
Background/Objectives: Vitamin D (VD) plays a crucial role in age-related diseases, and its influence on cellular senescence (CS) could help clarify its function in aging. Considering VD’s pleiotropic effects and the heterogeneity of CS. Methods: we utilized single-cell RNA sequencing (scRNA-seq) to explore these dynamics across multiple tissues. We analyzed three murine tissue datasets (bone, prostate, and skin) obtained from public repositories, enriching for senescence gene signatures. We then inferred gene regulatory networks (GRNs) at the tissue and cell-type levels and performed two cell communication analyses: one for senescent cells and another for interactions between senescent and non-senescent cells. Results: VD supplementation significantly decreased senescence scores in the skin (p = 3.96×10−134) and prostate (p=1.56×10−34). GRN analysis of the prostate revealed an altered macrophage–fibroblast regulatory relationship. In bone, distinct aging-related modules emerged for different bone lineages. In skin, contrary differentiation patterns between suprabasal and basal cells were observed. The main VD-modulated pathways were involved in inflammation, extracellular matrix remodeling, protein metabolism, and translation. VD reduced fibroblast–macrophage interactions in the prostate and skin but increased overall cellular crosstalk in bone. Conclusions: Our findings demonstrate that VD alleviates CS burden across tissues by modulating inflammation and metabolic processes and promoting differentiation. Key aging-related genes modulated by VD were linked to anabolism and cellular differentiation, suggesting VD’s potential for therapeutic interventions targeting age-related diseases.
... However, UVB radiation has a unique role in synthesizing vitamin D 3 in the skin. Vitamin D 3 protects against photodamage by repairing CPDs, mitigating oxidative stress, and reducing chronic inflammation [94]. In contrast, UVA exposure, while contributing to skin damage, is incapable of producing the skin protective vitamin D 3 . ...
Sunlight exposure plays an important role in human health, impacting processes such as mood, blood pressure regulation, and vitamin D3 production. Solar ultraviolet B radiation initiates vitamin D3 synthesis in the skin, which is subsequently metabolized into its biologically active form. UVB exposure plays a key role in enabling vitamin D3 synthesis, but it can also contribute to skin carcinogenesis, creating a complex interplay between its beneficial and harmful effects. Vitamin D deficiency, affecting over half the global population, is linked to a range of chronic diseases, including cancers, cardiovascular conditions, and autoimmune disorders. Simultaneously, excessive solar UVB exposure increases the risk of non-melanoma and melanoma skin cancers through mechanisms involving DNA damage and oxidative stress. This review examines the dual role of UVB radiation in health and disease, focusing on the mechanisms of cutaneous vitamin D3 synthesis, the epidemiology of skin cancer, and the protective roles of vitamin D3’s photoproducts and its active metabolite, 1,25-dihydroxyvitamin D3. Understanding these interconnections is critical for developing strategies that balance adequate sun-induced vitamin D3 production with skin cancer prevention.
Human skin is a physical and biochemical barrier that protects the internal body from the external environment. Throughout a person’s life, the skin undergoes both intrinsic and extrinsic aging, leading to microscopic and macroscopic changes in its morphology. In addition, the repair processes slow with aging, making the older population more susceptible to skin diseases. Intrinsic factors associated with advanced age gradually degrade the dermal collagen matrix, resulting in fine wrinkles and reduced elasticity; this is accelerated in post-menopausal women due to estrogen deficiency. In contrast, extrinsic factors associated with advanced age, primarily caused by exposure to ultraviolet (UV) radiation, lead to coarse wrinkles, solar elastosis, hyperkeratosis, irregular pigmentation, and skin cancers. UVB radiation, while contributing to skin photo-aging, also induces the cutaneous synthesis of vitamin D. Vitamin D, in turn, protects the skin from oxidative stress, inflammation, and DNA damage, thereby delaying both chronological and photo-aging. Moreover, research has demonstrated an association between lower vitamin D levels and a higher prevalence of certain cutaneous diseases. This review explores and summarizes the critical role of vitamin D in skin aging and age-related skin diseases. The data presented highlight the importance of maintaining vitamin D adequacy throughout life.
Introduction
The skin is a vital organ as the body’s largest barrier, but its function declines with aging. Therefore, research into effective regeneration treatments must continue to advance. Stem cell transplantation, a cell-based therapy, has become a popular skin-aging treatment, although it comes with drawbacks like host immune reactions. Stem cell-derived cell-free therapies have emerged as an alternative, backed by promising preclinical findings. Stem cell secretomes and extracellular vesicles (EVs) are the key components in cell-free therapy from stem cells. However, comprehensive reviews on the mechanisms of such treatments for skin aging are still limited.
Purpose
This review discusses stem cell-derived cell-free therapy’s potential mechanisms of action related to skin aging prevention by identifying specific molecular targets suitable for the interventions.
Methods
A search identified 27 relevant in vitro studies on stem cell-derived cell-free therapy interventions in skin aging model cells without restricting publication years using PubMed, Scopus, and Google Scholar.
Results
Stem cell-derived cell-free therapy can prevent skin aging through various mechanisms, such as (1) involvement of multiple regenerative pathways [NFkb, AP-1, MAPK, P-AKT, NRF2, SIRT-1]; (2) oxidative stress regulation [by reducing oxidants (HO-1, NQO1) and enhancing antioxidants (SOD1, CAT, GP, FRAP)]; (3) preventing ECM degradation [by increasing elastin, collagen, HA, TIMP, and reducing MMP]; (4) regulating cell activity [by reducing cell senescence (SA-β-gal), apoptosis, and cell cycle arrest (P53, P12, P16); and enhancing autophagy, cell migration, and cell proliferation (Ki67)] (5) Regulating the inflammatory pathway [by reducing IL-6, IL-1, TNF-⍺, and increasing TGF-β]. Several clinical trials have also revealed improvements in wrinkles, elasticity, hydration, pores, and pigmentation.
Conclusion
Stem cell-derived cell-free therapy is a potential novel treatment for skin aging by cell rejuvenation through various molecular mechanisms.
Objectives
Our aim was to analyze the results of published randomized controlled trials (RCTs) on vitamin D supplementation for psoriasis in order to explore its effectiveness and safety.
Patients and methods
As of July 7 2023, we conducted a systematic literature search in PubMed, Cochrane, Embase, and Web of Science Core Collection databases. The study outcomes included change values in Psoriasis Area and Severity Index (PASI) (at 3 months, 6 months, and end of follow-up)/Dermatology Life Quality Index (DLQI)/Psoriasis disability index (PDI)/C-reactive protein (CRP), and adverse events.
Results
333 patients from 4 studies were evaluated. Pooled analyses showed no significant effect of DLQI/PDI/CRP change value (P > 0.05) or PASI change value (3 months, end of follow-up; P > 0.05). Sensitivity analyses and statistical tests did not support the results of the PASI change values (6 months, P = 0.05). However, the results of subgroup analyses should not be ignored(supplementation with vitamin D2 or Asia would be more effective; P = 0.03). There were no serious adverse effects, and only a few individuals experienced nausea.
Conclusions
The efficacy and safety of vitamin D supplementation in the treatment of psoriasis remains unremarkable. The search for a new prognostic index that combines clinical and laboratory factors is needed to compensate for the shortcomings of existing measures and provide stronger evidence of validity.
Topical medications represent the most commonly used drugs in the treatment of psoriasis. However, topical steroids are mainly limited to short-term or intermittent use, and traditional non-steroidal topicals such as vitamin D analogues, topical calcineurin inhibitors, and topical retinoids are limited by low efficacy and poor local skin tolerability. Tapinarof (GSK2894512, DMVT-505) is a novel, topical aryl hydrocarbon receptor (AHR) agonist, which was recently approved by the FDA for the treatment of plaque psoriasis in adults. Tapinarof acts to improve psoriasis through diminished IL-17A production by CD4+ T cells, increased barrier gene expression in keratinocytes, and reduced production of reactive oxygen species. Both short-term and long-term efficacy and safety have been evaluated in two Phase II and two Phase III (PSOARING 1 and 2) clinical trials in addition to a long-term extension study (PSOARING 3). Overall, the drug has shown beneficial effects in achieving clear skin in adults with moderate-to-severe psoriasis, good local tolerability, and also a long duration of effect even after discontinuation of the drug. Therefore, this therapy provides a new, highly effective and safe non-steroidal option to add to our psoriasis treatment toolbox for both initial clearance and long-term maintenance of disease.
Simple Summary
Aging affects all cells of the body, leading to impaired system function. Although scientists are beginning to identify some mechanisms underlying the aging process, a complete understanding remains elusive. One characteristic of aged individuals is chronic low-level inflammation throughout the body. Since inflammation induces oxidative stress and other effects that can impact proper system functioning over time, this chronic inflammation is thought to promote aging, called inflamm-aging. The cause of inflamm-aging is unclear but likely involves immune system malfunction and various other age-related alterations. Excessive inflammation of the skin, the largest organ of the body, can result in widespread effects on other systems, as is seen with inflammatory skin diseases such as psoriasis and atopic dermatitis. An important function of skin is to serve as a barrier to prevent the entry of environmental insults, such as microorganisms, and to retain water and other important substances inside the body. Disruption of this barrier results in skin inflammation that can impact the whole individual. It is known that, with age, our skin becomes less able to maintain the barrier. Therefore, we propose and discuss evidence for the idea that a poorly functioning skin barrier contributes to inflamm-aging.
Abstract
With its unique anatomical location facing both the external and internal environment, the skin has crucial functions, including shielding the body from damage caused by ultraviolet radiation and chemicals, preventing water loss, acting as a primary barrier against pathogens, participating in metabolic processes like vitamin D production and temperature control and relaying information to the body through sensory and proprioceptor nerves. Like all organ systems, skin is known to undergo multiple changes with aging. A better understanding of the mechanisms that mediate aging-related skin dysfunction may allow the creation of targeted therapeutics that have beneficial effects not only on aged skin but also on other organs and tissues that experience a loss of or decline in function with aging. The skin is the largest organ of the body and can contribute to serum inflammatory mediator levels. One alteration known to occur with age is an impairment of skin barrier function; since disruption of the barrier is known to induce inflammation, skin may be a major contributor to the sustained, sub-clinical systemic inflammation associated with aging. Such “inflamm-aging” may underlie many of the deleterious changes observed in aged individuals. This review explores the role of age-related skin changes, skin inflammation and inflamm-aging.
Retinyl palmitate (RP) is a vitamin A derivative that has been widely used in anti-aging and skin treatment. The aim of this study is to investigate the effect of RP on UVB (Ultraviolet radiation B) induced photoaging and its potential mechanism. Immunofluorescence assay demonstrates that RP can reduce collagen degradation in skin cells by UVB radiation and reduce apoptosis of skin cells. Cell migration assay reveals that RP can increase cell migration rate, helping to repair skin damage and restore cell viability. Immunohistochemical assays indicate that RP can significantly reduce the expression of IL-6, IL-1β, TNF-α induced by UVB radiation. Moreover, metabolomics and transcriptomics results suggest that RP regulates several metabolic pathways and gene expression, particularly in inflammatory signaling pathways, collagen synthesis and apoptosis, exhibiting significant regulatory effects. Furthermore, network pharmacological analysis predicts that RP may affect UVB-induced photoaging by regulating multiple key proteins and signaling pathways. Overall, this study demonstrates that RP has significant anti-photoaging ability, acting through several pathways including inhibition of inflammatory response, promotion of collagen synthesis and inhibition of apoptosis. These results provide a scientific basis for the application of RP in skin anti-photoaging and therapy, enabling the potential usage of RP to skin care products.
Vitamin D is one significant prohormone substance in human organ systems. It is a steroidal hormone produced in the skin upon exposure to UVB rays. This paper presents a systematic review of the utilization of topical vitamin D, specifically cholecalciferol, calcipotriol, and tacalcitol, in the treatment of vitiligo. It considers the role of vitamin D in stimulating the synthesis of melanin and melanogenesis, which can help with the process of repigmentation. The inclusion of calcipotriol or tacalcitol in Narrowband Ultraviolet Phototherapy (NB-UVB) has shown the potential to enhance therapeutic outcomes for vitiligo. However, their effectiveness in combination with Psoralens Long Wave Ultraviolet Radiation (PUVA) and Monochromatic Excimer Light (MEL) treatment for vitiligo is limited. In contrast, combining topical corticosteroids with vitamin D analogues has demonstrated superior efficacy in treating vitiligo compared to using vitamin D analogues alone, while also providing the added benefit of reducing corticosteroid-related adverse effects. In addition, treating stable vitiligo with topical cholecalciferol and microneedling has shown success. Future studies are needed to ascertain an efficient method of administering vitamin D topically as an anti-vitiligo agent.
Atopic dermatitis (AD) is a chronic and recurrent inflammatory skin condition characterized by itching, eczematous plaques, and dry skin. Despite ongoing research, its exact cause remains elusive. In this study, we aimed to explore the factors that influence the severity of AD in children and assess the relationship between serum vitamin D levels and the disease’s severity. We enrolled 96 AD patients in our investigation, evaluated their clinical condition using the Scoring Atopic Dermatitis (SCORAD) index, and compared them to a group of 90 healthy controls. Our analysis revealed that serum vitamin D levels and eosinophil counts significantly impacted the SCORAD index (p < 0.001). According to standardized regression coefficients, for each incremental unit in serum vitamin D levels, the SCORAD index exhibited a decrease of 0.449 units. Similarly, a one-unit increase in eosinophil count resulted in a 0.009 unit increase in the SCORAD index. It is worth noting that the influence of serum vitamin D levels on disease severity surpasses that of eosinophil counts and atopic conditions. In our patient cohort, we uncovered a negative correlation (r = −0.419, p < 0.001) between serum vitamin D levels and the SCORAD index. Our findings suggest that low serum vitamin D levels may have a more substantial impact on AD severity than atopic conditions and eosinophilia. Furthermore, we observed a negative association between the severity of AD and serum 25(OH)D3 levels.
Both 25-autoimmunity and(25(OH)D: calcifediol) and its active form, 1,25-dihydroxyvitamin D (1,25(OH) 2 D: calcitriol), play critical roles in protecting humans from invasive pathogens, reducing risks of autoimmunity, and maintaining health. Conversely, low 25(OH)D status increases susceptibility to infections and developing autoimmunity. This systematic review examines vitamin D's mechanisms and effects on enhancing innate and acquired immunity against microbes and preventing autoimmunity. The study evaluated the quality of evidence regarding biology, physiology, and aspects of human health on vitamin D related to infections and autoimmunity in peer-reviewed journal articles published in English. The search and analyses followed PRISMA guidelines. Data strongly suggested that maintaining serum 25(OH)D concentrations of more than 50 ng/mL is associated with significant risk reduction from viral and bacterial infections, sepsis, and autoimmunity. Most adequately powered, well-designed, randomized controlled trials with sufficient duration supported substantial benefits of vitamin D. Virtually all studies that failed to conclude benefits or were ambiguous had major study design errors. Treatment of vitamin D deficiency costs less than 0.01% of the cost of investigation of worsening comorbidities associated with hypovitaminosis D. Despite cost-benefits, the prevalence of vitamin D deficiency remains high worldwide. This was clear among those who died from COVID-19 in 2020/21-most had severe vitamin D deficiency. Yet, the lack of direction from health agencies and insurance companies on using vitamin D as an adjunct therapy is astonishing. Data confirmed that keeping an individual's serum 25(OH)D concentrations above 50 ng/mL (125 nmol/L) (and above 40 ng/mL in the population) reduces risks from community outbreaks, sepsis, and autoimmune disorders. Maintaining such concentrations in 97.5% of people is achievable through daily safe sun exposure (except in countries far from the equator during winter) or taking between 5000 and 8000 IU vitamin D supplements daily (average dose, for non-obese adults, 70 to 90 IU/kg body weight). Those with gastrointestinal malabsorption, obesity, or on medications that increase the catabolism of vitamin D and a few other specific disorders require much higher intake. This systematic review evaluates non-classical actions of vitamin D, with particular emphasis on infection and autoimmunity related to the immune system.
Background:
Previous cross-sectional studies have failed to definitively establish a causal relationship between serum 25-hydroxyvitamin D (25OHD) concentrations and the onset of rosacea.
Objective:
To investigate the potential association between serum 25OHD levels, vitamin D receptor (VDR) polymorphisms, and the risk of developing incident rosacea.
Methods:
This cross-sectional population-based cohort study utilizing 370,209 individuals from the UK Biobank. Cox proportional hazard regression models and two-sample Mendelian randomization (MR) analyses were applied to explore the causative relationship between 25OHD and incident rosacea.
Results:
Our findings revealed that elevated levels of serum 25OHD were inversely correlated with the risk of incident rosacea. Specifically, compared to participants with 25OHD levels below 25 nmol/L, the multivariate-adjusted HR for incident rosacea was 0.81 (95% CI: 0.70, 0.94) in those with 25OHD levels exceeding 50 nmol/L. Further, in comparison to individuals with serum 25OHD less than 25 nmol/L and the rs731236 (TaqI) AA allele, those with serum 25OHD higher than 75 nmol/L and the TaqI GG allele had a multivariate-adjusted HR of 0.51 (95% CI 0.32 to 0.81) for developing rosacea. Results from the MR study supported a significant association, with each standard deviation increase in serum 25OHD concentrations correlating to a 23% reduced risk of rosacea (HR = 0.77, 95% CI: 0.63, 0.93).
Conclusions:
The findings of this cohort study indicate an inverse association between increased concentrations of serum 25OHD and the risk of developing incident rosacea. While our results highlight the potential protective role of vitamin D, the definitive efficacy of vitamin D supplementation as a preventive strategy against rosacea requires further investigation.
Apart from developmental disabilities, the prevalence of chronic diseases increases with age especially in those with co-morbidities: vitamin D deficiency plays a major role in it. Whether vitamin D deficiency initiates and/or aggravates chronic diseases or vice versa is unclear. It adversely affects all body systems but can be eliminated using proper doses of vitamin D supplementation and/or safe daily sun exposure. Maintaining the population serum 25(OH)D concentration above 40 ng/mL (i.e., sufficiency) ensures a sound immune system, minimizing symptomatic diseases and reducing infections and the prevalence of chronic diseases. This is the most cost-effective way to keep a population healthy and reduce healthcare costs. Vitamin D facilitates physiological functions, overcoming pathologies such as chronic inflammation and oxidative stress and maintaining broader immune functions. These are vital to overcoming chronic diseases and infections. Therefore, in addition to following essential public health and nutritional guidance, maintaining vitamin D sufficiency should be an integral part of better health, preventing acute and chronic diseases and minimize their complications. Those with severe vitamin D deficiency have the highest burdens of co-morbidities and are more vulnerable to developing complications and untimely deaths. Vitamin D adequacy improves innate and adaptive immune systems. It controls excessive inflammation and oxidative stress, generates antimicrobial peptides, and neutralizes antibodies via immune cells. Consequently, vitamin D sufficiency reduces infections and associated complications and deaths. Maintaining vitamin D sufficiency reduces chronic disease burden, illnesses, hospitalizations, and all-cause mortality. Vulnerable communities, such as ethnic minorities living in temperate countries, older people, those with co-morbidities, routine night workers, and institutionalized persons, have the highest prevalence of vitamin D deficiency—they would significantly benefit from vitamin D and targeted micronutrient supplementation. At least now, health departments, authorities, and health insurance companies should start assessing, prioritizing, and encouraging this economical, non-prescription, safe micronutrient to prevent and treat acute and chronic diseases. This approach will significantly reduce morbidity, mortality, and healthcare costs and ensure healthy aging.
Psoriasis is a chronic immune-dysregulated inflammatory disease and hypovitaminosis D is considered a risk factor. We conducted an online database search to review and meta-analyze the relationship between vitamin D, other bone metabolism parameters, and psoriasis. The efficacy of oral vitamin D supplementation in improving Psoriasis Area and Severity Index (PASI) was also evaluated. Non-original articles, case reports, and animal studies were excluded. Bias risk was assessed according to the Cochrane Collaboration's tool and the Newcastle-Ottawa scale in randomized controlled trials (RCTs) and case-control studies, respectively. Unstandardized mean differences were used for data synthesis. Twenty-three studies reported serum 25 hydroxyvitamin D (25(OH)D) levels in 1876 psoriasis patients and 7532 controls. Psoriasis patients had significantly lower 25(OH)D levels than controls (21.0 ± 8.3 vs. 27.3 ± 9.8, p < 0.00001). Conversely, 450 psoriasis patients had lower levels of parathormone than 417 controls (38.7 ± 12.8 vs. 43.7 ± 16.5, p = 0.015). Four RCTs examined the effect of oral vitamin D supplementation on psoriasis for 173 patients and 160 patients were treated with placebo. No significant differences were found in PASI after 3, 6, and 12 months of supplementation. It is shown that 25(OH)D serum levels are significantly lower in psoriasis, but, although the granularity of RCT methodology may have influenced the pooled analysis, vitamin D supplementation did not seem to improve clinical manifestations.
Objective:
Seborrheic dermatitis is a common papulosquamous skin disease with unknown pathogenesis. The aim of our study was to determine the serum level of 25-hydroxy vitamin D in patients with seborrheic dermatitis SD.
Methods:
A total of 53 patients and 60 healthy controls were included in the study. Serum vitamin D, calcium, phosphorus, and parathormone levels were measured in the patient and control groups, and a comparison was made between the two groups regarding these parameters.
Results:
Severe vitamin D deficiency was more frequent among patients with seborrheic dermatitisSD compared to controls (52.8 vs. 25.8%, p=0.003). In patients with severe vitamin D deficiency, seborrheic dermatitis SD was detected more frequently at an early age (p=0048) and in women (p=0.015). No correlation was found between the seborrheic dermatitis skin involvement site and vitamin D level.
Conclusion:
The fact that vitamin D levels decreased in patients with seborrheic dermatitis SD and patients with severe vitamin D deficiency develop seborrheic dermatitis SD earlier suggests that the low levels of vitamin D are related to seborrheic dermatitis.
The hormonal form of vitamin D3, 1,25(OH)2D3, reduces UV-induced DNA damage. UV exposure initiates pre-vitamin D3 production in the skin, and continued UV exposure photoisomerizes pre-vitamin D3 to produce “over-irradiation products” such as lumisterol3 (L3). Cytochrome P450 side-chain cleavage enzyme (CYP11A1) in skin catalyzes the conversion of L3 to produce three main derivatives: 24-hydroxy-L3 [24(OH)L3], 22-hydroxy-L3 [22(OH)L3], and 20,22-dihydroxy-L3 [20,22(OH)L3]. The current study investigated the photoprotective properties of the major over-irradiation metabolite, 24(OH)L3, in human primary keratinocytes and human skin explants. The results indicated that treatment immediately after UV with either 24(OH)L3 or 1,25(OH)2D3 reduced UV-induced cyclobutane pyrimidine dimers and oxidative DNA damage, with similar concentration response curves in keratinocytes, although in skin explants, 1,25(OH)2D3 was more potent. The reductions in DNA damage by both compounds were, at least in part, the result of increased DNA repair through increased energy availability via increased glycolysis, as well as increased DNA damage recognition proteins in the nucleotide excision repair pathway. Reductions in UV-induced DNA photolesions by either compound occurred in the presence of lower reactive oxygen species. The results indicated that under in vitro and ex vivo conditions, 24(OH)L3 provided photoprotection against UV damage similar to that of 1,25(OH)2D3.
Introduction: Vitiligo is an autoimmune disease that is caused by the destruction of melanocytes and is appeared as depigmented patches on skin and mucosa. There have been various reports of serum Vitamin D levels in patients with vitiligo. The present study aimed to Evaluation of serum Vitamin D levels in patients with vitiligo. Material and Methods: A case-control study was performed on 138 samples among people referring to Sabzevar Vasei clinic in the period of 2018-2019. The research units meeting the inclusion criteria were selected using convenience sampling and then divided into two group case and control (69 patients and 69 healthy people). After obtaining informed consent and completing the checklist of demographic characteristics, blood samples were taken from both groups and serum levels of Vitamin D in both groups were evaluated and compared. Data were analyzed using SPSS 20 via the independent t-test, chi-square test, Mann-Whitney test, Spearman correlation at a significance level of less than 0.01. Results: In total, 131 participants completed the study; the two groups did not differ significantly in terms of age nor gender. At the end of the study, the mean of serum levels of Vitamin D in was significantly lower in the patients with vitiligo than in the people without vitiligo (P <0.001). Conclusion: The results showed that serum Vitamin D levels in patients with vitiligo are lower than in those who do not have vitiligo. Therefore, it is recommended to measure the serum level of Vitamin D in these patients and if it is low, a treatment regimen should begin for these patients.
Vitamin D is essential for life—its sufficiency improves metabolism, hormonal release, immune functions, and maintaining health. Vitamin D deficiency increases the vulnerability and severity of type 2 diabetes, metabolic syndrome, cancer, obesity, and infections. The active enzyme that generates vitamin D [calcitriol: 1,25(OH)2D], CYP27B1 (1a-hydoxylase), and its receptors (VDRs) are distributed ubiquitously in cells. Once calcitriol binds with VDRs, the complexes are translocated to the nucleus and interact with responsive elements, up- or down-regulating the expression of over 1200 genes and modulating metabolic and physiological functions. Administration of vitamin D3 or correct metabolites at proper doses and frequency for longer periods would achieve the intended benefits. While various tissues have different thresholds for 25(OH)D concentrations, levels above 50 ng/mL are necessary to mitigate conditions such as infections/sepsis, cancer, and reduce premature deaths. Cholecalciferol (D3) (not its metabolites) should be used to correct vitamin D deficiency and raise serum 25(OH)D to the target concentration. In contrast, calcifediol [25(OH)D] raises serum 25(OH)D concentrations rapidly and is the agent of choice in emergencies such as infections, for those who are in ICUs, and for insufficient hepatic 25-hydroxylase (CYP2R1) activity. In contrast, calcitriol is necessary to maintain serum-ionized calcium concentration in persons with advanced renal failure and hypoparathyroidism. Calcitriol is, however, ineffective in most other conditions, including infections, and as vitamin D replacement therapy. Considering the high costs and higher incidence of adverse effects due to narrow therapeutic margins (ED50), 1α-vitamin D analogs, such as 1α-(OH)D and 1,25(OH)2D, should not be used for other conditions. Calcifediol analogs cost 20 times more than D3—thus, they are not indicated as a routine vitamin D supplement for hypovitaminosis D, osteoporosis, or renal failure. Healthcare workers should resist accepting inappropriate promotions, such as calcifediol for chronic renal failure and calcitriol for osteoporosis or infections—there is no physiological rationale for doing so. Maintaining the population’s vitamin D sufficiency (above 40 ng/mL) with vitamin D3 supplements and/or daily sun exposure is the most cost-effective way to reduce chronic diseases and sepsis, overcome viral epidemics and pandemics, and reduce healthcare costs. Furthermore, vitamin D sufficiency improves overall health (hence reducing absenteeism), reduces the severity of chronic diseases such as metabolic and cardiovascular diseases and cancer, decreases all-cause mortality, and minimizes infection-related complications such as sepsis and COVID-19-related hospitalizations and deaths. Properly using vitamin D is the most cost-effective way to reduce chronic illnesses and healthcare costs: thus, it should be a part of routine clinical care.
Various therapeutic approaches, including supplemental nutritional support, have been tried for the treatment of atopic dermatitis (AD). Previous studies have reported the role of vitamin D in the treatment of AD with inconsistent results. The aim of this study was to evaluate the effectiveness of vitamin D in the treatment of AD, with considerations on the heterogeneities of AD. Randomized controlled trials (RCTs) on the efficacy of vitamin D supplementation for AD treatment, published before June 30, 2021 were identified in the PubMed, EMBASE, MEDLINE, and Cochrane Library databases. The quality of evidence was assessed using the Grading of Recommendations, Assessment, Development and Evaluation system. This meta-analysis included 5 RCTs with 304 cases of AD. We found that vitamin D supplementation did not decrease AD severity, even when AD was classified as severe vs non-severe. However, vitamin D supplementation was found to be effective in the treatment of AD in RCTs that included both children and adults, but not in those that included only children. Geographic location was associated with a significant difference in the therapeutic effect of vitamin D supplementation. Moreover, vitamin D supplementation of > 2,000 IU/day decreased AD severity, but supplementation ≤ 2,000 IU/day did not. Vitamin D supplementation, in general, was not effective for the treatment of AD. However, vitamin D supplementation might provide a therapeutic effect depending on the geographic location and dose of supplementation. The results of the present meta-analysis suggest that vitamin D supplementation might be targeted for patients with AD who may benefit from vitamin D supplementation.
Vitamin D is a fat-soluble vitamin that plays an important role in the regulation of the immune system and has been linked to a variety of skin conditions. In this article, we will discuss the role of vitamin D deficiency in immunomodulation and its potential role in the etiology of dermatological disorders including psoriasis, atopic dermatitis, and vitiligo. This review examines the evidence linking vitamin D deficiency to these skin disorders, discusses potential mechanisms of action as well as possible management strategies.
Skin areas exposed to ultraviolet radiation (UV) from sunlight are more prone to photoaging than unexposed areas evidenced by several signs which include skin dryness, irregular pigmentation, lentigines, hyperpigmentation, wrinkling, and decreased elasticity. Plant-based natural product ingredients with therapeutic potential against skin photoaging are gaining more attention. This article aims the reviewing the research work done in exploring the cellular and molecular mechanisms involved in UV-induced skin photoaging, followed by summarizing the mechanistic insights involved in its therapeutics by natural product-based ingredients. In the mechanistic section of the convoluted procedure of photoaging, we described the effect of UV radiation (UVR) on different cellular macromolecules (direct damage) and subsequently, the deleterious consequences of UVR-generated reactive oxygen species (indirect damage) and signaling pathways activated or inhibited by UV induced ROS generation in various cellular pathologies of skin photoaging like inflammation, extracellular matrix degradation, apoptosis, mitochondrial dysfunction, and immune suppression. We also discussed the effect of UV radiation on the adipose tissue, and transient receptor potential cation channel V of photoaging skin. In the past few decades, mechanistic studies performed in this area have deciphered various therapeutic targets, opening avenues for different available therapeutic options against this pathological condition. So the remaining portion of the review deals with various natural product-based therapeutic agents available against skin photodamage.
The aim of this study was to investigate the protective function and mechanism of TCP3 (PKK), TCP6 (YEGGD) and TCP9 (GPGLM) from skipjack tuna cardiac arterial bulbs on skin photoaging using UVB-irradiated HaCaT cell model. The present results indicated that TCP3 (PKK), TCP6 (YEGGD) and TCP9 (GPGLM) had significant cytoprotective effect on UVB-irradiated HaCaT cells (p < 0.001). Hoechst 33342 staining showed that apoptosis of UV-irradiated HaCaT cells could be significantly reduced by the treatment of TCP3 (PKK), TCP6 (YEGGD) and TCP9 (GPGLM); JC-1 staining showed that TCP3 (PKK), TCP6 (YEGGD) and TCP9 (GPGLM) could protect HaCaT cells from apoptosis by restoring mitochondrial membrane potential (MMP); Furthermore, TCP3 (PKK), TCP6 (YEGGD) and TCP9 (GPGLM) could significantly down-regulate the ratio of Bax/Bcl-2 and reduce the expression level of the apoptosis-executing protein Caspase-3 by decreasing the expression of protein Caspase-8 and Caspase-9 (p < 0.05). The action mechanism indicated that TCP3 (PKK), TCP6 (YEGGD) and TCP9 (GPGLM) could up-regulate the expression levels of Nrf2, NQO1 and HO-1 (p < 0.05), which further increased the activity of downstream proteases (SOD, CAT and GSH-Px), and scavenged reactive oxygen species (ROS) and decreased the intracellular levels of malondialdehyde (MDA). In addition, molecular docking indicated that TCP3 (PKK) and TCP6 (YEGGD) could competitively inhibit the Nrf2 binding site because they can occupy the connection site of Nrf2 by binding to the Kelch domain of Keap1 protein. TCP9 (GPGLM) was inferred to be non-competitive inhibition because it could not bind to the active site of the Kelch domain of Keap1 protein. In summary, the antioxidant peptides TCP3 (PKK), TCP6 (YEGGD) and TCP9 (GPGLM) from cardiac arterial bulbs of skipjack tuna can effectively protect HaCaT cells from UVB-irradiated damage and can be used in the development of healthy and cosmetic products to treat diseases caused by UV radiation.
Background
Photoaging is mainly caused by ultraviolet radiations inasmuch they can damage the DNA, trigger ROS production, and activate p53/p21 pathway, which cause cell cycle arrest and senescence. The accumulation of senescent cells within the dermis contributes to tissue deregulation and skin carcinogenesis. However, the use of photoprotector molecules could reduce UV-induced damages and prevent photoaging. Therefore, the aim of this study is to evaluate whether the active forms of vitamin B3 (nicotinamide) and the analog of vitamin D3 (calcipotriol) might protect primary human dermal fibroblasts (HDFs) from UVB-induced photoaging.
Methods
HDFs were isolated from a healthy adult donor and stimulated with nicotinamide (25 μM) and calcipotriol (100 nM) for 24h before UVB exposure, and then, cultured for further 24h on vitamin-supplemented media. Then, cell viability, ROS production, DNA damages, senescence markers, protein and gene expression were evaluated.
Results
HDFs treated with nicotinamide and calcipotriol showed better proliferation properties and lower DNA damages due to a reduced UVB-induced ROS production. Consequently, p53/p21 pathway was less active which enhanced cell cycle progression and reduced senescence and cell death.
Conclusions
Overall, our results suggest that nicotinamide and calcipotriol can counteract UVB-induced effects responsible for the onset of skin photoaging.
The peculiarity of the skin is that it acts not only as a place of synthesis of vitamin D, but also as an organ targeted for its biologically active form. The aim of our study was to analyze the level of vitamin D in patients with atopic dermatitis. There were examined 48 people aged between 18 to 55 years; they are residents of Vinnytsia and Vinnytsia region. Serum levels of vitamin D, total IgE and eosinophilic cationic protein (ECP) were determined in the subjects. The average level of vitamin D in the serum of patients with atopic dermatitis was 19.2 [11.3-25.4] ng/ml, which corresponded to a deficiency. Among those surveyed, vitamin D deficiency was found in 68.4±4.7% (n=26) while vitamin D insufficiency in 31.6±4.5% (n=12). The severe course of the disease prevailed among patients aged 18-40 years (63.33±8.79) % more than in the age group of 41 years and older, (36.67±8.8%, p<0.05; OR=2.98, S=0.53, 95% SI:1.04-8.52). The proportion of people with vitamin D deficiency and moderate severity of atopic dermatitis was 62.5% (n=10) with a median level of 14 [8.3–19] ng/ml, and patients with severe atopic dermatitis made up 90.9% (n=20) (χ²=4.6; p=0.023), in which the median level of vitamin D was 14 [8.3-19] ng/ml. Serum vitamin D levels were in the zone of deficiency in patients with moderate and severe atopic dermatitis. Vitamin D deficiency was significantly more common in the group of patients with elevated levels of allergic inflammation markers. A positive correlation of medium strength between the level of vitamin D and ECP in the serum of patients with atopic dermatitis (rs=0.53, p<0.001), was revealed.
Psoriasis is a continuing, periodic, immune‑mediated, fiery skin disease branded by hyper proliferation of epidermal keratinocytes and accompanying with inflammatory cellular infiltrate in both dermis and epidermis. Immunomodulation could be an important effect of vitamin D in Psoriasis. This case-control study was designed to measure serum 25-hydroxy vitamin D levels in patients with psoriasis and healthy controls and to find out clinical correlation, if any. Six hundred two (n = 602) subjects (285 cases and 317 controls) were taken for the study. Cases and controls were frequency matched with respect to age and gender. Various demographic and clinical details were taken using a questionnaire. Chemiluminescence Micro Particle Immunoassay was used to estimate serum 25-hydroxy vitamin D levels. The vitamin D deficiency in psoriasis patients was 60.0% vs. 17.5% in controls (P < 0.001) with mean vitamin D levels of 28.3 ± 13.9 ng/ml in psoriasis patient’s vs. 37.9 ± 9.7 ng/ml in controls. Vitamin D deficiency was found to be associated with psoriasis independently of gender, age, smoking status, family history, hypertension, chronic medication, nail changes, duration of symptoms and severity of disease. Vitamin D levels were seven times lower in patients with Psoriasis as compared to controls. Reduced vitamin D levels are related to duration and clinical severity of the disease. Early detection of vitamin D deficiency and timely intervention could lead to better clinical outcome and improved quality of life in psoriasis patients.
Background:
Chronic plaque psoriasis is a chronic inflammatory skin disorder. Vitamin D has been shown to have effects on keratinocyte differentiation as well as immune regulation in the skin.
Objective:
The main objective of this study was to assess the 25hydroxyvitamin D [25 (OH) D] level in patients with psoriasis in comparison with healthy control subjects.
Materials and methods:
This case-control study included 180 persons (120 cases and 60 age- and sex-matched control subjects) from outpatient department of BPKIHS, a tertiary care hospital in eastern Nepal. Severity of psoriatic skin lesions was assessed using psoriasis area severity index (PASI) scoring. Serum vitamin D level was assessed by chemiluminescent immunoassay.
Results:
The mean serum 25(OH) D levels in psoriatic patients and controls were 19.57 ± 6.85 ng/mL and 23.63 ± 6.40 ng/mL, respectively. The difference was statistically significant even after adjusting for confounding factors in a multivariate analysis (aOR 2.929, 95% CI 1.376-6.230). Low serum 25(OH) D levels were negatively associated with the severity of disease (r= -0.628, P= 0.01).
Conclusion:
Serum 25(OH) D levels are significantly lower in psoriatic patients than in healthy control subjects. Deficiency of serum 25(OH) D was associated with severity of disease with an inverse relationship with PASI score.
Within solar ultraviolet (UV) light, the longest UVA1 wavelengths, with significant and relatively constant levels all year round and large penetration properties, produce effects in all cutaneous layers. Their effects, mediated by numerous endogenous chromophores, primarily involve the generation of reactive oxygen species (ROS). The resulting oxidative stress is the major mode of action of UVA1, responsible for lipid peroxidation, protein carbonylation, DNA lesions and subsequent intracellular signaling cascades. These molecular changes lead to mutations, apoptosis, dermis remodeling, inflammatory reactions and abnormal immune responses. The altered biological functions contribute to clinical consequences such as hyperpigmentation, inflammation, photoimmunosuppression, sun allergies, photoaging and photocancers. Such harmful impacts have also been reported after the use of UVA1 phototherapy or tanning beds. Furthermore, other external aggressors, such as pollutants and visible light (Vis), were shown to induce independent, cumulative and synergistic effects with UVA1 rays. In this review, we synthetize the biological and clinical effects of UVA1 and the complementary effects of UVA1 with pollutants or Vis. The identified deleterious biological impact of UVA1 contributing to clinical consequences, combined with the predominance of UVA1 rays in solar UV radiation, constitute a solid rational for the need for a broad photoprotection, including UVA1 up to 400 nm.
Vitamin D deficiency is a global public health problem, a pandemic that commonly affects the elderly and those with comorbidities such as obesity, diabetes, hypertension, respiratory disorders, recurrent infections, immune deficiency, and malignancies, as well as ethnic minorities living in temperate countries. The same groups were worst affected by COVID-19. Since vitamin D deficiency weakens the immune system, it increases the risk of infections, complications, and deaths, such as from sepsis and COVID-19. Deficiency can be remedied cost-effectively through targeted food fortification, supplementation, and/or daily safe sun exposure. Its endocrine functions are limited to mineral metabolism, musculoskeletal systems, specific cell membrane interactions, and parathyroid gland functions. Except for the rapid, endocrine, and cell membrane-based non-genomic functions, all other biological and physiological activities of vitamin D depend on the adequate intracellular synthesis of 1,25(OH)2D (calcitriol) in peripheral target cells via the genome. Calcitriol mediates autocrine (intracrine) and paracrine signalling in immune cells, which provides broader, protective immune functions crucial to overcoming infections. The synthesis of 1,25(OH)2D (calcitriol) in peripheral target cells is dependent on diffusion and endocytosis of D3 and 25(OH)D from the circulation into them, which requires maintenance of serum 25(OH)D concentration above 50 ng/mL. Therefore, in acute infections such as sepsis and respiratory infections like COVID-19, it is necessary to rapidly provide its precursors, D3 and 25(OH)D, through the circulation to generate adequate intracellular calcitriol. Immune defence is one of the crucial non-hormonal functions of vitamin D. A single oral (bolus) dose or divided upfront loading doses between 100,000 and 500,000 IU, using 50,000 IU vitamin D3 increase the serum 25(OH)D concentrations to a therapeutic level of above 50 ng/mL that lasts between two to three months. This takes three to five days to raise serum 25(OH)D. In contrast, a single oral dose of calcifediol (0.014 mg/kg body weight) can generate the needed 25(OH)D concentration within four hours. Considering both D3 and 25(OH)D enter immune cells for generating calcitriol, using the combination of D3 (medium-term) and calcifediol (immediate) is cost-effective and leads to the best clinical outcome. To maximise protection against infections, particularly to reduce COVID-19-associated complications and deaths, healthcare workers should advise patients on safe sun exposure, adequate vitamin D supplementation and balanced diets containing zinc, magnesium, and other micronutrients to support the immune system. Meanwhile, governments, the World Health Organisation, the Centers for Disease Control, and governments should consider similar recommendations to physicians and the public, change the outdated vitamin D and other micronutrient recommendations directed to their population, and organise targetted food fortification programs for the vulnerable groups. This article discusses a rational approach to maintaining a sustained serum 25(OH)D concentration above 50 ng/mL, necessary to attain a robust immune system for overcoming infections. Such would cost-effectively improve the population’s health and reduce healthcare costs. It also describes three cost-effective, straightforward protocols for achieving and sustaining therapeutic serum 25(OH)D concentrations above 50 ng/mL (>125 nmol/L) to keep the population healthy, reduce absenteeism, improve productivity, and lower healthcare costs.
Background
Excessive exposure of the skin to UV radiation (UVR) triggers a remodeling of the immune system and leads to the photoaging state which is reminiscent of chronological aging. Over 30 years ago, it was observed that UVR induced an immunosuppressive state which inhibited skin contact hypersensitivity.
Methods
Original and review articles encompassing inflammation and immunosuppression in the photoaging and chronological aging processes were examined from major databases including PubMed, Scopus, and Google Scholar.
Results
Currently it is known that UVR treatment can trigger a cellular senescence and inflammatory state in the skin. Chronic low-grade inflammation stimulates a counteracting immunosuppression involving an expansion of immunosuppressive cells, e.g., regulatory T cells (Treg), myeloid-derived suppressor cells (MDSC), and regulatory dendritic cells (DCreg). This increased immunosuppressive activity not only suppresses the function of effector immune cells, a state called immunosenescence, but it also induces bystander degeneration of neighboring cells. Interestingly, the chronological aging process also involves an accumulation of pro-inflammatory senescent cells and signs of chronic low-grade inflammation, called inflammaging. There is also clear evidence that inflammaging is associated with an increase in anti-inflammatory and immunosuppressive activities which promote immunosenescence.
Conclusion
It seems that photoaging and normal aging evoke similar processes driven by the remodeling of the immune system. However, it is likely that there are different molecular mechanisms inducing inflammation and immunosuppression in the accelerated photoaging and the chronological aging processes.
For full use of the by-products during Siberian sturgeon (Acipenser baerii) processing, gelatin was extracted from the cartilages using the hot water method, and its physico-chemical properties and protective function on ultraviolet-A injured human skin fibroblasts (HFSBs) were measured. Using single-factor and orthogonal experiments, the conditions for extracting gelatin from Siberian sturgeon cartilage were optimized as extraction time of 7 h, pH 9, material-to-liquid ratio (g/ml) of 1:5, and temperature of 45°C. The prepared gelatin (TCG) with a yield of 28.8 ± 1.53% had Gly (307 residues/1,000 residues) as the major amino acid and contained a lower amount (214 residues/1,000 residues) of imino acids than that (227 residues/1,000 residues) of pigskin gelatin (PSG). Sodium dodecyl sulfate–polyacrylamide gel electrophoresis (SDS-PAGE), ultraviolet spectrum, and infrared spectroscopy analysis indicated that TCG had the main spectral characteristics of fish gelatin and contained α chains (α1 and α2 chains) and β chain of type I collagen, but its structural stability was lower than that of PSG due to its low content of imino acids, which induced the smaller molecular bands observed in the SDS-PAGE pattern. TCG exhibited lower water content, gel strength, emulsion stability index, foam capacity, foam stability, and water-holding capacity but higher ash content, transmittance, emulsion activity index, and fat-binding capacity (P < 0.05). Moreover, TCG could significantly protect HFSBs against ultraviolet-A injury by enhancing the activity of superoxide dismutase, catalase, and glutathione peroxidase to scavenge excess reactive oxygen species and decrease the content of malondialdehyde. Therefore, gelatin from Siberian sturgeon cartilages could act as promising candidates when applied in health-promoting products against ultraviolet-A injury.
Background:
The role of vitamin D deficiency and vitamin D receptor (VDR) gene polymorphisms has been established in many autoimmune diseases, including vitiligo, but the result is still controversial.
Objectives:
The aim of this study was to investigate the serum vitamin D levels in vitiligo patients and to compare the association of VDR gene polymorphisms in vitiligo patients and healthy controls.
Methods:
We collected the data of age, sex, serum 25-hydroxy vitamin D (25[OH]D) level, thyroid autoantibodies, disease duration, types of vitiligo, family history and the affected body surface area of vitiligo from 172 patients. And we analyzed the VDR gene polymorphisms in 130 vitiligo and 453 age-sex-matched control subjects.
Results:
The mean serum level of 25(OH)D in 172 vitiligo patients was 18.75 ± 0.60 ng/mL, which had no significant difference with a mean serum value of 25(OH)D in the Korean population. However, there were significant differences according to the duration of the disease and family history. Also, there were no significant differences in the genotypic and allelic distributions of 37 examined SNPs of VDR gene between vitiligo patients and healthy controls.
Conclusion:
Serum level of 25(OH)D in vitiligo patients was not significantly different from the mean serum value of the Korean population. Also, there were no significant differences in the genotypic distributions of VDR gene between vitiligo patients and healthy controls.
Hidradenitis suppurativa (HS) is a chronic inflammatory disease of the apocrine gland bearing skin, presenting various stages of flexural skin pain, erythema, painful nodules, abscesses, sinuses, and fistulas. We aimed to assess serum vitamin D levels in patients with (HS) in Jordan. a cross-sectional comparative study conducted among 110 patients with HS and 110 matched controls, who didn’t previously receive vitamin D therapy. Serum vitamin D was measured and classified into normal (>30 ng/ml), insufficient (20–30 ng/ml), and low (<20 ng/ml). The mean age of the cases was 43.1 ± 12.9 years and the mean disease duration was 19.4 months. The mean body mass index among patients with HS was 30 and about 34% of them were smokers. The mean Vitamin D level was 8.4 ng/ml and all HS patients were vitamin D deficient. Patients of HS were more likely to have vitamin D deficiency compared to healthy controls. Most of the study subjects and particularly all of the patients with HS have low vitamin D levels. Smoking and high BMI, were associated with HS. We suggest the implementation standard public dietary recommendations of Vitamin D supplementation, smoking cessation, and weight reduction behaviors with further assessment of disease course among HS patients.
The paper highlights modern views on the metabolism of vitamin D in the human body. The analysis of the literature data on the mechanisms of the effect of vitamin D deficiency on the pathological processes occurring in the skin with psoriasis is carried out. It is known that psoriasis is associated with a high prevalence of metabolic syndrome, diabetes mellitus, and cardiovascular diseases. There is a direct correlation between a decrease in vitamin D levels and an increased risk of developing metabolic syndrome and cardiovascular mortality, including in patients with psoriasis. Data on the possibility of using vitamin D in dermatology are presented. Based on international and Russian clinical recommendations, the place of oral colecalciferol preparations in the prevention and correction of vitamin D deficiency and deficiency has been determined. The use of oral vitamin D for the simultaneous treatment of psoriasis and metabolic syndrome reduces the risk of cardiovascular diseases and type 2 diabetes mellitus. We analysed the international and domestic recommendations for the treatment of vitamin D deficiency and insufficiency, the use of which makes the oral administration of vitamin D3 (cholecalciferol) optimal for the treatment and prevention of vitamin D deficiency, as the results of several studies showed a higher efficacy of vitamin D3 vs vitamin D2. Vitamin D3 is found in vitamin D-fortified foods and is available as dietary supplements and drugs. The bioavailability of vitamin D in dietary supplements may differ depending on the used vehicle substance.
The epidermis maintains a cellular calcium gradient, that supports keratinocyte differentiation from its basal layers (low) to outer layers (high) leading to the development of the stratum corneum, which resists penetration of UV radiation. The calcium‐sensing receptor (CaSR) expressed in keratinocytes responds to the calcium gradient with signals that promote differentiation. In this study we investigated whether the CaSR is involved more directly in protection from UV damage in studies of human keratinocytes in primary culture and in mouse skin studied in vivo. siRNA‐directed reductions in CaSR protein levels in human keratinocytes significantly reduced UV‐induced direct cyclobutane pyrimidine dimers (CPD) by around 80% and oxidative DNA damage (8‐OHdG) by around 65% compared to control transfected cells. Similarly, in untransfected cells, the CaSR negative modulator, NPS‐2143 (500 nM), reduced UV‐induced CPD and 8‐OHdG by around 70%. NPS‐2143 also enhanced DNA repair and reduced reactive oxygen species (ROS) by around 35% in UV‐exposed keratinocytes, consistent with reduced DNA damage after UV exposure. Topical application of NPS‐2143 also protected hairless Skh:hr1 mice from UV‐induced CPD, oxidative DNA damage and inflammation, similar to the reductions observed in response to the well‐known photoprotection agent 1,25(OH)2D3 (calcitriol). Thus, negative modulators of the CaSR offer a new approach to reducing UV‐induced skin damage.
Background and objective
Cholecalciferol (vitamin D3) plays a physiological role in melanogenesis in human skin. Vitamin D3 deficiency has become a common complication encountered in daily clinical practice. Recently, there has been growing interest in the role of vitamin D3 in the pathogenesis of vitiligo and its relevance in the treatment of the same. We have also noticed an increase in the rate of vitiligo with an associated aggressive extension of the lesions. In light of this, we conducted this study to analyze the incidence of vitamin D deficiency in patients with vitiligo and explore the effect of this deficiency on disease extension and severity.
Materials and methods
This was a cross-sectional study involving 46 patients with vitiligo. The affected body surface area of the patients was assessed using the Vitiligo Extent Tensity Index (VETI) score.
Results
Most of the vitiligo patients had very low levels of vitamin D (p<0.05), and a majority of the vitiligo patients with low vitamin D levels were females; however, this difference between females and males was not statistically significant (p=0.642). There was no significant effect of vitamin D levels on VETI scores (p=0.184).
Conclusion
Based on our findings, patients with vitiligo have a high incidence of vitamin D deficiency, and this deficiency is more common among females than males.
Alopecia areata is a type of non-scarring hair loss. The dysregulation of numerous systemic Th1 (IL-2, IFN-γ, TNF, IL-12, and IL-18), Th2 (IL-4, IL-5, IL-6, IL-9, IL-10, IL-13, IL-17E, IL-31 and IL-33) and Th17 (IL-17, IL-17F, IL-21, IL-22, IL-23 and TGF-β) cytokines was observed in patients with alopecia areata. Positive correlations between the severity of alopecia areata and an increased serum level of various cytokines including IL-2, TNF, IL-12, IL-17, and IL-17E were reported in the literature. An increased serum level of numerous cytokines, such as IL-2, IL-6, TNF, IL-12, IL-17E, and IL-22, was described as positively correlated with the duration of the disease. Moreover, it was shown that increased pre-treatment serum level of IL-12 was a positive, while increased serum levels of IL-4 and IL-13 were negative prognostic markers for the efficacy of diphenylcyclopropenone. In conclusion, alopecia areata is associated with the dysregulation of systemic Th1, Th2 and Th17 cytokines with their role in the pathogenesis, clinical manifestations and prognosis of the disease. Available data indicate the most significant role of serum IL-2, TNF, IL-12, IL-17, and IL-17E as markers of disease activity. The serum levels IL-4, IL-12 and IL-13 may be useful as potential predictors of diphenylcyclopropenone efficacy.
Vitamin D status varies across all continents and countries. Vitamin D status usually is adequate in Latin America and Australia, but in contrast very low in the Middle East and some countries in Asia. Trends in vitamin D status, whether it improves or declines over the years, carry important messages. Trends usually are small, but can be predictors and indicators of general health. Vitamin D status has improved in the older population in the USA, and improvement relates to dairy use and vitamin D supplements. To the contrary, vitamin D status has declined in the Inuit population of Canada due to change from a traditional fish diet to a western diet. A large improvement was seen in Finland after mandatory fortification of dairy products was introduced. Determinants of decline are less sun exposure, increased use of sunscreen, increase of BMI, less physical activity and poor socioeconomic status. Determinants of increase are food fortification with vitamin D and vitamin D supplements. Food fortification can lead to a population‐wide increase in vitamin D status as shown by the Finnish example. This article is protected by copyright. All rights reserved.
Abstract Background Wound management is a critical factor when treating patients with the inherited skin fragility disease dystrophic epidermolysis bullosa (DEB). Due to genetic defects in structural proteins, skin and mucous epithelia are prone to blistering and chronic wounding upon minor trauma. Furthermore, these wounds are commonly associated with excessive pruritus and predispose to the development of life-threatening squamous cell carcinomas, underscoring the unmet need for new therapeutic options to improve wound healing in this patient cohort. Vitamin D3 is acknowledged to play an important role in wound healing by modulating different cellular processes that impact epidermal homeostasis and immune responses. In this study, we evaluate the safety and efficacy of low-dose calcipotriol, a vitamin D3 analogue, in promoting wound healing and reducing itch and pain in patients with DEB. Methods Eligible DEB patients, aged ≥ 6 years and with a known mutation in the COL7A1 gene, were recruited to a placebo-controlled, randomized, double blind, cross-over phase II monocentric clinical trial. Patients were required to have at least two wounds with a minimum size of 6 cm2 per wound. The primary objective was to evaluate efficacy of daily topical application of a 0.05 µg/g calcipotriol ointment in reducing wound size within a 4-week treatment regimen. Secondary objectives were to assess safety, as well as the impact of treatment on pruritus, pain, and bacterial wound colonization in these patients. Results Six patients completed the clinical trial and were included into the final analysis. Topical low-dose calcipotriol treatment led to a significant reduction in wound area at day 14 compared to placebo (88.4% vs. 65.5%, P
Objectives
Genetic association studies on alopecia areata (AA) performed in various populations have shown heterogeneous results. The aim of the current review was to synthesize the results of said studies to estimate the impact of FAS, FASL, PTPN22, CTLA4 and IL2RA gene polymorphisms on AA susceptibility.
Design
A systematic literature search was conducted in the Medline, Web of Science, Scopus, EMBASE and LILACS databases. Studies published up to June 2020 were included. The results available in the grey literature including the Open Grey and Google Scholar databases were also used. The texts of potentially related studies were screened by individual reviewers. Evidence of publication bias was assessed using the Newcastle-Ottawa scale and the quality of evidence was assessed using the GRADE system. The quantitative synthesis was performed using the fixed effect model.
Results
Out of 1784 articles, we identified 18 relevant articles for the qualitative synthesis and 16 for the quantitative synthesis. In a study of rs2476601 polymorphism of PTPN22 gene, including 1292 cases and 1832 controls, a correlation was found with the risk of developing AA in the allelic model (OR1.49 [95% C:1.13–1.95]), the heterozygous codominant (OR1.44 [95% CI:1:19–1.76]) and dominant model (OR1.43 [95% CI:1.18–1.73]). No association was found between the presence of FASL, PTPN22, CTLA and IL2RA gene polymorphisms with AA susceptibility.
Conclusions
The results suggest that the T allele of the single nucleoid polymorphism (SNP) rs2476601 in PTPN22 gene is a risk factor for developing alopecia areata. However, more robust studies defining the ethnic background of the population of origin are required, so that the risk identified in the present study can be validated. Additionally, a greater number of studies is necessary to evaluate the role of the FAS, FASL, PTPN22, CTLA4 and IL2RA genetic variants, given the heterogenous results found in the literature.
The active metabolites of vitamin D3 (D3) and lumisterol (L3) exert a variety of antiaging and photoprotective effects on the skin. These are achieved through immunomodulation and include anti-inflammatory actions, regulation of keratinocytes proliferation, and differentiation programs to build the epidermal barrier necessary for maintaining skin homeostasis. In addition, they induce antioxidative responses, inhibit DNA damage and induce DNA repair mechanisms to attenuate premature skin aging and cancerogenesis. The mechanism of action would involve interaction with multiple nuclear receptors including VDR, AhR, LXR, reverse agonism on RORα and -γ, and nongenomic actions through 1,25D3-MARRS receptor and interaction with the nongenomic binding site of the VDR. Therefore, active forms of vitamin D3 including its canonical (1,25(OH)2D3) and noncanonical (CYP11A1-intitated) D3 derivatives as well as L3 derivatives are promising agents for the prevention, attenuation, or treatment of premature skin aging. They could be administrated orally and/or topically. Other forms of parenteral application of vitamin D3 precursor should be considered to avoid its predominant metabolism to 25(OH)D3 that is not recognized by CYP11A1 enzyme. The efficacy of topically applied vitamin D3 and L3 derivatives needs further clinical evaluation in future trials.
Purpose
Vitiligo is a disease of acquired depigmentation characterized by the destruction of melanocytes. A theoretical association between low level of 25‐hydroxyvitamin D [25(OH)D] and vitiligo has been previously suggested. The objective of this study was to determine the efficacy of intramuscular injection of cholecalciferol with excimer laser compared with the excimer laser alone for vitiligo treatment.
Methods
This study included 26 patients diagnosed with non‐segmental vitiligo and low serum 25(OH)D levels (<20 ng/mL). The participants were randomly divided into two groups through randomization. The treatment using a 308‐nm excimer laser was administered to both groups, and the study group additionally received cholecalciferol injection.
Results
The Vitiligo Area Scoring Index (VASI) scores showed an 83.6% improvement over the initial score in the study group, whereas the control group showed a 54.7% improvement after 6 months of treatment. After 6 months of treatment, the study group showed a significantly higher proportion of patients who achieved VASI50 and VASI75 compared with the control group.
Conclusion
Intramuscular injection of cholecalciferol can be a supplemental option for the treatment of vitiligo patients with vitamin D deficiency with excimer laser therapy.
Objective: The objective was to compare the safety and efficacy of noncorticosteroid topical treatments for plaque psoriasis. Data Sources: A literature search of the PubMed database was performed (January 1978 to May 2023) using the keywords plaque psoriasis, tapinarof, benvitimod, Vtama, roflumilast, Zoryve, pimecrolimus, tacrolimus, tazarotene, tacalcitol, calcitriol, Vectical, calcipotriene, Dovonex, tacalcitol, vitamin D analogs, salicylic acid, non-corticosteroid topical, Investigator’s Global Assessment, and Physician’s Global Assessment. Study Selection and Data Extraction: Relevant English-language articles and clinical trial data were considered. Data Synthesis: Six noncorticosteroid topical classes for the treatment of plaque psoriasis were selected. The percentage of patients with plaque psoriasis who achieved Investigator’s Global Assessment (IGA) success after 8 weeks of treatment with tacalcitol, calcipotriene/betamethasone dipropionate compound, tazarotene/halobetasol propionate, and roflumilast was 17.9%, 39.9%, 40.7%, and 42.4%, respectively. For 12-week trials of tapinarof and coal tar, 37.4% and 58.2% of patients achieved IGA success, respectively. There were 48% and 71.4% reductions in IGA scores with salicylic acid (12 weeks) and pimecrolimus (4 weeks), respectively. Finally, 66.7% of patients achieved Physician’s Global Assessment success with 8 weeks of tacrolimus. There were no serious adverse events for the noncorticosteroid topicals. Conclusion: Noncorticosteroid topicals are suitable options for patients with plaque psoriasis who would like to avoid topical corticosteroids or have experienced adverse effects from chronic corticosteroid use. Due to treatment duration differences and varied outcome measures, it is unclear which noncorticosteroid topical is most efficacious; however, calcineurin inhibitors appear to exhibit the greatest efficacy. Each topical was efficacious in treating plaque psoriasis and had an adequate safety profile. Despite several treatment options for plaque psoriasis, medication adherence is a limiting factor.
Atopic Dermatitis (AD) is a chronically relapsing, highly pruritic, allergic inflammatory skin disease with significant cost and morbidity to the patients and their families. The underlying cause of AD has not been understood, however some studies have shown initial epidermal barrier defect with subsequent immune activation as the underlying mechanism of AD. Vitamin D is now recognized as an immunomodulator. The role played by vitamin D in atopic dermatitis is controversial and has been the focus of many studies. The aim of the study was to measure serum vitamin D in the form of 25-hydroxy vitamin D in patients with AD and to correlate them with disease severity. This cross-sectional study included 41 patients (25 males and 16 females) of any age with the clinical diagnosis of AD seen in Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka, Bangladesh from September 2015 to February 2017. Disease severity was determined using Scoring Atopic Dermatitis (SCORAD) index and the patients were divided into three groups: mild (SCORAD index <25), moderate (25-50) and severe (>50). Serum vitamin D levels were classified as sufficient (≥30ng/mL), insufficient (21-29ng/mL) and deficient (≤20ng/mL). Statistical analysis was performed using analysis of variance (ANOVA) and Pearson's correlation coefficient test. P value of <0.05 was considered as statistically significant. Among 41 patients 33 represent infantile and childhood AD and only 8 represent adolescent and adult AD. According to SCORAD index, 12 patients had mild, 20 had moderate and 9 had severe Atopic dermatitis. Levels of 25-hydroxyvitamin D were deficient or insufficient in 75.6% of patients and normal in 24.4% patients. There was no significant association between serum level of vitamin D and the severity of AD (r=-0.173). The mean±SD serum vitamin D level in mild AD (25.7±8.1) was higher compared with those with moderate (23.9±8.8) or severe (19.5±8.3) AD. But the result was not statistically significant (p=0.249). Variables such as sex, age, skin prototype, season and food allergy were not significantly associated with vitamin D levels. The results from this study suggesting that millions of children living in Bangladesh may have suboptimal levels of vitamin D, which should be a matter of public health concern. But these deficient results are not significantly related to AD severity. Thus, the study provides epidemiological evidence against the association of vitamin D status with atopic dermatitis for the first time in Bangladesh.
Ultraviolet B (UVB) irradiation causes skin damages. In this study, we focus on the involvement of mitochondrial disorders in UVB injury. Surprisingly, UVB irradiation increases the amounts of mitochondria in human immortalized keratinocytes HaCaT. However, further analysis shows that ATP levels decreased by UVB treatment in accordance with the collapse of mitochondrial membrane potential (MMP), suggesting an accumulation of dysfunctional mitochondria in UVB-irradiated HaCaT cells. Mitophagy, mainly mediated by PINK1 and parkin, is critical for the elimination of damaged mitochondria. Western blot results show that the levels of both PINK1 and parkin are decreased in UVB-irradiated cells, indicating the impairment of mitophagy. Silencing the expression of PINK1 or parkin by transfection of siRNA shows essentially the same damage to the cells as UVB irradiation does, including increased mitochondrial amount, decreased MMP and ATP production, and enhanced apoptosis, evidencing that repression of PINK1/parkin-mediated mitophagy plays a primary cause of UVB-caused cells damages. We previously found that HaCaT cells exposed to UVB showed activation of the cGAS-STING pathway and apoptosis. Here, silencing PINK1 or parkin also increases the protein levels of cGAS and STING, facilitates nuclear accumulation of NF-κB, and promotes the transcription of IFNβ, suggesting for the activation of STING pathway. Mitophagy impairment either by UVB-irradiation or by PINK1/parkin silencing initiates caspase-3-mediated apoptosis, as shown by the activation of caspase-3 and cleavage of PARP, as well as the increase of Hoechst-positive stained cells and Annexin V-positive cells. Further studies find that Bax-mediated permeabilization of mitochondrial membrane is critical for cell apoptosis, as well as the cytosolic leakage of mtDNA in UVB-treated cells, which results in cGAS-STING activation, and these processes are negatively-regulated by PINK1/parkin-mediated mitophagy. This study reveals the involvement of dysfunctional mitochondria due to impaired mitophagy in the damaging effect of UVB irradiation on HaCaT cells. Restoring the mitophagy has the potential to be developed as a new strategy to protect skin from UVB damages.
Vitamin D supplementation with standard treatment yielded positive clinical outcomes in mild and moderate atopic dermatitis; however, the potential benefit of vitamin D in severe cases remains unclear. This study aimed to evaluate the impact of vitamin D supplementation on response to standard treatment in pediatrics with severe atopic dermatitis. The patients were randomized to receive either vitamin D 3 1600 IU/day or placebo, plus baseline therapy of topical 1% hydrocortisone cream twice daily for 12 weeks. The primary endpoints were the change in mean Eczema Area and Severity Index (EASI) score at the end of the study and the mean percent change in EASI score from baseline to week 12. Eighty-six subjects completed the study. The treated group achieved a significant higher level of 25 hydroxy vitamin D (P < .001) compared to control group at week 12. The mean EASI score was significantly lower in the treatment group compared to placebo group (P = .035). The percent change in EASI score from baseline differed significantly between the sup-plementation (56.44 ± 29.33) and placebo (42.09 ± 19.22) groups after intervention (P = .039). Vitamin D supplementation could be an effective adjuvant treatment that improves the clinical outcomes in severe atopic dermatitis. K E Y W O R D S atopic dermatitis, Eczema, severe, vitamin D
For full use of Skipjack tuna (Katsuwonus pelamis) canning by-products, gelatins (STG) were extracted from tuna skins using acid (STG-A), enzyme (STG-E) and hot water (STG-H) methods with yields of 65.30 ± 1.56%, 39.83 ± 1.61%, and 50.97 ± 1.44%, respectively. Due to the high imino acid contents (228, 216, and 213 residues/1000 residues for STG-A, STG-E, and STG-H, respectively), STG-A showed the highest transparency and gel strength properties. Amino acid analysis, sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), ultraviolet (UV) and Fourier transform infrared spectroscopy (FTIR) analysis confirmed that STG-A, STG-E, and STG-H kept the main structure of type I collagen, but enzyme and hot water extraction methods showed much stronger hydrolysis ability on α and β chains. Moreover, neutrase hydrolysate (STG-AH) of STG-A showed the highest 1,1-diphenyl-2-picrylhydrazyl radical (DPPH•) scavenging activity and the fraction STG-AH-І (<3.5 kDa) from STG-AH prepared by ultrafiltration could significantly protect human skin fibroblasts (HSFBs) against ultraviolet-A (UVA) injury. Furthermore, nineteen peptides with high antioxidant activity were purified from STG-AH-І and identified. These results suggested that STG-AH and its derived antioxidant peptides could serve as potential ingredients applied in health benefiting products for preventing UVA injury.
Introduction: Vitiligo is a specific, common, often heritable acquired disorder characterized by well-circumscribed milky white cutaneous macules and patches devoid of identifiable melanocyte. Treatment of vitiligo, though quite frustrating, includes repigmentation therapies like Topical glucocorticoids, Topical calcipotrieinene, Topical PUVA (Psoralen + Ultraviolet Light A). The combination of calcipotriol and PUVA proves quite effective for management of this condition. Objectives: To compare the effectiveness of PUVA and the combination of topical calcipotriol and PUVA in treatment of vitiligo. Materials and Methods: This quasi experimental study was undertaken at Combined Military Hospital, Dhaka Cantonment, Dhaka from March to October 2015. A total of 32 patients suffering from vitiligo diagnosed clinically and confirmed by Wood’s lamp examination were selected as study population. Systemic PUVA, thrice weekly was given but Topical calcipotriol applied twice daily at one side of the body and other side used nothing Topically. Response was assessed clinically every 4 weeks along with photographic record and compared between two sides of the body. Results: During the course of the treatment, the calcipotriol plus PUVA treated side showed considerably better improvement than only PUVA treated side. The response was Excellent; 37.8% (12/32), Good; 31.3% (10/32), Fair; 18.8% (6/32), Poor; 12.5% (4/32) in calcipotriol plus PUVA treated side whereas Excellent; 12.5% (4/32), Good; 25% (8/32), Fair; 43.8% (14/32) and Poor; 18.8% (6/32) in only PUVA treated side. Conclusion: This study shown that concurrent topical calcipotriol potentiates the efficacy of PUVA in the treatment of vitiligo along with the fact that this combination achieves earlier pigmentation with a lower total UVA dosage in comparison to only PUVA therapy. JAFMC Bangladesh. Vol 18, No 1 (June) 2022: 23-25
Objectives
This systematic review was to assess the effects of phototherapies (psoralen plus ultraviolet A [PUVA], narrowband ultraviolet B [NBUVB], or 308 nm excimer laser [EL]) in combination with vitamin D analogs compared with phototherapy alone on vitiligo.
Methods
Four databases were searched up to 18 October 2021 for relevant studies. The primary outcome was the proportion of response to treatment (≥50% repigmentation) after treatment. Secondary outcomes included excellent response, treatment failure, and safety. The risk ratio (RR) was used as the estimate measure in meta-analyses.
Results
Fourteen studies (n = 642) were included. The meta-analyses showed that the combination of either calcipotriol or tacalcitol and NBUVB was superior to NBUVB monotherapy for vitiligo in the proportion of response to treatment (RR 1.67, 95% CI 1.21–2.31), treatment failure (RR 0.43, 95% CI 0.22–0.85), and excellent response (RR 7.48, 95% CI 1.09–51.13). The tacalcitol was more effective than calcipotriol in increasing the rate of response to treatment when combined with NBUVB (RR 2.25 versus 1.24, interaction p = 0.002). The results did not support better efficacy with the combination of PUVA or EL with vitamin D analogs over phototherapy alone in all outcomes. Adverse events were minor and transient.
Conclusions
The current evidence suggests that the additional use of topical calcipotriol or tacalcitol to NB-UVB may increase the treatment effect of vitiligo, and the effect of tacalcitol is greater than that of calcipotriol. None of the vitamin D analogs were found to enhance the efficacy of PUVA or EL for vitiligo.
Background:
Paediatric patients with Recessive Dystrophic Epidermolysis Bullosa (RDEB) are at risk of vitamin D deficiency due to large areas of skin being covered with dressings, reduced mobility and impaired nutritional intake.
Methods:
Patients attending the EB tertiary MDT clinic and diagnosed with RDEB were included. Serum levels of total 25 (OH) D were retrospectively recorded between 2012-2018. Data from clinical records on supplements, Bone Mineral Density (BMD) Z scores, compliance, enteral feeds and/or formula was also recorded.
Results:
24 patients met the inclusion criteria: 20 RDEB severe, 3 RDEB inversa and 1 had RDEB intermediate. 21/24 (88%) of patients were advised to take a vitamin D3 supplement, with the remaining three receiving sufficient intake from formula/enteral feeds. 13/24 (54%) showed vitamin D deficiency or insufficiency. Nine of these thirteen (69%) successfully took vitamin D supplements and levels became sufficient (>50nmol/L). The remaining four patients (31%) had persistent insufficient levels due to non-compliance with supplements. Reasons for non-compliance were palatability, forgetting or cost. The dose required to maintain sufficient serum levels increased with age, up to 300% of the RNI.
Conclusion:
All patients with RDEB require a supplement or formula/sip feed containing vitamin D to maintain sufficient serum vitamin D. The dose required increases with age and can be three times higher than the recommended nutrient intakes (RNI) for the normal population. Compliance may improve using a once-weekly loading dose of vitamin D3. Vitamin D deficiency was not solely causative of a low BMD Z score.
Background:
Alopecia areata (AA) is a common non-scarring, inflammatory type of hair loss that affects people of all ages and genders.
Aims:
To evaluate the safety and efficacy of Intralesional vitamin D3 injection in the treatment of alopecia areata.
Patients and methods:
A randomized- control clinical trial included a total of 60 adult patients with localized alopecia areata were randomly assigned into two groups . Group I consisted of thirty patients who received 1ml of intralesional injection of vitamin D3 every 4 weeks for a maximum of 3 sessions. Group II consisted of thirty patients who received intralesional injection of normal saline 0.9% every 4 weeks for 3 sessions as a control group. All patients had their serum levels of 25-hydroxy vitamin D, TSH, antithyroglobulin, and thyroid peroxidase antibodies estimated before starting treatment. The 5-point semiquantitative regrowth score (RGS) and dermoscopy were used to evaluate the therapeutic response.
Results:
There was statistically significant difference with p-value < 0.001 between two study groups regarding to degree of improvement. Dermoscopic findings that explain signs of activity were decreased, and signs of improvement were appeared after the 3rd months of treatment being better in intralesional vitamin D group.The adverse effects were negligible and transient, and there were no recurrence of lesions.
Conclusion:
Intralesional vitamin D3 is an effective treatment option for localized patchy (not more than 40% of scalp distribution) alopecia areata .There is no relation between serum vitamin D3 and efficacy of treatment, so measuring vitamin D3 before starting treatment is not advised.
The endophytes of medicinal plants play an important role in promoting the quality formation of the host. Therefore, this paper made a review of endophytes of medicinal plant Atractylodes lancea. According to previous studies, A. lancea boasts endophytes, such as fungi, bacteria, and actinomycetes, among which the beneficial microorganisms help the growth and development of A. lancea. There is a close interaction between the volatile oil of A. lancea and endophytes. Different endophytes vary in regulating the composition and content of the volatile oil of A. lancea, which might contribute to the quality formation of A. lancea. However, the information of the endophytic flora of A. lancea obtained by traditional culture and isolation is not enough to reflect the real situation of the endophytes of A. lancea. Little is known about the endophytes of A. lancea from different chemical types and different habitats, which is not conducive to the study of the ecological relationship between A. lancea and endophytes and limits the development and utilization of the endophytes. Therefore, at the end of this paper, the authors put forward suggestions for future research on endophytes in A. lancea, including:(1)mining the core endophyte resources of A. lancea by combining high-throughput sequencing with traditional culture and isolation;(2)exploring the relationship between the diversity of endophytes and chemical types of A. lancea;(3)strengthening the application of endophytes in A. lancea cultivation, in order to facilitate the cultivation efficiency and quality of A. lancea.
Alopecia areata (AA) is a relatively common nonscarring hairloss disease characterized by an autoimmune response to anagen hair follicles (HFs). Accumulated evidence suggests that collapse of the HF immune privilege subsequent to triggering events, represented by viral infection, leads to autoimmune response in which autoreactive cytotoxic CD8+NKG2D+ T cells mainly target exposed HF autoantigens. AA had been recognized as type 1 inflammatory disease, but recent investigations have suggested some roles of type 2- and Th17-associated mediators in AA pathogenesis. The significance of psychological stress in AA pathogenesis is less emphasized nowadays, but psychological comorbidities, such as depression and anxiety, attract greater interest in AA management. In this regard, the disease severity may not solely be evaluated by the extent of hair loss. Use of trichoscopy markedly improved the resolution of the diagnosis and evaluation of the phase of AA, which is indispensable for the optimization of treatment. For the standardization of AA management, the establishment of guidelines/expert consensus is pivotal. Indeed, the Japanese Dermatological Association (JDA) and other societies and expert groups have published guidelines/expert consensus reports, which mostly recommend intralesional/topical corticosteroid administration and contact immunotherapy as first-line treatments, depending on the age, disease severity, and activity of AA. The uniqueness of the JDA guidelines can be found in their descriptions of intravenous corticosteroid pulse therapy, antihistamines, and other miscellaneous domestically conducted treatments. Considering the relatively high incidence of spontaneous regression in mild AA and its intractability in severe subsets, the importance of course observation is also noted. Evidenced-based medicine for AA is currently limited, however, novel therapeutic approaches, represented by JAK inhibitors, are on their way for clinical application. In this review, the latest understanding of the etiopathogenesis and pathophysiology, and update on therapeutic approaches with future perspectives are summarized for AA, following the current version of the JDA AA management guidelines.