A randomized controlled double‐blind investigation of the effects of vitamin D dietary supplementation in subjects with atopic dermatitis

Subjects with atopic dermatitis (AD) have defects in antimicrobial peptide (AMP) production possibly contributing to an increased risk of infections. In laboratory models, vitamin D can alter innate immunity by increasing AMP production.

[1]  L. Deftos,et al.  PTH/PTHrP and Vitamin D Control Antimicrobial Peptide Expression and Susceptibility to Bacterial Skin Infection , 2012, Science Translational Medicine.

[2]  B. Salehi,et al.  Vitamin D supplementation in the treatment of atopic dermatitis: a clinical trial study. , 2012, Journal of drugs in dermatology : JDD.

[3]  M. Djalali,et al.  Randomized controlled trial using vitamins E and D supplementation in atopic dermatitis , 2011, The Journal of dermatological treatment.

[4]  A. Boner,et al.  Correlation between serum 25‐hydroxyvitamin D levels and severity of atopic dermatitis in children , 2011, The British journal of dermatology.

[5]  JoAnn E. Manson,et al.  The 2011 Report on Dietary Reference Intakes for Calcium and Vitamin D from the Institute of Medicine: What Clinicians Need to Know , 2010, The Journal of clinical endocrinology and metabolism.

[6]  J. Griggs,et al.  Casting light on 25-hydroxyvitamin D deficiency in ovarian cancer: a study from the NHANES. , 2010, Gynecologic oncology.

[7]  A. Pontecorvi,et al.  25‐Hydroxyvitamin D Concentration Correlates With Insulin‐Sensitivity and BMI in Obesity , 2010, Obesity.

[8]  T. Reunala,et al.  Narrowband ultraviolet B treatment improves vitamin D balance and alters antimicrobial peptide expression in skin lesions of psoriasis and atopic dermatitis , 2010, The British journal of dermatology.

[9]  James R Murphy,et al.  Decreased serum vitamin D levels in children with asthma are associated with increased corticosteroid use. , 2010, The Journal of allergy and clinical immunology.

[10]  T. Ruzicka,et al.  Control of cutaneous antimicrobial peptides by vitamin D3 , 2010, Archives of Dermatological Research.

[11]  J. Eisman,et al.  Adequacy of vitamin D replacement in severe deficiency is dependent on body mass index. , 2009, The American journal of medicine.

[12]  P. Elias,et al.  Vitamin D receptor and coactivators SRC2 and 3 regulate epidermis-specific sphingolipid production and permeability barrier formation. , 2009, The Journal of investigative dermatology.

[13]  J. Strain,et al.  Estimation of the dietary requirement for vitamin D in healthy adults. , 2008, The American journal of clinical nutrition.

[14]  P. Elias,et al.  Biopositive effects of low-dose UVB on epidermis: coordinate upregulation of antimicrobial peptides and permeability barrier reinforcement. , 2008, The Journal of investigative dermatology.

[15]  R. Gallo,et al.  Administration of oral vitamin D induces cathelicidin production in atopic individuals. , 2008, The Journal of allergy and clinical immunology.

[16]  J. Redzic,et al.  Th2 cytokines act on S100/A11 to downregulate keratinocyte differentiation. , 2008, The Journal of investigative dermatology.

[17]  R. Heaney Vitamin D in health and disease. , 2008, Clinical journal of the American Society of Nephrology : CJASN.

[18]  C. Camargo,et al.  Randomized controlled trial of vitamin D supplementation for winter‐related atopic dermatitis in Boston: a pilot study , 2008, The British journal of dermatology.

[19]  R. Gallo,et al.  Antimicrobial peptides, skin infections, and atopic dermatitis. , 2008, Seminars in cutaneous medicine and surgery.

[20]  J. Adams,et al.  Vitamin D and Innate Immunity , 2009 .

[21]  C. Albanesi,et al.  IL-4 and IL-13 Negatively Regulate TNF-α- and IFN-γ-Induced β-Defensin Expression through STAT-6, Suppressor of Cytokine Signaling (SOCS)-1, and SOCS-31 , 2007, The Journal of Immunology.

[22]  N. Hawker,et al.  Regulation of human epidermal keratinocyte differentiation by the vitamin D receptor and its coactivators DRIP205, SRC2, and SRC3. , 2007, The Journal of investigative dermatology.

[23]  Y. Helfrich,et al.  Injury enhances TLR2 function and antimicrobial peptide expression through a vitamin D-dependent mechanism. , 2007, The Journal of clinical investigation.

[24]  C. Albanesi,et al.  IL-4 and IL-13 negatively regulate TNF-alpha- and IFN-gamma-induced beta-defensin expression through STAT-6, suppressor of cytokine signaling (SOCS)-1, and SOCS-3. , 2007, Journal of immunology.

[25]  J. Adams,et al.  Toll-Like Receptor Triggering of a Vitamin D-Mediated Human Antimicrobial Response , 2006, Science.

[26]  John H. White,et al.  Cutting Edge: 1,25-Dihydroxyvitamin D3 Is a Direct Inducer of Antimicrobial Peptide Gene Expression , 2004, The Journal of Immunology.

[27]  John H. White,et al.  Cutting Edge: 1,25-Dihydroxyvitamin D3 Is a Direct Inducer of Antimicrobial Peptide Gene Expression1 , 2004, The Journal of Immunology.

[28]  J. Travers,et al.  Cytokine Milieu of Atopic Dermatitis, as Compared to Psoriasis, Skin Prevents Induction of Innate Immune Response Genes 1 , 2003, The Journal of Immunology.

[29]  Tomas Ganz,et al.  Endogenous antimicrobial peptides and skin infections in atopic dermatitis. , 2002, The New England journal of medicine.

[30]  T. Oppé,et al.  Vitamin D deficiency. , 1979, British medical journal.