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Vitiligo : What's new in 2012 - Howard Fox Memorial Lecture, New York Academy of Dermatology, Prof. Torello Lotti March 13, 2012

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NYAM Section on Dermatology Presents the 2012 Howard Fox, MD Memorial Lecture …

NYAM Section on Dermatology Presents the 2012 Howard Fox, MD Memorial Lecture
Date: March 13, 2012 to March 13, 2012
Time: 6:00 PM - 8:00 PM p.m., Lecture 7:00 p.m. – 8:00 p.m.
Speaker(s): Torello Lotti, MD, Professor of the Dermatology and Venereology Division at Guglielmo Marconi University, Rome, Italy - Honorary Professor of Dermatology - China Medical University Shenyang, 18 Dec.2011
Chair, Executive Scientific Committee Vitiligo Research Foundation, New York , NY , USA.

Sponsored by: NYAM Section on Dermatology
Location: The New York Academy of Medicine, 1216 Fifth Avenue at 103rd Street, New York, NY 10029

"Vitiligo: What's New – Update in 2012"
Vitiligo is a chronic acquired hypomelanotic disorder affecting 0.5-2% of the world's population. Different forms of vitiligo have been described, according to the distribution and the extent of the achromic lesion. Several hypotheses have been proposed to explain the pathogenesis of vitiligo. The two major pathogenetic hypotheses are focused on immune-mediated or toxic-mediated cell damage primarily directed at melanocytes. New data demonstrated an important involvement of the keratinocytes and dendritic cells in the pathogenesis of vitiligo.
According to our progress in understanding Vitiligo pathogenesis, new and experimental therapies, such as narrow-band ultraviolet B microphototherapy (NB-UVB), narrow-band ultraviolet B excimer laser and monochromatic excimer light are available for the treatment of the disease. In addition, there are new topical treatments such as antioxidants, tacrolimus and pimecrolimus, prostaglandin E, and vitamin D derivatives. Excellent therapeutic results can be achieved through combination treatments.
About the Speaker(s)
Torello Lotti, MD, Prof. Lotti is Professor of the Dermatology and Venereology Division at Guglielmo Marconi University, Rome, Italy. Previously, he was Professor of the Dermatology and Venereology Division at University of Florence School of Medicine, Florence, Italy.
The fields of his principal scientific investigations are focused on the study of neuropeptides in numerous skin diseases, of plasminogen activators in autoimmune dermatoses and in lichen planus, and the clinical aspects and treatment of psoriasis vulgaris with particular emphasis on new therapies with biological agents. Of particular relevance is his research on the pathogenesis and innovative treatments for vitiligo.
Dr. Lotti is Visiting Professor and Director, International Centre for Balneology, Cell Biology, and Physiotherapy, Thomas Jefferson University, Philadelphia (PA, USA), Visiting Professor of Dermatology in six international universities, and Key Note Lecturer, Japanese Society of Cosmetic Dermatology. Past activities: Past-President of the Italian Society of Dermatology and Venereology, Past President of International Society of Dermatology.

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  • Genetica: locus di suscettibilità autoimmune sul cromosoma 1, insieme alla suscettibilità per dermatite atopica, alopecia areata e forse altre cose. Immunità:il meccanismo principale è cellulo-mediato. Dopo si smascherano autoantigeni cutanei che montano una risposta anticorpale che rimane in secondo piano, a fare da spettatore innocente (innocent bystander-baistender). Metabolica: squilibrio fra i meccanismi di ossidazione e antiossidazione, con conseguente aumento dei radicali liberi e danno ossidativo sui melanociti. L’ipotesi virale è ormai da scartare.
  • .
  • I
  • I
  • Elenco dei gruppi analizzati e modalità di studio
  • A seconda dei vari ntipi di trattamento, la repigmentazione inzia prima o dopo. L’associazione che funziona prima è quella di bioskin + betametasone e bioskin + tacrolimus.
  • Tendenze di repigmentazione: gruppo di bioskin+betametasone raggiunge la massima repigmentazione (più del 90% dei pazienti raggiunge una pigmentazione >75% in 6 mesi di trattamento).
  • Transcript

    • 1. Vitiligo - what’s New: Update in 2012The 58th Annual Howard Fox, MD Memorial Lecture March 13, 2012 Torello Lotti Professor and Chair of Dermatology and Venereology at Guglielmo Marconi
    • 2. Hypomelanoses: Why ?1. Loss or reduction of melanocytes;2. Reduced melanine production from melanocytes (altered tyrosinase activity, altered structure/activity of rough endoplasmic reticulum, lack of specific melanocyte receptors…);3. Decreased melanine transfer from melanocytes to keratinocytes;4. Primary disorder of keratinocytes.
    • 3. Hypomelanoses Normal Albinism Functional defect in melanine synthesis VitiligoLocalized loss / inactivation of melanocytes
    • 4. Vitiligo: Definition Primitive acquired pigmentation disorder with focal depigmentation of the skin; Characterized by well circumscribed milky white cutaneous/mucous macules; Patches arise as a consequence of destruction and/or functional inactivation of melanocytes underlying a complex syndrome; Acquired (only in few cases congenital), often familial (23% of the cases).
    • 5. Vitiligo: Epidemiology Vitiligo affects 0.5-4% of the World population. The disease generally begins between the ages of 2 and 40. In a Dutch study, 50% of patients reported the occurrence before the age of 20.
    • 6. Vitiligo in 2012 Incidence ranges from 0,1% to 8,8%in different country of the globe. Thehighest incidence of the condition has been recorded in India, Mexico and Japan.
    • 7. Vitiligo: Epidemiology Adults and children of both sex are equally affected; No difference in races or skin type; The greater number of reports among females is probably due to greater social consequence to woman and girls affected by this condition; 50% of patients  before the age of 20; 25% of patients  before the age of 8.
    • 8. Vitiligo: ClinicalDiscrete, uniformly whitepatches with convex bordersand surrounded by normalskin, not painful and veryrarely itching.
    • 9. Vitiligo: Favorite Sitesface (periorificial),dorsal surface of the hands,nipples,axillae,umbilicus,sacrum,inguinal/anogenital regions,elbows,knees,digits,flexor wrists.
    • 10. Clinical Classification Localized  Focal: one or more macules in one area but not clearly in a segmental distribution;  Unilateral/segmental: one or more macules involving a unilateral segment of the body – lesions stop abruptely at the midline;  Mucosal: mucous membranes alone. Generalized  Vulgaris – scattered patches that are widely distributed;  Acrofacialis – distal extremities and face;  Mixed – acrofacialis and vulgaris; Universalis  Complete or nearly complete depigmentation.
    • 11. Vitiligo: Differential Diagnosis Alikhan A, Felsten LM, Daly M, Petronic-Rosic V. J Am Acad Dermatol. 2011;65(3):473-91.
    • 12. TUBEROUSIDIOPATHIC SCLEROSISGUTTATEHYPOMELANOSIS PIEBALDISM
    • 13. TINEA VERSICOLOR PINTALEPROSY
    • 14. HALO NEVUSNEVUS ANEMICUS MELANOMA ASSOCIATED MELANOMA LEUKODERMA WITH REGRESSION
    • 15. CHEMICAL INDUCED LEUKODERMA… Ghosh S.cIndian J Dermatol. 2010;55(3):255-8.
    • 16. Alikhan A, Felsten LM, Daly M, Petronic-Rosic V.J Am Acad Dermatol. 2011;65(3):473-91.
    • 17. Why?Loss of normal melanocytes Dopa stain
    • 18. ETIOPATHOGENESIS GENETIC PREDISPOSITION Autoimmune Susceptibility Locus (AIS1)NEURAL HYPOTHESIS AUTOIMMUNE HYPOTHESIS MELANOCYTE DESTRUCTIONAUTOCYTOTOXIC/RADICALIC HYPOTHESIS ECLECTIC HYPOTHESIS MELANOCYTORRAGY SYNERGISTIC THEORY
    • 19. Vitiligo: Etiopathogenesis GENETIC PREDISPOSITION  Autoimmune Susceptibility Locus (AIS1) AUTOIMMUNE  Umoral mechanism -Autoantibodies  Citotoxic mechanism – Cell mediated METABOLIC  Hydrogen peroxide accumulation  Abnormal expression of Tyrosine-Related Protein -1 OTHERS  Viral hypothesis  Neuronal toxicity
    • 20. Spritz RA. J Genet Genomics. 2011, 20;38(7):271-8
    • 21. Metabolic Pathogenesis Altered antioxidant Increased activity and scavenger of superoxide mechanism dismutase High levels of epidermic 7-BH4 and H2O2Inhibition of enzyme function (phenylalanine-hydroxilase and tyrosinase) and abnormal expression of Tyrosinase Related Protein-1 (TRP-1).  impaired melanine synthesis
    • 22. Convergence TheoryWesterhof, D’Ischia. Vitiligo puzzle: the pieces fall in place. Pigment Cell Res 2007 20; 345-359
    • 23. Vitiligo: what’s new in 2012Melanocytes are completely absent in the depigmented epidermis Nordlund JJ and Lerner AB – Arch Dermatol, 1982;118:5-8 Le Poole IC et Al. J Invest Dermatol, 1993;100:816-822 Vs.Melanocytes are not completely absent in the depigmented epidermis Bertosi KJ et Al. Eur J Dermatol 1998;8:95-97 Tobin DJ et Al. J Pathol 2000;191:407-416 Gottschalk GM, Kidson SH. Int J Dermatol. 2007;46(3):268-72
    • 24. Vitiligo: what’s new in 2012Melanocytes are not completely absentin the depigmented epidermis Normal Skin Perilesional Skin Lesional Skin Massi D. Histopathological and ultrastructural features of vitiligo. In: Lotti T & Hercogova J (Eds.) Vitiligo – Problems and solutions. Marcel Dekker Inc, New York 2004
    • 25. Vitiligo: what’s new in 2012Melanocytes are not completely absent in the depigmented epidermisComment: – A subpopulation of “resistant” epidermal melanocytes can persist independent of disease duration – Repigmentation can always occur independent of disease duration and with non-perifollicular pattern
    • 26. VITILIGO:NOT ONLY A MELANOCYTIC DISEASE?
    • 27. Imokawa G. Autocrine and paracrine regulation of melanocytes in human skin and inpigmentary disorders. Pigment Cell Res 2004
    • 28. What’s new in 2012: A focus on keratinocytes Impaired scavenging mechanisms can lead to ROS increase and subsequent melanocyte and keratinocyte damaging; Altered function of PAR-2 receptor can impair calcium homeostasis in keratinocytes and alter melanosome intake and processing.
    • 29. What’s new in 2012: the focus on keratinocytes The importance in mitochondria in keratinocytes from perilesional skin and the role of oxidative stress.Prignano F, et al. Ultrastructural and functional alterations of mitochondria in perilesional vitiligo skin. J Derm Sci 2009;54:157–167
    • 30. Mitochondrial alterations in perilesional keratinocytes Mitochondrial activity plays a crucial role in normal cell function Mitochondrial alterations observed in perilesional keratinocytes appear to be very similar to those described in the same cell types during apoptosis The mitochondrial damage is associated with an increase in ROS production and, hence, oxidative stress. Prignano F, et al. J Derm Sci 2009;54:157–167
    • 31. Functional alterations in vitiligo skin High levels of TNF-alpha and FasL in the depigmented epidermis (role in increasing apoptosis) – Kim NH, et al. J Invest Dermatol 2007;127:2612–7. mRNA for TNF-α and IL-6, with an inhibitory effect on pigmentation, was increased in the epidermis from vitiligo biopsies. This could contribute to keratinocyte apoptosis, which results in reduced release of melanogenic cytokines and in melanocyte disappearance. – Moretti S, et al. Histol Histopathol 2009:24:849-857
    • 32. Functional alterations in vitiligo skin Apoptotic keratinocytes may cause a decrease in SCF synthesis, which plays an important role in melanocyte survival and proliferation Keratinocyte apoptosis induces a decrease in the synthesis of other melanocyte growth factors, such as bFGF, resulting in melanocyte disappearance. – Lee AY, et al. Br J Dermatol 2004;151:995–1003. – Moretti S, et al. Histol Histopathol 2009:24:849-857
    • 33. Functional alterations in vitiligo skin Endothelin-1 (ET-1) mRNA seems to be significantly reduced in lesional as compared to perilesional epidermis SCF and ET-1 may contribute to melanocyte survival – Moretti S, et al. Histol Histopathol 2009:24:849-857
    • 34. Functional alterations in vitiligo skin Protease-activated receptor (PARs) 2 is abundantly expressed by keratinocytes, and seems to contribute to the pigmentation process PAR-2 impairment is seen in vitiligo, and may contribute to the epidermal pigment deficit through a reduced melanosome uptake in keratinocytes. To date, a precise cause and effect relationship between these two conditions cannot be determined. – Moretti S, et al. Pigment Cell Melanoma Res 2009;22:335–338
    • 35. Vitiligo in 2012: the importance of an evidence- based approach1. Is vitiligo an unmanageable disease?2. Is systemic evaluation useful?3. Is it everything about psychology?4. Should I suggest to buy a UV lamp?
    • 36. Is Vitiligo an unmanageable disease? Only 16% of dermatologists in The Netherlands are in favour of active treatment of vitiligo – Njoo MD et Al, Int J Dermatol 1999;38:866-872 84% of dermatologists in The Netherlands are reluctant to start any active treatment in vitiligo; 82% in the Mediterranean area either prescribe placebos or treatments of cosmetic relevance only – Lotti T. La vitiligine: nuovi concetti e nuove terapie. UTET – Torino, 2000
    • 37. Is systemic evaluation useful?  Vitiligo and tyroid disfunction: 8.7% to 38.5%  Polyglandular syndrome (type I and II): 2.8%  Diabetes mellitus type I: 1 to 7%  Pernicious anaemia: 1.6% to 13%  …Llambrich A & Mascaro MJ. Vitiligo: Focusing on Clinical Association. In: Lotti T &Hercogova J (eds.) Vitiligo: Problems and Solutions. Marcel Dekker Inc. – New York 2004,pp. 179-184El Mofti AM et Al. Disorders in healty relatives of vitiligo patients. In: Lotti T & Hercogova J(eds.) Vitiligo: Problems and Solutions. Marcel Dekker Inc. – New York 2004, pp. 51-65
    • 38. Vitiligo: Disease AssociationAlikhan A, Felsten LM, Daly M, Petronic-Rosic V. J Am Acad Dermatol. 2011;65(3):473-91.
    • 39. Is it everything about psychology? The psychosomatic hypothesis The somatopsychic rebound Punishment and Leprosy complex 33% cases of vitiligo are emotionally triggered, with a biological incubation period of 2-3 weeks between the stress event and the clinical manifestation – Griemser RD & Nadelson T, 1979 80% of patients never tried any treatments – Porter JR et Al, 1986 The effect on sexual relationship – Porter JR et Al, 1990
    • 40. Vitiligo and Psychology Vitiligo may impair quality of lifeThe dermatologist and the patient must openly discussthis burden and react positively with quality of lifeassessment.Women are generally more psychologically affected bythe disorder than menObservation of new pigmentation over the whitepatches brings optimism to the vitiligo subject alwaysPsychotherapy can be of help in selected cases, butonly after careful consideration.
    • 41. Should I suggest to buy a UV lamp? Dermatologists  no data availablePatient’s report  76% advised by dermatologists Short term side-effects: burning, ocular, viral infections 92%Long term side-effects: skin tumour, premature ageing… ???
    • 42. VITILIGO TREATMENT: AN OVERVIEWLotti T, Gori A, Zanieri F, Colucci R, Moretti S. Vitiligo: new and emergingtreatments. Dermatol Ther 2008; 21:110-117.
    • 43. VITILIGO TREATMENT: AN OVERVIEWLotti T, Gori A, Zanieri F, Colucci R, Moretti S. Vitiligo: new and emergingtreatments. Dermatol Ther 2008; 21:110-117.
    • 44. Vitiligo: what’s new in treatment Excimer laser / Monochromatic excimer light (MEL) Focused microphototherapy Calcineurine inhibitors with NB-UVB
    • 45. Vitiligo: what’s new in treatmentNarrow Band UVB Excimer Laser (XeCl) and MEL (Monochromatic Excimer Light) UVB 308 nm; Only the hypopigmented areas are treated; No contrast between normal and hypopigmented skin; Low dose of irradiation; Reduced short-term and long-term side effects; Treatment of limited body areas.
    • 46. BEFORE AFTER 20 TREATMENTS J Korean Med Sci 2005; 20: 273-8
    • 47. Narrow Band UVB Microphototherapy UVB 311 nm Only the hypopigmented areas are treated No contrast between normal and affected skin Low dose of radiation Reduced short-term and long-term adverse events
    • 48. BIOSKIN® emission spectrum Intensity10-100 mW/cm2
    • 49. Results of a study on734 patients after 2years of BIOSKIN® treatment
    • 50. Calcineurine inhibitors Tacrolimus ointment 0,03-0,1% Pimecrolimus cream 1% Alone or in association with XeCl laser/MEL Best results in photoexposed areas (face and neck) Inhibits T Lymphocyte activation and the release of pro-inflammatory cytokines
    • 51. Falbella R and Barone I. Update on skin repigmentation therapies in vitiligo.Pigment Cell Melanoma Res. 2008: 22; 42–65
    • 52. Calcineurine inhibitors: are they really effective?PROs•0.1% tacrolimus is as effective as 0.05% clobetasolpropionate. • Lepe V, Moncada B, Castanedo-Cazares JP, Torres-Alvarez MB, Ortiz CA, Torres- Rubalcava AB. Arch Dermatol 2003;139:581-5•Tacrolimus plus excimer laser is more effective thanexcimer laser alone • Kawalek AZ, Spences JM, Phelps RG. Dermatol Surg 2004;30(2 Pt 1):130-5CONs•The combination of NB-UVB and tacrolimus is no moreeffective than NB-UVB alone. • Mehrabi D, Pandya AG. Arch Dermatol 2006;142:927-9•Pimecrolimus is no more effective than placebo inachieving repigmentation. • Dawid M, Veensalu M, Grassberger M, Wolff K. J Dtsch Dermatol Ges 2006;4:942-6
    • 53. Combination therapy in 2012
    • 54. Combination therapy in 2012 Open study Tacrolimus 0.1% ointment, Pimecrolimus 1% cream, Betamethasone dipropionate 0.05% cream, Calcipotriol ointment 50mcg/g, 10% L-phenylalanine cream  alone or in combination with 311nm nb-UVB microphototherapy 470 patients affected by vitiligo (<10% skin surface) Lotti T et al. Dermatol Ther 2008;21 Suppl 1:s20-6
    • 55. Group 1 BIOSKIN® aloneGroup 2 0.1%Tacrolimus+ BIOSKIN®Group 3 1% Pimecrolimus+BIOSKIN®Group 4 Betamethasone dipropionate 0.05% +BIOSKIN®Group 5 Calcipotriol ointment 50mcg/g+BIOSKIN®Group 6 10% L-phenylalanine+BIOSKIN®Group 7 0.1% Tacrolimus aloneGroup 8 1% Pimecrolimus aloneGroup 9 Betamethasone dipropionate 0.05%Group 10 Calcipotriol ointment 50mcg/g aloneGroup 11 10% L-Phenylalanine alone
    • 56. Repigmentation rates: beginning of repigmentation (weeks) as assessed by clinical evaluation 14 12 10 8 Weeks 6 4 2 0 Treatment Groups Group I: Bioskin alone Group II: 0.1% Tacrolimus + Bioskin Group III: 1% Pimecrolimus + Bioskin Group IV: 0.05% Betamethasone dipropionate + Bioskin Group V: Calcipotriol ointment 50 mcg/g + Bioskin Group VI: 10% L-Phenylalanine + Bioskin Group VII: 0.1% Tacrolimus alone Group VIII: 1% Pimecrolimus alone Group IX: 0.05% Betamethasone dipropionate alone Group X: Calcipotriol ointment 50 mcg/g alone Group XI: 10% L-Phenylalanine alone
    • 57. Repigmentation rates and final repigmentation results: visual comparison of different treatment groups as assessed by clinical evaluation 100 90 Percentage of patients reaching >75% 80 70 repigmentation 60 50 40 30 20 10 0 Time (Months) Group I: Bioskin alone Group II: 0.1% Tacrolimus + Bioskin Group III: 1% Pimecrolimus + Bioskin Group IV: 0.05% Betamethasone dipropionate + Bioskin Group V: Calcipotriol ointment 50 mcg/g + Bioskin Group VI: 10% L-Phenylalanine + Bioskin Group VII: 0.1% Tacrolimus alone Group VIII: 1% Pimecrolimus alone Group IX: 0.05% Betamethasone dipropionate alone Group X: Calcipotriol ointment 50 mcg/g alone Group XI: 10% L-Phenylalanine alone
    • 58. General considerations: how to treat vitiligo Dermatologists are prescribing less PUVA in favour of UVB; Growing introduction of combined treatments targeted UVB + “active” topicals; Repigmentation rates show the therapeutic success of phocused microphototherapy which is more remarkable when used in combination.
    • 59. General considerations: how to treat vitiligo Both BIOSKIN® and Potent topical corticosterod preparations alone are the first line treatment in vitiligo vulgaris affecting less than 10% of the skin surface. Association of these 2 treatments gives better results, with very high repigmentation rate in more than 90% of patients. High repigmentation rates are observed also for other combination treatments, while Tacrolimus and Pimecrolimus but not phenylalanine are relatively active when applied without UVB irradiation .
    • 60. PSEUDOCATALASE CREAM catalase H2O2 H2O + O2 71 children with vitiligoPseudocatalase cream + NB-UVB vs NB-UVB alone > 75% repigmentation 70% disease progression (face, neck, trunk, and extremities) Schallreuter KU, Kru¨ ger C, Wu¨ rfel BA et al. From basic research to the bedside: efficacy of topical treatment with pseudocatalase PC-KUS in 71 children with vitiligo. Int J Dermatol 2008;47:743–753.
    • 61. PROSTAGLANDN EPGE2 has stimulant and immunomodulatory effects onmelanocytesExcellent response in neck scalp and trunk lesions.Kapoor R et al. Br J Dermatol 2009; 160(4) 861-3VITAMIN D ANALOGS•Possible role in melanocyte differentiation ?•Not effective alone.•Possible combination therapy with UV and steroids.Birlea SA et al. Med Res Rev. 2009; 29 (3): 514-546,
    • 62. Vitamin D analogs Calcipotriol and tacalcitol as topical therapeutic agents in vitiligo Vitamin D ligands target T cell activation, mainly by inhibiting the transition of T cells from early to late G1 phase and by inhibiting the expression of several pro- inflammatory cytokines genes, such as those encoding TNF- alpha and IFN-gamma. Vitamin D(3) compounds influence melanocyte maturation and differentiation and up-regulate melanogenesis through pathways activated by specific ligand receptors, such as endothelin receptor and c-kit.  Birlea SA, Costin GE, Norris DA. Curr Drug Targets. 2008 Apr;9(4):345-59.
    • 63. THERAPEUTIC ALGORITHM in CHILDREN 1. Potent/very potent topical steroid (max 2 months) 2. Topical pimecrolimus/tacrolimus (better short-term safety profile) 3. NB-UVB phototherapy (max 200 treatments) No recommendation for vitamin D anoalogues, PUVA, surgical treatments and systemic therapy
    • 64. THERAPEUTIC ALGORITHM in ADULTS 1. Potent/very potent topical steroid (max 2 months) 2. Topical pimecrolimus (segmental vitiligo) (better short-term safety profile) 3. NB-UVB (or PUVA) phototherapy (max 200 treatments NB-UVB; 150 PUVA) 4. Surgical treatments 5. Depigmentation with p-(benzyloxy)phenol (> 50% depigmentation, extensive depigmentation on the face or hands)No recommendation for vitamin D anoalogues and systemic therapy
    • 65. Felsten LM, Alikhan A, Petronic-Rosic V. J Am Acad Dermatol. 2011
    • 66. Vitiligo: an evidence-based approach Positive balance of active treatments of vitiligo patients*  Topical corticosteroids (max 6 months)  89%  PUVA treatment (max 12 months)  16%  PUVA treatment (max 9 months)  25%  UVB treatment (max 6 months)  87% (Broad + Narrow Band)  Surgical treatment (one shot + UVB)  68% *evaluation made by Dermatologists• Int J Dermatol 1999;38:866-872• Arch Dermatol 1999;135:1514-1521
    • 67. There is moderate evidencefor the use oftopical corticosteroids,although long-term use islikely to lead to adverseeffects.Topical non-steroidal immunomodulators such astacrolimus as alternatives to corticosteroids area form of care that appear promising,particularly in combination with light therapies(caution when combining topical immunomodulatorswith light:theoretical long term risk of skincancer).
    • 68. The use of a light source,either as monotherapy, or incombination with oral or topicalphotoactive chemical is the mostcommon method used inpractice. There is some evidence that excimer laser is more effective in combination with topical interventions such as hydrocortisone 17-butyrate, tacrolimus, or tacalcitol.
    • 69. Surgical therapies can be effective for smallareas in peoplewith stable disease.Suction blister grafts may result in adverseeffects, (precipitation of new areas of vitiligoat donor sites, Koebner phenomenon).
    • 70. In search for more evidence: the long road  The importance of mitochondria in keratinocytes from perilesional skin and the role of oxidative stress  The possible role of antioxidant supplementation in the treatment of vitiligo
    • 71. Positive effects of the supplementation of antioxidants in cultured cells Total Antioxidant Capacity (marker of cellular scavenging activity) Mitochondrial membrane depolarization (marker of mitochondrial and cellular integrity)
    • 72. Future perspectives Our study group is investigating on the positive effects of the supplementation of antioxidants in cultured cells form lesional, perilesional and healthy skin of selected vitiligo patients. The supplementation of curcumin and capsaicin at peculiar concentrations can dramatically improve the resistance of cultured cells to oxidative stress. Focus on keratinocytes from perilesional skin as the first actors in vitiligo pathogenesis .
    • 73. What’s new in surgery Punch micrografting seems to be very effective for the treatment of stable forms of vitiligo. Before Immediately after the surgery
    • 74. Before Immediately after surgery Before After 2
    • 75. CONCLUSIONS At the horizon of vitiligo therapy and cure we see a complex puzzle with some essential bricks already well positioned and installed in the right place. The Vitiligo Research Foundation (www.vrfoundation.org ; www.vitinomics.net ) is committed to find the cure for vitiligo and to bring the needing of the vitiligo subjects to the attention of the National Health Sysems.
    • 76. How to manage vitiligo Correct diagnosis Comorbidities Patient expectations Communication issue in 2012 and further
    • 77. OUR CONTRIBUTIONS
    • 78. Vitiligo Research Foundation Firmly committed  to curing   Vitiligo, the VR Foundation  is  a philanthropic organization  funding and fast-tracking medical research globally. Creating Synergy for Expedited Research. The world is now your R&D department. See Vitinomics.net for more details.
    • 79. VRF Leadership Team Mr. Dmitry Aksenov  established the Mr. Dmitr y Aksenov  Vitiligo Research Foundation as a MSc, MBA   continuation of his medical-  research VRF Founder and President initiatives. He joined  with leading physicians  and scientists in launching   the vitiligo research alliance to advance progress against  this annoying  skin  disease. Recently, he formalized  his philanthropic activities by founding the VR Foundation, which has become one of leading supporters of vitiligo research and treatment.  As an entrepreneur, Mr. Aksenov is often  said to have revolutionized Russian real estate development market and created  thousands of jobs. He has introduced  the first energy-efficient and affordable house to  the local market in 2010. He graduated with highest distinction and earned his Master of Science degree in 1989.
    • 80. VRF Leadership Team One of the Americas foremost dermatologists, Robert Schwartz is Professor and Head of Prof. Rober t A .  Dermatology at New Jersey Medical School, one of the eight medical schools in the New Schwar tz, MD, Professor York City metropolitan area. He is also and Head of Dermatology, Professor of Medicine, Professor of Pediatrics, Professor of Pathology and Laboratory Medicine New Jersey Medical School and Professor of Preventive Medicine and Community Health at the New Jersey Medical (US)  School. Professor Schwartz has authored several books, 10 monographs, and is the author of over 250 book chapters, 500 articles, and 150 other publications. Professor Schwartz has been elected a Member Honoris Causa of 15 National Dermatologic Societies in Europe. He has lectured widely, including eighteen consecutive years on the faculty of the annual meeting of the American Academy of Dermatology, as a featured speaker dozens of dermatological congresses. He is a past President of the Dermatology Section of the New York Academy of Medicine, and in 2009 began a five-year term on the Board of Directors of the International Society of Dermatology.
    • 81. VRF Leadership Team Torello Lotti, MD,  Full Professor of Dermatology, Dept of Dermatological Sciences, Professor of University of Florence, Italy. A Dermatology world-renown expert on vitiligo, a VRF Scientific Director key note lecturer at major and Chairman , Executive dermatology meetings, visiting professor at several universities in Scientific Committee homeland Italy and abroad, chairman and director of dermatology societies, a co-author , among many, of comprehensive book “Vitiligo: Problems and Solutions”, Professor Torello Lotti provides top scientific advisory to   the VRF.  www.torellolotti.it
    • 82. VRF Leadership Team•  Jana Hercogova, MD,  President-Elect of the European Academy of Dermatology and PhD Venereology, President of Scientific Director International Congress of Dermatology, Chair of the Communications Committee of International Society of Dermatology, Professor Jana Hercogova is best known for her excellence in research, education and training. A top presenter at key professional events, she is providing top scientific advisory to the VRF. 
    • 83. VRF Leadership Team Yan Valle, MSc, MBA  Dr. Yan Valle specializes in commercial applications arising from advanced VRF Executive technologies for almost 20 years. He currently leads our Director Cloud Medical Research and Managem  and oversees all VRF operations. Prior to joining the VRF, he was a Director of Business Development at a leading technology company in Toronto. Before 00’s, he co- owned a consulting company that served Fortune 500 companies, governments and venture funds in emerging markets of EEMEA and LATAM.
    • 84. VRF
    • 85.  Berti S, Bellandi S, Bertelli A, Colucci R, Lotti T, Moretti S. Vitiligoin an Italian outpatient center: a clinical and serologic study of 204patients in Tuscany. Am J Clin Dermatol. 2011;12(1):43-9.Prignano F, Ricceri F, Bianchi B, Guasti D, Bonciolini V, Lotti T,Pimpinelli N. Dendritic cells: ultrastructural andimmunophenotypical changes upon nb-UVB in vitiligo skin. ArchDermatol Res. 2010Arunachalam M, Sanzo M, Lotti T, Colucci R, Berti S, Moretti S.Common variable immunodeficiency in vitiligo. G Ital DermatolVenereol. 2010;145(6):783-8.Becatti M, Prignano F, Fiorillo C, Pescitelli L, Nassi P, Lotti T,Taddei N. The involvement of Smac/DIABLO, p53, NF-kB, andMAPK pathways in apoptosis of keratinocytes from perilesionalvitiligo skin: Protective effects of curcumin and capsaicin. AntioxidRedox Signal. 2010, 1;13(9):1309-1321.
    • 86.  Prignano F, Pescitelli L, Becatti M, Di Gennaro P, Fiorillo C,Taddei N, Lotti T. Ultrastructural and functional alterations ofmitochondria in perilesional vitiligo skin. J Derm Sci 2009;54:157–167;Moretti S, Fabbri P, Baroni G, Berti S, Bani D, Berti E, Nassini R,Lotti T and Massi D. Keratinocyte dysfunction in vitiligo epidermis:cytokine microenvironment and correlation to keratinocyteapoptosis. Histol Histopathol 2009;24:849-857; Moretti S, Nassini R, Prignano F, Pacini A, Materazzi S, Naldini A,Simoni A, Baroni G, Pellerito S, Filippi I, Lotti T, Geppetti P andMassi D. Protease-activated receptor-2 downregulation is associatedto vitiligo lesions. Pigment Cell Melanoma Res. 2009;22:335–338.Lotti T, Berti S, Moretti S. Vitiligo therapy.Expert OpinPharmacother. 2009;10(17):2779-85.
    • 87. Berti S, Buggiani G, Lotti T. Use of tacrolimus ointment in vitiligo aloneor in combination therapy. Skin Therapy Lett. 2009;14(4):5-7;Lotti T, Buggiani G, Troiano M, Assad GB, Delescluse J, De Giorgi V,Hercogova J. Targeted and combination treatments for vitiligo.Comparative evaluation of different current modalities in 458 subjects.Dermatol Ther 2008;21 Suppl 1:s20-6;Prignano F, Pescitelli L, Ricceri F, Lotti T. The importance of geneticallink in immuno-mediated dermatoses: psoriasis and vitiligo. Int J Dermatol2008;47:1060–1062;Prignano F, Betts CM, Lotti T. Vogt-Koyanagi-Harada disease andvitiligo: where does the illness begin? J Electron Microsc (Tokyo). 2008 Lotti T, Prignano F, Buggiani G. New and experimental treatments ofvitiligo and other hypomelanoses. Dermatol Clin. 2007;24(3):393-400 Hercogova J, Buggiani G, Prignano F, Lotti T. A rational approach to thetreatment of vitiligo and other hypomelanoses. Dermatol Clin.2007;24(3):383-392
    • 88. Thank you for your attention www.torellolotti.it