F A P A 2007 Congenital Dermatological Problems

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F A P A 2007 Congenital Dermatological Problems

  1. 1. Congenital Dermatological Problems We can help them before they can help themselves
  2. 2. Welcome FAPA Winter Symposium Attendees A d Dave Kotun, NSU PA Program, Orlando 2
  3. 3. Overview of Diseases Neurofibromatosis Vitiligo Alopecia areata Al i t Ichthyosis Erythropoetic porphyria Congenital nevus Melanoma Dave Kotun, NSU PA Program, Orlando 3
  4. 4. Objectives After completing this lecture, the participant will be able t bl to: 1. Recognize the most common congenital dermatologic problems in young children and list items f a focused history and physical exam. it for f d hi t dhil 2. Describe the prominent clinical features of each of the described problems. 3. List available treatment modalities f for the congenital dermatological problems. Dave Kotun, NSU PA Program, Orlando 4
  5. 5. And also: Recall the problems discussed from the p following list: 1. Neurofibromatosis 2. Congenital nevus 3. Melanoma 4. Vitiligo 5. Alopecia areata/totalis 6. Ichthyosis 7. Erythropoietic Porphyria Dave Kotun, NSU PA Program, Orlando 5
  6. 6. Neurofibromatosis Introduction – “Elephant Man Disease” Autosomal dominant Affects b Aff t bone, skin, and nervous system ki d t Eight clinical phenotypes Two genetic disorders Incidence Neurofibromatosis- Neurofibromatosis-1 (NF1), peripheral NF 1 in 25-33K births 25- Neurofibromatosis- Neurofibromatosis-2 (NF2), central NF 1 in 50-120K births 50- Segmental NF – single body region Due to segmental conditional hyperexpression, mosaicism, or heterozygosity loss Dave Kotun, NSU PA Program, Orlando 6
  7. 7. Neurofibromatosis Pathophysiology Neurocutaneous Any organ system may be involved yg y y No racial or gender preference Cutaneous manifestations can be mild to disfiguring Increased mortality derives from the increased malignant potential of the diseased tissues and neurofibrosarcomas NF – have up to 15% greater malignancy risk Dave Kotun, NSU PA Program, Orlando 7
  8. 8. Neurofibromatosis History and physical exam Café-au- Café-au-lait are not usually seen at birth Develop before age 3 Neurofibromas form in adolescence Patient complaints Skin discoloration Pain (due to neurofibromas) Pathologic fractures Hypertensive headache (due to pheochromocytoma) Dave Kotun, NSU PA Program, Orlando 8
  9. 9. Neurofibromatosis History and physical exam Unusual pigment patterns Irregularly shaped, evenly pigmented, light brown macules – café au lait 6 or more 1.5 cm spots for older children 15 5 or more 0.5 cm spots for younger children Less than 1% of healthy kids have 3 or more spots Lisch nodules Hamartomas in the iris on slit lamp Uncommon in healthy children Axillary and/or perineal f kli – C A ill d/ i l freckling Crowe sign i Develops during puberty Freckling and hypertrichosis can hide neurofibromas Dave Kotun, NSU PA Program, Orlando 9
  10. 10. Crowe Sign & Plexiform Nevus Dave Kotun, NSU PA Program, Orlando 10
  11. 11. Neurofibromatosis History and physical exam Neurofibromas – Schwann cells Any place along a nerve Types Cutaneous and subcutaneous Circumscribed Brown, pink, or eupigmented Invaginate when pressed Plexiform Noncircumscribed, thick, irregular Disfiguring Di fi i Dave Kotun, NSU PA Program, Orlando 11
  12. 12. Neurofibromatosis History and physical exam Neurologic abnormalities Acoustic nerve problems p Optic gliomas Other tumors Astrocytoma, meningioma, Astrocytoma meningioma imtramedullary glioma glioma, ependymoma Result – increased intracranial pressure, seizure, ataxia, other cranial nerve abnormalities Schwanomas Uncommon in NF-1 NF- Most common tumor in NF-2 NF- Dave Kotun, NSU PA Program, Orlando 12
  13. 13. Neurofibromatosis History and physical exam Learning disabilities NF- NF-1: 25 – 40 % Mental retardation: 5 – 10% Endocrine Short stature and GH deficiency Sexual precocity due to tumor Pheochromocytoma Dave Kotun, NSU PA Program, Orlando 13
  14. 14. Neurofibromatosis Diagnostic criteria review (NF-1), need 2 (NF-1) Café-au- Café-au-lait ≥ 6 (>5mm) prepubertal;(>15mm) postpubertal ≥ 2 neurofibromas or 1 plexiform neurofibroma Axillary or inguinal freckling y g g Optic glioma ≥2 iris hamartomas (Lisch nodules) Osseous lesions – sphenoid dysplasia, cortical thinning, ± pseudoarthrosis First degree relative with NF - 1 Dave Kotun, NSU PA Program, Orlando 14
  15. 15. Neurofibromatosis Diagnostic criteria for NF – 2 Bilateral CN VIII (Vestibulocochlear, Acoustic) masses on imaging First degree relative with NF – 2 and: CN VIII mass (unilateral) or 2 of the following: Neurofibroma Meningioma Glioma Schwannoma Posterior subcapsular opacity (juvenile) Dave Kotun, NSU PA Program, Orlando 15
  16. 16. Neurofibromatosis Causes Autosomal dominant NF – 1 gene on band 17q11 2 17q11.2 NF – 2 gene on band 22q11 Both encode neurofibromin Variable phenotypic expression both within families and as the disease changes with time Cutaneous (nuisance) to disfiguring and life threatening Dave Kotun, NSU PA Program, Orlando 16
  17. 17. Neurofibromatosis Diagnosis Genetic techniques are not readily available Imaging of suspected patients – MRI Orbits and auditory canals for NF – 1 and 2 respectively PET with 18 fl rodeo gl cose (FDG) ith flurodeoxyglucose For plexiform neurofibromas CT in NF – 1 Surface neurofibromas Focal thoracic scoliosis Vertebral scalloping Enlarged foramina Rib notching next t costal nerves – mass effect t hi t to tl ff t Slit lamp in children > 6 Café-au- Café-au-lait Wood’s lamp exam Dave Kotun, NSU PA Program, Orlando 17
  18. 18. Neurofibromatosis Care Excision of tumors Investigate epilepsy Consultations Ortho Plastics Psych y Speech Genetic counseling g Dave Kotun, NSU PA Program, Orlando 18
  19. 19. Neurofibromatosis Follow- Follow-up Yearly PE and ophthalmologic exam Monitor for growth pain or change in growth, pain, neurofibromas Neuro exams annually with imaging if indicated Complications Malignant transformations Reggie Bibbs from FOX Program, Orlando Dave Kotun, NSU PA 19 News interview
  20. 20. Vitiligo Introduction Unknown cause Melanocytes are destroyed Possibly autoimmune etiology 1% of the population is affected No gender preference Usually detected before 20 y.o. yo In a area of damaged skin Dave Kotun, NSU PA Program, Orlando 20
  21. 21. Vitiligo Pathophysiology Autoimmune Also affects mucosa, eyes, inner ear, hair Vitiligo vulgaris – common form Patients are predisposed to p p Alopecia Areata Thyroid disorders Addison’s di Addi ’ disease Pernicious anemia Diabetes mellitus Dave Kotun, NSU PA Program, Orlando 21
  22. 22. Vitiligo Diagnosis Straightforward on history and physical exam Complications Disfiguring Psychologically trying No serious health problems Dave Kotun, NSU PA Program, Orlando 22
  23. 23. Vitiligo Treatment Immune system suppression Surgical melanocytic transplant Repigmentation occurs slowly as new melanocytes return from the lesion edges Dave Kotun, NSU PA Program, Orlando 23
  24. 24. Vitiligo Modalities Topical steroids 2X daily for 3 – 6 months Caution – monitor for overabsorption Psoralen and UV light (PUVA) Causes sun sensitivity Ultra violet – B (UVB) May be safer than PUVA Dave Kotun, NSU PA Program, Orlando 24
  25. 25. Vitiligo Modalities (cont.) ( ) Surgery Autologus skin grafts Thigh or buttocks 90% response Can be spotty or irregular Excimer lasers Narrow band UV – B light Promote repigmentation P t i t ti Several treatments The XTRAC® excimer laser treatment system from PhotoMedexPA Program, Orlando Dave Kotun, NSU 25
  26. 26. Vitiligo Modalities (cont ) (cont.) Cosmetic covers Used when medical treatment is ineffective Covermark® Dermablend ® D bl d Sunless tanning preparations Avoid sun exposure to minimize contrast Dave Kotun, NSU PA Program, Orlando 26
  27. 27. Alopecia areata et al et.al. Etiology Multiple causes Signs and symptoms Hair loss – can be seen or the patient will tell you Treatment Cosmetic or underlying cause Dave Kotun, NSU PA Program, Orlando 27
  28. 28. Alopecia areata et al et.al. Etiology Types Nonscarring / diffuse Nonscarring / focal Scarring / focal g Dave Kotun, NSU PA Program, Orlando 28
  29. 29. Alopecia areata et al et.al. Nonscarring / diffuse Male and female pattern baldness Androgenic DHT conversion Male Begins at the temples and vertex Female Begins frontal, parietal and crown B i at f l ild Hair thinning is characteristic Dave Kotun, NSU PA Program, Orlando 29
  30. 30. Alopecia areata et al et.al. Nonscarring / diffuse g Telogen effluvium Hairs enter the resting phase simultaneously Shedding is noticed in the recovery phase Stress and nutritional deficiencies Drugs Chemotherapeutic agents H2-blockers oral contraceptives agents, H2-blockers, contraceptives, ACEIs, β-blockers, lithium, clofibrate, ibuprofen, benzafibrate, trimethadione, valproate, penicillamine, interferon, ranitidine, sulindac, tamoxifen, terfenadine, thiamphenicol Stress Endocrine changes Anagen effluvium g 2° to Chemo Dave Kotun, NSU PA Program, Orlando 30
  31. 31. Alopecia areata et al et.al. Nonscarring / diffuse Anagen effluvium Loss in the growth phase Causes Radiation and chemotherapy Hg, Tl, boric acid, vitamin A Alopecia totalis Dave Kotun, NSU PA Program, Orlando 31
  32. 32. Alopecia areata et al et.al. Nonscarring diffuse Hair shaft abnormalities (trichodystrophies) Trichorrhexis invaginata (bamboo hair) Associated with ichthyosis and Netherton syndrome Wooly hair nevus Trichorrhexis nodosa Monilethrix Dave Kotun, NSU PA Program, Orlando 32
  33. 33. Alopecia areata et al et.al. Nonscarring focal Most are not congenital Traction alopecia Braids, trichotollomania, T. capitus, Late 2° syphyllis 2° Most common congenital g Alopecia areata Dave Kotun, NSU PA Program, Orlando 33
  34. 34. Alopecia areata et al et.al. Scarring focal Fibrotic denegration of follicle Usually not congenital y g Trauma, scarring, disease Burns, trauma, radiation therapy, infections (both primary and secondary), sarcoidosis, SLE, secondary) sarcoidosis SLE malignancy Primary disease (rare) Lichen planouplaris LP of the scalp Folliculitis decalvans – scarring alopecia with pustules and “clumped hairs” Pseudopelade of Brocq ( p q (really rare) y ) Dave Kotun, NSU PA Program, Orlando 34
  35. 35. Alopecia areata et al et.al. Possibly due to anagen phase antibodies Prevalence is 1.7% lifetime No significant preponderance by race or gender Most occur at ages 15 – 29 with many younger but not many over 40 S g t association t Slight assoc at o with DM Often can be traced to stress or disease onset Dave Kotun, NSU PA Program, Orlando 35
  36. 36. Alopecia areata et al et.al. History Hair loss Itching – may or may not lead to a specific cause g y y p Scarring Warrants a check of the entire skin and mucosa for systemic disease The usual questions Timing New drugs or health products Family history both historically and in the present living situation Dave Kotun, NSU PA Program, Orlando 36
  37. 37. Alopecia areata et al et.al. Physical exam y Hair loss is visible Pull test Grab ≈ 60 hairs X3 and pull gently pg y Count hairs - < 6 telogen-phase telogen- hairs should come out > 6 is abnormal Telogen hairs have bulbs without g sheaths, anagen hairs have sheaths Pluck test – same except the hairs are pulled out painfully and swiftly Both tests – 85 – 90% are in anagen phase Dave Kotun, NSU PA Program, Orlando 37
  38. 38. Alopecia areata et al et.al. Physical exam Biopsy for persistent mystifying alopecia Daily hair counts - > 100 are abnormal except after shampooing (250) Alopecia areata – broken hairs at the margins Nails may be pitted or rough Dave Kotun, NSU PA Program, Orlando 38
  39. 39. Alopecia areata et al et.al. Treatment Male pattern baldness Minoxidil – topical 1ml to scalp Best with vertex alopecia as it prolongs the anagen phase 30 – 40% effective ff ti Finesteride 5-α reductase inhibitor 5- 1 mg p daily g po y Pregnant women should not be in the same room as these pills Treat for 24 months Dave Kotun, NSU PA Program, Orlando 39
  40. 40. Alopecia areata et al et.al. Alopecia areata p TAC injections – 0.1 ml/site (10mg/mL suspension) Topicals must be potent as many cannot penetrate to the hair bulb Betamethasone 0.05% has a chance Oral steroids are effective but hair loss reoccurs as therapy is ended Anthralin 0.5 – 1% 10 min daily and washed off Titrate to 30 min. as titrated Minoxidil topically Induction of dermatitis Diphencyprone , squaric acid squaric dibutylester Cyclosporine, tacrolimus, dapsone Dave Kotun, NSU PA Program, Orlando 40
  41. 41. Alopecia areata et al et.al. Surgical options Follicle transplant Scalp flaps pp Alopecia reduction Secondary alopecia is treated symptomatically Traction reduction, fungal treatments, psychotropics, Coverings Hair pieces or tattooing Dave Kotun, NSU PA Program, Orlando 41
  42. 42. Follicule Transplant Dave Kotun, NSU PA Program, Orlando 42
  43. 43. ichthyosis Introduction Congenital or acquired Four inherited types ichthyosis vulgaris Appears at puberty Most common Epidermolytic hyperkeratosis Red, moist, tender, Red moist tender bullous skin at birth Lamellar ichthyosis Rear, autosomal recessive “Colloidion babies” X-linked ichthyosis Present shortly after birth Due to sulfatase deficiency Dave Kotun, NSU PA Program, Orlando 43
  44. 44. ichthyosis vulgaris Symptoms Dry scaly hyperkeratinized skin Frequency Higher in Mexico, China, and UK Lower in Denmark and Italy All races affected equally Increased risk of testicular cancer Acquired ichthyosis can occur with HIV in IV drug users after T-cell depletion T- Dave Kotun, NSU PA Program, Orlando 44
  45. 45. ichthyosis vulgaris Eye exam Corneal abnormalities especially abrasion Ectropion Blephritis Retinitis pigmentosa Tortuous vessels Dave Kotun, NSU PA Program, Orlando 45
  46. 46. ichthyosis vulgaris Skin biopsy can differentiate py Genetic testing for the rarer types CBC TFTs Acquired ichthyosis Angiotensin converting enzyme and lysozyme Chest X-ray (lymphoma, HIV, TB, sarcoid) X- In t I utero U/S for excessive debris, polyhadraminos, footlength Biopsy Dave Kotun, NSU PA Program, Orlando 46
  47. 47. ichthyosis vulgaris Treatment Isotrenitoin PO 2mg/Kg daily – Adults Liarozole 150mg bid – cytochrome P450 inhibitor Urea topical cream 2 10 and 20% 2,10, Carboxymethylcellulose 0.5 – 1.0% N-acetylcystine 10% emulsion Don’t forget antibiotics if bacterial infection crop up Dave Kotun, NSU PA Program, Orlando 47
  48. 48. ichthyosis vulgaris Eye care Petrolatum/mineral oil to cornea Eyelid care is important Amniotic membrane transplant for corneal wound healing Follow up with dermatology and ophthalmology if needed Surgery may be needed for scarring or transplants g p Dave Kotun, NSU PA Program, Orlando 48
  49. 49. ichthyosis vulgaris Continued care Bathing with tar soap Removing surface scales Applying barrier products Dave Kotun, NSU PA Program, Orlando 49
  50. 50. Erythropoetic Porphyria Introduction Inborn error of heme synthesis in the bone marrow Autosomal recessive Porphyrins buildup causing cutaneous py p g photosensitivity Port wine urine and skin blistering Dave Kotun, NSU PA Program, Orlando 50
  51. 51. Erythropoetic Porphyria Günther s Günther's disease Very rare – less than 200 nationwide Clinical variability is wide Most patients survive into adulthood No predilection for: Race Age But, most patients are younger Gender Dave Kotun, NSU PA Program, Orlando 51
  52. 52. Erythropoetic Porphyria History CC is blistering of light exposed skin Jaundice at birth Physical exam Skin Vesicles and bullae Fragility Hypertrichosis Oral Reddish teeth that fluoresce Dave Kotun, NSU PA Program, Orlando 52
  53. 53. Erythropoetic Porphyria Physical exam Urine Pink staining Ocular Blepharitis, ectropion Blepharitis ectropion, conjunctivitis Scleral fissures and pink fluorescence Corneal scarring g Skeletal Bones fluoresce pink Bone loss Dave Kotun, NSU PA Program, Orlando 53 Osteopenia and acro-osteolysis acro-
  54. 54. Erythropoetic Porphyria DD Erythropoetic protoporphyria Porphyria cutanea tarda Pseudoporphyria Variegate porphyria Xeroderma pigmentosa Dave Kotun, NSU PA Program, Orlando 54
  55. 55. Erythropoetic Porphyria Labs Urine porphyria and derivatives Increased uroporphyrin in RBCs p py Increased Coprophyrin Decreased uroporphyrin III synthase activity Fluorescence microscopy of blood and bone marrow CBC Hemolytic anemia Hepato and splenomegaly Dave Kotun, NSU PA Program, Orlando 55
  56. 56. Erythropoetic Porphyria Medical care Avoid sun Sunscreens with ZnOxide or Titanium dioxide Sun protective clothing Avoid trauma to skin Oral β-carotene slight benefit Transfusions Bone marrow transplant Oral α-tocopherol and vitamin C Dave Kotun, NSU PA Program, Orlando 56
  57. 57. Erythropoetic Porphyria Consults Dermatology Ophthalmologist Hematologist Surgeon (splenectomy) Oral surgeon Dave Kotun, NSU PA Program, Orlando 57
  58. 58. Congenital Nevus Types Nevus sebaceous Hairy nevus Café-au- Café-au-lait All present f t from birth bi th Acquired nevi occur after birth when groups of melanocytes occur l t Congenital hairy nevus is our focus Dave Kotun, NSU PA Program, Orlando 58
  59. 59. Congenital Nevus Congenital nevomelanocytic nevus (CNN) Congenital hairy nevus Carcinogenic potential ≈ 6-8.5% of large/giant nevi have potential for 6- cutaneous melanoma 5% lifetime risk f any size CNN lif ti i k for i Incidence Found in 1% of newborns Most are small Large are present in 1 in 20K – 500K babies Dave Kotun, NSU PA Program, Orlando 59
  60. 60. Congenital Nevus Incidence Equal in males and females Found in all races but higher in blacks Some rare types have delay in pigment appearance 1 month to 2 years Dave Kotun, NSU PA Program, Orlando 60
  61. 61. Congenital Nevus Physical exam Size Small < 1.5 cm Med 1.5 – 20 cm Large > 20 cm Bigger than your fist Borders Surface Shape Color Location Distribution Associated findings NF for example Dave Kotun, NSU PA Program, Orlando 61
  62. 62. Congenital Nevus Treatment is usually surgical with the following f ll i considerations id ti Aesthetics Large at 6 mo. old L t ld Small at adolescence Excision and reconstruction Follow small ones with photodocumentation (Try using the copier when possible) Dave Kotun, NSU PA Program, Orlando 62
  63. 63. Congenital Nevus Other treatment Phenol chemical peel with possible additional dermabrasion Normal mode ruby laser Pulsed CO2 laser Dave Kotun, NSU PA Program, Orlando 63
  64. 64. Melanoma Introduction Not the most common skin cancer, but the most deadly UV light exposure increases risk Sun damage is contributory Development is usually on these areas, but look for the unusual presentations Most people have between 10 and 40 moles (by age 20) Dave Kotun, NSU PA Program, Orlando 64
  65. 65. Melanoma Incidence 1 in 75 people 75% of skin cancer deaths Rate is increasing from 1994 Rate of increase peaked in the 70’s and the rate of 70 s increase is declining Rate has gone down in women g Dave Kotun, NSU PA Program, Orlando 65
  66. 66. Melanoma Risk factors Fair skin Sunburn history Sunny/high elevation climates yg Moles Dysplastic More than 50 Family history Immune compromise Carcinogenic exposure g p ACS says avoid radium, coal tar, creosote, arsenic Xeroderma pigmentosa Rare, genetic Dave Kotun, NSU PA Program, Orlando 66
  67. 67. Melanoma Unusual locations Under a nail Mouth Urinary tract Vagina Eye Don’t forget the amelanocytic melanoma!! Please examine your dark skinned patients also Pl i d k ki d ti t l Dave Kotun, NSU PA Program, Orlando 67
  68. 68. Melanoma Diagnosis g Screening exam Head to toe Biopsy Punch or excisional NEVER SHAVE Staging St i Thickness Depth Dh Spread Dave Kotun, NSU PA Program, Orlando 68
  69. 69. Melanoma A – asymmetry B – border C – color Dark or changing D – diameter > 6 mm Changes Scaling, itching, texture change, spreading, oozing, bleeding oozing Dave Kotun, NSU PA Program, Orlando 69
  70. 70. Melanoma Stages 0 – Melanoma in situ I – IV Lower numbers are less invasive and more importantly have better survival/recovery rates Simple surgeries work well for early stage or thin lesions Dave Kotun, NSU PA Program, Orlando 70
  71. 71. Melanoma Treatment options Surgery Chemotherapy Radiation therapy Immunotherapy Biological therapy Synthetic compound called CP-31398 helped CP- stabilize damage in the tumor-suppressing p53 tumor- gene (from AAPA’s Medical Watch) Dave Kotun, NSU PA Program, Orlando 71
  72. 72. Melanoma Therapy in trial Chemoimmunotherapy Gene therapy Replacement Splicing Targeted anti – growth or proliferation therapy Vaccine Dave Kotun, NSU PA Program, Orlando 72
  73. 73. Melanoma Prevention Avoid sun from 1000 – 1600 Always wear sunscreen Protective clothing Avoid tan accelerators Tanning beds Lotions Know sun sensitizing meds Regular skin checks by you and your PA Dave Kotun, NSU PA Program, Orlando 73
  74. 74. N i P Q . e m h u . a a o e . l g t w s M e o a t o s i r o o o s f f h n e a a q M d u a l Q e r a a u s k r e t s g s i q e t o u c i n e a o q s r n u m t t e a i o M s r o o a t k n n r i b k o m . 5 u n a j t r p - t m k g c e a a r o r 3 t f n k 0 a l 0 l 3 y i o 8 t x g 9 . . 8 . 3 x 0 . . 0 3 0 Dave Kotun, NSU PA Program, Orlando 74 . 0 3 1 . 4 8 0 x - 0 6 5 0 x 4 4 - 5 k 8 4 1
  75. 75. References Hall HI et al. Update on the incidence and mortality from melanoma in the United States. J Am Acad Dermatol 1999 40 35-42. 35- Mayo Cllinic Staff Paper, Mayo Foundation for Medical Education and Research (MFMER), June 1, 2007 The Merck Manuals Online Medical Library, Alopecia, Nov, 2005. Bolduc, C., Lui, H., & Shapiro, J., 2006. Alopecia Areatai E-Medicine Online. Gomuwka, P 2006 Gomuwka P, 2006. Congenital Hairy Nevi E-Medicine Online Mar 10, 2006 Online. 10 Nevi, Lehrer, M. S. Nevus review provided by VeriMed Healthcare Network., Oct. 16, 2006 Hebel, J. L., Poh-Fitzpatrick, M. B., 2006, Erythropoietic Porphyria, E-Medicine Online, Oct. 19, Poh- 2006 Goins, K., 2006, Ichthyosis, E-Medicine Online, 2006 update. Intillehealth.com Intillehealth com Information Sheet, Reviewed by Harvard Medical School, March 24, 2007 Sheet School 24 U.S. National Library of Medicine & National Institutes of Health, Neurofibromatosis, Medline Plus, Neurofibromatosis, 23 September 2007 Kam, J. R., Helm, T. N. Neurofibromatosis, E-Medicine Online, Jan 2, 2007. Hann, S-K, Vitiligo, E-Medicine Online, 2006. S- Vitiligo, E- American O t A i Osteopathic College of Dermatology, 2007. D thi C ll fD tl 2007 Dermatologic Di t l i Disease Database, Vitiligo, Dtb Vitiligo, Vitili 2007. American Academy of Physician Assistants, Medical Watch, December 10, 2007 Gary M. White & Neil H. CoxDiseases of the Skin, from www.merckmedicus.com/.../white-ch-028- www.merckmedicus.com/.../white-ch-028- s007.htm Dave Kotun, NSU PA Program, Orlando 75

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