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. 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. 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. 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. 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. 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. Crowe Sign & Plexiform Nevus
Dave Kotun, NSU PA Program, Orlando 10
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. 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. 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. 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. 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. 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. 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. Neurofibromatosis
Care
Excision of tumors
Investigate epilepsy
Consultations
Ortho
Plastics
Psych
y
Speech
Genetic counseling
g
Dave Kotun, NSU PA Program, Orlando 18
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. 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. 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. Vitiligo
Diagnosis
Straightforward on history and physical exam
Complications
Disfiguring
Psychologically trying
No serious health problems
Dave Kotun, NSU PA Program, Orlando 22
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. 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. 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. 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. 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. Alopecia areata et al
et.al.
Etiology
Types
Nonscarring / diffuse
Nonscarring / focal
Scarring / focal
g
Dave Kotun, NSU PA Program, Orlando 28
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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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
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. 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. ichthyosis vulgaris
Eye exam
Corneal abnormalities especially abrasion
Ectropion
Blephritis
Retinitis pigmentosa
Tortuous vessels
Dave Kotun, NSU PA Program, Orlando 45
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. 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. 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. ichthyosis vulgaris
Continued care
Bathing with tar soap
Removing surface scales
Applying barrier products
Dave Kotun, NSU PA Program, Orlando 49
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. 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. 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. 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-
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. 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. Erythropoetic Porphyria
Consults
Dermatology
Ophthalmologist
Hematologist
Surgeon (splenectomy)
Oral surgeon
Dave Kotun, NSU PA Program, Orlando 57
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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. Melanoma
Therapy in trial
Chemoimmunotherapy
Gene therapy
Replacement
Splicing
Targeted anti – growth or proliferation therapy
Vaccine
Dave Kotun, NSU PA Program, Orlando 72
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. 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. 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
