Atopic Dermatitis, Eczema, and Noninfectious Immunodeficiency Disorders

1
Atopic Dermatitis, Eczema, and Noninfectious
Immunodeficiency Disorders

• Kristy P. Gilbert, D.O.
• November 29, 2005

2
Atopic Dermatitis

• atopic eczema
• infantile eczema
• flexural eczema
• disseminated neurodermatitis
• prurigo diathsique

3
Atopic Dermatitis

• Pruritis is the hallmark of AD
• Itch that rashes -itching commonly precedes
  the appearance of lesions
• Eczematous eruption often leads to lichenified
  dermatitis

4
Atopic Dermatitis

• Commonly associated with xerosis and
  susceptibility to irritants and proteins, as well
  as an atopic diathesis (tendency towards asthma,
  allergic rhinitis, IgE mediated systemic
  manisfestations)
• IgE bound to Langerhans cells in atopic skin
• Food exacerbates symptoms in some patients soy,
  eggs, peanuts, cows milk represent up to 75 of
  positive tests for food allergies- most commonly
  seen in infants kids w/ mod-severe AD (up to
  40 of pts.)
• Most frequent allergens leading to respiratory
  allergies are dust mites, pollen, animal fur,
  molds- (seen in up to 70 of pts and associated
  w/ adult AD)

5
Atopic Dermatitis

• Triggering Factors
• Temperature change
• Sweating
• Excessive washing
• Contact with irritating substances (wool, soaps,
  detergents, cigarette smoke)
• Contact allergy
• Aeroallergens
• Microbial agents
• Food
• Stress

6
(No Transcript)
7
(No Transcript)
8
AD 3 Stages

• Infantile
• 2 months to 2 years
• Childhood
• 2 years to 10 years
• Adult
• adolescence to adulthood

9
Infantile Atopic Dermatitis

• 60 of AD present in the first year of life,
  after 2 months of age
• Begin as itchy erythema of the cheeks
• Distribution include scalp, neck, forehead,
  wrist, and extensors
• May desquamate leading to erythroderma
• Buttocks and diaper area frequently spared

10
Infantile Atopic Dermatitis

• Partial or even complete remission in summer and
  relapse in winter are the rule
• Worsening observed after immunizations and viral
  infections

11
Infantile Atopic Dermatitis

• In most cases the symptoms will disappear toward
  the end of the second year.
• Egg, peanut, milk, wheat, fish, soy, and chicken
  may exacerbate infantile AD

12
(No Transcript)
13
Childhood Atopic Dermatitis

• Characterized by less acute lesions
• Distribution antecubital and popliteal fossae,
  flexor wrist, eyelids, and face.
• Severe atopic dermatitis involving more than 50
  of body surface area is associated with growth
  retardation.

14
(No Transcript)
15
Adult Atopic Dermatitis

• Distribution antecubital and popliteal fossae,
  the front side of the neck, the forehead, and
  area around the eyes.
• Atopic individuals are at greater risk of
  developing hand dermatitis than are the rest of
  the population
• 70 develop hand dermatitis sometime in their
  lives
• Common in women after birth of their 1st child,
  when increased exposure to soaps and water
  trigger disease

16
(No Transcript)
17
(No Transcript)
18
Cutaneous stigmata

• Dennie-Morgan folds
• Pityriasis alba
• Keratosis pilaris
• Hertoghes sign thinning of the lateral
  eyebrows
• Keratosis punctata palmaris et plantaris
• Xerosis
• Icthyosis vulgaris
• Palmarplantar hyperlinearity
• Cheilitis
• LSC
• Prurigo Nodularis

19
(No Transcript)
20
(No Transcript)
21
(No Transcript)
22
AD and Ichthysosis vulgaris

• Up to 50 of AD will have Ichthysosis vulgaris
• Autosomal dominant
• Excessive scaling most prominent on shins
• White, translucent, quadrangular scales on the
  extensor aspects of the arms and legs common with
  atopy

23
Vascular Stigmata

• Headlight sign perinasal and periorbital pallor
• White dermographism blanching of the skin at
  the site of stroking with a blunt instrument
  cause edema and obscure color of underlying
  vessels.

24
Infection

• Pts w/ AD more prone to certain cutaneous infx,
  may have more widespread infx, may have
  exacerbations of their AD provoked by skin infx
• Staph aureus 90 of chronic lesions
• Eczema herpeticum generalized herpes simplex
  infection. Young children usually.
• Secondary to reduced cell-mediated immunity
• Vaccination against smallpox is contraindicated
  in person with atopic dermatitis. Even when
  condition is in remission, widespread and even
  fatal vaccinia can occur.
• Also more prone to other cutaneous viral diseases
  such as flat warts and molluscum contagiosum

25

• Eczema herpeticum typical vesicular lesions on
  the hand, around the eye, and on the face

26
Immunology

• T helper cell type 2 (Th2) dominance
• Th2 produces IL-4, 5, and 10
• IL-4 and IL-5 produce elevated IgE and
  eosinophilia
• IL-10 inhibits delayed type hypersensitivity
• Th2 may be sensitive to house mites or grass
  pollen

27
(No Transcript)
28
Immunology

• Monocytes produces elevated amount of
  prostaglandin E2 (PGE2)
• PGE2 reduces gamma-interferon production, but not
  IL-4 from helper cells thereby enhancing the Th2
  dominance
• PGE2 also directly enhances IgE production from B
  cells

29
(No Transcript)
30
Immunology

• Langerhans cells of AD patient stimulate helper T
  cells into Th2 phenotype without the presence of
  antigen
• Langerhans cells have IgE bound to their suface
  receptors. These IgE are associated with atopic
  antigens, such as house dust mites

31
Differential Diagnosis

• Seborrheic Dermatitis
• Contact dermatitis
• Nummular eczema
• Scabies
• Psoriasis
• LSC
• Asteatotic eczema
• Dermatophytosis
• HIV or HTLV-1 Associated dermatoses
• Chronic mucocutaneous candidiasis
• Impetigo
• Congenital syphilis
• Dermatitis herpetiformis
• GVHD
• Dermatomyositis
• Pemphigus foliaceus
• Lupus erythematosis

• Wiskott- Aldrich
• Hyperimmunoglobulin-E syndrome
• SCID
• DiGeorge Syndrome
• CTCL
• Langerhans Cell histiocytosis
• Nethertons syndrome
• Ectodermal dysplasias
• Familial KP
• Ataxia telangiectasia
• Hartnuo disease
• PKU
• Zinc deficiency
• Drug eruption
• Photoallergic dermatitis
• Chronic actinic damage

32
Histology

• Spongiotic dermatitis
• Lichen simplex chronicus
• Eosinophils may be seen

33
(No Transcript)
34
Management

• Protect from scratching
• Adequate cleansing but not over bathing or
  rubbing
• Gentle cleansers- mild, non-alkali soaps
• Anti-histamines, especially at night
• Bathing protocol
• Food allergy identification and dietary
  restrictions.
• Hydrate skin daily with moisturizers

35
Management

• Topical steroids
• Wet compress of Burows solution such as
  Domeboro.
• Crude coal tar/liquor corbonis detergens (LCD)
• PUVA
• Cyclosporine

36
Management

• Topical FK506 (Tacrolimus) is dramatically
  beneficial in SEVERE atopic dermatitis
• 95 showed good improvement in Alaiti and Rusicka
  study in JAAD 1998, Archives 1999

37
(No Transcript)
38
Regional Eczema

• Ear eczema
• Eyelid dermatitis
• Nipple eczema
• Hand eczema
• Diaper dermatitis
• Infectious eczematoid dermatitis
• Juvenile plantar dermatosis

39
Ear Eczema

• Most frequently caused by seborrheic or atopic
  dermatitis
• Staph, Strep, or Pseudomonas
• Earlobe is pathognomonic of nickel allergy

40
(No Transcript)
41
Eyelid dermatitis

• When on one eye only, it is most frequently
  caused by nail polish, and usually affects the
  upper eyelid
• When both eyes are involved, consider mascara,
  eye shadow, eyelash cement, eyeliner, etc
• In contrast, atopic dermatitis affects both upper
  and lower eyelid.

42
Nipple eczema

• Painful fissuring, seen especially in nursing
  mothers
• Maybe an isolated manifestation of atopic
  dermatitis
• If persist more than 3 months, and/or unilateral,
  biopsy is mandatory to rule out Pagets

43
(No Transcript)
44
Hand eczema

• Spongiosis histologically
• Irritant hand dermatitis- seen in homemakers,
  nurses. Resulting from excessive exposure to
  soaps
• Pompholyx- tapioca vesicles, on sides of fingers,
  palms, and soles
• Differentials Bullous tinea, id, allergic
  contact dermatitis

45
(No Transcript)
46
(No Transcript)
47
Treatment

• Barrier
• Moisturizer
• Systemic Corticosteroids
• Phototherapy UVA, PUVA, Radiotherapy (Grenz
  Ray)
• New research suggests use of oral retinoids for
  severe recalcitrant hand eczema

48
Diaper (Napkin) Dermatitis

• Erythematous, papulovesicular dermatitis
  distributed over the lower abdomen, genitals,
  thighs, and the convex surfaces of the buttocks
• Irritation caused by bacteria, change in the
  environment (moisture, lower PH, feces)
• Candida albicans secondary infection.

49
(No Transcript)
50
(No Transcript)
51
Diaper dermatitis - complications

• Jacquets erosive diaper dermatitis
• Punched out ulcers/erosions with elevated borders
• Pseudoverrucous papule and nodules
• Granuloma gluteal infantum

52
Jacquets diaper dermatitis with eroded nodules
on the labia
53
Granuloma gluteale infantum
54
Diaper Dermatitis

• Differential diagnosis Napkin psoriasis,
  seborrheic dermatitis, atopic dermatitis,
  langerhans cell histiocytosis, tinea cruris,
  allergic contact dermatitis, acrodermatitis
  enteropathica, biotin deficiency, congenital
  syphillis
• Treatment prevention

55
Juvenile plantar dermatosis

• Begins as a patchy symmetrical, smooth, red,
  glazed macules on the base of the great toes
• Affect age 3 to puberty.
• Symmetrical lesions on weight bearing area
• toxic sock syndrome caused by repeated
  maceration of the feet by occlusive shoes and
  nonabsorbent synthetic socks
• Virtually always resolve after puberty

56
Juvenile plantar dermatosis
57
(No Transcript)
58
Xerotic Eczema

• Aka winter itch, nummular eczema, eczema
  craquele, and asteototic eczema.
• Anterior shins, extensor arms, and flank
• Elderly person predisposed.
• Use of bath oils in bath water is recommended to
  prevent water loss
• Moisturizers urea or lactic acid.

59
Xerotic eczema
60
Hormone Induced Dermatoses

• Autoimmune progesterone dermatitis Appear 5-10
  days before menses. Oophorectomy, danazol, and
  tamoxifen are treatment modalities- Urticaria-
  Angioedema- Eczema- Erythema multiforme-
  Stomatitis- Folliculitis- Papulopustular/papulov
  esicular lesions- Stephens-Johnson syndrome-
  Vesiculobullous reactions- Dermatitis
  herpetiformis-like rash- Mucosal lesions
• Autoimmune estrogen dermatitis a cyclic skin
  disorder with variable morphologies. Exacerbate
  premenstrually or occur only immediately before
  the menses. Treatment with tamoxifen maybe
  effective.

61
Immunodeficiency Syndromes

• X-Linked Agammaglobulinemia
• Isolated IgA Deficiency
• Common Variable Immunodificiency
• Isolated Primary IgM Deficiency
• Immunodificiency with Hyper-IgM
• Thymic Hypoplasia
• Thymic Dysplasia with Normal Immunoglobulins
  (Nezelof Syndrome)

62
Immunodeficiency Syndromes

• Purine Nucleoside Phosphorylase Deficiency
• Miscellaneous T-Cell Deficiencies
• Severe Combined Immunodeficiency Disease (SCID)
• Thymoma with Immunodeficiency
• Ataxia-Telangiectasia (Louis-Bars S.)
• Wiskott-Aldrich Syndrome

63
Immunodeficiency Syndromes

• X-Linked Lymphoproliferative Syndrome
• Chronic Granulomatous Disease
• Myeloperoxidase Deficiency
• Leukocyte Adhesion Molecule Deficiency
• Chediak-Higashi Syndrome
• Hyperimmunoglobulinemia E Syndrome
• Complement Deficiency
• Graft-Versus-Host Disease

64
X-Linked Agammaglobulinemia

• Aka Brutons syndrome, sex-linked
  agammaglobulinemia.
• Patients develop recurrent bacterial infections
  in the first year of life. The skin is the most
  common site of infection, usually manifest as
  furuncles and cellulitis, and occasionally
  ecthyma gangrenosum.
• Staphylococcus, Streptococcus, Haemophilus and
  Pneumococcus are the most common organisms.
• Increased susceptibility to hepatitis B and
  enteroviral infections.
• Increased risk of eczema.
• Associated papular dermatitis may result from
  extensive lymphohistiocytic infiltration of the
  skin.
• Non-infectious cutaneous granulomas have been
  described.
• Small percentage of patients develop a
  dermatomyositis-like disorder with slowly
  progressive neurologic involvement, usually
  related to echoviral meningoencephalitis.
• May develop leukemia, lymphoma, fatal
  encephalitis, pulmonary fibrosis

65
X-Linked Agammaglobulinemia

• Defect lies in the maturation block in pre-B-cell
  to B-cell differentiation
• IgA, IgM, IgD, and IgE are absent in the serum.
  IgG present in small amount
• Cell-mediated immunity intact. T lymphocytes are
  normal, B cells are completely lacking
• Protein tyrosine kinase (PTK) gene deletion and
  point mutation
• Tx gamma globulin

66
Selective IgA Deficiency

• Most common immunoglobulin deficiency
• Usually asymptomatic
• Clinical manifestations 10-15
• Sinopulmonary bacterial infections
• Giardia gastroenteritis
• 1/3 with clinical disease develop autoimmune
  disorders
• SLE, Vitiligo, chronic mucocutaneous candidiasis,
  lipodystrophia centrifugalis abdominalis, ITP
• No sexual predilection
• A number of patients have severe atopic-like
  dermatitis, asthma, cow's milk allergy, and/or
  allergic rhinoconjunctivitis.
• An extremely rare selective immunoglobulin
  deficiency, IgM deficiency, is apparently caused
  by an inability of T-helper cell function to
  stimulate IgM production. In addition to
  recurrent bacterial infections, severe eczema and
  extensive large warts have been described.

67
Hyperimmunoglobulinemia M syndrome
68
Isolated IgA Deficiency

• Absence or marked reduction of serum IgA
• 1600 in white population, most are entirely
  well.
• Malignancy is increased in adult with IgA
  deficiency.

69
Common Variable Immunodificiency

• Aka acquired hypogammaglobulinemia
• HLA marker B8 and DR3 are affected
• B cells present but not terminally differentiated
• T cell dysfunction evident
• Recurrent sinopulmonary infections- patients are
  especially predisposed to pyogenic upper and
  lower respiratory tract infections

70
Common Variable Immunodeficiency

• Increased risk of autoimmune disorders
• Vitiligo, alopecia areata, vasculitis
• 8- to 13-fold increased risk of cancer overall
• Increased incidence of lymphoma
• 400 fold increase risk in female patients
• Giardia infections are more common in CVID than
  in the X-linked form. Patients frequently have
  cutaneous pyodermas and eczema.
• Abnormalities of cell-mediated immunity may occur
  in addition to the Ig deficiency and may manifest
  in the skin as widespread warts and extensive
  dermatophyte infections.
• Pts may develop non-caseating granulomas of the
  lungs, liver, spleen, and/or skin that are not
  due to microorganisms.
• Death in patients with CVID usually results from
  infection, respiratory insufficiency, or
  neoplasia.

71
(No Transcript)
72
Isolated Primary IgM Deficiency

• Eczematous dermatitis presents in 1/5 of patients
  with this condition
• Predisposition to bacterial infection
• Defect in maturation of IgM producing plasma cell.

73
Immunodificiency with Hyper-IgM

• Low or absent IgG, IgE, and IgA level. Normal or
  elevated IgM and IgD
• X-linked form caused by mutation or deletion of
  Xq26.3-27.1 region, which encodes a ligand of
  CD40, gp39
• Gp39-CD40 interaction signals for Ig isotype
  switching.
• Tx IVGG, and allogenic bone marrow transplant

74
Thymic Hypoplasia

• DiGeorge anomaly, aka III and IV pharyngeal pouch
  syndrome
• Facies notched and low-set ears, micrognathia,
  shorten philtrum, hypertelorism
• Congenital absence of the parathyroid, thymus,
  and abnormal aorta
• Hypocalcemia is the first sign
• Aortic and cardiac defects are the most common
  cause of death
• Deletions within proximal long arm of chromosone
  22

75
Noninfectious, persistant cutaneous granulomas in
a patient with DiGeorge Syndrome. The granulomas
are indistinguishable clinically from cutaneous
granulomas associated with other
immunodeficiencies.
76
Thymic Dysplasia with Normal Immunoglobulins
(Nezelof Syndrome)

• Faulty development of thymus gland
• Autosomal recessive
• Thymus is present but underdeveloped no cardiac
  abnormalities
• Contrast to DiGeorge syndrome

77
Purine Nucleoside Phosphorylase Deficiency

• Greatly reduced T-Cell counts, depressed cell
  mediated immunity
• B cells and antibody formation intact
• Mutation on 14q13
• Usually die of overwhelming viral infection

78
Miscellaneous T-Cell Deficiencies

• Cartilage-hair hypoplasia syndrome
• AR, patient with short-limbed dwarfism, fine
  sparse, hypopigmented hair, defective cell
  mediated immunity. Some may also have deecreased
  humoral immunity.
• Most common in Amish and Finns
• May have doughy skin secondary to degenerated
  elastic tissue
• Increased risk of non-Hodgkins lymphoma and
  basal cell carcinomas
• Patients are highly susceptible to severe
  disseminated varicella

79
Miscellaneous T-Cell Deficiencies

• Omenns syndrome
• AR
• Mimics GVHD
• exfoliative erythroderma, eosinophilia, recurrent
  infection, hypogammaglobulinema, diarrhea,
  hepatosplenomegly, alopecia
• Early death by 6 months
• Inefficient and abnormal generation of T-Cell
  receptors.

80
SCID Severe Combined Immunodeficiency Disease

• Severe impairment of humoral and cellular
  immunity
• 75 of pts are males
• Recurrent infections, diarrhea, and failure to
  thrive are apparent by 3-6 months of age
• Triad of Moniliasis of the oropharynx and skin,
  intractable diarrhea, and pneumonia.
• Overwhelming viral infection is the cause of
  death.
• Deficiency or total absence of circulating
  lymphocytes
• Infants can present with diffuse skin
  involvement seborrheic-like dermatitis or
  morbilliform eruptions.
• Common early infections are mucocutaneous
  candidiasis, virus-induced chronic diarrhea with
  malabsorption, and pneumonia due to bacteria,
  viruses, or Pneumocystis carinii.
• Cutaneous infections are most often caused by C.
  albicans, S. aureus, and S. pyogenes.

81
Ataxia-Telangiectasia (Louis-Bar Syndrome)

• Distinctive telangiectasia in bulbar conjuctiva
  and flexural suraces of the arm developing during
  the 5th year of age
• Telangiectasia occurs on butterfly area of the
  face, palate, ear, and exposed skin. Café au
  lait patches, and graying hair also present.
• Cerebellar ataxia is the first sign of this
  syndrome, beginning in the second year of life.
• Choreic and athetoid movement present.

82
(No Transcript)
83
Ataxia-Telangiectasia

• Progeric changes seen in 90
• Subcutaneous fat is lost
• Facial skin becomes atrophic and sclerotic early
  on
• Poikiloderma
• Sinopulmonary infections in 80
• Defects in cell mediated immunity
• Most common cause of death is bronchiectasis with
  respiratory failure

84
(No Transcript)
85
Wiskott-Aldrich Syndrome

• Exclusively in boys
• Triad chronic eczematous dermatitis resemble AD,
  increase suseptibility to infections (OM), and
  thrombocytopenic purpura/hepatosplenomegly
• Thrombocytopenia, petechiae and hemorrhagic
  episodes
• Death by age 6
• Accelerated IgA, IgM and IgE synthesis
• T-cell decline in numbers and activity
• Xp11 gene mutation. Codes for WASP protein which
  reorganize cytoskeleton
• Bone marrow transplant is tx of choice

86
(No Transcript)
87
Petechiae and ecchymoses in a young boy with WAS
88
X-Linked Lymphoproliferative Syndrome

• Aka Duncans disease
• Inability to control Epstein-Barr virus
  infection.
• Pt normal until develop infectious Mono.
• Necrotic hepatitis and exanthem are common
• Xq26 abnormailty
• B-cell lymphoproliferative disease with acquired
  hypoglobulinemia.

89
Chronic Granulomatous Disease

• Recurring purulent and granulomatous infections
  involving long bones, lymphatic tissue, liver,
  skin, and lung.
• Deficient in one of the component of
  NADPH-oxidase complex, which generates
  superoxide.
• Leads to inability to destroy bacteria per
  radical mechanism
• Patients develop granulomas as a compensatory
  effort to confine organisms

90
Chronic Granulomatous Disease

• 65 of cases are the X-linked form, lacks the
  subunit of cytochrome b 558(gp91-phox)
• Female carrier has mixed, normal and abnormal
  cells thus shows an intermediate phenotype.

91
Chronic Granulomatous Disease

• Myeloperoxidase producing bacteria
  characteristically cause infections because their
  destruction requires generation of oxygen free
  radicals
• Staph. Aureus
• Serratia

92
Chronic Granulomatous Disease

• Screening test Nitroblue tetrazolium (NBT)
  reduction assay
• NBT is normally yellow
• 80-90 of normal leukocytes reduce NBT during
  phagocytosis to insoluble precipitate, turning it
  blue
• Only 5-10 of leukocytes from patients with CGD
  are able to reduce NBT during phagocytosis

93
(No Transcript)
94
Leukocyte Adhesion Molecule Deficiency

• Autosomal recessive
• Affects the adherence of neutrophils, cytolytic T
  lymphocytes, and monocytes
• Faulty complexing of the CD11 and CD18 integrins
• Necrotic ulcerations resembling pyoderma
  gangrenosum
• Frequent skin infections, mucositis, and otitis
• Poor wound healing
• Delayed separation of the umbilical cord
• Death usually occurs by 5 years of life unless
  bone marrow transplant is undertaken.

95
A minor scratch from his sister evolved during
the subsequent weeks into a large ulcer on the
arm of a boy with leukocyte adhesion disorder.
96
Chediak-Higashi Syndrome

• Autosomal recessive
• Abnormal pigmentation with silvery hair
• Photophobia
• Partial oculocutaneous albinism, cutaneous and
  intestinal infections early in childhood
• Ocular albinism is accompanied by nystagmus and
  photophobia
• Parental consanguinity common

97
Chediak-Higashi Syndrome

• Defect in the gene LYST, resulting in defective
  vesicular transport to and from the lysosome and
  melanosome
• Causes the giant intracytoplasmic granules
  found within leukocytes, melanocytes, hair
  shafts, renal tubular cells, CNS neurons, and
  other tissues

98
(No Transcript)
99
Hyperimmunoglobulinemia E Syndrome

• Autosomal dominant with variable expressivity
• Consists of atopic-like eczematous dermatitis,
  recurrent pyogenic infection, high level of IgE,
  elevated IgD, IgE anti-staphlococcal antibodies,
  and eosinophilia.
• Face is consistently involved. Begin early in
  life (2 month to 2 years)
• Lesions resemble prurigo
• Keratoderma of the palms and soles

100
(No Transcript)
101
Jobs syndrome

• AKA Buckley Syndrome
• Subset of HIE.
• Mainly affect girls with red hair, freckles, and
  blue eyes.
• Hyperextensible joints
• Cold abscesses occur.

102
(No Transcript)
103
Graft-Versus-Host Disease

• Immunocompetent cells are introduced as graft or
  blood transfusion to host who is unable to reject
  the graft cell.
• Most commonly after bone marrow transplant.
• Begins between 4-5th weeks after transplant.
• Result in exfoliative erythroderma.

104
Early, chronic graft-versus-host reaction with
widespread, almost confluent hyperpigmented
lichenoid papules and toxic epidermal
necrosis-like appearance on knee 
105
Late, chronic graft-versus -host reaction with
hyperpigmented sclerotic plaques on the back
106
Acute graft-versus-host reaction with vivid
palmar erythema 
107
Graft-versus-host reaction with early, chronic,
diffuse, widespread lichenoid changes of lips
108
Acute erosions of the buccal mucosa in
graft-versus-host reaction
109
Graft-versus-host reaction acute basal cell
hydropic degeneration with interepidermal
necrotic keratinocytes 
110
Graft-versus-host reaction early chronic
hyperkeratosis and hypergranulosis, irregular
acanthosis, cytoid body and basal cell hydropic
degeneration reminiscent of lichen planus
111
(No Transcript)
112
THE END