common skin inflammatory diseases.pptx

SHUKRALLAH
ZAYNOUN,M.D.
CLINICAL PROFESSOR
DEPARTMENT OF DERMATOLOGY
AMERICAN UNIVERSITY OF BEIRUT

SOME COMMON INFLAMMATORY SKIN
DISORDERS
 Handout : An introduction, a skeleton.
Gives you a bird’s eye view.
 Details not necessary at present.
 Impossible to cover all skin diseases in
such a short period.
 No need to take notes. Slides are
exactly as the text. Treatment will be
brief.
 No side talks!

DERMATITIS
 The terms dermatitis and eczema are
often used interchangeably.
 Derma=skin, itis= inflammation.
Dermatitis means inflammation of the
skin.
 Affects one in every five people at some
time in their lives.

DERMATITIS
 ACUTE
 SUBACUTE
 CHRONIC

ACUTE DERMATITIS
 Erythema
 Edema
 Vesiculation

CHRONIC DERMATITIS
 Mild erythema
 Scaliness
 Lichenification : thickening of
epidermis with accentuation of skin
markings, with or without
hyperpigmentation

CHRONIC DERMATITIS
Color atlas of Pediatric Dermatology by Weinberg et al 1975
Figure 224

SUBACUTE
 An in-between state.

DERMATITIS
 Secondary bacterial infection may
occur.

CLASSIFICATION OF
DERMATITIS
A- EXOGENOUS = CONTACT DERMATITIS:
DERMATITIS
FOLLOWS CONTACT OF A SUBSTANCE WITH
SKIN.
1. Primary irritant contact dermatitis
2. Allergic contact dermatitis
B- ENDOGENOUS = CONSTITUTIONAL DERMATITIS

PRIMARY IRRITANT CONTACT
DERMATITIS
 The most common type of contact
dermatitis.
 Includes chemical burns (acids and
alkalies).
 A primary skin irritant is a substance that
causes damage at the site of contact
because of its direct chemical or physical
action on the skin.
 Not immunologic. No antecedent
immunologic sensitization is required.
Reaction can be elicited in all individuals.

PRIMARY IRRITANT CONTACT
DERMATITIS
 Certain factors may affect the severity of
the dermatitis. These include the strengths
of the irritant substance, frequency of
exposure and skin sensitivity as occurs in
atopic dermatitis.
 The hands are most commonly affected
usually from repeated exposure to water,
soaps and detergents.
 No diagnostic test for irritant contact
dermatitis.

PRIMARY IRRITANT
CONTACT DERMATITIS- Acute

PRIMARY IRRITANT CONTACT DERMATITIS-
chronic

PRIMARY IRRITANT CONTACT DERMATITIS -
chronic

TREATMENT OF PRIMARY IRRITANT
CONTACT DERMATITIS
 Preventive measures. In the case of hand
dermatitis the use of cotton gloves inside
rubber gloves is helpful.
 Topical corticosteroid preparations.

ALLERGIC CONTACT DERMATITIS
 A form of cell-mediated hypersensitivity
(tuberculin-like, type IV response), based on
a specific immunologic alteration requiring
an incubation period of several days.
Sensitization occurs about one week after
the first exposure.
 Re-exposure to allergen causes dermatitis
that appears eight to ninety six hours after
exposure.
 Only small quantities of allergen are
necessary to induce the reaction.

MECHANISM OF SENSITIZATION
 Most environmental allergens are haptens,
that is, simple chemicals that must link to
proteins to form a complete antigen before
they sensitize.
 The complete antigen combines with binding
sites on membrane of Langerhans cell.
Langerhans cells are bone marrow-derived
dendritic cells and are located within the
suprabasal layer of the epidermis. They
possess HLA-DR or class II antigens on their
surface, which act as binding sites (carriers)
for contact allergens.

MECHANISM OF
SENSITIZATION
 The antigen is taken up and processed by
the Langerhans cell which then migrates
from the epidermis to the draining lymph
node where it presents the processed
antigen to the T cell. T cells become
sensitized and start proliferating.
 Sensitized lymphocytes enter the blood
circulation. The whole skin becomes
sensitized.

AFFECTED SITES
 The dermatitis is generally confined to
the site of contact with the allergen.
 Sometimes the allergen is transferred
from the hands to other sites.

AAD Occupational Dermatoses

ALLERGIC CONTACT
DERMATITIS
A color atlas of Dermatology by Levene & Calnan 1974
Figure 30

ALLERGIC CONTACT
DERMATITIS
Atlas of Contact Dermatitis 1999 Figure 4.102

Atlas of Contact Dermatitis 1999
Figure 7.67.b

ALLERGIC CONTACT
DERMATITIS
Atlas of Contact Dermatitis 1999 Figure 7.52.a

Atlas of Contact Dermatitis 1999 Figure 7.52.b

MANAGEMENT
 A detailed history is important in evaluating
individuals with allergic contact dermatitis
and identifying the allergen.
 Patch testing will confirm the nature of the
material causing the dermatitis.

TREATMENT
 Avoid the allergen.
 Topical corticosteroids are the mainstay of
treatment. In severe cases systemic
corticosteroids may be indicated.

ENDOGENOUS DERMATITIS
 It is the most common form of dermatitis.
 Several types exist. The commonest are:
1. Atopic dermatitis
2. Seborrheic dermatitis
3. Dyshidrotic dermatitis

ATOPIC DERMATITIS
 Occurs in association with a personal or
family history of atopy.
 Atopy is a heritable state of increased
susceptibility to atopic diseases, e.g.
asthma, hay fever, urticaria, allergic
conjunctivitis and systemic drug allergy.
There is increased production of IgE
antibodies, the role of which in dermatitis is
not fully clarified.
 Skin is dry, irritable (sensitive), with a low
threshold for itching. Itching leads to
scratching and lichenification.

CLINICAL MANIFESTATIONS
 The dermatitis usually starts in early
infancy.
 Infants less than one year old often
have widely distributed eczema.
 The cheeks of infants are often the first
place to be affected by eczema.
 Flexures are affected in childhood and
later on in life.

PATHOGENESIS
 Abnormalities in the skin barrier that
causes increased permeability.
 May be due to a) immune-mediated
mechanisms
b) inherited structural gene
mutations.

Immune-mediated mechanisms
 There is generally an equilibrium of the two
main types of T Helper lymphocytes, Th- 1
and Th-2.
 In atopic dermatitis, there is often an
imbalance, with far more Th-2 cells and
their associated chemical messengers
(cytokines) particularly IL-4 and IL-13 (Th2
pathway cytokines) and IL-22 (the Th22
axis cytokine).
 This leads to barrier defects
and inflammation that result in the clinical

Inherited structural gene
mutations
 Mutations in the gene for the production of filaggrin
strongly increases the risk for developing atopic
dermatitis.
 Filaggrin is a protein that plays an important role in
the retention of water in the stratum corneum, and a
mutation in this protein leads to dry skin.
 A defect in skin barrier function makes the skin more
susceptible to irritants, weather changes and other
triggers.
 However, the majority of patients with AD do not
have filaggrin mutations, and, in these patients, the
downregulation of epidermal filaggrin expression
may be caused by several important factors
including Th2 skin inflammation and environmental

Atopic dermatitis in a 6 months old
infant

ATOPIC DERMATITIS IN
CHILDHOOD

TOPICAL TREATMENT OF ATOPIC
DERMATITIS
 Avoid aggravating factors such as contact with
irritants and chemical and rough materials e.g.
wool, extremes of weather, excessive bathing,
exposure to chlorinated water in swimming
pools.
 Patients should stop rubbing and scratching.
 Emollients to keep the skin moist.
 Topical corticosteroids to suppress the
inflammation.
 Topical immunomodulators such as tacrolimus
may be helpful.

ORAL TREATMENT OF ATOPIC
DERMATITIS
 Oral medications are reserved for severe
eczema.
 Oral corticosteroids, ciclosporin and
methotrexate.
 Biologic medications (biologicals) that are
monoclonal antibodies or recombinant
proteins targeted at specific components of
the immune system mainly Th2 cytokines
are being developed.

PROGNOSIS OF ATOPIC
DERMATITIS
 54% CLEAR BY AGE 2

SEBORRHEIC DERMATITIS
 Cause is unknown.
 Associated with excessive sebaceous
secretion (seborrhea) and is usually
localized in the areas of greatest sebaceous
activity such as the scalp, face (nasolabial
folds), and trunk (including presternal
region, axillae and crural region).

 Onset is during the first few months of life
and at puberty. It may affect infants as cradle
cap or napkin dermatitis and usually clears
by one year of age.
 Lesions consist of subacute dermatitis
covered by greasy scales.

 Dandruff is a form of seborrheic
dermatitis.
 The dermatitis is frequently associated
with acne.
 Activity is increased in winter and early
spring. It improves during summer.
 The condition in adults lasts for a
lifetime.

Seborrheic dermatitis(cradle
cap)

TREATMENT OF SEBORRHEIC
DERMATITIS
 Shampoos containing ketoconazole, tar, zinc
pyrithione.
 Topical ketoconazole.
 Topical corticosteroids.

DYSHIDROTIC DERMATITIS
(ECZEMA)
 Also known as dyshidrosis or pompholyx.
 Recurrent vesicles and/or bullae appear on the
palms and sides of fingers and sole of feet.
 Blisters normally last for about three weeks then
dry and end up in scales.
 Cause is unknown. It is not due to sweat
dysfunction but hyperhidrosis may be an
aggravating factor. It is more commonly seen in
warmer climates and during spring and summer.

DIFFERENTIAL DIAGNOSIS OF
DYSHIDROTIC DERMATITIS
 Allergic contact dermatitis.
 Id reaction to inflammatory tinea
pedis.

Tinea Pedis and Id Reaction over
Hands

TREATMENT OF DYSHIDROTIC
DERMATITIS
 High-strength topical corticosteroids and
cold compresses.
 Short courses of oral steroids as the
second line of treatment for acute flares.
 Oral antibiotics for secondary infection.

PAPULOSQUAMOUS
DISORDERS
 PSORIASIS
 LICHEN PLANUS
 PITYRIASIS ROSEA

PSORIASIS
 Genetic disorder.
 Several clinical expressions. Most common
is
psoriasis vulgaris which affects 2% of the
population.
 Primary lesion in psoriasis vulgaris is a
well-demarcated erythematous papule or
plaque, covered by silvery scales.

PSORIASIS
 Usually affects extensor surfaces, scalp and
glans penis.
 Nails may be affected (commonly pitting and
onycholysis).
 In up to 30% of patients, the joints are also
affected.

Proto-type lesion: erythematous papule
or plaque covered by silvery scales

PATHOPHYSIOLOGY
 Psoriasis involves hyperproliferation of the
keratinocytes in the epidermis, with an increase in
the epidermal cell turnover rate (4 days from basal
cell layer to stratum corneum compared with 27 days
in normal skin).
 Psoriasis is a complex immune-mediated disease
in which T lymphocytes, dendritic cells, and
increased production of cytokines play a
significant role in the development of this disease.
Early investigational studies presumed a
dominating role for Th1 cells which produce an
array of proinflammatory cytokines, including IFN-
gamma, IL-2, and TNF-alpha.; However, Th17 cells
are now believed to play the more critical role.

INCREASED EPIDERMAL TURNOVER
RATE

Factors that may precipitate or aggravate
psoriasis
 Physical and emotional stress.
 Psoriasis tends to localize at sites of friction.
Isomorphic response may occur following
trauma.
 Infections may cause flares of psoriasis; in
particular streptococcal throat infection may
result in guttate psoriasis .
 Several medications can precipitate or
aggravate psoriasis e.g. lithium, beta-
blockers, anti-malarials and non-steroidal
anti- inflammatory agents.

Koebner phnenomenon or isomorphic
response

Post-streptococcal guttate
psoriasis

PSORIASIS & METABOLIC
SYNDROME
 There is a relationship between psoriasis
and metabolic syndrome.
 Metabolic syndrome refers to the
combination of obesity, hypertension,
dyslipidemia and insulin resistance.
 Patients with psoriasis have a higher
prevalence of metabolic syndrome, and
patients with more severe psoriasis are
more likely to have metabolic syndrome
than those with milder psoriasis.

TREATMENT
 There is no cure for psoriasis but there is
ongoing search for new therapy.
 The first line of therapy consists of topical
medications and short wave ultraviolet
radiation (UVB) or sun exposure.
 Topical treatments include topical steroids,
vitamin D analogues (cacipotriene), coal tar,
salicylic acid, and moisturizers.

TREATMENT (ctd)
 Systemic therapy is reserved for more extensive and
more difficult cases.
 The more commonly used systemic medications are
methotrexate, oral retinoids, cyclosporine and
immunomodulators.
 Photochemotherapy which involves oral psoralens plus
long wave ultraviolet radiation is more effective than UVB
but has fallen into disrepute because of potential
carcinogenesis.
 The most recent drugs are the biologicals. These include
inhibitors of TNFα, interleukins 17, 23, and 12. To assess
the degree of improvement the Psoriasis Area and
Severity Index (PASI) is the most widely used. PASI
combines the assessment of the severity of lesions and
the area affected into a single score. A near 100 %
clearing of psoriasis has been achieved with some

LICHEN PLANUS
 Unknown etiology.
 Primary lesion is a violaceous lichen,
sometimes with whitish streaks on surface.
Lacy white lesions on buccal mucosa.
 Affects skin, mucous membranes, nail, and
hair. Itching is a fairly consistent feature.
 Koebner phenomenon or isomorphic
response.
 Distribution of lesions: inner wrists, lumber
region, shins, scalp, and glans penis.

Koebner phenomenon or isomorphic
response

SOME OTHER FORMS OF LICHEN
PLANUS
 Actinic lichen planus: occurs on sun-
exposed sites.
 Lichenoid drug eruption: e.g Gold,
antimalarials (hydroxycholorquine),
captopril (ACE inhibitor),
hydrochlorothiazide, non- steroidal anti-
inflammatory drugs (NSAIDs).

TREATMENT OF CLASSICAL LICHEN
PLANUS
 Topical and systemic steroids

PITYRIASIS ROSEA
 A self-limited disease, thought to be viral in
origin, commonly seen in early spring and
later summer (early autumn).
 Lasts about six weeks.
 Primary lesion is an erythematous, oval scaly
macule with a scale trailing just inside the
edge of the lesion like a collaret.
 The rash is preceded by a large, usually
annular lesion with a scaly border resembling
ringworm infection, called the “herald patch”.

PITYRIASIS ROSEA
 The rash is symmetrical and affects mainly
the trunk and proximal part of the
extremities.
 The lesions are oriented in the planes of
cleavage running parallel to the ribs.
 The rash is usually asymptomatic.
 The differential diagnosis includes
secondary syphilis and drug eruptions.
 No treatment is necessary. Sun is
beneficial.

Oval scaly macules with a scale trailing just
inside the edge of the lesion like a collaret

Rash is preceded by a large, usually annular lesions with a scaly
border
resembling ringworm infection, called the “herald patch”.

The lesions are oriented in the planes of
cleavage running parallel to the ribs

ACNE VULGARIS
 Acne vulgaris is a chronic inflammatory
disorder of the pilosebaceous follicle
associated with seborrhea.
 Genetically determined.
 Onset is at puberty.
 Lesions are distributed over the face, neck,
upper trunk, and proximal part of the upper
extremities where sebaceous glands are
largest and most numerous.

HORMONAL CONTROL OF SEBACEOUS
GLANDS
 Testosterone : increase size and secretion.
 Estrogen : decrease size and secretion.
 Progesterone :
a. Physiologic amounts : no effect.
b. Pharmacologic dose : increase size and
secretion.

ACNE FOLLICLE
 Broad canal.
 Rudimentary hair.
 Hyperplastic sebaceous gland.
 Abnormal keratinization of lining epithelium
of the sebaceous duct and follicle with
resultant comedo formation and plugging.

PATHOGENESIS
 The comedo (or comedone) is the initial
acne lesion. Plugging leads to rupture of
hair follicular epithelium with resultant
inflammation leading to the formation of
papules, pustules, nodules, and cysts.
 The mechanism of comedo formation is
disputed but is probably influenced by
sebum and free fatty acids derived from
sebum triglycerides under the effects of
lipase enzyme.

Primary lesion: comedo
(comedone)

FACTORS THAT MAY WORSEN ACNE
 Cosmetic agents and hair pomades.
 Medications such as steroids, androgens,
lithium, some antiepileptics, and iodides.
 Diet: Studies indicate that certain dietary
factors, including dairy products and
carbohydrate-rich foods — such as bread,
bagels and chips, which increase blood
sugar — may trigger acne.

POLYCYSTIC OVARY SYNDROME
Women with polycystic ovary syndrome
often experience dermatologic
manifestations of hyperandrogenism,
including hirsutism, acne vulgaris, and
androgenic alopecia. Also, irregular
menstrual bleeding.

TREATMENT
 Topical preparations containing benzoyl
peroxide, acids (e.g. salicylic acid, retinoic
acid), antibiotics (erythromycin and
clindamycin).
 Oral antibiotics mainly doxycycline.
 Isotretinoin, a vitamin A derivative, is used
for severe nodulocystic acne.
 Intralesional steroid injections.
 Manual extraction of comedones (acne
surgery).

ROSACEA
 The cause is unknown.
 Some cases are genetic.
 Red papules and sometimes pustules but
no comedones.
 Erythema and telangiectasia usually in a
butterfly distribution.
 History of flushing.

ROSACEA
 Patient with rosacea have a sensitive skin with
burning and stinging, especially in reaction to
make-up, sunscreens and other facial creams .
 Dry and flaky facial skin.
 Rosacea is worsened by exposure to sun and heat.
Common triggering factors include hot or cold
temperatures, hot drinks, alcohol, spicy food,
caffeine, emotions, topical irritants, and
medications that cause flushing, e.g. nicotinic
acid. Potent topical corticosteroids worsen
rosacea.

Rhinophyma
Some patients with rosacea may develop enlarged unshapely
nose with prominent pores (sebaceous hyperplasia) and
fibrous thickening called rhinophyma. It is a slowly
progressive condition and is often seen in cases of long-
standing disease.

Eye involvement
 Blepharitis.
 Conjunctivitis.
 Styes.

Blepharo-kerato-conjuctivitis
Eye and Skin Disease - Mannis 1996 p
338 Patient with severe active rosacea
blepharo-kerato-conjuctivitis. Note the
lid inflammation posterior lamellar
disease, interpalpebral conjunctival
hyperemia, corneal vascularization and
sterile corneal infiltrates.
Eye and Skin Disease - Mannis 1996 p
337 Characteristic interpalpebral
bulbar conjuctival injection in rosacea
blepharoconjuctivitis.

Differential diagnosis of
rosacea
Rosacea may be confused with or accompanied
by acne vulgaris. The latter has comedones and
usually starts at a younger age.

Treatment of rosacea
 Avoid sun, heat and spicy foods. Use oil-free
cosmetics including sunscreens. Avoid topical
corticosteroids as they may aggravate the
condition.
 Topical metronidazole and topical ivermectin.
 Oral doxycycline & minocycline.

VESICULOBULLOUS
DISEASES
 Epidermolysis bullosa
 Pemphigus vulgaris
 Bullous pemphigoid
 Dermatitis herpetiformis

BASEMENT MEMBRANE ZONE
 The cutaneous basement membrane zone connects the basal cell
cytoskeletal network with the network of interstitial collagen fibrils in
the dermis.
 Made up of anchoring complexes.
 At the superior aspect of the basement membrane zone, keratin-
containing intermediate filaments of the basal cell cytoskeleton insert
on basal cell plasma membrane condensations termed hemi-
desmosomes.
 Anchoring filaments extend from the basal cell plasma membrane into
the extracellular environment and span the lamina lucida, connecting
hemidesmosomes with the lamina densa.
 At the most inferior aspect of the basement membrane zone, type VII
collagen-containing anchoring fibrils extend from the lamina densa into
the papillary dermis, connecting the lamina densa to anchoring plaques,
trapping interstitial collagen fibrils.

The ultrastructural elements of the dermal-
epidermal basement membrane
Dermatology in General Medicine 1999 Figure 65-1

The ultrastructural elements of the dermal-
epidermal basement membrane

EPIDERMOLYSIS BULLOSA
 Epidermolysis bullosa is a group of
inherited bullous disorders characterized
by blister formation on the skin and
mucous membranes in response to
mechanical trauma, usually on hands and
feet.
 The condition usually shows up in infancy
or early childhood. Some people don't
develop signs and symptoms until
adolescence or early adulthood.

CLASSIFICATION OF EPIDERMOLYSIS
BULLOSA
Classified into 3 major types based on site
of blister formation. Various subtypes exist
within each type.
1. Epidermolysis bullosa simplex
(epidermolytic).
2. Junctional epidermolysis bullosa: Herlitz
or
lethal form (basement membrane zone).
3. Dystrophic epidermolysis bullosa
(dermolytic).

CLASSIFICATION OF EPIDERMOLYSIS
BULLOSA

Junctional epidermolysis
bullosa
DIGM 1999 Figure 65-5

Dominant dystrophic epidermolysis
bullosa

Recessive dystrophic epidermolysis
bullosa

Recessive dystrophic epidermolysis bullosa-
Older patient

Management of epidermolysis
bullosa
 Reduce blister formation.
 Supportive therapy.
 Prevent complications such as secondary
infection.
 No cure.

PEMPHIGUS VULGARIS
 Pemphigus vulgaris is an autoimmune, intraepithelial, blistering disease
affecting the skin and mucous membranes particularly the mouth but
may also affect the genitals and conjunctiva.
 The primary lesion of pemphigus vulgaris is a flaccid blister filled with
clear fluid that easily ruptures producing painful erosions.
 The disease is more common in Jews. The age of onset is commonly
between 50 and 60 years of age.
 It is a potentially life-threatening disease and has a mortality rate of
approximately 10%

Pemphigus vulgaris of mucous
membranes
Dermatology in
General
Medicine 1999
Figure 60-2
Pemphigus
vulgaris. A.
Flaccid blisters.
B. Oral erosions.
Br J Derm 140,
945,1999 Fig1.
Pemphigus vulgaris
localized to the
vagina presenting as
chronic vaginal
discharge An erosion
is evident on the
anterior vaginal wall
(arrow).

Pathogenesis
 There is binding of IgG autoantibodies to
keratinocyte desmosomes.
 This results in a loss of cell-to-cell adhesion
(acantholysis) and subsequent blister formation.

Histopathologic findings
The skin biopsy shows a blister above the
basal cell layer of the epidermis containing
acantholytic cells (rounded-up separated
keratinocytes).

Histopathology of pemphigus
vulgaris
Suprabasilar acantholysis
DIGM 1999 Figure 5-4 Single as well as
clusters of acantholytic cells are seen.
The round shapes result from the loss of
intercellular connections.
Cytologic smear preparation.

Immunofluorescence in
pemphigus
Immunofluorescence in
pemphigus. A. Direct
immunofluorescence for
IgG of perilesional skin from
a patient with pemphigus
vulgaris. Note
cell surface staining
throughout the epidermis.
B. Indirect
immunofluorescence with
the serum from a patient
with pemphigus
foliaceus on normal human
skin. Note IgG on the cell
surface
throughout the epidermis.

Treatment
 Oral corticosteroids are the mainstay of
treatment. Immunosuppressive agents such as
azathioprine should be considered early the
course of the disease as a steroid-sparing agent.
Oral antibiotics for secondary infection.

BULLOUS PEMPHIGOID
 A chronic, subepidermal, autoimmune, blistering
skin disease which primarily affects middle-aged
or elderly individuals.
 The lesions consist of tense, fluid-filled, bullae
that heal without scarring or milia formation.
 Mucous membranes are not usually affected.

Pathogenesis
IgG autoantibodies and activated T lymphocytes
attack components of the basement membrane,
particularly a protein known as the BP antigen
BP180, or less frequently BP230.

Diagnosis
 The diagnosis is usually made clinically but may be
confirmed by a skin biopsy and immunoflurescence
studies.
 The histopathologic findings consist of subepidermal
blister and a polymorphous inflammatory infiltrate with an
eosinophil predominance.
 Direct immunofluorescence on a perilesional skin biopsy
specimen shows a linear band of immunoglobulin G deposit
along the dermoepidermal junction.

Diagnosis
JAAD 58,41-48,2008.
Tense blisters. D, Western
blot analysis of serum and
blister fluid in patient 7
demonstrating IgG
antibodies against 180 and
230 kd, typical of BP. E,
Subepidermal vesicle with
few intravesicular
eosinophils, hydropic
degeneration of basal cell
layer, and mixed
mononuclear and
eosinophilic infiltrates in
papillary dermis.
(Hematoxylin-eosin stain;
original magnification: ×40.)
F, Direct
immunofluorescence
demonstrating linear
deposition of IgG along
dermoepidermal junction of
lesional skin.

Treatment
Treatment usually includes oral corticosteroids,
and other drugs that suppress the immune
system such as azathioprine.

DERMATITIS HERPETIFORMIS
 Dermatitis herpetiformis is an autoimmune
subepidermal blistering disorder associated with
celiac disease, a gluten-sensitive enteropathy, and
is a cutaneous manifestation of gluten sensitivity.
 Like other forms of celiac disease, it involves IgA
antibodies and intolerance to the gliaden fraction
of gluten found in wheat, rye and barley.

CELIAC DISEASE
 Autoimmune disorder of the small intestine.
 Patients have intolerance to gliaden fraction of gluten,
which is found in wheat, rye, barley and oats.
 May be mild and asymptomatic or severe leading to
atrophy of the intestinal villi. This interferes with absorption
of nutrients.
 Common gastrointestinal symptoms include chronic
diarrhea, abdominal discomfort (pain), bloating, flatulence
and distension. Weight loss and failure to thrive.

Clinical features of dermatitis
herpetiformis
 The disease is characterised by extremely pruritic
papulovesicles or excoriated papules on extensor surfaces.
 They tend to be distributed symmetrically and are most
often found on the scalp, shoulders, buttocks, elbows and
knees.
 The name dermatitis herpetiformis means that it is a skin
inflammation having an appearance similar to herpes.
Grouped or ‘herpetiform’ papulovesicles with an
erythematous base are characteristic of dermatitis
herpetiformis.
 The blisters rupture upon scratching and result in erosions
and crusting.

Diagnosis
 Skin biopsy is usually required for diagnosis. It
shows neutrophilic infiltration of the dermal
papillae with vesicle formation at the dermal–
epidermal junction.
 Direct immunofluorescence of clinically normal-
appearing skin adjacent to a lesion exhibits
granular deposition of IgA in the dermal papillae
(versus linear IgG deposition in bullous
pemphigoid).

Skin biopsy
Dermatology in General Medicine 1999 Figure 5-11 Two
papillae show microabscesses composed of neutrophils.
Vacuolization and early cleft formation are evident in both
papillae.

Direct immunofluorescence
Dermatology in General
Medicine 1999 Figure 67-5
showing granular dermal
papillary deposits of IgA.
Textbook of Dermatology-
Rook 1998. Fig. 40.56
demonstrating granular IgA
deposition in the dermal
papillae.

Treatment
 A strict gluten-free diet is strongly
recommended.
 There is a dramatic response of the skin,
but not intestinal disease, to dapsone
therapy.

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