Bercak merah

ATOPIC DERMATITIS

DEFINITION
Atopic dermatitis is a chronic, relapsing, intensely pruritic,
inflammatory condition of the skin that is associated with
a personal or family history of atopic disease (e.g., asthma,
allergic rhinitis, or atopic dermatitis). The cause of atopic
dermatitis is thought to be altered skin barrier and immune
function. P

INCIDENCE
Atopic dermatitis is predominantly a disease of childhood,
with 17% of children and 6% of adults affected. It usually
starts after 2 months of age, and by 5 years of age, 90% of
the patients who will develop atopic dermatitis have manifested the disease. It is uncommon for adults to
develop
atopic dermatitis without a history.

Manifestasi klinis DA

TERAPI
THERAPY
The treatment of atopic dermatitis is the same as for other
eczematous eruptions and includes topical steroids, topical
macrolide immunosuppressants, and systemic antihistamines. However, the use of antihistamines to reduce
pruritus
is largely unproven. Only sedating antihistamines may be
effective for itching that interferes with sleep. Treatment
should be given in appropriate strength and frequency to
reduce inflammation and itching significantly. A common
error is under treatment. Occasionally, a short course of systemic steroids (prednisone) is necessary to bring the
disease
under control. Wet dressings (plain water) and bleach baths
are helpful in treating acute atopic dermatitis. Avoidance of
environmental factors that enhance itching, such as woolen clothes, emotional stress, and uncomfortable
climatic
conditions, is important. Moisturizers reduce dry skin and
itching. Ultraviolet radiation B (UVB), psoralen plus ultraviolet radiation A (PUVA), or other systemic
immunosuppressants – cyclosporine (Neoral), azathioprine (Imuran),
mycophenolate mofetil (CellCept), and dupilumab
(Dupixent) – may be considered if satisfactory control is
not achieved with initial treatment.

PATHOGENESIS
Atopic dermatitis is a multifactorial cutaneous inflammatory disease caused, in part, by gene
polymorphismisms
affecting the innate and adaptive immune response and
the epidermal barrier function.

1. A disrupted skin barrier

(filaggrin gene mutation) and
2. disturbed immunologic
response (Th2+Th1 cytokines, and IgE) have been
implicated in the etiology of atopic dermatitis.
3. The epidermal barrier defect results in dry skin and penetration
of irritants, microbes, and antigens.
4. The immunologic
changes are most notable and frequent in patients with
severe atopic dermatitis. These changes include raised
serum IgE levels, defective cellmediated immunity,
decreased chemotaxis of mononuclear cells, increased
Tlymphocyte activation with production of T helper Th1
and Th2 cytokines, and hyper stimulatory Langerhans
cells. The increased IgE concentration is thought to reflect
decreased numbers of Tsuppressor cells and uninhibited
production of IgE. Depressed cellmediated immunity is
manifested by an increased susceptibility to cutaneous
viral and bacterial infections. In addition, responses to
in vitro tests of cellmediated immunity such as lymphocyte blastogenesis to mitogens and antigens are
blunted.
There are also low levels of antimicrobial peptides in
lesional skin resulting in increased susceptibility to
pathogens such as S. aureus, herpes simplex virus, and
vaccinia virus
CONTACT DERMATITIS

DEFINITION
Contact dermatitis (Fig. 8.3) is an inflammatory reaction
of the skin precipitated by an exogenous chemical. The
two types of contact dermatitis are irritant and allergic.
Irritant contact dermatitis is produced by a substance that
has a direct toxic effect on the skin. Allergic contact dermatitis triggers an immunologic reaction that
causes tissue inflammation. Examples of irritants include acids,
alkalis, solvents, and detergents. Innumerable chemicals
cause allergic contact dermatitis, including metals, plants,
medicines, cosmetics, and rubber compounds. Clinical
appearance can range from acute (vesicles) to chronic
(lichenification) eczematous reactions.
Bacterial and viral skin infections are common in atopic
dermatitis.
Disruption of the skin barrier and immune dysfunction contribute to the development of atopic dermatitis.
Key Points
1. Irritant or allergic etiology
2. Distribution conforms to areas of contact
3. Avoidance of the contactant results in cure
PATHOGENESIS
Irritant contact dermatitis is a nonspecific inflammatory
reaction resulting from toxic injury of the skin. Allergic
contact dermatitis is a cellmediated, delayed type IV
immunologic reaction. It is divided into a sensitization

ESSENTIAL DERMATITIS

DEFINITION
Essential (nonspecific) dermatitis is an epidermal eruption that may be acute (Fig. 8.8) or chronic (Fig. 8.9),
and localized or generalized. It is a diagnosis that is
made by exclusion when an underlying cause such as an
allergen or irritant cannot be found, and its distribution
Allergic contact dermatitis is a cell-mediated, delayed type IV
immunologic reaction.
Key Points
1. Idiopathic etiology
2. Diagnosis of exclusion
3. Treatment is symptomatic: suppress inflammation and
itching phase and an elicitation phase. The sensitization phase
occurs when a chemical (hapten) is applied to the skin
of a nonsensitized individual. This chemical in itself is
unable to induce an allergic reaction because of its small
molecular size, which is usually less than 500 Daltons
(Da). It must combine with an epidermal protein thought
to be on the surface of the Langerhans cell (epidermal
macrophage). After the formation of the hapten–protein
complex, the Langerhans cell presents the allergen to T
lymphocytes in the lymph node, where effector, memory,
and suppressor lymphocytes are produced. The period
of sensitization requires approximately 7 to 10 days. The
elicitation phase occurs in sensitized individuals 1 to
2 days after reexposure to the antigen. After presentation
of the antigen by Langerhans cells to memory T cells in
the skin, effector T cells produce lymphokines, which
recruit other inflammatory cells and produce allergic
contact dermatitis. The dermatitis usually appears
clinically 1 to 2 days after the elicitation exposure. The
reaction is thought ultimately to be extinguished by
suppressor T cells
 LICHEN SIMPLEX CHRONICUS
DEFINITION
Lichen simplex chronicus (also called “neurodermatitis”) is a chronic eczematous eruption of the skin that
is the result of scratching (Fig. 8.13). Pruritus precedes
the scratching and may be precipitated by frustration,
depression, and stress. The scratching then causes the
lichenification and further itching, resulting in an “itch–
scratch–itch” cycle that perpetuates the process.
PHYSICAL EXAMINATION
The patient may appear anxious and may talk with pressured speech. There may be little insight into the cause
of
the eruption. The lichenified plaque always occurs within
reach of scratching fingers.
 SEBORRHEIC DERMATITIS
Key Points
1. Face and scalp most commonly involved
2. Treat with antiyeast and antiinflammatory agents
3. Check HIV status in severe cases

DEFINITION
Seborrheic dermatitis is a chronic, superficial, inflammatory process affecting the hairy regions of the body,
especially the scalp, eyebrows, and face (Fig. 8.15). Its cause is
thought to be an inflammatory reaction to the Malassezia
yeast (formerly Pityrosporum ovale). Dandruff is scaling of
the scalp without inflammation.,

NCIDENCE
Seborrheic dermatitis is a common problem affecting 3%
to 5% of the healthy population.

.l
PHYSICAL EXAMINATION
Seborrheic dermatitis has a predilection for the hairy
regions of the skin, where sebaceous glands are numerous
(Fig. 8.16). These regions are the scalp, eyebrows, eyelids,
nasolabial creases, ears, chest, intertriginous areas, axilla,
groin, buttocks, and inframammary folds

Bilateral

STASIS DERMATITIS
DEFINITION
Stasis dermatitis is an eczematous eruption of the
lower legs secondary to peripheral venous disease
(Fig. 8.17). Venous incompetence causes increased
hydrostatic pressure and capillary damage with
extravasation of red blood cells and serum. In some
patients, this condition causes an inflammatory
eczematous process.

INCIDENCE
Stasis dermatitis is a disease of adults, predominantly of
middle and old age.
HISTORY
Patients have a history of a chronic, pruritic eruption of the lower legs preceded by edema and swelling. Patients
with stasis dermatitis have often had
thrombophlebitis.
PHYSICAL EXAMINATION
Varicose veins are often prominent, as is pitting edema
of the lower leg. The peripheral pulses are intact. The
involved skin has brownish hyperpigmentation, dull
erythema, petechiae, thickened skin, scaling, or weeping.
Any portion of the lower leg may be affected, but the predominant site is above the medial malleolus.
PATHOGENESIS
Venous incompetence results in increased venous
pressure of the lower legs. This increased hydrostatic
pressure results in swelling and edema. Capillary
proliferation and leakage of red blood cells and vascular fluids result in inflammation. If the condition
is unchecked, fibrin deposition will occur around the
capillaries, resulting in tissue hypoxia, sclerosis, and
necrosis with ulceration.
 uNCommoN ECzEmATouS
APPEARING DISEASES
DARIER’S DISEASE
Darier’s disease, also known as keratosis follicularis, is a rare,
autosomal dominantly inherited genodermatosis. It is characterized by a chronic, waxing and waning course
beginning
in childhood and lasting a lifetime. The eruption (Fig. 8.18)
involves the scalp, face, neck, trunk, and extremities with
accentuation in the seborrheic areas. It has tan, pink, brown,
roughfeeling papules that coalesce into large plaques that
can become secondarily infected, resulting in crusting and
weeping. The skin biopsy is diagnostic, demonstrating epidermal suprabasilar clefts with acantholytic
keratinocytes.
Mutations in the ATP2A2 gene result in markedly reduced
calciumdependent epidermal adhesion molecules

GLUCAGONOMA SYNDROME
Glucagonoma syndrome is a multisystem disorder characterized by migrating erythematous, scaling, and crusted
papules, patches, and plaques along with the occasional
vesicle and pustule (Fig. 8.19). The skin biopsy demonstrates characteristic superficial epidermal necrosis.
Hence,
this condition is also known by the descriptive name,
necrolytic migratory erythema. The eruption is periorificial,
flexural, and acral, with associated glossitis. It is caused by
a pancreatic tumor of the islet alpha cell, which secretes
raised plasma glucagon levels. Besides the skin findings,
patients with this syndrome also have weight loss, anemia, diarrhea, and diabetes
LANGERHANS CELL HISTIOCYTOSIS
Langerhans cell histiocytosis is a neoplasm of Langerhans
cells that affects the skin and extracutaneous organs, particularly bone, bone marrow, spleen, liver, lungs, central
nervous system, and lymph nodes. It can be acute and
disseminated, chronic and multifocal, and localized. The
acute, disseminated form (Fig. 8.20) typically presents in
infancy and involves the scalp, trunk, and intertriginous
areas (recalcitrant diaper dermatitis). There are tan, pink,
sometimes hemorrhagic, papules, and scaling, slightly
eroded, patches. The skin biopsy demonstrates a proliferation of Langerhans cells in the epidermis and dermis

LICHEN SCLEROSUS
Lichen sclerosus can initially be confused with a pruritic
eczematous patch, especially in the anogenital region of
females (Fig. 8.21). On close inspection, or with time, the
typical ivory white papules and atrophic patches are seen
(see Chapter 13)

PEMPHIGUS FOLIACEUS
This rare, milder form of pemphigus affects the superficial epidermis, causing erythematous scaling with some
crusting (Fig. 8.22), and a few flaccid bullae and erosions.
Like pemphigus vulgaris (see Chapter 10), a skin biopsy
with immunofluorescence is diagnostic. This reveals
subcorneal/granular layer acantholysis with intercellular
IgG staining.

WISKOTT–ALDRICH SYNDROME
Wiskott–Aldrich syndrome is a rare Xlinked recessive
disorder that may appear like atopic dermatitis. Recurrent,
severe infections suggest an immunodeficiency that is
characterized by increased IgA and IgE levels, decreased
IgM concentration, and impaired cellmediated immunity.
Petechiae (Fig. 8.23) and bleeding episodes are a manifestation of thrombocytopenia, as well as platelet
dysfunction. Infection, bleeding, and lymphoreticular malignancy
are causes of childhood death in these patients.

ZINC DEFICIENCY
Zinc deficiency is an inherited (acrodermatitis enteropathica)
or acquired (parenteral nutrition) malady characterized
by perioral (Fig. 8.24), genital, and acral dermatitis plus
diarrhea. It usually begins in infancy, with the diagnosis
confirmed by low serum zinc levels. Essential fatty acid and
biotin deficiencies have a similar dermatitic appearance.