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Section 1.

Disorders of Sebaceous and


Apocrine Glands
ICD-9: 706.1 ICD-10: L70.0

An inflammation of pilosebaceous units, very common

Appears in certain body areas (face, trunk, rarely buttocks)

Most frequently in adolescents

Manifests as comedones, papulopustules, nodules, and cysts

Results in pitted, depressed, or hypertrophic scars

Epidemiology
Occurrence
Very common, affecting approximately 85% of young people.

Age of Onset
Puberty10 to 17 years in females, 14 to 19 in males; however, may appear first at
25 years or older.

Sex
More severe in males than in females.

Race
Lower incidence in Asians and Africans.

Genetic Aspects
Multifactorial genetic background. Familial predisposition: majority of individuals with
cystic acne have parent(s) with a history of severe acne. Severe acne may be
associated with XYY syndrome.

Pathogenesis
Key factors are follicular keratinization, androgens, and Propionibacterium
acnes (5185637).

IMAGE 1-1
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AD. Acne pathogenesis [From Zaenglein AL et al. Acne vulgaris and acneiform eruptions, in Wolff
K et al (eds): Fitzpatrick's Dermatology in General Medicine, 7th ed. New York, McGraw-Hill, 2008.]

Acne results from a change in the keratinization pattern in the pilosebaceous unit,
with the keratinous material becoming more dense and blocking secretion of sebum.
These keratin plugs are called comedones and represent the time bombs of acne.
Linoleic acid, which regulates keratinocyte proliferation, is decreased in acne.
Comedonal plugging and a complex interaction between androgens and bacteria (P.
acnes) in the plugged pilosebaceous units lead to inflammation. Androgens
(qualitatively and quantitatively normal in the serum) stimulate sebaceous glands to
produce larger amounts of sebum. Bacteria contain lipase, which converts lipid into
fatty acids, and produce proinflammatory mediators, [interleukin 1, tumor necrosis
factor TNF ]. Fatty acids and proinflammatory mediators cause a sterile
inflammatory response to the pilosebaceous unit. The distended follicle walls break,
and the contents (sebum, lipids, fatty acids, keratin, bacteria) enter the dermis,
provoking an inflammatory and foreign-body response (papule, pustule, nodule).
Rupture plus intense inflammation lead to scars.

Contributory Factors
Acnegenic mineral oils, rarely dioxin and others.

Drugs
Lithium, hydantoin, isoniazid, glucocorticoids, oral contraceptives, iodides, bromides
and androgens (e.g., testosterone), danazol.
Others
Emotional stress can definitely cause exacerbations. Occlusion and pressure on the
skin, such as by leaning face on hands, very important and often unrecognized
exacerbating factor (acne mechanica). Acne is not caused by chocolate or fatty foods
or, in fact, by any kind of food.

Clinical Manifestation
Duration of Lesions
Weeks to months.

Section 2. Eczema/Dermatitis
The terms eczema and dermatitis are used interchangeably, denoting a polymorphic
inflammatory reaction pattern involving the epidermis and dermis. There are many etiologies and
a wide range of clinical findings. Acute eczema/dermatitis is characterized by pruritus, erythema,
and vesiculation; chronic eczema/dermatitis, by pruritus, xerosis, lichenification, hyperkeratosis,
fissuring.

ICD-9 : 692-9 ICD-10 : L25

Contact dermatitis is a generic term applied to acute or chronic inflammatory reactions to


substances that come in contact with the skin. Irritant contact dermatitis (ICD) is caused by a
chemical irritant; allergic contact dermatitis (ACD) by an antigen (allergen) that elicits a type IV
(cell-mediated or delayed) hypersensitivity reaction.

The acute form of ICD occurs after a single exposure to the offending agent that is toxic to the
skin (e.g., croton oil, phenols, kerosene, organic solvents, sodium and potassium hydroxide, lime
acids) and in severe cases may lead to necrosis. It is dependent on concentration of the
offending agent and occurs in everyone, depending on the penetrability and thickness of the
stratum corneum. There is a threshold concentration for these substances above which they
cause acute dermatitis and below which they do not. This sets acute ICD apart from acute ACD,
which is dependent on sensitization and thus occurs only in sensitized individuals. Depending on
the degree of sensitization, minute amounts of the offending agents may elicit a reaction. Since
ICD is a toxic phenomenon, it is confined to the area of exposure and is therefore always sharply
marginated and never spreads. ACD is an immunologic reaction that tends to involve the
surrounding skin (spreading phenomenon) and may even spread beyond affected sites.
Generalization may occur.

FIG. 2E-CD1
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Acute irritant contact dermatitis following the application of a cream containing nonylvanillanidand nicotinic
acid-butoxyethylester that had been prescribed for lower back pain. The streaky pattern indicates an outside
job, the eruption is characterized by massive erythema with vesiculation and blister formation and is confined to
the sites exposed to the toxic agent.

FIG. 2E-CD2
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Acute irritant contact dermatitis on the hand due to an industrial solvent. There is massive blistering on the palm.

FIG. 2E-CD3
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Acute irritant contact dermatitis in resolution. This is a florist who had contact with croton, poinsettias, and butter
cup so that it could not be determined which of these was the eliciting plant. Note the streaky pattern of the
eruption on the left hand.

FIG. 2E-CD4
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Early chronic irritant contact dermatitis in a housewife. This has resulted from repeated exposure to soaps and
detergents. Note glistening finger tips (pulpitis).