Transcript Slide 1

ACNE VULGARIS

DEFINITION

 Acne is a chronic inflammatory disease of the pilosebaceous units.  It is characterized by the formation of comedones,  erythematous papules and pustules,  less frequently by nodules or pseudocysts and, in some cases, is accompanied by scaring.

EPIDEMIOLOGY  Acne affects more than 85 percent of teenagers but frequently continues into adulthood.

 Although there are more than 2 million visits to office based physicians per year for patients in the age range of 15 to 19 years, the mean age at presentation for treatment is 24 years,  Only10 % of visits taking place when patients are between the ages of 35 and 44 years.

2  The condition usually starts in adolescence and frequently resolves by the mid-twenties Some degree of acne affects 95% and 83% of 16-year-old boys and girls, respectively

In about 20%, the disease necessitates the help of a physician. Acne develops earlier in females than in males.  The direct cost of acne in the United States is estimated to exceed $1 billion per year, with $100 million spent on over-the-counter acne products

 The social, psychological, and emotional impairment that can result from acne has been reported to be similar to that associated with epilepsy, asthma, diabetes, and arthritis.

 Patients evaluated at tertiary care centers are prone to depression, social withdrawal, anxiety, and anger and are more likely to be unemployed than persons without acne.

 Scarring can lead to lifelong problems in regard to self-esteem.

 Questionnaire studies have shown that many acne patients experience  shame (70%),  embarrassment and anxiety (63%),  lack of confidence (67%),  impaired social contact (57%)  And a significant problem with unemployment

 Only rarely is prepubertal acne occurs as a cutaneous marker of an endocrine abnormality such as an adrenogenital late-onset syndrome.  Comedonal acne can be the first sign of pubertal maturation; significant comedones usually precede inflammatory lesions by 2-3 year  It is not known why acne resolves or why it is more persistent in females.

 Active sebaceous glands are a prerequisite for the development of acne.  Acne patients, male and female, excrete on average more sebum than normal subjects, and the level of secretion correlates reasonably well with the clinical picture . Sebaceous activity is predominantly dependent on androgenic sex hormones of gonadal or adrenal origin. Abnormally high levels of sebum secretion could thus result from high overall androgen production,

increased availability of free androgen, because of a deficiency in sex hormone-binding globulin (SHBG).  Equally, they could involve an amplified target response mediated through 5 alfa reduction of testosterone

Predisposing causes

 Patients dealing with oil undoubtedly develop an acneiform oil folliculitis, particularly on their trunks and limbs. The induction of chloracne by accidental release of halogenated hydrocarbons or other chemicals.

 DIET  STRESS  PREMANSTURAL

PILOSEBACEOUS UNIT

PATHOGENESIS

 Four major factors are involved in the pathogenesis:  increased sebum production,  an abnormality of the microbial flora,  cornification of the pilosebaceous duct  and the production of inflammation.

Pathogenesis ANDROGENS SEBOCYTES KERATINOCYTES SEBORRHEA ABNORMAL FOLLICULAR KERATINIZATION ALTERATION IN FOLLICULAR MILIEU COLONIZATION WITH P. ACNES INFLAMMATION

Clinical features

  Acne is a polymorphic disease, which occurs predominantly on   On the face (99%) on the back (60%)  chest (15%)

Non-inflamed lesions (comedones)

more frequent in the younger patients consist of blackheads (open comedones), in which the black colour is due to melanin not dirt, whiteheads (closed comedones)

Inflammatory lesions

  may be superficial or deep, and many arise from non inflamed lesions. The superficial lesions are usually papules and pustules (5mm or less in diameter   Deep lesions are nodules ,sinuses Rarely scars & keloids

ACNE SCAR

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Types of acne form lesions

Acne excoriée Drug-induced acne/acneiform eruptions Endocrine' acne Externally induced acne Tropical acne (hydration acne) Infantile and juvenile acne Pilosebaceous naevoid disorders  Severe acne variants     Pyoderma faciale Acne conglobata ** Acne fulminans *** Gram-negative folliculitis

THERAPY

 Choice of therapy  Topical treatment  Oral therapy -Side-effects of conventional therapy  Hormonal treatments  Isotretinoin  Other oral treatments - ORAL ATIBIOTICS  Physical modalities  Treatment of scars

DRUG THERAPY

ANTIBACTERIAL RETINOIDS OTHERS PHYSICAL MODALITIES TETRACYCLINE DOXICYCLINE MINOCYCLINE CLINDAMYCIN ERYTHROMYCIN ISOTRETINOIN ADALPALENE TAZAROTENE BENZOYL PEROXIDE AZEAIC ACID ANTIANDROGENS CYPOTERON ACETATE SPIRONOLECTONE FLTAMIDE GLUCOCORTICOID OCPS CRYOTHERAPY UV THERAPY

EFFECT OF ORAL ISOTRETINOIN