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Acne a common problem in youth, specailly the teens. So lets find out the causes, symptoms, preventation & treatment of this disese.
Acne vulgaris develop in sebaceous follicles, which consist of a large, multilobular sebaceous gland that drains its products into the follicular canal. The initial lesion of acne is a microcomedone, which progresses to a comedone. A comedone is a dilated epithelium-lined follicular sac filled with lamellated keratinous material, lipid, and bacteria. An open comedone, known as a blackhead, has a patulous pilosebaceous orifice that permits visualization of the plug. An open comedone becomes inflammatory less commonly than does a closed comedone or whitehead, which has only a pinpoint opening. An inflammatory papule or nodule develops from a comedone that has ruptured and extruded its follicular contents into the subadjacent dermis, inducing a neutrophilic inflammatory response. If the inflammatory reaction is close to the surface, a papule or pustule develops. If the inflammatory infiltrate develops deeper in the dermis, a nodule forms. Suppuration and an occasional giant cell reaction to the keratin and hair are the cause of nodulocystic lesions. These are not true cysts but liquefied masses of inflammatory debris.
The primary pathogenetic alterations in acne are (1) abnormal keratinization of the follicular epithelium, resulting in impaction of keratinized cells within the follicular lumen; (2) increased sebaceous gland production of sebum; (3) proliferation of Propionibacterium acnes within the follicle; and (4) inflammation. Comedonal acne ( Fig. 668-1 ), particularly of the central face, is frequently the 1st sign of pubertal maturation. At puberty, the sebaceous gland enlarges and sebum production increases in response to the increased activities of androgens of primarily adrenal origin. Most patients with acne do not have significant endocrine abnormalities. Hyper-responsiveness of the sebocyte to androgens is likely involved in determining the severity of acne in a given individual. Sebocytes and follicular keratinocytes contain 5α-reductase, 3β- and 17β-hydroxyl-steroid dehydrogenase which are capable of metabolizing androgens. A significant number of women with acne (25–50%), particularly those with relatively mild papulopustular acne, note that their acne flares ≈1 wk before menstruation. The pathogenesis of this phenomenon is unknown.
TREATMENT.
No evidence shows that early treatment, with the exception of isotretinoin, alters the course of acne. Acne can be controlled and severe scarring prevented, however, by judicious maintenance therapy that is continued until the disease process has abated spontaneously. Therapy must be individualized and aimed at preventing microcomedone formation through reduction of follicular hyperkeratosis, sebum production, the P. acnes population in follicular orifices, and free fatty acid production. Initial control takes at least 6–8 wk, based on the severity of the acne ( Table 668-2 ). It is also important to address the potentially severe emotional impact of acne on adolescents
Classification of Acne
SEVERITY DESCRIPTION
Mild Comedones (noninflammatory lesions) are the main lesions.Papules and pustules may be present but are small and few in number (generally <10).
Moderate
Moderate numbers of papules and pustules (10–40) and comedones (10–40) are present.Mild disease of the trunk may also be present.
Moderately severe
Numerous papules and pustules are present (40–100), usually with many comedones (40–100) and occasional larger, deeper nodular inflamed lesions (up to 5).Widespread affected areas usually involve the face, chest, and back
Severe
Nodulocystic acne and acne conglobata with many large, painful nodular or pustular lesions are present, along with many smaller papules, pustules, and comedones
Source: Nelson Textbook of PEDIATRICS>