Acne Medication For Severe Acne

If acne becomes severe, it may take a long time to heal. This severity of acne also causes deep abscesses and scars after healing. The main and severe form of acne vulgaris is known as acne conglobata. In acne conglobata, infected nodules form around comedones. The nodules become more inflamed and spread deep inside. As they burst, they leave deep scars. Blackheads are very common in this acne. It can form on trunk, buttocks, face, etc. The treatment of acne conglobata is commonly done with isotretinoin.

Other severe types are acne fulminans and gram-negative folliculitis. If acne suddenly flares up causing inflammation, ulcers, and fever, it is called as acne fulminans. This is generally treated with steroids.

Gram-negative folliculitis is a severe form of folliculitis that damages the hair follicle and infects the pore. Isotretinoin is the treatment of choice for this. Any acne that keeps flaring up instead of settling down can become severe acne. Such acne forms deep scars, infects the skin and causes inflammation. You should be under the care of a doctor if you have severe acne.

BIOSKINCARE is a natural skin care cream made with the same substance that a cute little creature, living under the sun, uses to bathe his own skin to protect it from environmental hazards and to repair it when damaged. On human skin the natural fluid performs two functions: a) fights opportunistic bacteria that always thrive on injured cells, b) restores a healthy skin whenever damaged by acne or other inflammatory reactions triggered by rosacea, accidents, trauma, burns, or folliculitis, boils or warts.

BIOSKINCARE also keeps hair follicles opened and opens up clogged pores, vanishes post inflammatory marks quickly, destroys microbes and creates an environment that stimulates the regeneration of normal collagen. It also improves the water holding capacity of the skin and thus elasticity, density and skin firmness.

BIOSKINCARE contains enzymes that gently "digests" or dissolve scar tissues and damaged cells and regulate the organized production of new skin cells. It also improves skin resilience and elasticity and helps to plump the underlying structure of the skin, reducing the depth and appearance of icepick acne scars.

Common concerns about treating acne

When treating acne as many of the factors that cause it as possible should be targeted.

Excessive sebum production: At puberty, increasing levels of androgens, the major sebotrophic hormones, begin to drive an increase in sebum production. However, while androgenic stimulation is important in the pathogenesis of acne, the typical acne patient does not have significant endocrine abnormalities. Hormonal therapy is not indicated in the initial management of mild to moderate acne, although females who require oral contraception may be candidates for anti-androgen therapy early in the course of treatment.

Abnormal desquamation of the follicular epithelium: In acne, keratinocytes, hyperproliferate and accumulate within the sebaceous follicle. As these abnormally desquamated cells accumulate in the sebaceous follicle, they lead to microcomedo formation. The microcomedo, is the precursor to all acne lesions and is present in 80% of acne papules but is invisible to the unaided eye. However, as the already clogged follicle begins to fill with lipids, bacteria and cell fragments, the microcomedo progresses to open or closed comedones (blackheads and whitehead, respectively), both of which are non-inflammatory lesions. If P. acnes proliferates, inflammatory mediators are generated and inflammatory papules and pustules occur.

Bacterial proliferation: The microenvironment of the follicle in acne is conducive to colonization with P. acnes. This leads to inflammation and the production of the visible papules and pustules with which acne patients typically present to dermatologists.

Inflammation: Inflammation in acne occurs as a result of humoral and cellular immune reactions to P. acnes proliferation. It has been suggested that changes in sebum production or composition irritate infundibular keratinocytes leading to the release of interleukin 1a (IL-1a). In addition, CD4 lymphocytes and neutrophils migrate to the follicle. Rupture of the follicular duct leads to the extravasation of lipids, corneocytes and bacteria into the dermis, causing further inflammation.

Last modified: November 30, 2007

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