Drugs and Acne
April 25th, 2008Some medications are known to cause acne. Some cortisones, few anti-tuberculosis medications and some anti-epileptic and anti-seizure medications can cause acne. Also medications that include anabolic steroids, and lithium and iodine-based medications.
Hormone preparations like contraceptive agents and older oral contraceptives may make acne worse. Other medications known to exacerbate acne include certain antidepressants, and cyclosporin.
Thyroid Medications: recommended to stimulate the thyroid gland in patients with weak thyroid function. Acne is a side effect.
Disulfuram - recommended for alcoholic patients trying to achieve sobriety. Regular use can trigger acne.
Immunosuppressants - recommended to suppress the immune system; primarily used to prevent organ rejection in patients enduring transplants. Immune suppression permits bacteria to flourish, including the bacteria that causes acne, Proprionibacterium acnes.
Oral Vitamin A: Retinoids (derivatives of vitamin A) are applied topically and orally to treat acne under medical supervision. Vitamin A does not treat acne. If you take excessive vitamin A, hoping that it will cure acne, your health may become worse. Keep in mind that Vitamin A in excess quantity can have negative consequences on the body.
Hereditary: Acne can be hereditary. If your parents suffered acne, you may be more prone to it.
Hormonal Changes: Hormonal variations bring on acne. The hormone androgen is responsible for excess production of sebum. Females can suffer acne episodes during menstruation and pregnancy.
Acne-Like Conditions: Some other conditions such as folliculitis may appear like acne. There are many other diseases that may look like acne. Some of them are rosacea, keratosis pilaris, perioral dermatitis, etc. Always visit a dermatologist instead of trying self-treatment.
Usual concerns about treating acne
Exaggerated sebum production: At puberty, increasing levels of androgens, the major sebotrophic hormones, begin to drive an elevation in sebum production. However, while androgenic stimulation is crucial in the pathogenesis of acne, the typical acne patient does not have important endocrine abnormalities. Hormonal therapy is not indicated in the initial treatment of mild to moderate acne, but women who require oral contraception may be candidates for anti-androgen therapy early in the application of treatment.
Abnormal desquamation of the follicular epithelium: In acne, keratinocytes hyperproliferate and accumulate inside 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 blemishes and is present in 80% of acne papules but is imperceptible to the naked eye. However, as the already clogged follicle starts to fill with lipids, bacteria and cell fragments, the microcomedo progresses to open or closed comedones (blackheads and whiteheads, respectively), both of which are non-inflammatory lesions. If P. acnes grows, inflammatory promoters are produced and inflammatory papules and pustules occur.
Microbial growth: The microenvironment of the follicle in acne is conducive to colonization with P. acnes. This produces inflammation and the formation of the noticeable papules and pustules with which acne patients typically present to dermatologists.
Inflammation: Inflammation in acne occurs as a result of humoral and cellular defensive responses to P. acnes growth.
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