Recent Articles of Interest

Some 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-containing medications.

Hormone preparations like contraceptive agents and older oral contraceptives can make acne worse. Other medications known to boost acne include certain antidepressants, and cyclosporin.

Thyroid Medications: recommended to activate the thyroid gland in people with low thyroid function. Acne is a side effect.

Disulfuram - recommended for alcoholic people trying to achieve sobriety. Constant use can trigger acne.

Immunosuppressants - recommended to suppress the immune system; mainly used to prevent organ rejection in patients awaiting transplants. Immune suppression permits bacteria to grow, including the bacteria that starts acne, P. acnes.

Oral Vitamin A: Retinoids (derivatives of vitamin A) are used locally and orally to alleviate acne under professional supervision. Vitamin A does not alleviate acne. If you take excessive vitamin A, hoping that it will cure acne, your health may become worse. Remember that Vitamin A in excess quantity can have negative effects on the body.

Hereditary: Acne can be inherited. If your parents suffered acne, you may be more prone to it.

Hormonal Variations: Hormonal changes bring on acne. The hormone androgen is responsible for excess secretion of sebum. Women can suffer acne episodes during menstruation and pregnancy.

Acne-Like Conditions: Some other conditions like folliculitis may appear like acne. There are many other conditions that may look like acne. Some of them are keratosis pilaris, perioral dermatitis, rosacea, etc. Always ask a dermatologist instead of trying self-treatment.

Usual concerns about treating acne

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

Aberrant desquamation of the follicular epithelium: In acne, keratinocytes hyperproliferate and gather within the sebaceous follicle. As these abnormally desquamated cells gather 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 unaided eye. However, as the already clogged follicle starts to fill with lipids, bacteria and cell fragments, the microcomedo changes to open or closed comedones (blackheads and whiteheads, respectively), both of which are non-inflammatory lesions. If P. acnes grows, inflammatory mediators are produced and inflammatory papules and pustules appear.

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

Inflammation: Inflammation in acne happens as a consequence of humoral and cellular defensive responses to P. acnes proliferation.