Some drugs are known to cause acne. Some cortisones, few anti-tuberculosis medications and some anti-epileptic and anti-seizure drugs can cause acne. Also drugs that include anabolic steroids, and lithium and iodine-containing drugs.

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

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

Disulfuram - prescribed for alcoholic people trying to achieve sobriety. Regular use can produce acne.

Immunosuppressants - prescribed to deactivate the immune system; mainly used to prevent organ rejection in patients enduring transplants. Immune suppression allows bacteria to grow, including the bacteria that starts acne, P. acnes.

Oral Vitamin A: Retinoids (derivatives of vitamin A) are used topically and orally to treat acne under professional supervision. Vitamin A does not treat 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 adverse effects on the body.

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

Hormonal Changes: Hormonal changes produce acne. The hormone androgen is responsible for excess production of sebum. Females can suffer acne outbreaks 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 perioral dermatitis, rosacea, keratosis pilaris, etc. Always ask a doctor instead of trying self-treatment.

Usual concerns about treating acne

Excessive sebum production: At puberty, increasing levels of androgens, the major sebotrophic hormones, start to produce an increase in sebum production. 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, although women 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 gather within the sebaceous follicle. As these aberrantly desquamated cells gather in the sebaceous follicle, they lead to microcomedo formation. The microcomedo is the initiator to all acne blemishes and is present in 80% of acne papules but is imperceptible to the unaided eye. However, as the already blocked follicle starts to fill with lipids, microbes 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 proliferates, inflammatory promoters are produced and inflammatory papules and pustules appear.

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

Inflammation: Inflammation in acne happens as a result of humoral and cellular immune responses to P. acnes growth.