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

Hormone medications like contraceptive solutions and older oral contraceptives can make acne worse. Other medications known to exacerbate 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 trigger acne.

Immunosuppressants - prescribed to deactivate the immune system; primarily used to avoid organ rejection in patients awaiting transplants. Immune suppression allows bacteria to flourish, including the bacteria that starts acne, P. acnes.

Oral Vitamin A: Retinoids (derivatives of vitamin A) are used locally 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. Remember that Vitamin A in excess quantity can have negative consequences 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 secretion of sebum. Females can suffer acne outbreaks during menstruation and pregnancy.

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

Common concerns about treating acne

Excessive sebum secretion: At puberty, increasing levels of androgens, the major sebotrophic hormones, begin to drive an increase in sebum secretion. However, while androgenic stimulation is important in the pathogenesis of acne, the average acne patient does not have significant endocrine irregularities. 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.

Aberrant 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 produce microcomedo development. The microcomedo is the initiator to all acne lesions and is present in 80% of acne papules but is imperceptible to the naked eye. However, as the already blocked follicle begins 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.

Bacterial growth: The microenvironment of the follicle in acne is conducive 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 result of humoral and cellular immune reactions to P. acnes growth.