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

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

Thyroid Medications: recommended to stimulate the thyroid gland in patients with low 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; mainly used to avoid organ rejection in patients awaiting transplants. Immune suppression permits bacteria to flourish, including the bacteria that causes acne, Proprionibacterium 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 treat acne, your health may become worse. Keep in mind that Vitamin A in excess quantity can have negative effects on the body.

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

Hormonal Variations: Hormonal variations produce acne. The hormone androgen is responsible for excess secretion of sebum. Women can have acne episodes during menstruation and pregnancy.

Acne-Like Ailments: Some other conditions like folliculitis may appear like acne. There are several other conditions that may look like acne. Some of them are keratosis pilaris, rosacea, perioral dermatitis, etc. Always visit 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 produce an increase in sebum secretion. However, while androgenic stimulation is crucial in the pathogenesis of acne, the typical acne patient does not have important endocrine irregularities. Hormonal therapy is not indicated in the initial management of mild to moderate acne, although women who use oral contraception may be candidates for anti-androgen therapy early in the application of treatment.

Aberrant 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 development. The microcomedo is the initiator 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 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 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 production of the noticeable papules and pustules with which acne sufferers commonly present to dermatologists.

Inflammation: Inflammation in acne occurs as a consequence of humoral and cellular immune reactions to P. acnes growth.