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 stimulate the thyroid gland in patients with weak thyroid function. Acne is a side effect.

Disulfuram - prescribed for alcoholic patients trying to achieve sobriety. Regular use can trigger acne.

Immunosuppressants - prescribed to suppress the immune system; primarily used to prevent 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 medical supervision. Vitamin A does not alleviate acne. If you take excessive vitamin A, hoping that it will treat acne, your health can become worse. Keep in mind that Vitamin A in excess quantity can have adverse effects 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 outbreaks during menstruation and pregnancy.

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

Common concerns about treating acne

Excessive sebum production: At puberty, increasing levels of androgens, the major sebotrophic hormones, begin to drive an increase in sebum production. However, while androgenic stimulation is crucial in the pathogenesis of acne, the average acne patient does not have significant endocrine irregularities. Hormonal therapy is not recommended in the initial management of mild to moderate acne, but women who use oral contraception can be candidates for anti-androgen therapy early in the course of treatment.

Abnormal desquamation of the follicular epithelium: In acne, keratinocytes hyperproliferate and gather inside 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 blemishes and is present in 80% of acne papules but is invisible to the naked 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 generated and inflammatory papules and pustules appear.

Microbial proliferation: The microenvironment of the follicle in acne is conducive to colonization with P. acnes. This produces inflammation and the formation of the visible 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 proliferation.

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