Several drugs are known to provoke acneiform reactions.
Oral corticosteroids and adrenocorticotropic hormone produce acne-like lesions that are usually more monomorphic and symmetric in distribution than those seen in adolescent and postadolescent acne. Lesions are located primarily on the trunk. The precise mechanism is uncertain.
Androgens, including anabolic steroids and gonadotrophins, may precipitate acne, especially in athletes who take such drugs.
Antiepileptic drugs, especially phenytoin, have been held responsible for causing or exacerbating acne; however, modern anticonvulsants do not appear to have acne as a potential side effect.
Patients taking isoniazid, especially those who slowly inactivate the drug, appear to be prone to develop acne.
The management of drug-induced or drug-exacerbated acne includes discontinuation of the causative drug, decreasing the dosage, or substituting the drug with another agent. Then, proceed with the treatment of acne as described earlier in this chapter.
This refers to acne that is routinely picked at by the patient, who is almost invariably is female (Fig. 12.21).
Many of these patients deny that they manipulate their skin, but it is rather obvious because there are usually no primary lesions present and all, or most, have crusts.
Some of these patients may benefit from selective serotonin receptor inhibitors and/or psychotherapy.
The presence of acne, coupled with other signs or symptoms, may indicate an endocrinopathy.
Hormonal disorders that can produce excessive androgens (e.g., polycystic ovary syndrome), as well as those that can manifest with elevated cortisol levels (e.g., congenital adrenal hyperplasia) can be responsible for producing or aggravating pre-existing acne (see Chapter 20: Hirsutism).
Outline