Novel cycle changes in scalp hair are caused by etretinate therapy.

The scalp hair of 15 patients, who were treated with etretinate for at least 6 months, was investigated, with the aims of confirming the previously described reduction in the duration of anagen and establishing the mechanism of etretinate alopecia. An increase in hair shedding rate and an increase in plucked telogen count, both of which continued for 6 months of treatment, were found, whereas there was no significant increase in the proportion of new, or regrowing, anagen hairs in a cut sample (NAH). The sustained decrease in the duration of anagen was confirmed, and it was further shown that this decrease was progressive. This would appear to be the main cause of the observed increased shedding associated with etretinate treatment. In relation to the mechanism of the alopecia, it was concluded that an arrest at the onset of anagen and a follicular anchorage defect in telogen were causes. The evidence for an arrest at the onset of anagen was a failure of NAH to rise on treatment, and a large increase in NAH on stopping treatment. The evidence for a follicular anchorage defect was a rise in shed rate very early in treatment, and an observed shed rate greater than expected, on the basis of plucked telogen results, later in treatment. These pathogenic mechanisms have never been described previously in drug-induced alopecia, or in the majority of hair disorders in general. However, it would seem highly unlikely that these mechanisms are exclusive to etretinate therapy.