Griseofulvin therapy in acne vulgaris

To the Editor,

The idea of treating acne vulgaris with griseofulvin arose by chance, when a patient suffering from both tinea corporis and acne vulgaris was receiving griseofulvin. It was interesting to note that in the course of the treatment marked improvement occurred in acne lesions. Thus we planned to perform a clinical trial to find out the effect of griseofulvin in acne vulgaris.

Our trial included 20 patients having acne vulgaris. Out of 20 patients, 11 were males and 9 were females, their age ranging from 16-28 years. At the first visit patients were examined and number of inflammed acne lesions (papules, pustules, cysts and nodules) and non-inflammed acne lesions (comedones) were counted. Then griseofulvin 250 mg twice daily was started and patients were routinely followed up every 2 weeks for a total of 8 weeks. At each follow up visit number of lesions were again counted to assess the effect of griseofulvin. Our results were as follows:

Both subjective and objective impovement in the condition of the patients started within 2 weeks following the commencement of griseofulvin therapy. After 8 weeks of therapy there was a statistically singnificant decrease in the number of papules (p<0.001). Similarly in all the patients the decrease in the number of pustules after 8 weeks of therapy with griseofulvin was statistically significant (p<0.01). But it was noted that the decrease in number of comedones, cysts and nodules before and after 8 weeks of therapy was not statistically significant.

Thus the maximum benefit was observed in inflammatory acne lesions. Improvement was slow and less dramatic in non-inflammed lesions. No serious side-effects were noted with griseofulvin.

It is difficult to conjecture the mode of action of griseofulvin in acne vulgaris. It has been suggested recently that pathogenesis of acne also involves immune mechanisms,[1] evidence of which includes the observation of complement component C3 in the walls of dermal blood vessels and basement membrane zone of acne lesions and demonstration of cell mediated immunity directed towards P acnes in patients with severe acne. Attraction and killing of leucocytes by comedonal components, the resultant inflammatory cascade and specific immunological events all contribute to the final appearance of inflammed acne lesions. Thus one factor may be that griseofulvin may act as an immunomodulator as Tamaki et al have shown that griseofulvin can be used as an immunomodulator.[2] But still the mode of action of griseofulvin in acne vulgaris is unclear and further double blind controlled studies are essential to confirm our observations.