Low-dose daily aspirin reduces topical minoxidil efficacy in androgenetic alopecia patients.

Topical minoxidil is the only US FDA approved OTC drug for the treatment of androgenetic alopecia (AGA). Minoxidil is a pro-drug converted into its active form, minoxidil sulfate, by the sulfotransferase enzymes in the outer root sheath of hair follicles. Previously, we demonstrated that sulfotransferase activity in hair follicles predicts response to topical minoxidil in the treatment of AGA. In the human liver, sulfotransferase activity is significantly inhibited by salicylic acid. Low-dose OTC aspirin (75-81 mg), a derivative of salicylic acid, is used by millions of people daily for the prevention of coronary heart disease and cancer. It is not known whether oral aspirin inhibits sulfotransferase activity in hair follicles, potentially affecting minoxidil response in AGA patients. In the present study, we determined the follicular sulfotransferase enzymatic activity following 14 days of oral aspirin administration. In our cohort of 24 subjects, 50% were initially predicted to be responders to minoxidil. However, following 14 days of aspirin administration, only 27% of the subjects were predicted to respond to topical minoxidil. To the best of our knowledge, this is the first study to report the effect of low-dose daily aspirin use on the efficacy of topical minoxidil.

[Experimental allergic encephalomyelitis as an animal model for multiple sclerosis]. / Eksperimentalni alergijski encefalomijelitis kao zivotinjski model multiple skleroze.

Experimental allergic encephalomyelitis is an animal model for demyelinating autoimmune disease of central nervous system, whose clinical and pathological characteristics resemble those in human disease multiple sclerosis. Multiple sclerosis is a chronic inflammatory disease followed by central nervous system demyelination, which is the result of an autoimmune process followed by central nervous system infiltration with autoreactive lymphocytes, activated macrophages and by local production of proinflammatory cytokines. Finally, the destruction of oligodendrocytes and myelin sheath occurs, caused by immunologic effector mechanisms. In this paper we reviewed fundamental and new facts about the most used models, induction, clinical and immunological characteristics of the experimental allergic encephalomyelitis in comparison with multiple sclerosis. Aethology and pathogenesis of multiple sclerosis are still unknown, but experiments on its animal models have improved our knowledge, not only about multiple sclerosis, but autoimmune diseases in general.