Influence of Psoralen and Ultraviolet Therapy on Platelet Function and Arachidonic Acid Metabolism in Patients with Vitiligo
Shortwave ultraviolet light (UVC; 200-290 nm) can cause irreversible aggregation in stirred samples of human platelet-rich plasma (PRP). Patients with vitiligo are commonly treated with oral psoralen and longwave ultraviolet light (UVA; 320-400 nm) to induce repigmentation. The effect of this treatment on platelet function has not been evaluated. In the present study, we evaluated platelet function in eight patients with vitiligo, one of whom was receiving oral psoralen and UVA treatment (PUVA). Platelets from the seven nontreated patients with vitiligo aggregated normally with all agents. The platelets of the patient who was receiving PUVA therapy did not aggregate to the addition of arachidonate (0.45 mM; AA), but did aggregate after exposure to collagen (3 μg/ml) and a combination of epinephrine (5 μM) and AA. In vitro studies showed that exposure of platelets to 8-methoxsalen (0.5 mM) blocked arachidonate-induced aggregation. All patients’ cells converted 14C-arachidonic acid through the cyclooxygenase and lipoxygenase pathways to eicosanoid products as efficiently as control cells. Platelet prostaglandin synthesis, AA metabolism, and aggregation were also studied from two patients with nontreated vitiligo before ingestion of 20 mg of oxsoralen (8-MOP), 2 hours after psoralen ingestion, and immediately following the administration of UVA radiation. No significant changes in arachidonate-induced activation or prostaglandin synthesis were found. The results of our study demonstrate that (a) platelets from patients exposed to PUVA therapy do not show any alterations in arachidonate-induced activation or prostaglandin synthesis; and (b) PUVA therapy is associated with the induction of a specific refractory state to arachidonate by an unknown mechanism.
KeywordsArachidonic Acid Platelet Function Arachidonic Acid Metabolism Vitiligo Patient PUVA Therapy
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