AA is the precursor of oxygenated metabolites called the eicosanoids, that are generated by the cyclooxygenase, lipoxygenase, or cytochrome P450 enzymatic pathways. The biologically active eicosanoids are labile, usually but not always, act near their site of synthesis, and are not stored in any tissue to any appreciable degree. In most tissues, there is a continuous low-level synthesis that is probably essential to normal function. Injury or surgical trauma can evoke a dramatic change in the quality and quantity of the metabolites. Pharmacologic manipulation of the pathways of AA metabolism, or alteration of the effects of AA metabolites, can significantly improve tissue perfusion in a variety of clinical situations. (See Figure 1 for a schematic summary of the pathways involved in arachidonic acid metabolites.
To examine the contribution of arachidonic acid (AA) metabolites to the maintenance of cutaneous vasomotor tone after thermal injury, enzyme inhibitors were topically applied to the hamster cheek pouch before and after a spot burn. By use of video microscopy, blood flow was measured in adjacent arterioles that supplied the injured site. Ringer's solutions containing no drug (vehicle), indomethacin (cyclooxygenase inhibitor), BW755c (cyclooxygenase/lipoxygenase inhibitor), or ketoconazole (lipoxygenase/cytochrome P450 inhibitor) continuously suffused the entire tissue. There were no effects of these drugs on preburn blood flow at concentrations that blocked the vascular effects evoked by topical AA. In all groups, blood flow transiently increased after burn and thereafter decreased to levels that were altered by treatment. These results could not be attributed to alterations in vascular reactivity because neither the burn nor the drugs altered the vasodilation evoked by adenosine or prostacyclin. Relative to Ringer's, indomethacin had no effect, BW755c caused vasodilation, and ketoconazole caused vasoconstriction, which suggests that cytochrome P450 products might be vasoactive mediators in injured tissue. Therefore, purified synthetic compounds were compared with known vasodilators.
Rhinophyma is the final stage in the evolution of acne rosacea, a common vasoactive dermatosis. Individuals with rhinophyma present with a typical, disfiguring nasal appearance consisting of bulbous enlargement, erythema, and telangiectasia with a sebaceous, oily skin surface. This classic appearance permits a facile diagnosis but may also lead the physician to overlook a coexistent malignancy. We report the occurrence of a diffuse large B-cell lymphoma (DLBCL) arising synchronously with a marked rhinophyma. A wide local excision of the malignancy was performed, and the defect was reconstructed with forehead flaps. The rhinophyma was treated with a skin graft and cheek flaps. Following surgery, chemotherapy was used to manage the systemic disease. This case demonstrates the necessity for clinical scrutiny in the diagnosis and treatment of rhinophyma. It is imperative to entertain a high degree of suspicion when non-typical changes are observed within a rhinophymatous lesion or in adjacent areas of the nose.
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