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Microvenular hemangioma (MVH) is a rare, slowly growing, benign vascular tumor that typically presents as a solitary enlarging plaque or nodule on the trunk or the extremities of young to middle-aged adults. A minority of MVH present with multiple lesions that are either gradually or suddenly acquired (eruptive MVH). Herein, we report a case of a 53-year-old woman who progressively developed numerous bilateral MVHs presenting as enlarging, blanching, erythematous to violaceous macules, patches, and plaques over the proximal thighs and axillae. Two biopsies exhibited the irregular branching venules with inconspicuous lumina lacking endothelial atypia and associated with dermal fibrosis characteristic of MVH. Immunophenotypically, the endothelium expressed Wilms Tumor 1, CD31, CD34, and erythrocyte-type glucose transporter protein (GLUT-1) GLUT-1 focally and was negative for Human herpes virus 8 and the lymphatic marker D2-40. In addition, numerous dermal spindle cells expressing CD34 and procollagen, putative fibrocytes, surrounded the thickened dermal collagen bundles and small vessels of MVH implicating a reactive/reparative (proliferative) process due to an unrecognized cutaneous injury. A review of MVH summarizing its clinicopathologic findings and its natural history is presented.

Simvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, has been shown to lower serum cholesterol levels and normalize endothelial cell function. Moreover, HMG-CoA reductase inhibitors exert beneficial effects in coronary artery and cerebrovascular diseases. We examined the effects of simvastatin on leukocyte-endothelial cell interaction in vivo by intravital microscopy. Simvastatin (12.5 or 25 microg per rat) was given 18 hours before study. Superfusion with the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME, 50 micromol/L) significantly increased leukocyte rolling from 12+/-2 to 60+/-8 leukocytes per minute, increased adherence to the mesenteric endothelium from 1.8+/-0.5 to 17+/-1.2 leukocytes per 100 microm of venular length, and raised leukocyte transmigration from 2.5+/-1.0 to 10+/-2 leukocytes per perivessel area (P<0.01). Similar results were obtained with thrombin (0.5 U/mL) superfusion of the mesentery. In contrast, pretreatment with simvastatin (25 microg per rat IP) significantly attenuated L-NAME-stimulated leukocyte rolling, to 12+/-2 (P<0.01); adherence, to 5+/-0.5 leukocytes per 100 microm (P<0.01); and leukocyte transmigration, to 3.5+/-1.5 leukocytes per perivessel area (P<0.01). Similar results were obtained in thrombin-superfused mesenteries. Moreover, immunohistochemical analysis demonstrated significantly increased P-selectin expression on the mesenteric venular endothelium after superfusion with either L-NAME (P<0.01) or thrombin (P<0.01), which was significantly attenuated by simvastatin. These results clearly demonstrate that simvastatin is a potent and effective endothelium-protective agent that reduces leukocyte-endothelial cell interactions independently of its well-known lipid-lowering effects. This effect was found to be at least partially mediated via downregulation of P-selectin expression on the microvascular endothelium. Thus, HMG-CoA reductase inhibitors like simvastatin have important anti-inflammatory effects besides their well-known lipid-lowering action.