The precise mechanism of<unk>  is not known. The current line of thinking goes that vasospasms in the cutaneous arteries and arterioles produce cyanotic discoloration, while compensatory dilatation in the postcapillary venules causes sweating. Arteriovenous subpapillary plexus shunting also occurs. Persistent vasoconstriction at the precapillary sphincter creates a local hypoxic environment, thus releasing adenosine into the capillary bed. Vasospasms force adenosine to enter the capillary bed, where it vasodilates the postcapillary venules. Such differences in vessel tone create a countercurrent exchange system that attempts to retain heat. Profuse sweating would then be caused by an overwhelmed countercurrent exchange system. In addition to adenosine, other hormones may contribute to<unk>  such as increase blood levels of serotonin. This would seem to support case studies reporting<unk>  as an unusual side effect for pediatric patients taking tricyclic antidepressants, as these medications can inhibit the reuptake of serotonin and thus increase their blood concentrations.<unk>  has been reported in association with many other medications and substances.
Acrocyanosis
Nail clubbing
Cyanosis
Maculopathy
Rhagades
Retinopathy
Hyperthecosis
Pathergy