Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The division of the venous circulation in to two sectors, one constituted by the superficial and deep venous trunks (macrocirculation) and the other by the capillaries and precapillary venules (microcirculation), is surely schematical but aids the comprehension of many hemodynamic effects connected to hampered venous return and to the incompetence of the valvular devices. In fact many of the effects of stasis and venous hypertension (oedema, red cell diapedesis, skin dystrophies) cannot be explained merely by hydraulic mechanisms but require a primary alteration of the microvascular wall associated with structural changes of the perivascular connective tissue. The alterations that occur in microcirculation are of the utmost importance in the formation of the venules ulcerations. The passage of fibrinogen through large pores in the venules of the patients affected by venous hypertension derived from venous insufficiency creates a pericapillary fibrin deposition that cannot be removed because of inadequate blood and tissue fibrinolysis. This accumulation acts as a barrier to the diffusion of oxygen and other nutrients, determining a stasis dermatitis that may lead to tissue necrosis and ulceration. The more precise knowledge of the phenomena connected with the venous stasis at the level of microcirculation (pericapillary fibrin deposition, endothelial ischemia, blocked lymphatic drainage) will not only allow a deeper comprehension of the clinical signs but hopefully will lead to a more effective treatment of the postphlebitic syndrome.
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PMID:[Physiopathology of venous stasis at the microcirculation level]. 129 20

The 48,XXYY syndrome is a form of hypergonadotropic hypogonadism, characterized by tall statures, aggressive behavior, mental retardation, and stasis changes reflecting vascular insufficiency. We report a 25-year-old male with this syndrome showing a peripheral neuropathy and stasis dermatitis which were both reversed by administration of testosterone. Electrophysiologic studies, plethysmography, and thermography indicated that this treatment improved nerve conductivity and peripheral circulation. We postulate that in 48,XXYY syndrome a decrease in testosterone may result in peripheral neuropathy via nerve ischemia.
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PMID:Improvement of peripheral neuropathy by testosterone in a patient with 48,XXYY syndrome. 1112 5