The authors of this editorial [Gladwin and Kato, 2008: (http://www.haematologica.com/cgi/content/full/93/1/1)(http://www.ncbi.nlm.nih.gov/pubmed/18166776)] discussed research showing that measures of the rate of intravascular (as opposed to intramedullary, I suppose) hemolysis, in people who had had sickle-cell disease, had correlated positively with markers of hemostasis and the activation of the coagulation cascade. This type of research (http://scholar.google.com/scholar?hl=en&q=hemolysis+thrombosis+OR+thrombogenic+OR+hypercoagulability+OR+coagulopathy), along with that editorial and accompanying article [Ataga et al., 2008: (http://haematologica.com/cgi/content/full/93/1/20)(http://www.ncbi.nlm.nih.gov/pubmed/18166781)], suggests to me that the hemolysis that not-uncommonly occurs (http://scholar.google.com/scholar?hl=en&q=hemolysis+hypophosphatemia) in the context of hypophosphatemia, for example, could contribute to some of the complications associated with hypophosphatemia (or with the depletion of intracellular phosphate). It's interesting that hemolysis can produce transient elevations in serum phosphate, but hemolysis per se, as in the context of autoimmune hemolytic anemia, can cause hypophosphatemia, given that the kidneys simply excrete more phosphate in response to the hemolysis-induced elevations. Over time, those types of cycles of phosphate loss, through hemolysis or exercise-induced glycolytic activity or glycolytic activity due to thrombosis due to hemolysis, would lead to hypophosphatemia. A lot of the articles on exercise and serum phosphate report hypophosphatemia, but it's conceivable to me that hypophosphatemia-induced hemolysis could "falsely" and intermittently elevate serum phosphate to normal levels and confound attempts to diagnose the condition. Thatte et al. (1995) [Thatte et al., 1995: (http://www.ncbi.nlm.nih.gov/pubmed/7573122)] discussed research showing that hemolysis can induce hyperphosphatemia. The thrombogenic state associated with hemolysis could contribute to the intracranial hypertension that researchers have associated with hypophosphatemia and could contribute to exercise-induced rhabdomyolysis, given that rhabdomyolysis has commonly been reported in the context of hypophosphatemia.
Part of the reason this is interesting is that the combination of thrombocytopenia, which is not uncommon in association with hypophosphatemia (http://scholar.google.com/scholar?q=thrombocytopenia+hypophosphatemia&hl=en), with hemolysis-induced thromboses and activation of the coagulation cascade is an especially dangerous combination and is one reason that heparin-induced thrombocytopenia, for example, is such a dangerous and difficult-to-manage condition. My understanding of it is that thromboses are constantly reforming and undergoing thrombolysis and that this causes small injuries and basically amounts to diffuse ischemia and hypoxia. But one explanation for the bleeding that accompanies thrombogenic conditions, such as heparin-induced thrombocytopenia, is that localized smooth muscle cell necrosis results from localized thromboses and that the small-scale reperfusion or recanalization at the site of "arterionecrosis" or microcapillary damage produces the hemorrhages. Then platelets adhere to the site of the microhemorrhage, etc. Gladwin and Kato (2008), cited above, discussed the fact that the scavenging of nitric oxide by deoxyhemoglobin can be drastically increased during hemolysis and that that, along with the generation of reactive oxygen and nitrogen species by the hemoglobin, can then produce ischemia. Nitric oxide also generally inhibits platelet function, etc., and that effect would be decreased during hemolysis.
That type of discussion, in the editorial by Gladwin and Kato (2008), is helpful to me, as far as understanding the elevations in intracranial pressure that result from so many different causes and that occur in so many different contexts. In a lot of the cases of intracranial hypertension due to retinoids or excess vitamin A (http://scholar.google.com/scholar?hl=en&q=%22intracranial+pressure%22+ischemic+OR+ischemia+OR+ischaemia+OR+ischaemic), the condition is described as being an ischemic encephalopathy or something similar. To say that intracranial hypertension is caused by or is associated with venous sinus thrombosis is basically to say that it's partly sustained by ischemia, for example, and it's almost inconceivable to me that there could ever be a total absence of ischemia, mild or not-mild, in the context of intracranial hypertension. The article by Gladwin and Kato (2008) gets at that. Thromboses, by definition, impair tissue oxygenation and would be expected to impair blood-flow regulation by augmenting the rate of formation of reactive oxygen and nitrogen species,etc. This doesn't necessarily mean that every effort to restore cerebral blood flow would be effective in the treatment of intracranial hypertension, but I think it's an important consideration. Also, one way of describing this might be to consider the distinction between venous ischemia and arterial ischemia, and intracranial hypertension has been shown to occur in association with venous ischemia (http://scholar.google.com/scholar?hl=en&q=venous+sinus+thrombosis+%22venous+ischemia%22+intracranial+pressure); (http://scholar.google.com/scholar?hl=en&q=%22venous+ischemia%22+intracranial+pressure); (http://scholar.google.com/scholar?hl=en&q=%22venous+ischemia%22+cerebral+OR+intracranial+OR+brain); (http://scholar.google.com/scholar?hl=en&q=%22venous+ischemia%22)].
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