Dysfunction in the coagulation system and XXXX .

@entity1 @entity4889 @entity1456 @entity1150 @entity3190 @entity161 @entity716 @entity3562 @entity1229
UNASSIGNED: Although different hypotheses have been formulated to explain @entity161 pathogenesis, the links between them are weak. The observation that five @entity716 @entity1 on chronic @entity1229 therapy for @entity1150 showed long-term remission of @entity716 made us suspect that abnormalities in the coagulation pathway, specifically low @entity1456 ( @entity1456 ) activity, could be one of the missing links. Our hypothesis is supported by a high prevalence of conditions affecting @entity1456 activity in drug-naive @entity161 , such as antiphospholipid antibodies, elevated cytokine levels, @entity3190 and @entity3562 . We recently screened a group of @entity161 @entity1 and controls for conditions affecting @entity1456 activity. @entity4889 was highly prevalent among @entity1 , but not found in controls. Free-protein S and functional protein C are natural anticoagulants that form complexes that inhibit @entity1456 inhibitors. All @entity1 had normal protein C levels, suggesting that protein S could have a role in @entity161 , independent of protein C. Chronic @entity1 and those studied during acute episodes had between three and six conditions affecting @entity1456 and/or protein S activity, while @entity1 in remission had up to two, which led us to postulate that multiple conditions affecting @entity1456 and/or protein S activity could contribute to the full expression of @entity161 phenotype. This paper describes the physiological roles of @entity1456 and protein S, reviewing how their activity influences pathogenesis and comorbidity of @entity161 . Next, it analyzes how activity of @entity1456 and protein S is influenced by biochemical abnormalities found in @entity161 . Last, it suggests future directions for research, such as studies on animal models and on therapeutic approaches for @entity161 aiming at increasing @entity1456 and protein S activity.
