Narayan, "
Hyperfibrinogenemia in patients of diabetes mellitus in relation to glycemic control and urinary albumin excretion rate," The Journal of the Association of Physicians of India, vol.
Laboratory data showed leukopenia (1900 cells/[micro]L), microcytic anemia (8.2 g/dl), platelets of 173,000 cells/[micro]L, erythrocyte sedimentation rate (ESR) of 85 mm/h1, elevated C reactive protein (CRP) of 2 mg/dl, hypoalbuminemia (2.6 g/dl),
hyperfibrinogenemia (546 mg/dl), elevated lactate dehydrogenase (1279 IU/L), and hyperferritinemia (12,000 pg/L).
Wolberg, "Causal relationship between
hyperfibrinogenemia, thrombosis, and resistance to thrombolysis in mice," Blood, vol.
Cause-effect relation between
hyperfibrinogenemia and vascular disease.
Note that these changes proceeded in background of hemostasis significant (P<0.01)
hyperfibrinogenemia.
Thus, taken together, it is reasonable to suggest that the observed impairment in the endothelial functions could result from chronic exposure to toxic particulate matters, hydrocarbons, oxygenated organics, free radicals (28-30), and carbon monoxide (33), oxidative stress (31, 32), increased endothelin levels and plasma viscosity,
hyperfibrinogenemia, and enhanced platelet activity (9-11).
Hyperfibrinogenemia. An important risk factor for vascular complications in diabetes.
These differences were detected in healthy persons as well as in patients with
hyperfibrinogenemia. The results remained unaffected when we used variations of the ethanol precipitation method as described by Qiu et al.
Hyperfibrinogenemia as a cause of prolonged thrombin dotting time.
These include normalization of bleeding times, increased platelet counts, alterations in platelet function, reduction in protein C and protein S levels, and
hyperfibrinogenemia. However, it is not clear that the changes in these parameters that affect hemostasis are responsible for an increased incidence of vascular access thrombosis (Standage et al., 1993).
Including fibrinogen level as a risk factor enables physicians to more accurately identify patients who require lipid-lowering measures, according to standard recommendations; ie, those who have a traditional risk factor and previously unrecognized
hyperfibrinogenemia as a second risk factor.
At high plasma fibrinogen concentrations, the FXIII Leu34 variant showed a protective effect through the formation of more permeable fibrin clots that are more susceptible to lysis, while at low fibrinogen concentration the effect was reversed, suggesting that protection against thrombosis by FXIII 34Leu only occurs in
hyperfibrinogenemia [23].
