Acquired protein C and S deficiency, inflammatory bowel disease and cerebral arterial thrombosis

Jorens, Philippe G.; Hermans, Colette R.; Haber, I; Kockx, Mark; Vermylen, Jozef; Parizel, G

doi:10.1007/bf01732883

Cited by 49 publications

(28 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Our results revealed that factor IXa, Xa, Va, VIIIa and AT-III levels were higher in active UC and IC than inactive UC, and suggested that common pathways were initiated by extrinsic and intrinsic pathways. (2,17,26). On the other hand, the present results suggested that there were no cases of hereditary thrombophilia in our study, since AT-III, protein C and protein S were within the normal range among all patients.…”

Section: Discussionsupporting

confidence: 43%

“…Normalization of markers of the coagulation system has been documented during treatment, which suggests that the observed abnormalities are secondary to the disease state (5,13). There have been no complete studies on the hypercoagulable state in UC on the total coagulation system, although there have been many reports on a part of the system (1)(2)(3)(4)(5)(6)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32). Therefore, the first aim of this study was to compare active with inactive UC in relation to the hypercoagulable tendency in the total coagulation system.…”

Section: In Patients With Inflammatory Bowel Disease (Ibd) Mucosal Amentioning

confidence: 99%

See 1 more Smart Citation

Activations of Coagulation and Fibrinolysis Secondary to Bowel Inflammation in Patients with Ulcerative Colitis

et al. 2007

View full text Add to dashboard Cite

Background Recent investigations suggest that activation of coagulation and fibrinolysis occurs in patients with ulcerative colitis (UC). activated partial thromboplastin time (APTT), thrombin time (TT), prothrombin time (PT), serum concentrations of von Willebrand factor (vWF), activated factors XII, XI, X, IX, VIII, VII, V, II, fibrinogen, prothrombin fragments 1+2 (F1+2), thrombin-antithrombin complexes (TAT), protein S, protein C, plasminogen, α-2 plasminogen inhibitor (α-2PI) and D-dimer (D-D). Results Median serum vWF concentrations, F1+2, TAT, fibrinogen, activated factor XI, IX, VIII and V were significantly elevated in patients with active UC and IC compared to those in patients with

show abstract

Section: Discussionsupporting

confidence: 43%

Section: In Patients With Inflammatory Bowel Disease (Ibd) Mucosal Amentioning

confidence: 99%

Activations of Coagulation and Fibrinolysis Secondary to Bowel Inflammation in Patients with Ulcerative Colitis

et al. 2007

View full text Add to dashboard Cite

show abstract

“…Deficiency of the proteins C and S in IBD patients was proposed by the studies of Jorens et al [38] gree of inflammatory activity and prothrombotic abnormalities has been found [19]. Studies using sensitive and Aadland et al [39,40].…”

Section: Hypercoagulability In Inflammatory Bowel Diseasementioning

confidence: 99%

Role of Thrombotic Vascular Risk Factors in Inflammatory Bowel Disease

Koutroubakis

2000

Dig Dis

View full text Add to dashboard Cite

Thromboembolic disease is a significant cause of morbidity and mortality in patients with inflammatory bowel disease (IBD). It is recognized that a hypercoagulable state exists in IBD which involves all components of the clotting system. It has been suggested that this hypercoagulable state is closely linked to the disease pathogenesis. Recent studies have shown that genetic defects such as factor V Leiden mutation and C677T methylenetetrahydrofolate reductase polymorphism associated with hyperhomocysteinemia seem to interfere in the thrombotic manifestations of IBD. Acquired factors such as antiphospholipid antibodies could also participate in the development of the thrombotic process. Deficiencies of other anticoagulant factors play a less important role in the thrombosis, and therefore it is not surprising that the results on these factors in IBD are contradictory. In conclusion the resultant gene–gene and gene–environment interactions between risk factors are the key to the understanding of why an IBD patient develops thrombosis at a specific point in time.

show abstract

“…Cerebral arterial thrombosis was reported after acquired protein S deficiency related to nephrotic syndrome [22] and inflammatory bowel disease [23], Acquired free pro tein S deficiency by using oral contraceptives is controver sial [25][26][27][28], A high prevalence of free protein S deficiency was found in hospitalized patients over 60 years of age, even in the absence of a predisposing condition [7]; our control and patient groups were composed o f younger subjects and no case of free protein S deficiency was found in healthy subjects.…”

Section: Discussionmentioning

confidence: 99%

Free Protein S Spectrum in Young Patients with Stroke

Nighoghossian¹,

Berruyer²,

Getenet³

et al. 1994

Cerebrovasc Dis

View full text Add to dashboard Cite

Up to 4% of strokes in young people are attributed to hematologic disorders. Deficiencies of natural anticoagulant proteins have recently been associated with ischemic strokes. The aim of this study was to determine the frequency of protein S deficiency following stroke in young patients and the course of these deficiencies. We studied natural anticoagulant proteins in a group of 26 patients under 45 years of age, hospitalized for a first ischemic stroke. Blood samples were collected with a mean delay of 1.91 (± 0.97) months after stroke onset. Free protein S (FPS) deficiency was found in 2 patients (7.69%): inherited FPS deficiency in 1 case and transient FPS deficiency in 1 case. No abnormality of protein C or antithrombin III was observed. A significant decrease in FPS was found in patients with respect to a control group of 27 age- and sex-matched healthy subjects. In conclusion, a decrease of FPS following ischemic stroke might be transient and could be related to thrombogenesis.

show abstract

Acquired protein C and S deficiency, inflammatory bowel disease and cerebral arterial thrombosis

Cited by 49 publications

References 20 publications

Activations of Coagulation and Fibrinolysis Secondary to Bowel Inflammation in Patients with Ulcerative Colitis

Activations of Coagulation and Fibrinolysis Secondary to Bowel Inflammation in Patients with Ulcerative Colitis

Role of Thrombotic Vascular Risk Factors in Inflammatory Bowel Disease

Free Protein S Spectrum in Young Patients with Stroke

Contact Info

Product

Resources

About