Persistence of Hemostatic Alterations in Patients Affected by Crohn's Disease After Bowel Surgery

Chiarantini, E; Valanzano, Rosa; Liotta, Agatina Alessandrello; Cellai, Anna Paola; Ilari, I.; Prisco, Domenico; Antonucci, Emilia; Tonelli, Francesco; Abbate, Rosanna

doi:10.1016/s0049-3848(97)00183-7

Cited by 20 publications

(9 citation statements)

References 24 publications

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“…The high platelet number correlates well with disease severity. [38] In agreement with the previously mentioned study, our results showed significantly elevated platelet counts in patients with active CD compared with that in the control group, but they were not significantly increased in active UC.…”

Section: Discussionsupporting

confidence: 93%

Assessment of thrombophilic abnormalities during the active state of inflammatory bowel disease

Maher

Soloma

2008

Saudi J Gastroenterol

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Background/Aims:Thromboembolic disease has been recognized as a complication of inflammatory bowel disease (IBD). The relative contributions of inherited or acquired thrombophilia and the inflammatory response to the mechanism of this tendency are unclear. Thrombotic events are more common in active disease although significant numbers also occur spontaneously. The aim of this study was to investigate common thrombophilic markers in patients with active IBD.Methods:Twenty-six patients with IBD who had active disease, and 40 sex- and age-matched non-IBD patients were recruited into the study. For all the subjects, complete blood counts, C-reactive protein levels, erythrocyte sedimentation rate, International normalized ratio, activated partial thromboplastin time, and levels of lupus anticoagulant, anticardiolipin antibodies (ACA IgG), proteins C and S, antithrombin-III (AT-III), and factor V were measured.Results:The International normalized ratio, activated partial thromboplastin time, and levels of proteins C and S were comparable between the two groups. However, antithrombin-III levels were significantly lower in the IBD group as compared with that in the healthy control group (P < 0.001). ACA IgG was detected in one patient in the IBD group. Factor V Leiden mutation was present in 3.8% of the patients in the IBD group, whereas the prevalence was 2.5% in the control group. Significantly elevated platelet counts were observed in patients with active Crohn's disease compared with that in the control group (P < 0.001), but they were not significantly increased in active ulcerative colitis (P = 0.231).Conclusions:The present study failed to establish a strong association between the common thrombophilic markers and the active clinical course of IBD, with the exception of high platelet counts and lower levels of AT-III in the IBD group as compared with those in the control group. All other parameters of thrombophilia were comparable between the two groups.

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Section: Discussionsupporting

confidence: 93%

Assessment of thrombophilic abnormalities during the active state of inflammatory bowel disease

Maher

Soloma

2008

Saudi J Gastroenterol

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“…However, autoantibodies against factor XIII have been found in sporadic cases of patients with a spontaneous hemorrhagic syndrome, 198 either in the elderly, 199,200 in the context of drug reactions, 201 in SLE, 202 or in celiac or inflammatory bowel disease. 203,204 In one of these cases, the antibody did not inhibit the activation of factor XIII but it bound to a fibrin-binding site of XIIIa. 200 …”

Section: The Role Of Apl Antibodies and Their Respective Antigens mentioning

confidence: 93%

Antiphospholipid Antibodies: Laboratory and Pathogenetic Aspects

Vlachoyiannopoulos

Samarkos

Sikara

et al. 2007

Critical Reviews in Clinical Laboratory Sciences

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Antiphospholipid antibodies (aPL) constitute a heterogeneous group of autoantibodies that share the ability to bind phospholipids (PL) alone, protein-PL complexes, or PL-binding proteins. They have been detected in isolation, in association with autoimmune diseases such as systemic lupus erythematosus (SLE), and during the course of different infections. aPL have been associated with an array of clinical manifestations in virtually every organ, although deep vein and arterial thrombosis as well as pregnancy morbidity are predominant. The co-occurrence of these clinical findings with aPL constitutes the so-called antiphospholipid syndrome (APS). aPL can be detected by immunological methods [e.g., anticardiolipin antibodies (aCL)] or by functional methods that exploit the effect of aPL on blood coagulation [lupus anticoagulant (LA)]. Since aPL are heterogeneous, numerous immunological and coagulation assays have been developed. These assays have not been fully standardized, and, therefore, problems such as high interlaboratory variation are relatively frequent. Recently, recommendations have been published regarding LA and aCL testing. Not all aPL are pathogenic. However, when they are not associated with infections, they have a role in the pathogenesis of APS. Clinical and experimental data have shown that aPL exert their pathogenic activity by interfering with the function of coagulation factors, such as thrombin and factors X, XI and XII, and with the function of anticoagulant proteins of the protein C system. In addition, aPL interaction with platelets and endothelial cells induces a pro-adhesive activated phenotype.

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“…Other plateletrelated abnormalities identified in patients with IBD are increased spontaneous and induced platelet aggregation which correlated with a history of thromboembolism in seven of eight patients [107,120]. Surgical resections in patients with CD result in significant decreases in platelet counts, fibrinogen levels and spontaneous platelet aggregation supporting the concept that the underlying bowel disease contributes to the hypercoagulable state [121]. Increased platelet mass in IBD is due to systemic increases in thrombopoietin and IL-6 [122].…”

Section: Disorders Of Coagulationmentioning

confidence: 76%