Factor XII deficiency associated with coronary stent thrombosis

Helft, Gérard; Feuvre, Claude Le; Metzger, J. P.; Vacheron, A; Monsuez, J.-J.; Lachurie, Marie Laure; Ahlenc‐Gelas, Martine

doi:10.1002/1096-8652(200008)64:4<322::aid-ajh18>3.0.co;2-b

Cited by 7 publications

(3 citation statements)

References 5 publications

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“…Congenital deficiency of factor XII results in the laboratory finding of an elevated activated partial thromboplastin time. Although factor XII levels appear to modify the risk of arterial and venous thrombosis 7–11, even complete deficiency is generally thought to be of minimal clinical consequence. However, a report in the literature describes a child with a subdural hematoma who was found to have factor XII deficiency 12.…”

Section: Discussionmentioning

confidence: 99%

Low factor XII level in an individual with Sotos syndrome

Shen

Kurotaki

Patel

et al. 2005

Pediatr. Blood Cancer

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Sotos syndrome is an overgrowth disorder that manifests characteristic dysmorphic features, neurological problems, and an increased risk for cancers and heart defects. Alterations of NSD1 are responsible for this disease. A subset of cases arise from deletions, which is of interest as the factor XII locus lies in close proximity to NSD1. This case report describes an individual with Sotos syndrome and factor XII deficiency, providing a potential link between these two genes and, consequently, expanding the clinical phenotype of Sotos syndrome.

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Section: Discussionmentioning

confidence: 99%

Low factor XII level in an individual with Sotos syndrome

Shen

Kurotaki

Patel

et al. 2005

Pediatr. Blood Cancer

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“…[27][28][29] Most patients with FXII deficiency have presented with thromboembolic complications, usually venous thromboembolic disease or myocardial infarction. 4,6,7,[10][11][12][13]23) FXII deficiency is one of the rare congenital blood protein defects associated with thrombosis, in contrast to the more common deficiencies of antithrombin III, protein C, and protein S. 2) Analysis of 121 patients (including case histories) with Hageman trait found an 8% incidence of thromboembolism and several cases of myocardial infarction. 7) The prevalence of partial FXII deficiencies was 8% in patients with exclusively recurrent venous thromboembolism.…”

Section: Discussionmentioning

confidence: 99%

Subdural Hematoma in a Patient With Hageman Trait-Case Report-

Kaspera

Rothkegel²,

Stadnicki

2005

Neurol. Med. Chir.(Tokyo)

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A 61-year-old man with severe factor XII deficiency presented with a subdural hematoma appearing as mixed but mainly high density by computed tomography in the left frontotemporoparietal region. No cranial injury was reported in the medical history of the patient. Clotting system study showed less than 1% functional activity of factor XII, whereas the levels of the other clotting factors were within the normal ranges. Partially clotted and hemolyzed subdural hematoma was removed through a craniotomy. The postoperative course was uneventful. The patient later died of severe circulatoryrespiratory failure. We believe that the subdural hematoma may have developed as a result of a minor head trauma sustained in the past. We suggest that impairment of fibrinolytic activation related to severe factor XII deficiency might have contributed to the delay of dissolution of the subdural hematoma which, under ordinary circumstances, would have formed chronic subdural hematoma.

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“…However, there have been conflicting reports on thrombotic tendency in Factor XII deficiency. Some reports showed an increased incidence of thrombotic complications in patients with Factor XII deficiency because of less activity of Factor XII-dependent plasmin production (30), but others reported that there was no difference in the thromboembolic incidence between normal and Factor XII-deficient patients (31).…”

Section: Components Of the Kallikrein-kinin System In Plasmamentioning

confidence: 99%

Roles for the Kallikrein-Kinin System in Inflammatory Exudation and Pain: Lessons From Studies on Kininogen-Deficient Rats

Ueno¹,

Oh‐ishi²

2003

J Pharmacol Sci

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Abstract. Roles for the kallikrein-kinin system in inflammation have been investigated extensively, and many reviews on this topic have been published during the 50 years since the discovery of bradykinin in 1949. Recent progress in the field has been remarkable with the help of experiments using gene-targetted transgenic or knockout mice, which have added further valuable information in addition to previous results obtained from pharmacological and biochemical studies using purified and isolated components of the system. Furthermore, much knowledge has been accumulated as a result of the development of various bradykinin agonists and antagonists. In this review, we focused on the data obtained from the kininogen-deficient rat, which is a natural mutant, and discuss the results in comparison with those from bradykinin receptor knockout mice. These data have clarified that endogenous bradykinin exerts a most important role in inflammatory exudation along with prostanoids, preferentially to histamine, serotonin, or neuropeptides. In inflammatory pain perception also, bradykinin produced in the local perivascular spaces stimulates polymodal pain receptors in conjunction with co-helpers such as prostanoids, vanilloids, and neuropeptides. These important roles are concluded based on consistent results obtained from experiments using several antagonists of bradykinin, kininogen-deficient rats, and bradykinin receptor knockout mice.

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Factor XII deficiency associated with coronary stent thrombosis

Cited by 7 publications

References 5 publications

Low factor XII level in an individual with Sotos syndrome

Low factor XII level in an individual with Sotos syndrome

Subdural Hematoma in a Patient With Hageman Trait-Case Report-

Roles for the Kallikrein-Kinin System in Inflammatory Exudation and Pain: Lessons From Studies on Kininogen-Deficient Rats

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