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Results for “Factor XII Deficiency”

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PubMed2004

Periodic painful purpura: fact or factitious?

A 60-year-old woman with multiple psychosocial issues presented with a history of spontaneous painful bruising on her left upper arm. Extensive investigations did not reveal any abnormality apart from an elevated activated partial thromboplastin time as a result of factor XII deficiency. An autoerythrocyte sensitization test reproduced the tender bruises on her back. Our patient reported relief of pain with promethazine injections. She was subsequently referred to the psychiatric team for ongoing assessment and management. Having an awareness of this rare condition will assist in the prevention of unnecessary investigation of such cases and will allow the early referral of patients for appropriate psychological counselling.

Diagnosis, Differential↗
PubMed1982

Deficiency and urinary losses of factor XII in adult nephrotic syndrome.

Factor XII was measured in the plasma and urine of 16 adult patients with nephrotic syndrome and 10 normal volunteers using a monospecific antibody to human factor XII. In addition plasma factor XII procoagulant activity was determined in both groups. Plasma immunoreactive factor XII level was significantly lower in the nephrotic group than the control group. This was associated with a significant reduction of plasma factor XII procoagulant activity. To examine the effect of albumin concentration on factor XII procoagulant activity purified human serum albumin was added in the in vitro system. Manipulation of albumin concentration failed to alter plasma factor XII activity. Considerable amounts of factor XII were recovered in the urine of all but one of the tested nephrotic patients while none were found in the urine of the control group. Plasma factor XII concentration was within normal limits in the single patient whose urine contained no detectable factor XII. Moreover, there was a significant negative correlation between plasma and urinary factor XII concentrations (r = -0.79; p less than 0.01). In addition, plasma factor XII concentration showed a significant correlation with serum albumin concentration (r = 0.63; p less than 0.05). It thus appears that renal losses of this plasma protein contribute to its low plasma concentration in our patients.

Adult↗
PubMed1980

The first cases of Fitzgerald factor deficiency in the Orient: three cases in one family.

Asymptomatic, female, 56-year-old identical Japanese twins were found to have a severe abnormality in the surface-mediated intrinsic coagulation, fibrinolysis and esterolytic activity. These defects were thought to be due to the lack of Fitzgerald factor, because of the prolongations of kaolin-activated partial thromboplastin time and kaolin-activated euglobulin lysis time that were not corrected by the addition of Fitzgerald trait-plasma but were corrected to normal levels by the addition of isolated bovine high-molecular-weight kininogen, Fletcher trait-plasma or Hageman trait-plasma.

Animals↗
PubMed2001

[Antiphospholipid antibodies in asymptomatic pediatric patients].

BACKGROUND: Findings of prolonged activated partial thromboplastin time (APTT) and lupus anticoagulant are rare in asymptomatic children and are often preceded by certain types of surgery. Clinical behaviour is usually favorable. PATIENTS AND METHODS: We assessed the biological and clinical features of antiphospholipid antibodies found in 13 children diagnosed between January 1996 and September 2000 (mean age at diagnosis: 5 years). The patients were prospectively followed-up for a median of 16 months (range: 15-60). The diagnosis of lupus anticoagulant was based on the guidelines of the International Society of Thrombosis and Hematosis and included coagulation-based assays as well as enzyme-linked immunosorbent assay for anticardiolipin and anti-beta 2 glycoprotein I. RESULTS: In all patients lupus anticoagulant was detected after investigation of prolonged APTT prior to surgery (adenoidectomy in eight patients, orchidopexy in one and eye surgery in one). The antibody was associated with infectious mononucleosis in one patient and was detected during routine laboratory investigations in two. All antibodies were primary and 53.6% of events were transient. In all patients lupus anticoagulant IgG and anti-beta 2 glycoprotein I were negative. Slightly reduced factor XII:C plasma concentrations (mean: 38.2 UI/dl) were found in 30.7% of the patients. No clinical manifestations of antiphospholipid symptoms were associated with the diagnosis of antiphospholipid antibodies and none of the patients experienced bleeding after surgery. CONCLUSIONS: Primary antiphospholipid antibodies were infrequent in asymptomatic pediatric patients and were typically associated with certain types of surgery (adenoidectomy, tonsillectomy) or viral infections. They were usually transient and clinically irrelevant. These antibodies may be associated with slightly reduced plasma concentrations of factor XII and consequently a differential diagnosis with a mild factor XII deficiency should be considered.

Adenoidectomy↗
PubMed2002

[Effect of oxidized cellulose on fibrin formation and blood platelets].

BACKGROUND: Haemostyptic materials initiate and hasten blood clotting at the site of their application. The properties of haemostyptic materials are used for treatment of capillary and parenchymatous haemorrhage along with surgical treatment. Celluloses one of the biopolymers studied for a long time, suitable because of its biocompatibility and non-toxicity. METHODS AND RESULTS: In the submitted study the authors used microdispersed calcium-sodium salt of oxidized cellulose which is formed by oxidation of cellulose in position C6 (patent Alltracel Pharmaceuticals). The authors investigated the effect of oxidized cellulose on fibrin formation and platelets. Using the optic method of the surface plasmon resonance they investigated the initial stage of interaction between fibrinogen and oxidized cellulose. Oxidized cellulose retards and reduces the interaction of the immobilized fibrin monomer with fibrinogen. Fibrin formation was investigated spectrophotometrically at 350 nm. In the presence of cellulose the period of formation of fibrin gel was prolonged and its turbidity increased, depending on the concentration of the cellulose used. The platelet activation by cellulose was assessed by measuring the released serotonin. For the activation of platelets by cellulose the presence of plasma is necessary, rinsed platelets were not activated by cellulose. It was revealed that direct, interaction of rinsed platelets or fibrinogen with cellulose plays a secondary role. CONCLUSIONS: These data and the retarded activation of platelets in plasma with factor XII deficiency indicate that due to negatively charged oxidized cellulose probably activation of the contact coagulation system occurs and this leads to the activation of platelets and fibrin formation.

Blood Platelets↗
PubMed1991

Effect of heparin on the activation of factor XII and the contact system in plasma.

We examined in purified systems and in human plasma whether heparin serves as a contact system activating compound. Purified human factor XII zymogen was not activated by heparin through an autoactivation mechanism, but was activated in the presence of purified prekallikrein. Zn2+ (12 microM) did not support autoactivation by heparin. The activation of factor XII and the contact system by heparin in plasma anticoagulated with citrate or with hirudin (not chelating ions) was examined by the cleavage of 125I-labeled factor XII and high molecular weight kininogen (HK). Heparin at 1.6 and 16 USP U/ml was not able to produce activation, in contrast to dextran sulfate (20 micrograms/ml) which supported activation of both factor XII and HK. This study indicates that heparinized plasma does not support activation of the contact system mediated through activation of factor XII. It is not expected that heparin anticoagulant therapy will contribute to activation of the contact system.

Complement C1 Inactivator Proteins↗
PubMed1979

Reduction of salivary tissue factor (thromboplastin) activity by warfarin therapy.

The coagulant of normal human saliva has been identified as tissue factor (thromboplastin, TF) by virtue of its ability to cause rapid coagulation in plasmas deficient in first-stage coagulation factors and to activate factor x in the presence of factor VII and by virtue of the fact that its activity is expressed only in the presence of factor VII and is inhibited by an antibody to TF. The TF is related to cells and cell fragments in saliva. Salivary TF activity has been found to be significantly reduced in patients taking warfarin. The decline in TF activity during induction of warfarin anticoagulation occurs during the warfarin-induced decline in vitamin-K-dependent clotting factor activity, as judged by the prothrombin time. The decrease in TF activity is not related to a reduction in salivary cell count or total protein content or to a direct effect of warfarin on the assay. It is hypothesized that the mechanism by which warfarin inhibits TF activity may be related to the mechanism by which it inhibits expression of the activity of the vitamin-K-dependent clotting factors. Inhibition of the TF activity may be involved in the antithrombotic effect of warfarin.

Factor VII↗