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PubMed2004

-455G/A beta-fibrinogen gene polymorphism, factor V Leiden, prothrombin G20210A mutation and MTHFR C677T, and placental vascular complications.

Hyperfibrinogenaemia is associated with systemic arterial and venous thromboembolism and therefore may contribute to placental vascular disease associated with obstetric complications. The fibrinogen-raising -455G/A beta-fibrinogen gene polymorphism may enhance the physiological increase in fibrinogen levels during pregnancy and thereby predispose to obstetric complications. This retrospective case-control study looked at the association between the beta-fibrinogen gene polymorphism -455G/A, the hereditary thrombophilic markers factor V Leiden, prothrombin G20210A mutation (PGM) and C677T methylene tetrahydrofolate reductase (MTHFR), and obstetric complications associated with placental vascular disease. The study group (n = 247) comprised 147 women (90 Caucasian) who met the clinical criteria and a control group of 100 parous women (90 Caucasian) with no history of obstetric or medical complications. No significant differences were observed in the -455A allelic frequencies of the patient and normal control groups, with (allelic frequencies, 0.156 and 0.178, respectively; P = 0.5716, chi2 test, odds ratio = 1.17, 95% confidence interval = 0.65-2.13) or without (allelic frequencies, 0.129 and 0.170, respectively; P = 0.2077, chi2 test, odds ratio = 1.38, 95% confidence interval = 0.81-2.35) the exclusion of non-Caucasian women. There was an increased prevalence of factor V Leiden among Caucasian patients compared with normal controls (allelic frequencies, 0.056 and 0.017, respectively; P = 0.048, chi2 test, odds ratio = 0.29, 95% confidence interval = 0.05-1.15) but there were no differences in the prevalences of PGM or MTHFR. These data suggest that factor V Leiden is associated with an increased risk of obstetric complications, but that the -455A allele of beta-fibrinogen, PGM and MTHFR do not appear to be implicated.

3' Untranslated Regions↗
PubMed2004

Successful control of massive coumarol-induced acute upper gastrointestinal bleeding and correction of prothrombin time by recombinant active factor VII (Eptacog-alpha, NovoSeven) in a patient with a prosthetic aortic valve and two malignancies (chronic lymphoid leukaemia and lung cancer).

Severe, life-threatening acute upper gastrointestinal bleeding may occasionally occur in patients receiving coumarol prophylaxis for prosthetic heart valves. These patients are exposed to two potential, serious risks: bleeding due to the severe blood loss induced by excessive anticoagulant effect or as a consequence of the cessation of anticoagulation subsequent thrombotic occlusion of the valve and loss of patency. Herein a short case report is presented. The elderly male patient had a prosthetic valve in the aortic position and also suffered from two malignant diseases: chronic lymphocytic leukaemia and a more recently developed lung cancer with metastatic spread into both lungs. The patient had a major gastrointestinal bleed, leading to a sudden fall of haematocrit (0.09), and to a collapse of peripheral circulation due to too excessive a coumarol effect (International Normalized Ratio > 8). An acute left ventricular failure developed during the early period of the emergency blood transfusion, so the correction of prothrombin time by fresh-frozen plasma (due to the large volume requirement) was not feasible. The patient received 50 microg/kg intravenous bolus of NovoSeven (recombinant active factor VII) in an almost desperate situation. The International Normalized Ratio changed to 2.1 in 30 min; bleeding had stopped immediately. There was neither evidence of disseminated intravascular coagulation (in spite of the age and underlying diseases) nor loss of valve patency or infective endocarditis during follow-up. This modest report may call attention to the potential use of recombinant active factor VII in the coumarol-induced severe bleeding episodes of prosthetic heart valve patients.

Acute Disease↗
PubMed2005

Early cerebral sinovenous thrombosis in a child with acute lymphoblastic leukemia carrying the prothrombin G20210A variant: a case report and review of the literature.

This paper describes the case of a male child with acute lymphoblastic leukemia who developed cerebral sinovenous thrombosis on day 6 of induction therapy with intrathecal methotrexate and methylprednisolone. A central venous catheter had been implanted the day before. The heterozygous prothrombin G20210A variant was found together with acquired activated protein C resistance and a reduced activated partial thromboplastin time. Clinical course and magnetic resonance imaging with magnetic resonance venography gradually improved over the following days after starting anticoagulant therapy (heparin and nadroparin). Cerebral sinovenous thrombosis is a serious disease in leukemic children, occurring in up to 6% of these patients. Data from the literature are in favor of anti-coagulant treatment, even though the efficacy and safety of thromboprophylaxis during chemotherapy in leukemic children with inherited thrombophilic conditions remain to be demonstrated.

Activated Protein C Resistance↗
PubMed1984

Mother-infant prothrombin precursor status at birth.

Previous work from this laboratory has suggested there is a risk of hemorrhagic disease of the newborn (HDNB) in approximately one-third of term neonates, presumably as a result of vitamin K deficiency. Using the same assay for PIVKA (protein induced by vitamin K absence, prothrombin precursor), we studied 46 normal mother-infant pairs at term to investigate the relationship between neonatal and maternal PIVKA status. PIVKA was found in 13 infants (28%) and in seven mothers (15%). Maternal PIVKA status correlated with infant status (p less than 0.03). These data suggest that fetal vitamin K deficiency and risk of HDNB may be a consequence of maternal deficiency of the vitamin.

Adult↗
PubMedDate not supplied

Acarboxy prothrombin (PIVKA-II) as a marker of hepatoblastoma in infants.

We evaluated plasma PIVKA-II (protein induced by vitamin K absence or antagonist-II, acarboxy prothrombin) levels in three infants with hepatoblastoma as a tumor marker. PIVKA-II levels were highly elevated in all three patients. Vitamin K administration, performed in two patients, resulted in only moderate reduction of PIVKA-II levels. Chemotherapy against tumor cells reduced the PIVKA-II levels without exception. Immunohistochemical study of the liver tissue indicated the presence of PIVKA-II in the hepatoblastoma cell. These findings suggest that elevated PIVKA-II in these patients was not due to nutritional vitamin K deficiency, but to excess production of tumor cells. A measurement of plasma PIVKA-II may be useful as a new marker of hepatoblastoma.

Biomarkers↗
PubMed2002

Prevalence of factor V G1691A (Leiden), prothrombin G20210A, and methylene tetrahydrofolate reductase C677T thrombophilic mutations in children with inflammatory bowel disease.

BACKGROUND: Patients with inflammatory bowel disease (IBD) have an increased incidence of thromboembolic events. This risk may be caused by an increased frequency of thrombophilic mutations such as factor V Leiden G1691A (FVL), prothrombin G20210A (PT), or methylene tetrahydrofolate reductase C667T (MTHFR). Prevalence rates of heterozygous mutations in FVL, PT, and MTHFR are reported for whites (1.8%, 1.3%, 26.6%, respectively), blacks (0.8%, 0.3%, and 12.4%, respectively), and Hispanics (1.2%, 2.4%, and 41.5%, respectively). We sought to determine the prevalence of these thrombophilic mutations in a large cohort of children with IBD. METHODS: Children aged 21 years or younger with IBD were genotyped for FVL, PT, and MTHFR mutations by polymerase chain reaction amplification and restriction enzyme digestion. Prevalence rates were compared with established rates in the respective populations. RESULTS: Of 92 patients enrolled, 89 (62 with Crohn disease, 24 with ulcerative colitis, and 3 with indeterminate colitis) had genotype results available. The mean age was 13.3 +/- 4.2 years (range, 2-21 years). Statistical analysis was performed on 89 FVL, PT, and MTHFR allele pairs. Polymerase chain reaction genotyping identified 5 patients with heterozygous FVL mutations, 3 patients heterozygous for the PT mutation, and 36 patients heterozygous and 4 patients homozygous for the MTHFR mutation. The thrombophilic allele mutation frequencies in our sample were not significantly different from predicted weighted average values: FVL, 2.8% versus 1.5%; PT, 1.7% versus 1.1%; and MTHFR, 24.7% versus 24.4%. In 24 patients with a family history of thrombosis, 1 was heterozygous for FVL and for MTHFR, 1 was heterozygous for FVL and homozygous for MTHFR, 2 were heterozygous for PT, and 9 were heterozygous MTHFR. There was no significant correlation between family history of thrombosis and presence of a thrombophilic mutation. The four patients with homozygous mutations for MTHFR, two of whom also were heterozygous for FVL, did not have either a personal history of thrombosis or a family history of thrombotic events. Two patients had thrombotic events without mutations in these genotypes: one had protein S deficiency and the other had no identifiable cause. CONCLUSIONS: The presence of genetic mutations that predispose to hypercoagulable states does not appear to correlate with the prevalence of IBD or to thromboembolic events in patients with IBD. There was no statistical difference between the proportions of the mutated allele frequency in our study patients and the general population.

Adolescent↗
PubMed1994

Prolongation of the prothrombin time after organophosphate poisoning.

Prolongation of the prothrombin time owing to a transient reduction in factor VII activity is described in a 14-month-old child with organophosphate poisoning. Correction after vitamin K administration suggested an organophosphate-related effect on vitamin K-dependent factor VII activity. Historically, coagulation screening has not been routinely recommended after organophosphate intoxications. We suggest, however, that routine screening in such patients may be important. A brief review of organophosphate poisoning and the unique features of our case are presented.

Acetylcholinesterase↗
PubMed1999

Clinical utility of simultaneous measurement of serum high-sensitivity des-gamma-carboxy prothrombin and Lens culinaris agglutinin A-reactive alpha-fetoprotein in patients with small hepatocellular carcinoma.

OBJECTIVE: To evaluate the diagnostic efficacy of simultaneous measurements of high-sensitivity des-gamma-carboxy prothrombin (H-DCP) and Lens culinaris agglutinin A-reactive alpha-fetoprotein (AFP-L3) in small hepatocellular carcinoma (HCC). METHODS: Sixty-one patients with small HCCs < or = 2 cm in diameter and 134 controls (chronic hepatitis: 59 cases; cirrhosis: 75 cases) were examined. H-DCP was measured by electrochemiluminescence immunoassay (cut-off 40 mAU/ml (milli-arbitrary units/ml) and AFP-L3% (percentage of AFP-L3/total AFP) by lectin-affinity electrophoresis coupled with the antibody-affinity blotting method (cut-off 10%). Fifty-six patients were histologically diagnosed and the remaining five patients were diagnosed clinically. RESULTS: Of 61 patients, 27 (44.3%) were positive for H-DCP and 14 (23.0%) were positive for AFP-L3. There was no correlation between H-DCP and AFP-L3%. Nineteen patients (31.1%) had positive H-DCP alone. Six patients (9.8%) had positive AFP-L3 alone, and in eight patients (13.1%) both markers were positive. In combination assay, 33 of 61 patients (54.1%) were positive for either marker; specificity and accuracy were 97.8% and 84.1%, respectively. There was a tendency for the AFP-L3% to be elevated in patients with moderately or poorly differentiated HCC (P= 0.0564) and multiple HCC nodules (P= 0.0316), while the H-DCP showed no elevation related to the tumour type. CONCLUSION: The detection rate of small HCC was improved by combination assay with H-DCP and AFP-L3%. Our results indicate that the markers are complementary and useful for the diagnosis and evaluation of small HCC when measured simultaneously.

Biomarkers↗
PubMed2002

Alpha-fetoprotein- and des-gamma-carboxy prothrombin-producing advanced gastric cancer.

A case of alpha-fetoprotein (AFP) and des-gamma-carboxy prothrombin (DCP) producing gastric cancer with multiple liver metastasis is reported. The simultaneous presence of Borrmann I gastric cancer and IIa aggregating type gastric cancer was noted. Borrmann I gastric cancer was a poorly differentiated adenocarcinoma, while IIa aggregating type gastric cancer was a moderately differentiated adenocarcinoma. Plasma levels of AFP and DCP were 247,000 ng/ml and 320,000 mAU/ml, respectively. Immunohistochemical staining confirmed the production of these two proteins in Borrmann I gastric cancer.

Adenocarcinoma↗
PubMed2002

Prothrombin index decrease: a useful and reliable marker of extensive fibrosis?

Non-invasive serum markers of extensive liver fibrosis are required in clinical practice for several reasons: (1) although histological analysis is considered to be the gold standard for the diagnosis of extensive fibrosis and cirrhosis, the rate of false-negative results is approximately 15-20%; (2) liver biopsy is an invasive method with a 1/10 000 mortality rate, even though occurrence of death is exceptional in patients with diffuse liver disease; (3) patients with chronic viral hepatitis have to undergo multiple liver biopsies during follow-up to assess the progression of tissue injury. In this leading article, we briefly overview the recent progress in non-invasive serum markers for the prediction of the extent of liver fibrosis. Among those serum markers, we focused on prothrombin index, which seems to be a reliable and non-expansive marker for the diagnosis of extensive fibrosis.

Apolipoprotein A-I↗
PubMed2005

The administration of N-acetylcysteine causes a decrease in prothrombin time in patients with paracetamol overdose but without evidence of liver impairment.

OBJECTIVE: To explore the effect of intravenous N-acetylcysteine (NAC) on the prothrombin time (PT) in patients with paracetamol overdose and persistent normal liver profile. MATERIALS AND METHODS: This retrospective case series study examined all admissions with a diagnosis of paracetamol poisoning in a tertiary hospital between 1989 and 2002. Patients were included if they had ever received NAC infusion, had no biochemical evidence of liver damage, and had more than two measurements of PT. Patients who had also ingested other drugs were excluded. RESULTS: Of 65 admissions wtih paracetamol poisoning, 18 patients (10 men) met the inclusion criteria. The median age was 29 years, and the median quantity of paracetamol ingested was 186 mg/kg. The mean number of PT measurements per patient was 4.8. The baseline PT (as a percentage) 8.6 h after paracetamol ingestion was 89.6%. During NAC infusion the PT fell in all patients (range, 4.8-53.4% relative to baseline; P < 0.0001) at 14 h. The PT was less than 60% in 28% of the patients. Eight hours after the initiation of NAC there was a 16% fall in PT (range, 4.3-34%; P < 0.0001). At the end of NAC infusion all PTs returned to values close to baseline. Nine patients were hospitalized. CONCLUSIONS: In patients with paracetamol overdose without evidence of liver damage a marked decrease in PT often occurs, which seems to be due to the overload of NAC infused at the beginning of treatment. This particular feature should be noted in clinical practice guidelines as a potentially misleading indicator of the development of severe liver dysfunction.

Acetaminophen↗
PubMed2002

Recombinant plasminogen activator therapy for cerebral vein thrombosis in a child carrier of prothrombin gene mutation.

Venous thrombosis of transverse and sigmoid sinuses was diagnosed in a 3-year-old child who is a carrier of the G20210A prothrombin gene mutation. Recombinant tissue plasminogen activator (rt-PA) treatment was started 9 days following the onset of neurologic signs. Nine days of rt-PA therapy completely dissolved the thrombus. This case provides further evidence that rt-PA is useful and safe in children with thrombosis.

Brain↗
PubMed2003

Familial thrombophilia is an oligogenetic disease: involvement of the prothrombin G20210A, PROC and PROS gene mutations.

Population-based case-control studies and cases previously published suggest that the prothrombin G20210A mutation is a weak risk factor for thrombosis, leading to clinical expression mainly in the presence of other risk factors. We report the results of plasma and genetic analyses performed in a 13-year-old symptomatic boy homozygous for the 20210A allele and in his family, which are in accordance with this suggestion. These analyses demonstrated the presence of several PROC (R-5W, R87H) and PROS (R60C, T103N) gene mutations in this family. These additional mutations have modulating effects on clinical expression of the G20210A mutation. The present family study illustrates the concept of 'mild' mutation and the hypothesis that familial thrombophilia is a multifactorial disease.

Adolescent↗
PubMed2003

Evaluation of the Roche LightCycler: a simple and rapid method for direct detection of factor V Leiden and prothrombin G20210A genotypes from blood samples without the need for DNA extraction.

The Roche LightCycler is a micro-volume thermocycler that combines extremely rapid polymerase chain reaction with fluorescence resonance energy transfer analysis of amplified products. We have evaluated the use of minimally processed blood samples for detection of two point mutations known to increase the risk of venous thromboembolism. Results from the LightCycler using the supernatant of diluted heated blood were compared with those gained by traditional methods based on polymerase chain reaction and restriction enzyme digestion. For factor V Leiden mutation, there was complete agreement between both methods in detection of wild-type (n = 82), heterozygous (n = 100) and homozygous (n = 18) genotypes. Similarly, the prothrombin G20210A mutation showed complete agreement for wild-type (n = 135), heterozygous (n = 63) and homozygous (n = 2) subjects.

3' Untranslated Regions↗
PubMed2006

Effect of phosphatidylcholine, phosphatidylethanolamine and lysophosphatidylcholine on the activated factor X-prothrombin system.

Membrane phospholipids are essential in blood coagulation reactions. The importance of negatively changed phosphatidylserine has been shown. The roles of other phospholipids in the blood coagulation system, however, are not clear. This study examined the effects of phosphatidylcholine on the blood coagulation system using liposomes containing varying concentrations of phosphatidylcholine in the presence of phosphatidylserine at a constant concentration. In addition, with phosphatidylserine and phosphatidylcholine at constant concentrations, the effects of phosphatidylethanolamine and lysophosphatidylcholine on the blood coagulation system were examined. Using an in vitro reconstructed system of the activated factor X-prothrombin system, blood coagulation was measured by the rate of thrombin formation after the addition of liposome preparations. The results showed suppression of the system by phosphatidylcholine and phosphatidylethanolamine and acceleration by lysophosphatidylcholine. The results of the present study suggest that the cell membrane, the 'location' of blood coagulation, is one of the regulatory factors, and that changes in phosphatidylcholine content and phospholipid composition of the cell membrane regulate the coagulation reaction.

Animals↗
PubMed2004

Prothrombin time international normalized ratio monitoring by self-testing.

PURPOSE OF REVIEW: The increasing numbers of patients on oral anticoagulants may challenge the traditional organization of patient monitoring. The availability of portable coagulometers capable of measuring prothrombin time (PT) international normalized ratio (INR) in a drop of capillary blood facilitates decentralization of monitoring by self-testing. This article reviews the literature on use of portable coagulometers. RECENT FINDINGS: Numerous studies have evaluated the reliability of portable coagulometers in testing the PT-INR. This has been assessed by statistically as well as clinically relevant criteria. Other studies have been devoted to developing calibration models fulfilling the criteria recommended by the World Health Organization (WHO) for the calibration of INR measuring systems. Finally, studies have assessed the value of schemes for patient training and for the long-term quality assurance of portable coagulometers. SUMMARY: It can be concluded from the published studies that PT-INR self-testing may be considered as a suitable alternative to conventional laboratory testing. For the PT-INR to be reliable, manufacturers of portable coagulometers should calibrate their devices against international standards for thromboplastin with procedures similar to those recommended by WHO for conventional measuring systems. Training of patients and implementation of appropriate quality assessment schemes are also essential prerequisites for the success of PT-INR self-testing.

Administration, Oral↗
PubMed2003

Prothrombin G20210A mutation and sudden death.

The authors present a case of sudden death in a previously healthy 36-year-old male. At autopsy there were bilateral pulmonary thromboemboli and right ventricular dilatation. Histologic findings in the lungs included recanalized, old thrombi and evidence of pulmonary hypertension. Genetic analysis for hereditary risk factors was heterozygous positive for the prothrombin G20210A mutation. Implications of this finding, its history and the diagnostic technique shall be discussed. The authors recommend that all cases of deep venous thromboses and pulmonary thromboemboli lacking known risk factors be evaluated for newly described genetic variations associated with an increased risk for venous thrombosis.

Adult↗
PubMed2005

Thromboembolism in heart transplantation: role of prothrombin G20210A and factor V Leiden.

BACKGROUND: Thromboembolism has been reported as a frequent complication after cardiac transplantation. Many risk factors for thrombosis may explain this, such as metabolic alterations and the use of cyclosporine. In the general population, two single nucleotide polymorphisms (SNPs), factor V Leiden and prothrombin G20210A (PT G20210A), have been associated with a significant increase in the risk of thrombosis. However, these mutations have not been analyzed in cardiac transplant patients. We describe the protracted history of recurrent thromboembolism in a rare case of homozygosity for the PT G20210A variant. This prompted us to analyze the entire cardiac transplant cohort for the incidence of thromboembolic events and their association with these genetic polymorphisms. METHODS: We report the study of 84 cardiac transplant recipients. We retrospectively analyzed the frequency of thromboembolic episodes. The genotypes for FVL and PT G20210A were determined and correlated with those episodes. RESULTS: Our results confirm a very high incidence of thromboembolism in this population. We also found a significant increase in the likelihood of thromboembolism in subjects with the PTB G20210A variant (odds ratio 3.08; 95% confidence interval: 1.7-5.5). CONCLUSIONS: The incidence of thromboembolic complications after heart transplantation is increased and may be related in part to genetic predisposition.

Adult↗