Rotation thromboelastography (ROTEM) parameters are influenced by age, gender, and oral contraception.

Rotation thromboelastography (ROTEM) is a screening method that allows the rapid detection of plasma- and platelet-related haemostatic abnormalities. To use this procedure more efficiently, reference values depending on gender, age, and oral contraception are required. In this study, five cohorts of healthy subjects were examined by ROTEM upon activation of the extrinsic or intrinsic pathway of coagulation, or recalcification alone. The cohorts comprised male subjects below (1) and above (2) 45 years of age, female subjects below 45 years of age with (3) or without (4) oral contraception, and female subjects above 45 years (5) without hormone replacement therapy. A significant influence of gender, age, and oral contraception on parameters determined by ROTEM was observed. Thus, adjustment for age, gender, and oral contraception is required when ROTEM is used to screen for distinct abnormalities of haemostasis.

Platelet-function analyzer closure times indicate shear stress-induced hemostatic abnormalities in patients with aortic valve stenosis and correlate with perioperative transfusion requirements.

BACKGROUND: Shear stress-induced hemostatic abnormalities are highly prevalent in patients with aortic valve stenosis. In this study, we determined closure times with a platelet-function analyzer (PFA-100, Dade Behring, Marburg, Germany) in patients admitted for aortic valve replacement to assess the correlation with the severity of aortic valve stenosis, blood loss, perioperative transfusion requirements, and need for re-thoracotomy. PATIENTS AND METHODS: Fifty consecutive patients (mean age [+/- SD] 68 +/- 9 years) were enrolled. Closure times of epinephrin/collagen and adenosine diphosphate (ADP)/collagen cartridges were determined at least ten days after discontinuation of antiplatelet medication and compared to those of healthy control subjects without medication. RESULTS: Closure times of epinephrin/collagen (210 +/- 69 sec vs. 140 +/- 50 sec, p < 0.0001) and ADP/collagen (145 +/- 58 sec vs. 108 +/- 45 sec, p < 0.0001) cartridges were prolonged in patients with aortic valve stenosis. Intraoperative transfusion of red blood cell units was associated with the closure times of epinephrin/collagen (r = 0.28, p = 0.04) and ADP/ collagen cartridges (r = 0.28, p = 0.04). Total transfusion of red blood cell units was associated with ADP/ collagen closure times (r = 0.31, p = 0.02), but not epinephrin/collagen closure times (r = 0.26, p = 0.07). No significant association of closure times with intraoperative, postoperative and total transfusion of fresh frozen plasma units was observed. CONCLUSIONS: Prolongation of closure times determined with a platelet-function analyzer is highly prevalent in patients with aortic valve stenosis and appears to reflect shear stress-induced hemostatic abnormalities. Since prolonged closure times are associated with increased perioperative transfusion of red blood cell units, the assay could significantly contribute to the identification of individuals at risk.

[Relevance of a single dose of 270 microg/kg recombinant factor VIIa for the treatment of patients with haemophilia and inhibitors - Recommendations from the GTH experts]. / Stellenwert der Einzelgabe von 270 microg/kg rekombinantem Faktor VIIa in der Behandlung von Hämophilie-Patienten mit Hemmkörpern - Empfehlungen der Experten.

Recombinant factor VIIa (rFVIIa; NovoSeven) is, besides other indications, authorised for the treatment of bleeding episodes in patients with hereditary haemophilia A or B and inhibitors. Based on the results of three clinical studies, marketing authorisation was granted for the single dose of 270 microg/kg body weight rFVIIa for the treatment of mild to moderate bleeding episodes in patients with haemophilia A or B with inhibitors in March 2007. Thereupon, an expert group analysed the relevance of this additional treatment option for clinical routine. Compared with the repeated application of 90 microg/kg body weight rFVIIa, quality of life may be improved if the single dose of 270 microg/kg body weight rFVIIa reduces the number of injections. The single dose has a benefit for those patients who require several rFVIIa applications or who do not respond adequately to low doses. Moreover, patients with poor venous access or patients who fear injections or reject them (especially children) may benefit from the single dose. The prescription of 270 microg/kg body weight rFVIIa as a single dose instead of multiple dosing of 90 microg/kg body weight is basically an individual and indication-related decision.

Rotational thrombelastometry for the bedside monitoring of recombinant hirudin.

BACKGROUND: Recombinant hirudin is used as an alternative anticoagulant, particularly in patients with heparin-induced thrombocytopenia type II. However, bedside monitoring for hirudin is not available. The present study aims to evaluate rotational thrombelastometry regarding its suitability to detect the effects of recombinant hirudin on whole blood coagulation. Hirudin was added to whole blood samples from healthy donors (n=5) and thrombelastometry variables resulting from activation of samples with tissue factor, ellagic acid, and ecarin were determined. METHODS: Hirudin (0.1-10 microg/ml) was added to citrated blood. Thereafter, rotational thrombelastometry was performed by initiating coagulation via recalcification and addition of tissue factor, ellagic acid, and ecarin, respectively, using the commercially available assays. RESULTS: In the absence of hirudin, clotting times (CT) induced by ellagic acid, tissue factor, and ecarin, respectively, were 141.7+/-18.0, 54.0+/-7.6, and 64.5+/-4.1 s. Increasing concentrations of hirudin led to dose-dependent prolongation of the clotting time with the three activators. All assays were capable to detect hirudin concentrations in the range of 0.5-5 microg/ml. At a final hirudin concentration of 1 microg/ml, clotting time increased to 268.0+/-25.1, 84.0+/-9.3, and 107.5+/-9.9 s, respectively, with the above-mentioned activators. The other thrombelastographic variables, including clot formation time, angle alpha, and maximum clot firmness, were not altered by hirudin at concentrations up to 5 microg/ml. CONCLUSIONS: Our study demonstrates the suitability of rotational thrombelastometry to detect anticoagulant effects of recombinant hirudin.

[Thrombophilia in pregnancy: venous thromboembolism, fetal loss, preeclampsia, intrauterine growth restriction]. / Thrombophile Hämostasestörung in der Schwangerschaft: Thrombose, Abort, Präeklampsie, intrauterine Wachstumsretardierung.

Women with acquired and hereditary thrombophilia are at increased risk of developing venous thromboembolism and other associated gestational vascular complications like fetal loss, preeclampsia, intrauterine growth restriction, and placental abruption during pregnancy. These complications are a major cause of maternal and fetal morbidity and mortality. In view of the data showing an association between thrombophilia and these adverse pregnancy outcomes, clinicians are increasingly using antithrombotic therapy in women at risk of these complications. Aside from recurrent pregnancy loss in antiphospholipid syndrome and prevention of venous thromboembolism, there is limited evidence on the benefit of antithrombotic interventions to guide therapy. The data in favour of antithrombotic therapy in women with hereditable thrombophilia and vascular placental complications consist predominantly of small uncontrolled trials or observational studies. Randomized, placebo-controlled trials are lacking as most patients do not accept placebo. Further randomised controlled trials are urgently required to explore this therapeutic option.

Platelet receptor HPA-1 polymorphism of alphaIIbbeta3 and 807 C/T polymorphism of alpha2beta1 and Buerger's disease.

Thromboangiitis obliterans or Buerger's disease is an episodic and segmental inflammatory and thrombotic process of the medium and small arteries of the lower extremities. Even though the disease was described 90 years ago, the etiopathogenesis is still under consideration. Afflicted patients are mostly young male cigarette smokers without signs of atherosclerosis or other risk factors for peripheral arterial occlusive disease. This indicates that hereditary thrombophilic factors could play a role in the etiopathogenesis. Recently, increasing evidence shows that platelet receptor polymorphisms (HPA-1 polymorphism of beta3 subunit of alphaIIbbeta3 and 807 C/T polymorphism alpha2beta1) are associated with early onset of arterial thrombosis (myocardial infarction, stroke). This case-control study was designed to assess whether the 807 C/T polymorphism or the HPA-1 polymorphism is involved in the pathogenesis of Buerger's disease or has any influence on the clinical course of Buerger's disease. Eighteen patients with Buerger's disease and 81 (sex and age matched) healthy control subjects (mean age 44 +/- 10 vs 45 +/- 8 years, respectively) were genotyped for platelet receptor HPA-1 and GPIa 807 C/T polymorphism. The gene frequency of HPA-1 and GPIa 807 C/T polymorphisms was identical in both groups. Prevalence of hetero- and homozygous carriers of the HPA-1b allel (1a1b and 1b1b genotype) as well as the prevalence of the 807 C/T and 807 T/T carriers did not differ significantly between the two groups, p >0.05. The grade of clinical disease manifestation as well as disease progression did not reveal any significant relationship with HPA-1 and 807 C/T polymorphisms. A relationship between the age at onset of the disease and HPA-1 polymorphism was not found. Otherwise analysis of the GPIa 807 C/T platelet receptor polymorphism showed that the average age of patients who are carriers of the T allele at early onset of disease was 32 +/- 6 years (range 27-48 years) compared to 42 +/- 6 years (range 34-53 years) of the C/C carriers (p <0.05). This indicates that the GPIa 807 C/T polymorphism does not represent a risk factor for Buerger's disease itself, but could be associated with premature onset of this disorder in predisposed individuals.

[Recombinant factor VIIa in patients with platelet function disorders or thrombocytopenia]. / Rekombinanter Faktor VIIa bei Patienten mit Plättchenfunktionsstörungen oder Thrombozytopenien.

Apart from on-label indications, recombinant factor VIIa (rFVIIa) is increasingly administered for treatment of life threatening bleeding events when appropriate standard therapy fails. Case reports and short treatment series document the efficacy and safety of rFVIIa to achieve haemostasis in patients with platelet function disorders and thrombocytopenias of various origin. An established on-label indication for the use of rFVIIa is given in patients with Glanzmann thrombasthenia with refractoriness to transfusions of platelet concentrates. Bolus applications of rFVIIa at dosages between 80 and 120 microg/kg body weight every 1.5 to 3 h are also administered successfully in patients with Bernard-Soulier syndrome, platelet storage pool defects, and other acquired platelet function disorders. In patients with Glanzmann thrombasthenia, at least three bolus injections are required to achieve effective haemostasis. In approximately half of the patients with thrombocytopenias, a single bolus of rFVIIa has been shown to be sufficient in managing otherwise untreatable bleeding complications. In these patients, haemostasis was achieved even at platelet counts <20,000/microl, although the efficacy of rFVIIa increases at higher platelet concentrations.

[Monitoring of NOAC]. / Monitoring von NOAK.

BACKGROUND: Monitoring non-vitamin K antagonist oral anticoagulants (NOAC) is usually not necessary; however, in some patients it may prove beneficial. OBJECTIVES: Patient subgroups who may profit from monitoring were identified, and methods of monitoring (including assessment of which coagulation parameters are affected by NOAC) are described. MATERIALS AND METHODS: We searched the PubMed database for each of the search terms, "NOAC", "DOAC", "rivaroxaban", "dabigatran", and "apixaban", in combination with one of the terms, "monitoring", "measurement", "measuring", or "assessment". The results were compiled and reviewed. RESULTS: Monitoring is most advantageous in emergency cases with severe bleeding where drug activity needs to be assessed. It can also help in deciding for or against lysis therapy after acute stroke in patients taking NOAC. Furthermore, it can also identify compliance problems and help in planning periprocedural management. There are quantitative measurement methods which measure plasma concentrations exactly and qualitative methods which only allow for a rough estimate or a general confirmation of drug activity. Recommended quantitative measurement methods are diluted thrombin time for dabigatran, and anti-factor Xa activity (calibrated) for rivaroxaban and apixaban. CONCLUSIONS: Several patient subgroups may profit from monitoring of NOAC plasma concentration. One should, however, take several issues into consideration before measurements, such as the objective of each individual measurement, possible consequences (e. g., dose adjustment), and which measurement method to pick.

[Pregnancy-associated venous thromboembolic disease: prediction, prevention, and therapy]. / Venöse Thrombose in der Schwangerschaft. Prädiktion, Prävention und Therapie.

Thromboembolic disease remains a leading cause of maternal mortality during pregnancy and the puerperium. Rational and risk-adapted administration of heparin prophylaxis depends on 1. the identification of those women who have an increased risk of thrombosis and 2. the accurate quantification of this risk. In women without prior thrombosis, the presence of a heterozygous factor V Leiden or heterozygous G20210A mutation in the prothrombin gene is associated with a pregnancy-associated thrombotic risk of approximately 1 in 400. Thus, in pregnant carriers of either one of these mutations the risk of venous thromboembolism is low. Therefore, no heparin prophylaxis is recommended. A combination of the two genetic risk factors can increase the risk to a modest level of 1 in 25. In women with a single episode of prior thrombosis associated with a transient risk factor, e.g. surgery or trauma, and no additional genetic risk factor, the probability of a pregnancy-associated thrombosis appears also to be low. However, data are sparse and conflicting. In contrast, in women with a prior idiopathic venous thrombosis who carry an additional hereditary risk factor or who have a positive family history of thrombosis, a high risk (>10%) can be expected supporting the indication for active antepartum and postpartum heparin prophylaxis. Despite the remarkable progress in risk stratification, the absolute magnitude of risk and the optimal management in many cases is an issue of ongoing debate.

Associations between thrombophilic risk factors and determinants of atherosclerosis and inflammation in patients with non-arteritic anterior ischaemic optic neuropathy.

UNLABELLED: Non-arteritic anterior ischaemic optic neuropathy (NAION) is caused by ischaemia of the optic nerve head. The pathophysiology of NAION is unclear, and no proven effective treatment exists. PATIENTS, METHODS: We analyzed thrombophilic risk factors and determinants of atherosclerosis and inflammation in 109 consecutive patients and 109 age- and sex-matched volunteers using a case-control design. RESULTS: High levels of fibrinogen (>384 mg/dl; OR 3.2, p = 0.003), factors VIII:C (>183%; OR 2.6, p = 0.02), IX (>153%; OR 2.6, p = 0.026), XI (>142%; OR 3.4, p = 0.006), von Willebrand factor (activity >205%; OR 3.1, p = 0.005; antigen >194%; OR 3.5, p = 0.002), and triglycerides (>228 mg/dl; OR 2.8, p = 0.026), higher platelet counts (>294,000/µl; OR 2.5, p = 0.04), low levels of HDL cholesterol (<40 mg/dl; OR 2.7, p = 0.032), and an accelerated erythrocyte sedimentation rate (>20 mm/h; OR 4.4, p = 0.003) were associated with NAION. CONCLUSION: Our findings support the contention of a complex pathogenesis of NAION resulting from the coincidence of proatherogenic, prothrombotic and proinflammatory processes. The alterations described could be causative, side effects, or just coincidental findings.

Association of polymorphisms of platelet membrane integrins alpha IIb(beta)3 (HPA-1b/Pl) and alpha2(beta)1 (alpha807TT) with premature myocardial infarction.

Conflicting results of an association of the human platelet antigen 1b (HPA-1b/PlA2), localized on the beta-subunit of the integrin alpha(IIb)beta3, and the alpha(2)807TT genotype of the integrin alpha2beta1 with coronary atherosclerosis and myocardial infarction have been reported. Both platelet receptor polymorphisms were genotyped in 3261 patients who had undergone coronary angiography, including 1175 survivors of a myocardial infarction, 1211 individuals with coronary artery disease but no history of myocardial infarction, and 571 control patients without angiographic coronary artery disease, and in 793 blood donors. In a case-control design, the prevalence of HPA-1b and alpha(2)807TT genotypes did not differ significantly between the patient groups with coronary artery disease or myocardial infarction and patient controls or blood donors. By contrast, using a multivariate case-only design, it was found that the median age of onset of myocardial infarction was 5.2 years earlier (P = 0.006) in carriers of the HPA-1b allele and 6.3 years earlier (P = 0.006) in carriers of the alpha(2)807TT genotype in the 264 survivors of myocardial infarction of recent onset with one- or two-vessel coronary artery disease. A significant interaction with the conventional risk factors hypercholesterolemia, smoking, diabetes, hypertension, and hyperfibrinogenemia was excluded. Human platelet antigen 1b and alpha(2)807TT are associated with premature myocardial infarction but not with coronary artery disease, suggesting a role of distinct integrin genotypes for increased platelet thrombogenicity. This association requires confirmation in follow-up studies.

The G20210A prothrombin-gene mutation and the plasminogen activator inhibitor (PAI-1) 5G/5G genotype are associated with early onset of severe preeclampsia.

Hereditary risk determinants of venous thrombosis have been reported to be associated with severe preeclampsia. So far there are no data to support whether these risk determinants are related to the time of onset of severe preeclampsia. We used a case-control design, studying 97 women with severe preeclampsia in previous pregnancies and 277 normal women, to assess hereditary risk factors of venous thrombosis as risk determinants for severe preeclampsia. A case-only design comprising solely the 97 women with a history of preeclampsia was used to evaluate these risk factors as risk determinants for early onset of severe preeclampsia. Using the case-control design, there was no significant risk association of the hereditary risk factors with severe preeclampsia [factor V Leiden, odds ratio (OR) 0.9, 95% confidence interval (CI) 0.4, 2.2; prothrombin mutation, OR 1.9, 95% CI 0.5, 7.0; methylentetrahydrofolate reductase 677TT genotype, OR 0.8, 95% CI 0.4, 1.8; plasminogen activator inhibitor (PAI-1) 4G/4G genotype, OR 1.2, 95% CI 0.7, 2.1; PAI-1 5G/5G genotype, OR 1.0, 95% CI 0.5, 1.8]. However, the onset of severe preeclampsia was significantly earlier in women with the G20210A prothrombin gene mutation (24.5 weeks vs. 30.1 weeks, P = 0.046) and in women with the PAI-1 5G/5G genotype (25.7 weeks vs. 30.8 weeks, P = 0.024). Hereditary risk factors for venous thrombosis do not predispose for severe preeclampsia. However, women who are carriers of the G20210A prothrombin gene mutation and the PAI-1 5G/5G genotype are at risk for early onset of severe preeclampsia. It appears that these risk factors do not induce the pathomechanism but accelerate the course of preeclampsia.

Value of an extended monoethylglycinexylidide formation test and other dynamic liver function tests in liver transplant donors.

Measuring monoethylglycinexylidide (MEGX) formation after intravenous administration of lidocaine in potential organ donors (MEGX test) has been advocated as a useful test to select donor livers for transplantation, but some groups have demonstrated a low test efficacy. We, therefore, investigated the value of an extended MEGX formation test and the value of other dynamic liver function tests, in selecting suitable human donor livers. In 51 human multi-organ donors, we measured elimination of galactose, indocyanine green, and lidocaine, as well as formation of MEGX, at 15, 30, and 60 min after administration of the test substances. In the early postoperative period, the function of the transplanted liver was then classified as good or poor, as defined by a prothrombin time above or below 65% by day 4 and fibrinogen concentration above or below 300 mg/dl by day 7. Donor characteristics and preservation modalities were very similar between the two groups. Galactose, indocyanine green, and lidocaine metabolism failed to predict good or poor graft function in the early postoperative period. MEGX serum concentrations, however, were significantly higher in the group of donors whose organs functioned well in the recipients, as compared with donors whose organs functioned poorly in the recipients. This was true for MEGX concentrations at 15 min (117+/-9 vs. 90+/-9 ng/ml; P=0.03), 30 min (108+/-8 vs. 86+/-8 ng/ml; P=0.04), and 60 min (100+/-6 vs. 73+/-5 ng/ml; P=0.006). Extending the MEGX formation test from 15 to 60 min improved test efficacy. Maximal MEGX concentration in 9 or up to 12 consecutive blood samples, drawn between 3 and 120 min after lidocaine infusion, was also significantly higher in donors whose organs functioned well, than in donors whose organs functioned poorly (129+/-10 vs. 101+/-10 ng/ml; P=0.03). Although the groups with good and poor organ function differed significantly with respect to their MEGX serum concentrations, and although efficacy of the MEGX test was improved by extending the test from 15 to 60 min, the overlap in individual MEGX serum concentrations was still so wide that it is virtually impossible to predict early graft function only on the basis of the MEGX test in the donor. Therefore, the MEGX test, although of potential scientific interest, does not predict early graft function with an accuracy necessary for clinical use.

Mutation in the gene coding for coagulation factor V and resistance to activated protein C: detection of the genetic mutation by oligonucleotide ligation assay using a semi-automated system.

Resistance of coagulation factor Va to inactivation by activated protein C (APCR) is associated with a point mutation in which adenine is substituted for guanine at nucleotide 1691 in the gene coding for factor V (FV Leiden). To date, this mutation of factor V is the most frequent genetic risk factor for venous thrombophilia. In this report, we describe the adaptation of an automatable oligonucleotide ligation assay (OLA) to detect the mutation in polymerase chain reaction-amplified DNA samples from 40 normal, 20 affected heterozygous, and 3 affected homozygous individuals. The genotypes determined by conventional allele-specific restriction enzyme site analysis were in complete concordance with the results obtained by ELISA-based oligonucleotide-ligation assay. The automated oligonucleotide ligation assay provides a rapid, reliable, nonisotopic method to detect the mutation responsible for APCR that can rapidly be applied to large population screening.

Prospective analysis after coronary-artery bypass grafting: platelet GP IIIa polymorphism (HPA-1b/PIA2) is a risk factor for bypass occlusion, myocardial infarction, and death.

Recently, we have demonstrated that human platelet antigen 1b (HPA-1b or P1A2) is a hereditary risk factor for platelet thrombogenicity leading to premature myocardial infarction in preexisting coronary artery disease. However, HPA-lb does not represent a risk factor for coronary artery disease itself. The aim of our present study was to evaluate the role of HPA-lb on the outcome in patients after coronary-artery bypass surgery. We prospectively determined the HPA-1 genotype in 261 consecutive patients prior to saphenous-vein coronary-artery bypass grafting. The patients were followed for one year. Among patients with bypass occlusion, myocardial infarction, or death more than 30 days after surgery, the prevalence of HPA-lb was significantly higher than among patients without postoperative complications (60 percent, 6/10, vs. 24 percent, 58/241, p <0.05, odds ratio 4.7). Using a stepwise logistic regression analysis with the variables HPA-1b, age, sex, body mass index, smoking (pack-years), hypertension, diabetes, cholesterol and triglyceride concentration, only HPA-lb had a significant association with bypass occlusion, myocardial infarction, or death after bypass surgery (p = 0.019, odds ratio 4.7). This study shows that HPA-1b is a hereditary risk factor for bypass occlusion, myocardial infarction, or death in patients after coronary-artery bypass surgery.

Polymorphism of platelet membrane glycoprotein IIIa: human platelet antigen 1b (HPA-1b/PlA2) is an inherited risk factor for premature myocardial infarction in coronary artery disease.

Conflicting results of an association between the human platelet antigen 1b (HPA-1b or PlA2) allele and the risk of myocardial infarction and coronary artery disease have been reported. To assess the reason for this discrepancy, we determined the HPA-1 genotype in 298 men who had undergone coronary angiography, including 124 individuals with myocardial infarction, 83 individuals with coronary artery disease but no history of myocardial infarction, and 91 control patients. Among patients with acute or recent onset myocardial infarction (< 1 year), the prevalence of HPA-1b was higher than among patients with coronary artery disease but without myocardial infarction (33 percent vs. 14 percent, p = 0.016). In patients under 60 years of age this difference was even more pronounced (45 percent vs. 15 percent, p = 0.003). Unlike conventional risk factors HPA-1b does not represent a risk factor for coronary artery disease itself but appears to be associated with increased platelet thrombogenicity.

Hemostatic changes due to the venom gland extract of the red-necked keelback snake (Rhabdophis subminiatus).

After a bite by the aglyphous red-necked keelback snake Rhabdophis subminiatus a complete defibrinogenation syndrome with severe hemorrhagic diathesis developed in a 25-year-old man. In vitro studies showed that the venom gland extract of the snake contains a very active prothrombin (Factor II) activator. The thrombin generated is inhibited neither by antithrombin III nor the antithrombin-III-heparin complex. The venom gland extract stimulated also the tissue plasminogen activator; however, it did not cause direct activation of plasminogen, protein C, Factor X or direct degradation of fibrinogen.

Successful thrombolysis of st. Jude medical aortic prosthesis with tissue-type plasminogen activator in a pregnant woman: a case report.

Mechanical valve thrombosis is a life-threatening event. Pregnancy is associated with a hypercoagulable state that further emphasizes the importance of adequate anticoagulation. This is associated with a therapeutic dilemma. Continued anticoagulation with warfarin throughout the first trimester can result in fetopathic effects, while replacement of warfarin by heparin between 6 and 12 weeks of gestation does not completely prevent the risk of valve thrombosis. There are a small number of reported cases of pregnant women with prosthetic heart valve thrombosis under low molecular weight heparin and consecutive lytic therapy. The authors report a 33-year-old pregnant woman with a St. Jude Medical aortic prosthesis, anticoagulated with a therapeutic dosage of low molecular weight heparin from 6 weeks of gestation, who developed prosthetic heart valve thrombosis at 17 weeks of gestation. A thrombolysis with recombinant tissue-type plasminogen activator (50 mg for 2 hours) was performed. Under thrombolysis, ST-segment elevation in leads II, III, aVF, V5, and V6 developed electrocardiographically with a maximal creatine kinase (CK) of 349 U/L (CK-MB isoenzyme of 48 U/L). Echocardiography revealed normal function of the St. Jude Medical aortic prosthesis 2 hours after thrombolysis and normal wall motions. Short-course thrombolytic therapy appears to be an effective alternative to surgical intervention for the treatment of thrombotic dysfunction of valve prostheses in pregnancy.

[Serology and culture diagnosis of Campylobacter jejuni infections]. / Serologische und kulturelle Diagnose von Campylobacter-jejuni-Infektionen.

Campylobacter jejuni is known today as one of the most common pathogens in acute infectious enteritis. In 77 patients serological testing by complement fixation as well as stool cultures were performed. A campylobacter jejuni infection was identified in 53% by culture and in 64% by serology, only in 17% the diagnosis was made with both methods. We conclude, that because of these data stool culture and serological testing should be used simultaneously. The complement fixation technique shows an increase in serum titer one to three weeks after beginning of the illness and a decrease in serum titer after four to eight weeks. For this reason it is an appropriate method for the identification of acute infections.