scholarly journals Coagulation Status in Women With Missed Abortion

2021 ◽  
Author(s):  
Shuo Yang ◽  
Dandan Chen ◽  
Junxiong Wang ◽  
Rui Qiao ◽  
Liyan Cui
Keyword(s):  
Platelet Aggregation ◽  
Lupus Anticoagulant ◽  
Protein C ◽  
Antithrombin Iii ◽  
Protein S ◽  
Missed Abortion ◽  
Coagulation Function ◽  
Healthy Pregnancy ◽  
At Iii ◽  
D Dimer

Abstract Background: Missed abortion is a special type of spontaneous miscarriage, as well as a complex and multifactorial reproductive health problem that affects people all over the world. The purpose of this study was to assess the status of coagulation function in a large series of reproductive-age women diagnosed as missed abortion. Likewise, we want to explore the association between coagulation and missed abortions, in order to evaluate whether they could be used as early predictive factors for missed abortions.Methods: A total of 11182 women who suffered from missed abortion from Peking University Third Hospital and 5298 healthy age –matched early pregnancy women were enrolled in our study. Coagulation function test (prothrombin time, activated partial thromboplastin time), fibrinolysis status detection (fibrinogen, D-Dimer), anticoagulation function tests (protein C, protein S and antithrombin III) and lupus anticoagulants (LAC) were examined on an automated coagulation analyzer. In addition, platelet counts were detected by automated hematology analyzer. Platelet aggregation (PAgT) were tested by light transmission aggregometry (LTA). All tests were taken according to standard operating procedures of the instruments.Results: Compared with healthy pregnancy, the level of D-Dimer and platelet count were higher, and the antithrombin III (AT-III) activity was lower(P<0.05). 13.1% patients with missed abortion were positive for LAC, and platelet aggregation was increased in 47.4% patients. There were no significant differences in the levels of PT, aPTT, TT, fibrinogen, protein C and protein S between the patients with missed abortion and healthy pregnancy. Moreover, multivariate logistic regression analysis showed that D-Dimer, dRVVT-R, AT-III and PAgT had significant predictive value for missed abortion.Conclusion: These findings provide evidence of hypercoagulability in patients with missed abortion. Lupus anticoagulant, PAgT and D-Dimer were the strongest predictors of missed abortion. These data suggest that treatment of the lupus anticoagulant and antiplatelet aggregation could be considered in missed abortion.

Molekularbiologische Grundlagen und Diagnostik der hereditären Defekte von Antithrombin III, Protein C und Protein S

2002 ◽  
Vol 22 (02) ◽  
pp. 57-66
Author(s):  
I. Witt
Keyword(s):  
Protein C ◽  
Antithrombin Iii ◽  
Protein S ◽  
Klinische Relevanz ◽  
At Iii

ZusammenfassungDie enormen Fortschritte in der Molekularbiologie in den letzten Jahren ermöglichten sowohl die Aufklärung der Nukleotidsequenzen der Gene für Antithrombin III (AT III), Protein C (PROC) und Protein S (PROS) als auch die Identifizierung zahlreicher Mutationen bei hereditären Defekten dieser wichtigen Inhibitoren des plasmatischen Gerinnungssystems. Da die Gene für AT III (13,8 kb) und PROC (11,2 kb) nicht groß und relativ leicht zu analysieren sind, gibt es bereits umfangreiche »databases« der Mutationen (50, 73). Für AT III sind 79 und für PROC 160 unterschiedliche Mutationen beschrieben.Sowohl beim AT-III-Mangel als auch beim Protein-C-Mangel hat die Mutationsaufklärung neue Erkenntnisse über die Struktur-Funktions-Beziehung der Proteine gebracht. Beim Protein-C-Mangel steht die klinische Relevanz der DNA-Analyse im Vordergrund, da die Diagnostik des Protein-C-Mangels auf der Proteinebene nicht immer zuverlässig möglich ist.Das Protein-S-Gen ist für die Analytik schwer zugänglich, da es groß ist (80 kb) und außerdem ein Pseudogen existiert. Es sind schon zahlreiche Mutationen bei Patienten mit Protein-S-Mangel identifiziert worden. Eine Database ist bisher nicht publiziert. Die klinische Notwendigkeit zur Mutationsaufklärung besteht ebenso wie beim Protein-C-Mangel. Es ist zu erwarten, dass zukünftig die Identifizierung von Mutationen auch beim Protein-S-Mangel beschleunigt vorangeht.

Haemostatic Studies in Carbohydrate-deficient Glycoprotein Syndrome Type I

1996 ◽  
Vol 76 (04) ◽  
pp. 502-504 ◽  
Author(s):  
A Fiumara ◽  
R Barone ◽  
P Buttitta ◽  
R Musso ◽  
L Pavone ◽  
...  
Keyword(s):  
Plasma Levels ◽  
Protein C ◽  
Antithrombin Iii ◽  
Plasma Concentrations ◽  
Protein S ◽  
Coagulation Factors ◽  
Type I ◽  
Clotting Factors ◽  
Blood Coagulation Factors ◽  
D Dimer

SummaryCDG syndrome (CDGS) type I is the most frequent form of a group of metabolic disorders characterised by a defect of the carbohydrate moiety of glycoproteins. A large number of plasma glycoproteins, including clotting factors and inhibitors, are decreased and stroke-like episodes have been described in about half of the reported patients. We studied blood coagulation factors, inhibitors and D-dimer plasma levels in four subjects, aged 12-23 years, with CDGS type I. Factors VIII, XI, antithrombin III activity, antigen plasma levels of antithrombin III, free protein S and protein C were decreased whereas protein C as activity was normal. In addition two patients had reduction of factors II, V, VII, IX, X reflecting the phenotypic heterogeneity associated with CDGS type I. D-dimer plasma concentrations were elevated in all subjects. The hypercoagulable state as consequence of the combined deficiencies of coagulation inhibitors could contribute to the stroke-like phenomena in CDGS type I.

Molekularbiologische Grundlagen und Diagnostik der hereditären Defekte von Antithrombin III, Protein C und Protein S

1994 ◽  
Vol 14 (04) ◽  
pp. 199-208
Author(s):  
Irene Witt
Keyword(s):  
Protein C ◽  
Antithrombin Iii ◽  
Protein S ◽  
Klinische Relevanz ◽  
At Iii

ZusammenfassungDie enormen Fortschritte in der Molekularbiologie in den letzten Jahren ermöglichten sowohl die Aufklärung der Nukleotidsequenzen der Gene für Antithrombin III (AT III), Protein C (PROC) und Protein S (PROS) als auch die Identifizierung zahlreicher Mutationen bei hereditären Defekten dieser wichtigen Inhibitoren des plasmatischen Gerinnungssystems. Da die Gene für AT III (13,8 kb) und PROC (11,2 kb) nicht groß und relativ leicht zu analysieren sind, gibt es bereits umfangreiche »databases« der Mutationen (50, 73). Für AT III sind 79 und für RPOC 160 unterschiedliche Mutationen beschrieben.Sowohl beim AT-Ill-Mangel als auch beim Protein-C-Mangel hat die Mutationsaufklärung neue Erkenntnisse über die Struktur-Funktions-Beziehung der Proteine gebracht. Beim Protein-C-Mangel steht die klinische Relevanz der DNA- Analyse im Vordergrund, da die Diagnostik des Protein-C-Mangels auf der Proteinebene nicht immer zuverlässig möglich ist.Das Protein-S-Gen ist für die Analytik schwer zugänglich, da es groß ist (80 kb) und außerdem ein Pseudogen existiert. Es sind schon zahlreiche Mutationen bei Patienten mit Protein-S-Mangel identifiziert worden. Eine Database ist bisher nicht publiziert. Die klinische Notwendigkeit zur Mutationsaufklärung besteht ebenso wie beim Protein-C-Mangel. Es ist zu erwarten, daß zukünftig die Identifizierung von Mutationen auch beim Protein-S-Mangel beschleunigt vorangeht.

Patients with APC Resistance Compared with Those with Other Clotting Inhibitor Deficiencies Show Later Onset of Venous Thrombosis During Oral Contraception

1995 ◽  
Vol 1 (4) ◽  
pp. 274-276 ◽  
Author(s):  
Antonio Girolami ◽  
Paolo Simioni ◽  
Sandra Zanardi ◽  
Luigi Scarano ◽  
Bruno Girolami
Keyword(s):  
Deep Vein Thrombosis ◽  
Protein C ◽  
Antithrombin Iii ◽  
Activated Protein C ◽  
Protein S ◽  
Oral Contraception ◽  
Vein Thrombosis ◽  
Apc Resistance ◽  
At Iii ◽  
Deep Vein

The prevalence of deep vein thrombosis in female patients with antithrombin III (AT III), protein C, or protein S deficiency who are on oral contraception has been compared with that of patients with activated protein C (APC) resistance. In the latter case the prevalence was lower (36.4%) than in the AT III deficiency group (71.4%) but similar to that seen in the protein C and protein S group (25%).' Furthermore, venous thrombosis occurred with APC resistance much later than with AT III, protein C, or protein S defects. The time lag between onset of oral contraception and thrombosis (~16 cycles) was not statistically different from that seen in a group of women who were known to have no antithrombin III, protein C, or protein S defects. It appears that as far as the interaction with oral contraception is concerned APC resistance is a much less severe condition compared with other clotting inhibitor defects. Key Words: Oral contraceptive—Activated protein C resistance—Deep vein thrombosis.

scholarly journals Effect of CMF-chemotherapy on blood coagulation in patients with breast cancer

2002 ◽  
Vol 10 (2) ◽  
pp. 61-66
Author(s):  
Dragana Petrovic
Keyword(s):  
Breast Cancer ◽  
Metastatic Breast Cancer ◽  
Cancer Patients ◽  
Protein C ◽  
Antithrombin Iii ◽  
Metastatic Breast ◽  
Breast Cancer Patients ◽  
Significant Difference ◽  
At Iii ◽  
D Dimer

BACKGROUND: Influences of CMF (cyclophosphamide, methotrexate,5-fluorouracil) chemotherapy on blood coagulation were investigated in 30 patients receiving adjuvant chemotherapy and in 30 patients receiving chemotherapy for metastatic breast cancer. METHODS: In plasma samples of 60 patients (median age 49.5), we evaluated the following parameters 1)Markers of in vivo clotting activation thrombin-antithrombin complex (ELISA) and D-dimer (ELISA), 2) Natural anticoagulants (protein C [PC] and antithrombin III [AT III] by chromogenic methods). The coagulation studies were performed at the beginning and at the end of the first cycle of CMF protocol. RESULTS: Before CMF therapy, significant difference was observed between patients with early stage and patients with metastatic breast cancer in the PC (p<0.01), AT III (p<0.01) and TAT (p<0.01) levels. After CMF therapy, patients with stage II (adjuvant) disease manifested a significant decrease in the level of PC and AT III activity (p<0.01) and an increase in TAT level (p<0.01). In patients with disseminated breast cancer CMF therapy provoked an increased level of TAT and D-dimer with a decreased activity of protein C and antithrombin III. There was significant difference in value of TAT, D- dimer, protein C and antithrombin III between the patients with adjuvant and metastatic breast cancer patients after CMF chemotherapy CONCLUSION: Our results suggest that the application of cytotoxic therapy provokes hypercoagulable condition in breast cancer patients. This effect should be considered when chemotherapy is employed in advanced cancer patients at high risk for thrombosis, or in patients with other risk factors.

Hämostaseologische Risikoindikatoren im Verlauf der tiefen Venenthrombose und ihre Beziehung zur Entzündungsreaktion (CRP)

1995 ◽  
Vol 15 (02) ◽  
pp. 109-116
Author(s):  
O. Anders ◽  
H. Auel ◽  
C. Burstein ◽  
H. Ehrensberger ◽  
V. Hossmann ◽  
...  
Keyword(s):  
Protein C ◽  
Antithrombin Iii ◽  
Protein S ◽  
C Protein ◽  
At Iii

ZusammenfassungIn dieser Studie sollte bei Patienten mit tiefer Venenthrombose im Verlauf des akuten Ereignisses und bei ambulanter Nachuntersuchung die Beziehung zwischen bekannten hämostaseologischen Risikoindikatoren der Thrombophilie und der Akute-Phase-Reaktion untersucht werden. 73 Patienten mit phlebographisch gesicherter Venenthrombose wurden am Tag der Klinikaufnahme, am zweiten Tag und bei Entlassung aus dem Krankenhaus untersucht, bei 63 Patienten erfolgte eine ambulante Nachuntersuchung nach Abklingen der akuten Symptomatik. Bestimmt wurden die Parameter Plasminogenaktivator-Inhibitor (PAI), Ristocetin-Kofaktor, Plasminogen, Antithrombin III (AT III), Protein C, Protein S, Fibrinogen und C-reaktives Protein (CRP). Es zeigte sich ein deutlicher Abfall der bei 90% der Patienten pathologisch erhöhten CRP-Werte vom Zeitpunkt der Klinikaufnahme bis zur Entlassung aus dem Krankenhaus, 1/3 der Patienten hatte auch zum Zeitpunkt der ambulanten Nachuntersuchung noch erhöhte CRP-Konzehtrationen >0,5 mg/dl. Diese Patienten hatten eine Häufigkeit pathologisch erhöhter Werte von Fibrinogen (84,2%) und Ristocetin-Kofaktor (47,4%) wie zum Zeitpunkt der Akutveränderung bei Klinikaufnahme. Bei 2/3 der Patienten konnte bei der ambulanten Nachuntersuchung anhand unauffälliger CRP-Werte <0,5 mg/dl eine Akute-Phase-Reaktion ausgeschlossen werden. Diese Patienten hatten zu 49% pathologisch erhöhte Fibrinogenwerte, zu 41 % pathologisch erhöhte PAI-Werte und zu 25% pathologisch erhöhte Ristocetin-Kofaktor-Werte; 39% dieser Patienten mit normalem CRP hatten gleichzeitige Erhöhungen von zwei der drei Parameter Fibrinogen, Ristocetin-Kofaktor und PAI.Fibrinogen, Ristocetin-Kofaktor und PAI sind auch als Risikoindikatoren arterieller Thrombosen bekannt. Dies führt zu dem Schluß, daß der Pathomechanismus und die Risikokonstellation bezüglich thromboembolischer Ereignisse zwischen arteriellem und venösem System ähnlicher sind als bisher angenommen.CRP hat sich nach den vorliegenden Ergebnissen als prognostisch wichtiger Risikomarker bei der tiefen Venenthrombose erwiesen. Die vorgelegten Daten können Hinweise darauf geben, daß die Entzündungsreaktion im Pathomechanismus der tiefen Venenthrombose eine kausale und nicht nur sekundäre Rolle spielt. Die prospektive Bedeutung dieser Ergebnisse muß noch durch weitere Untersuchungen geklärt werden.

Different Incidence of Venous Thrombosis in Patients with Inherited Deficiencies of Antithrombin III, Protein C and Protein S

1994 ◽  
Vol 71 (01) ◽  
pp. 015-018 ◽  
Author(s):  
G Finazzi ◽  
T Barbui
Keyword(s):  
Venous Thrombosis ◽  
Protein C ◽  
Antithrombin Iii ◽  
Protein S ◽  
Total Period ◽  
Total Incidence ◽  
S Deficiency ◽  
At Iii ◽  
Antithrombin Iii Deficiency

SummaryA cohort study was undertaken to compare the incidence of thrombosis in patients with inherited deficiency of Antithrombin III (n = 9), Protein C (n = 36) and Protein S (n = 36). The patients were stratified for schedule of antithrombotic prophylaxis and followed for a total period of 160 patient-years. Seven venous thrombosis were observed for a total incidence of 4.3% pts.-ys. The incidence of thrombosis was not significantly different in patients of different age, sex and schedule of prophylaxis, although there was a trend to a lower incidence in young individuals and in those receiving long-term oral anticoagulation. Patients with AT III deficiency had an higher incidence of thrombosis than patients with Protein C or Protein S deficiency (12 vs. 2.8 vs. 3.3% pts.-ys., p <0.05), despite the fact that they were, on average, younger and more prophylaxed. This study suggests that congenital Antithrombin III deficiency constitutes a greater risk of thrombosis than congenital deficiences of Protein C and Protein S.

APC Resistance and other Haemostatic Variables during Pregnancy and Puerperium

1999 ◽  
Vol 81 (04) ◽  
pp. 527-531 ◽  
Author(s):  
U. Kjellberg ◽  
N.-E. Andersson ◽  
S. Rosén ◽  
L. Tengborn ◽  
M. Hellgren
Keyword(s):  
Factor Viii ◽  
Plasminogen Activator ◽  
Protein C ◽  
Activated Protein C ◽  
Plasminogen Activator Inhibitor ◽  
Protein S ◽  
Reference Level ◽  
Soluble Fibrin ◽  
Prothrombin Fragment ◽  
D Dimer

SummaryForty-eight healthy pregnant women were studied prospectively and longitudinally. Blood sampling was performed at 10-15, 23-25, 32-34 and 38-40 weeks of gestation, within one week and at eight weeks postpartum. Classic and modified activated protein C ratio decreased as pregnancy progressed. In the third trimester 92% of the ratios measured with the classic test were above the lower reference level whereas all modified test ratios were normal. Slight activation of blood coagulation was shown with increased levels of prothrombin fragment 1+2, soluble fibrin and D-dimer. Fibrinogen, factor VIII and plasminogen activator inhibitor type 1 and type 2 increased. Protein S and tissue plasminogen activator activity decreased. Protein C remained unchanged. No correlation was found between the decrease in classic APC ratio and changes in factor VIII, fibrinogen, protein S, prothrombin fragment 1+2 or soluble fibrin, nor between the increase in soluble fibrin and changes in prothrombin fragment 1+2, fibrinogen and D-dimer.

The Frequency of Type I Heterozygous Protein S and Protein C Deficiency in 141 Unrelated Young Patients with Venous Thrombosis

1988 ◽  
Vol 59 (01) ◽  
pp. 018-022 ◽  
Author(s):  
C L Gladson ◽  
I Scharrer ◽  
V Hach ◽  
K H Beck ◽  
J H Griffin
Keyword(s):  
Venous Thrombosis ◽  
Protein C ◽  
Antithrombin Iii ◽  
Young Patients ◽  
Protein S ◽  
Type I ◽  
Protein S Deficiency ◽  
Protein C Deficiency ◽  
Low Protein ◽  
S Deficiency

SummaryThe frequency of heterozygous protein C and protein S deficiency, detected by measuring total plasma antigen, in a group (n = 141) of young unrelated patients (<45 years old) with venous thrombotic disease was studied and compared to that of antithrombin III, fibrinogen, and plasminogen deficiencies. Among 91 patients not receiving oral anticoagulants, six had low protein S antigen levels and one had a low protein C antigen level. Among 50 patients receiving oral anticoagulant therapy, abnormally low ratios of protein S or C to other vitamin K-dependent factors were presented by one patient for protein S and five for protein C. Thus, heterozygous Type I protein S deficiency appeared in seven of 141 patients (5%) and heterozygous Type I protein C deficiency in six of 141 patients (4%). Eleven of thirteen deficient patients had recurrent venous thrombosis. In this group of 141 patients, 1% had an identifiable fibrinogen abnormality, 2% a plasminogen abnormality, and 3% an antithrombin III deficiency. Thus, among the known plasma protein deficiencies associated with venous thrombosis, protein S and protein C. deficiencies (9%) emerge as the leading identifiable associated abnormalities.

The Influence of Insulin, ß-Estradiol, Dexamethasone and Thyroid Hormone on the Secretion of Coagulant and Anticoagulant Proteins by HepG2 Cells

1995 ◽  
Vol 74 (02) ◽  
pp. 686-692 ◽  
Author(s):  
René W L M Niessen ◽  
Birgit A Pfaffendorf ◽  
Augueste Sturk ◽  
Roy J Lamping ◽  
Marianne C L Schaap ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Protein C ◽  
Protein Production ◽  
Culture Medium ◽  
Protein S ◽  
Cell Protein ◽  
Hepatoma Cell Line ◽  
Factor X ◽  
Factor Ii ◽  
At Iii

SummaryAs a basis for regulatory studies on the influence of hormones on (anti)coagulant protein production by hepatocytes, we examined the amounts of the plasma proteins antithrombin III (AT III), protein C, protein S, factor II, factor X, fibrinogen, and prealbumin produced by the hepatoma cell line HepG2, into the culture medium, in the absence and presence of insulin, β-estradiol, dexamethasone and thyroid hormone. Without hormones these cells produced large amounts of fibrinogen (2,452 ± 501 ng/mg cell protein), AT III (447 ± 16 ng/mg cell protein) and factor II (464 ± 31 ng/mg cell protein) and only small amounts of protein C (50 ± 7 ng/mg cell protein) and factor X (55 ± 5 ng/mg cell protein). Thyroid hormone had a slight but significant effect on the enrichment in the culture medium of the anticoagulant protein AT III (1.34-fold) but not on protein C (0.96-fold) and protein S (0.91-fold). This hormone also significantly increased the amounts of the coagulant proteins factor II (1.28-fold), factor X (1.45-fold) and fibrinogen (2.17-fold). Insulin had an overall stimulating effect on the amounts of all the proteins that were investigated. Neither dexamethasone nor ß-estradiol administration did substantially change the amounts of these proteins.We conclude that the HepG2 cell is a useful tool to study the hormonal regulation of the production of (anti)coagulant proteins. We studied the overall process of protein production, i.e., the amounts of proteins produced into the culture medium. Detailed studies have to be performed to establish the specific hormonal effects on the underlying processes, e.g., transcription, translation, cellular processing and transport, and secretion.

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