scholarly journals Prevalence and role of antithrombin III, protein C and protein S deficiencies and activated protein C resistance in Kosovo women with recurrent pregnancy loss during the first trimester of pregnancy

2015 ◽  
Vol 8 (4) ◽  
pp. 224 ◽  
Author(s):  
Agon Mekaj ◽  
Ymer Mekaj ◽  
Shefqet Lulaj ◽  
Fetie Daci ◽  
Naser Rafuna ◽  
...  
Keyword(s):  
Protein C ◽  
Pregnancy Loss ◽  
Recurrent Pregnancy Loss ◽  
Antithrombin Iii ◽  
Activated Protein C ◽  
Protein S ◽  
First Trimester ◽  
Activated Protein C Resistance ◽  
First Trimester Of Pregnancy

scholarly journals Lack of Association between Recurrent Pregnancy Loss and Inherited Thrombophilia in a Group of Colombian Patients

Thrombosis ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Henry Cardona ◽  
Serguei A. Castañeda ◽  
Wálter Cardona Maya ◽  
Leonor Alvarez ◽  
Joaquín Gómez ◽  
...  
Keyword(s):  
Protein C ◽  
Pregnancy Loss ◽  
Recurrent Pregnancy Loss ◽  
Methylenetetrahydrofolate Reductase ◽  
Statistical Significance ◽  
Activated Protein C ◽  
Factor V Leiden ◽  
Prothrombin G20210a ◽  
Activated Protein C Resistance ◽  
Inherited Thrombophilia

Studies have shown an association between recurrent pregnancy loss and inherited thrombophilia in Caucasian populations, but there is insufficient knowledge concerning triethnic populations such as the Colombian. The aim of this study was to evaluate whether inherited thrombophilia is associated with recurrent pregnancy loss. Methods. We conducted a case-control study of 93 patients with recurrent pregnancy loss (cases) and 206 healthy multiparous women (controls) in a Colombian subpopulation. Three single nucleotide polymorphisms (SNPs) markers of the inherited thrombophilias factor V Leiden, prothrombin G20210A, and methylenetetrahydrofolate reductase C677T were genotyped by PCR-RFLP. Activated protein C resistance and plasma levels of antithrombin, protein C, and protein S were also measured. Results. The frequency of thrombophilia-associated SNPs, activated protein C resistance, and anticoagulant protein deficiencies, was low overall, except for the methylenetetrahydrofolate reductase C677T SNP. The differences between patients and controls had no statistical significance. Conclusion. Our study confirms the low prevalence of inherited thrombophilias in non-Caucasian populations and it is unlikely that the tested thrombophilias play a role in the pathogenesis of recurrent pregnancy loss in this Colombian population.

Lack of Association between Inherited Thrombophilic Risk Factors and Idiopathic Sudden Sensorineural Hearing Loss in Italian Patients

2006 ◽  
Vol 115 (3) ◽  
pp. 195-200 ◽  
Author(s):  
Gabriella Cadoni ◽  
Simona Scipione ◽  
Bianca Rocca ◽  
Stefania Agostino ◽  
Carmelo La Greca ◽  
...  
Keyword(s):  
Risk Factors ◽  
Protein C ◽  
Antithrombin Iii ◽  
Activated Protein C ◽  
Protein S ◽  
Mthfr C677t ◽  
Sudden Sensorineural Hearing Loss ◽  
Prothrombin G20210a ◽  
Factor V ◽  
Activated Protein C Resistance

Objectives: We investigated the presence of congenital thrombophilic risk factors in a population of consecutive Italian patients affected by idiopathic sudden sensorineural hearing loss (SSNHL). Methods: We investigated 48 patients with idiopathic SSNHL for the presence of congenital thrombophilic risk factors. The factor V Leiden G1691A, the prothrombin G20210A allele, and methylenetetrahydrofolate reductase (MTHFR) C677T genotypes were investigated. Allele frequencies and genotype distribution of all factors found in patients were compared to those of 48 healthy subjects of the same ethnic background by χ2 and odds-ratio analysis. Odds ratios and 95% confidence intervals were calculated for allele and genotype frequencies of all thrombophilia variants. Statistical significance was accepted with a p value of less than .05. We also performed the following blood tests: hemacytometric analysis including platelet count, prothrombin time, activated partial thromboplastin time, fibrinogen, erythrocyte sedimentation rate, C-reactive protein, protein S, protein C, antithrombin III, and activated protein C resistance. Results: In our series, we did not find an association between SSNHL and abnormal levels of antithrombin III, protein C, protein S, D-dimer, or fibrinogen; activated protein C resistance; or factor V G1691 A, prothrombin G20210A, or MTHFR C677T mutations. Conclusions: At present, the few studies regarding genetic polymorphisms of congenital thrombophilic factors in SSNHL are not conclusive. According to our data, factor V G1691A, prothrombin G20210A, and MTHFR C677T variants should be not considered risk factors for SSNHL. Further large prospective studies are needed to provide currently lacking information and to improve our knowledge in the field before we recommend the determination of genetic polymorphism in SSNHL as routine practice.

DEVELOPMENT OF A PROTEIN C CONCENTRATE

1987 ◽  
Author(s):  
Prabir Bhattacharya ◽  
Carolyn L Orthner ◽  
Dudley K Strickland
Keyword(s):  
Protein C ◽  
Antithrombin Iii ◽  
Activated Protein C ◽  
Protein S ◽  
Exchange Chromatography ◽  
Factor Ix ◽  
Human Protein ◽  
Red Cross ◽  
American Red Cross ◽  
Protein C Concentrate

A Protein C (PC) concentrate may be useful in treating patients with congenital or acquired Protein C deficiencies. A method for preparation of a human Protein C concentrate has been developed using a by-product of American Red Cross Factor IX production as the starting material (Menache et. al. Blood, 64, 1220). Levels of other vitamin K dependent proteins in the Protein C concentrate were measured and found to be <10 units per 100 units of PC, except for Protein S. The level of Protein S as judged by immunological assay was 30 u/100 u PC. Assay of the PC concentrate using chrcmogenic substrates revealed that levels of thrombin, Factor 3�a and Factor IXa were less than 0.006 u/mL. In addition, Antithrombin III and ax -macroglobulin were not detected. The vivo effects of Protein C concentrate and Protein C activated by thrombin have been tested in anesthetized rabbits. Thrombin was removed from the activated Protein C by ion-exchange chromatography; depletion was verified by S-2238 or by a clotting assay (< 0.006 u/mL). Rabbits were injected with Protein C concentrate (400 ug/kg) or activated Protein C 24 - 48 ug/Kg). The activated partial thromboplastin time (APTT), FactorV (FV) and Factor VIII (FVIII) levels were measured in samples collected over the next three hours. Infusion of PC concentrate elevated the level of PC to 150% of the preinfusion level within 30 min. It did not change the levels of FV, FVIII, fibrinogen or platelet count. In contrast, infusion of activated Protein C produced progressive prolongation of the APTT. Levels of FV and FVIII were decreased to 25% and 50% of preinfusion levels, respectivelv, three hours after the infusion. Fibrinogen and platelet levels were unchanged during that period. These data demonstrate that activated human Protein C concentrate induces an anticoagulant effect that can be readily measured in rabbits.

Acquired activated protein C resistance is associated with lupus anticoagulants and thrombotic events in pediatric patients with systemic lupus erythematosus

Blood ◽  
2001 ◽  
Vol 97 (4) ◽  
pp. 844-849 ◽  
Author(s):  
Christoph Male ◽  
Lesley Mitchell ◽  
James Julian ◽  
Patricia Vegh ◽  
Penny Joshua ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Protein C ◽  
Pediatric Patients ◽  
Activated Protein C ◽  
Factor V Leiden ◽  
Protein S ◽  
Activated Protein C Resistance ◽  
Systemic Lupus ◽  
Lupus Anticoagulants

Abstract Acquired activated protein C resistance (APCR) has been hypothesized as a possible mechanism by which antiphospholipid antibodies (APLAs) cause thrombotic events (TEs). However, available evidence for an association of acquired APCR with APLAs is limited. More importantly, an association of acquired APCR with TEs has not been demonstrated. The objective of the study was to determine, in pediatric patients with systemic lupus erythematosus (SLE), whether (1) acquired APCR is associated with the presence of APLAs, (2) APCR is associated with TEs, and (3) there is an interaction between APCR and APLAs in association with TEs. A cross-sectional cohort study of 59 consecutive, nonselected children with SLE was conducted. Primary clinical outcomes were symptomatic TEs, confirmed by objective radiographic tests. Laboratory testing included lupus anticoagulants (LAs), anticardiolipin antibodies (ACLAs), APC ratio, protein S, protein C, and factor V Leiden. The results revealed that TEs occurred in 10 (17%) of 59 patients. Acquired APCR was present in 18 (31%) of 58 patients. Acquired APCR was significantly associated with the presence of LAs but not ACLAs. Acquired APCR was also significantly associated with TEs. There was significant interaction between APCR and LAs in the association with TEs. Presence of both APCR and LAs was associated with the highest risk of a TE. Protein S and protein C concentrations were not associated with the presence of APLAs, APCR, or TEs. Presence of acquired APCR is a marker identifying LA-positive patients at high risk of TEs. Acquired APCR may reflect interference of LAs with the protein C pathway that may represent a mechanism of LA-associated TEs.

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