Biomedical subjects

M Bokarewa

Publications and source records attributed to M Bokarewa.

3 recordsLinked to original sources

PubMed2000

Decrease in protein C inhibitor activity and acquired APC resistance during normal pregnancy.

BACKGROUND: Since protein C inhibitor (PCI) inhibits activated protein C (APC) and a number of proteases, one would expect lower concentrations of PCI in a hypercoagulable state due to increased consumption of the inhibitor. Normal pregnancy is associated with a state of activated hemostasis, where response to APC is depressed. We aimed to study whether PCI function varies during normal pregnancy, and assess the relationship between this inhibitor and acquired APC resistance. METHODS: PCI activity in plasma was tested during pregnancy and postpartum in 28 healthy pregnant women without factor V Leiden Arg(506) - Gln mutation and in 14 non-pregnant female controls. The PCI levels determined in the present study was compared to the APC ratio (APC-r), we investigated previously, in the same samples. RESULTS: The levels of PCI in the pregnant group, as compared to that in the control group (4.74 +/- 0.48), gradually decreased from the first to the third trimester, i.e., 3.30 +/- 1.31 microg/mL in week 12 (p < 0.001), 2.66 +/- 1.44 microg/mL in week 20 (p < 0.001), 1.92 +/- 1.18 microg/mL in week 28 (p < 0.001), 1.30 +/- 0.94 microg/mL in week 32 (p < 0.001) and 1.49 +/- 1.12 microg/mL in week 37 (p < 0.001). After delivery, they rose to 5.02 +/- 1.93 microg/mL, similar to that in the controls (p > 0.05). The values of APC-r showed the same tendency during gestation and postpartum. CONCLUSION: With advance of normal pregnancy, decreasing PCI function corresponds to increasing APC resistance, probably due to that activated hemostasis acts as a link connecting the two variables.

Activated Protein C Resistance↗

PubMed1996

Elastin degradation in systemic vasculitis.

The elastin peptide level (EP) and elastase-type activity (EA) were investigated in 89 patients with different types of systemic vasculitis (polyarteritis nodosa-14, non-specific aortoarteritis-33, temporal arteritis-23 and thromboangiitis obliterans-18) and compared to the controls: 31 patients with leg atherosclerosis and 12 aged subjects with no evident vascular pathology. EP and EA levels in patients with thromboangiitis obliterans were significantly lower as compared to leg atherosclerosis and the aged control group (p < 0.02 for EA, p < 0.05 for EP). The increase of EP predominated in giant-cell arteritis as compared to the other vasculitic groups (18/56 vs. 5/32, p < 0.05); EA in these patients was the lowest. The activation of elastin degradation after corticosteroid treatment was demonstrated by an increase of EP in temporal arteritis (p < 0.05) and of EA in thromboangiitis obliterans (p < 0.03). We suggest that the determination of the above parameters of elastin degradation may be helpful in the search for differences in mechanisms of vascular damage between atherosclerosis and inflammatory vascular diseases.

Adolescent↗

PubMed1994

Heterogeneity of the APC-resistance phenomenon.

We developed an amidolytic assay for the determination of APC-resistance by inhibition of factor Xa (F Xa) generation, expecting it to be a result of factor VIIIa (F VIIIa) inactivation. Thirty-nine samples were tested with the proposed assay and compared to an APTT-based assay performed using the APC-resistance kit (Chromogenix, Mölndal, Sweden). In both assays APC was added at the last stage of the reaction together with CaCl2. The response to APC was calculated as a ratio of absorbances (or of clotting times) of a sample tested with or without APC and as the amount of F VIII activity generated in the presence of APC. An APC-ratio less than 2.0 and residual F VIII activity over 55% indicated APC-resistance. The results demonstrated that APC-response was heterogenic and dependent on the assay used for the determination. Only 1/3 of the tested samples were resistant in both APTT-based and in amidolytic assays. A number of samples developed an adequate decrease in F VIII activity, but the APC-resistance was still registered by the APTT-based assay. Other samples had a sufficient APC-response in APTT-based assay, in spite of diminished inactivation of F VIIIa. The obtained data presented the response to APC as a complex process with a chain of reactions. It indicated that poor degradation of coagulation factors may not be sufficient for its development.

Adult↗