Biomedical subjects

J J Sidelmann

Publications and source records attributed to J J Sidelmann.

3 recordsLinked to original sources

PubMed2006

Relationship of glucose concentrations with PAI-1 and t-PA in subjects with normal glucose tolerance.

AIM: To study metabolic risk factors for the development of cardiovascular disease (CVD), including markers of the fibrinolytic system in relation to blood glucose levels in subjects with normal glucose tolerance and fasting blood glucose levels below 5.6 mmol/l. METHODS: Cross-sectional, community-based study from a primary health-care centre of adult subjects with normal glucose tolerance. Analysis of fasting and 2-h post-load blood glucose concentrations were centralized and related to anthropometric characteristics, metabolic variables, inflammatory markers, and coagulation and fibrinolytic variables. RESULTS: Increasing fasting blood glucose concentrations within the normal range in subjects with normal glucose tolerance were associated with increasing age, body mass index, and waist circumference, and with increasing concentrations of metabolic risk factors for development of CVD. After adjustment for gender, age, body mass index (BMI), and fasting insulin, levels of plasmin activator inhibitor (PAI-1) and tissue type plasminogen activator (t-PA) increased significantly with increasing levels of fasting glucose within the normal range (P = 0.012 and P < 0.0001, respectively). CONCLUSIONS: We found risk factors for CVD, specifically key components of the fibrinolytic system, PAI-1 and t-PA, increased with increasing fasting glucose levels even in subjects with normal glucose tolerance. This observation may help to explain the increased risk of CVD with increasing values of fasting glucose in the normal range.

Adult↗

PubMed2003

Hormone replacement therapy and hypercoagulability. Results from the Prospective Collaborative Danish Climacteric Study.

OBJECTIVE: To assess the influence of a variety of HRT regimens on the haemostatic balance using markers of fibrin turnover and inhibitors of coagulation. DESIGN: An open randomised study allocating women to either a control group or five different HRT treatment groups. SETTING: Gentofte Hospital, Hellerup, and Rigshospitalet, Copenhagen, Denmark. POPULATION: One hundred and forty-nine postmenopausal women without previous venous thromboembolic disease. METHODS: Prothrombin fragment 1+2 (F(1+2)), fibrin degradation products, antithrombin, protein C, total protein S and activated protein C-normalised ratio were measured at baseline and after 6 and 12 months of HRT in six groups of healthy postmenopausal women: (A). no HRT (reference group), (B). continuous oestradiol valerate (E(2)V) plus cyproterone acetate, (C). cyclic E(2)V plus cyproterone acetate, (D). continuous combined oestrogen (E(2)) plus norethindrone acetate, (E). E(2) combined with local delivery of levonorgestrel and (F). E(2)V plus medroxyprogesterone. HRT-induced changes in the concentration of inhibitors of coagulation and markers of fibrin turnover during 12 months of treatment. RESULTS: Significant decreases of antithrombin and protein S were found in all treatment groups, of protein C in Groups C, D, E and F and of activated protein C-normalised ratio in Groups E and F. Fibrin degradation products increased after three months of treatment, whereas F(1+2) was persistently increased after three months in Group F. The cumulative response of antithrombin was significantly lower in Groups D, E and F than in the reference group. The cumulative response of protein S and activated protein C-normalised ratio was lower, whereas that of F(1+2) was significantly higher in Group F than in the reference group. CONCLUSION: HRT reduces the inhibitory potential of coagulation significantly. The effect is related to the type of E(2)/progestin combination administered, but seems to be oestrogen-derived as the most pronounced effect is found with only quarterly progestin intake. Such procoagulant activity of HRT may well translate into clinical manifestations in thrombosis-prone individuals.

Adult↗

PubMed2000

Fibrin clot formation and lysis: basic mechanisms.

The hemostatic balance, introduced more than 40 years ago, addresses the components and reactions involved in fibrin turnover. Fibrin is placed in the core of this delicate balance. Defects in the mechanisms responsible for fibrin turnover might lead to thrombosis or bleeding, and fibrin consequently is an important substrate in the physiology of hemostasis. This review describes the components and processes involved in fibrin formation and fibrin degradation. Particular emphasis is put on the reactions involved in the conversion of fibrinogen to fibrin, the polymerization of fibrin molecules induced by coagulation factor XIII (FXIII), and the degradation of fibrinogen and fibrin mediated by plasmin and elastase. Furthermore, factors influencing fibrin structure and fibrin breakdown are addressed; in particular polymorphisms in the genes coding for fibrinogen and FXIII, but also the physical and biochemical conditions in which fibrin is formed. The past decades have produced a bulk of biochemical publications reviewing fibrin turnover and fibrin structure, and it has been shown that alterations in fibrin structure are important for the development of various disease conditions, whereas, the architecture of fibrin can be modified by certain drugs and chemical compounds. However, these topics deserve increased attention in clinical settings. Of particular importance might be more detailed clinical studies that review the influence of polymorphisms in the genes coding for the key factors involved in fibrin metabolism on the development of hemostatic diseases, but also the role of elastase-induced fibrin degradation deserves increased attention.

Antithrombins↗