Related Experiment Video
Updated: Jul 18, 2026

In Vivo Osteo-organoid Approach for Harvesting Therapeutic Hematopoietic Stem/Progenitor Cells
Published on: February 16, 2024
[The changes of general potential of hemocoagulation in children, suffering an acute hematogenic osteomyelitis]
Insights
Children with acute hematogenic osteomyelitis exhibit secondary hypocoagulation due to soluble fibrin-monomer complexes. This condition, despite initial appearances, reflects an underlying hypercoagulation state in the blood
Area of Science:
- Hematology
- Pediatric Medicine
- Biochemistry
Context:
- Acute hematogenic osteomyelitis is a serious pediatric infection.
- Coagulation disorders are frequently observed in patients with severe infections.
- Understanding these disorders is crucial for effective treatment.
Purpose:
- To investigate the hemostatic balance in children with acute hematogenic osteomyelitis.
- To elucidate the mechanisms behind observed coagulation abnormalities.
- To determine the true coagulation status in these patients.
Summary:
- Children with acute hematogenic osteomyelitis display chronometric hypocoagulation.
- This is characterized by prolonged coagulation times and altered fibrinogenesis.
- Lowered anticoagulant capacity and increased platelet activity contribute to this state.
- Accumulation of soluble fibrin-monomer complexes inhibits fibrinogenesis, masking an underlying hypercoagulable state.
Impact:
- Identifies soluble fibrin-monomer complexes as key mediators of hypocoagulation.
- Reclassifies the overall coagulation potential in affected children as structural hypercoagulation.
- Provides critical insights for managing coagulation disturbances in pediatric osteomyelitis.
Abstract:
Chronometric hypocoagulation was observed in children, suffering an acute hematogenic ostheomyelitis, witnessed by processes of thrombin formation according to internal (the prolonged time of the blood plasm recalcification and activated partial thromboplastin time) and external (the thrombin time enhancement) ways of the blood coagulation process, as well as changes in fibrinogenesis mechanisms (the thrombin time prolongation). The lowering of anticoagulant capacity of the blood (the antithrombin III activity inhibition by 18.5%) was combined with significant increase of the thrombocytes functional activity (the rising of their adhesive and aggregational properties) in more than two times, which have occurred on the background of constant content of fibrinogen in the blood. Changes in the system of the plasm fibrinolysis in an acute hematogenic ostheomyelitis was characterized by inhibition of cofermental and, mainly, fermental fibrinolytic activity of the blood plasm, in conjunction with Hageman-dependent fibrinolysis intensification and was accompanied by accumulation of soluble complexes of fibrin-monomer in the blood. So far, chronometric hypocoagulation is secondary process, caused by the influence of soluble complexes of fibrin-monomer, which blocks fibrinogenesis. That's why the general potential of the blood coagulation system in children with an acute hematogenic ostheomyelitis must be regarded as a structural hypercoagulation.
Related Concept Videos
Introduction to Hemostasis
The three phases of hemostasis involve many clotting factors present in plasma and several substances released by platelets and injured tissue cells. It is a fast, localized, and...
Extrinsic and Intrinsic Pathways of Hemostasis
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...
Hemorrhagic Stroke ll: Pathophysiology
Overview of Hematopoiesis
Developmental Phases of Hematopoiesis
Initially, HSCs are formed in the embryonic yolk sac, a critical site for early blood cell production. These stem cells subsequently migrate to other...
Disorders of Hemostasis
Thromboembolic Disorders
Two factors primarily cause thromboembolic conditions.
Anticoagulant Drugs: Low-Molecular-Weight Heparins
