Heghine Khachatryan: The discussion of Thrombophilia, APS and Coagulation Testing
Heghine Khachatryan, Heghine Khachatryan, Editor-in-Chief of Hemostasis Today, Head of Hemophilia and Thrombosis Center at Yeolyan Hematology and Oncology Center, shared a post on LinkedIn:
“Thrombophilia, APS and coagulation testing.
The second part of Professor Jeko Thachil’s lecture offered a focused analysis of thrombophilia, antiphospholipid syndrome and coagulation testing. Its central message was that laboratory investigations have value only when they answer a defined clinical question and are interpreted in context.
The lecture began with the regulation of thrombin. When thrombin binds thrombomodulin, it activates protein C; activated protein C, together with protein S, limits coagulation by inactivating factors Va and VIIIa. Deficiencies of protein C, protein S or antithrombin increase thrombotic susceptibility, but thrombosis usually results from interaction with acquired triggers such as surgery, immobility, pregnancy, inflammation, malignancy or hormonal therapy.
Factor V Leiden, the prothrombin G20210A variant and deficiencies of natural anticoagulants do not carry equal clinical significance. Their identification should not automatically determine indefinite anticoagulation. Management must also consider whether the event was provoked, its location, recurrence risk and bleeding risk.
Particular attention was given to patient selection and timing. Functional measurements of protein C, protein S and antithrombin may be distorted by acute thrombosis or anticoagulant therapy; testing at the wrong time can therefore create false diagnoses. MTHFR testing should not be included in routine thrombophilia panels because it provides no clinically useful information about venous thromboembolic risk.
Thrombosis at unusual sites, including cerebral or splanchnic veins, requires broader assessment for APS, JAK2-associated myeloproliferative neoplasms, paroxysmal nocturnal haemoglobinuria, malignancy and local factors.
The discussion of APS was especially relevant. It should be considered in younger patients with unexplained venous or arterial thrombosis, ischemic stroke, pregnancy morbidity or autoimmune disease. One positive antibody result is insufficient: diagnosis requires an appropriate clinical event and persistent laboratory positivity. Correct recognition may change treatment; in high-risk APS, particularly after arterial thrombosis, vitamin K antagonists remain the established therapy.
Finally, bleeding during anticoagulation should not be attributed only to the drug. Treatment may reveal a silent lesion, including malignancy; the bleeding source must therefore always be investigated.
Thank you, Professor Jeko Thachil, for connecting complex haemostatic mechanisms with practical clinical reasoning.”
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