HAEMATOLOGY DEPARTMENT

Oral anticoagulant therapy (Sintrom) is primarily monitored using prothrombin time (PT or Quick time). The World Health Organisation recommends that PT results be expressed using the International Normalised Ratio (INR). PT should not be used for therapeutic evaluation during the first 2–3 days of oral anticoagulant therapy, as it is known that the desired hypocoagulability takes 4–5 days to achieve. It usually takes several days or weeks for the anticoagulant effect to stabilise. Most patients require moderate-intensity anticoagulation, which typically corresponds to an INR of 2–3. In addition to the INR, the test results include the patient’s time and the control time in seconds. The test is performed by collecting blood via venipuncture into a special vial.

APTT is currently the most used test for monitoring heparin therapy. It is also known as activated kallikrein time and/or kallikrein-kaolin time. Measuring a patient’s PT and APTT before starting any anticoagulant therapy is essential. APTT is influenced by various factors unrelated to heparin, resulting in cases where there is no linear relationship between clotting time and heparin concentration. Low-molecular-weight heparins (LMWHs), when administered prophylactically, do not prolong the APTT; therefore, laboratory monitoring of the APTT is not recommended.  When administering a therapeutic dose of LMWH, the use of APTT has certain limitations, the main one being its low sensitivity. In this case, the use of other methods to monitor treatment is recommended, such as measuring anti-CoA activity. This is performed by collecting blood via venipuncture into a special vial.

Oral anticoagulant therapy (Sintrom) is primarily monitored using the prothrombin time (PT or Quick time). The World Health Organisation recommends that PT results be expressed using the International Normalised Ratio (INR). PT should not be used for therapeutic evaluation during the first 2–3 days of oral anticoagulant therapy, as it is known that the desired hypocoagulability takes 4–5 days to achieve. It usually takes several days or weeks for the anticoagulant effect to stabilise. Most patients require moderate-intensity anticoagulation, which typically corresponds to an INR of 2–3. In addition to the INR, the test results include the patient’s time and the control time in seconds. It is performed by collecting blood via venipuncture into a special vial.

At the haematology department of AEGEAN Medical.

Τα D-διμερή (D-dimers) αποτελούν προϊόντα αποδομής του ινώδους. Η μέτρηση των επιπέδων D-dimers είναι απαραίτητη στον αποκλεισμό της εν τω βάθει φλεβικής θρόμβωσης και της πνευμονικής εμβολής. Αυξημένα επίπεδα D-dimers παρατηρούνται και σε ασθενείς με αυξημένη δημιουργία ινώδους, όπως στο τραύμα, στην προεκλαμψία, στις κακοήθειες και στη διάχυτη ενδαγγειακή πήξη. Ελαφρώς αυξημένα επίπεδα παρατηρούνται με την πάροδο της ηλικίας και κατά την εγκυμοσύνη. Πραγματοποιείται με συλλογή αίματος κατόπιν φλεβοκέντησης σε ειδικό μπουκαλάκι.

Antithrombin III belongs to the group of natural anticoagulants, along with proteins C and S. It is the most important natural anticoagulant and is synthesised in the liver and in the endothelial cells of blood vessels. As its name suggests, it acts by forming a stable complex with thrombin, thereby inactivating it. A decrease in antithrombin, therefore, leads to increased thrombin activity and thrombogenesis due to activation of the blood coagulation mechanism. The clinical presentation typically manifests as a venous thromboembolic event and rarely as an arterial one. Antithrombin deficiency may be acquired or inherited. Measurement of antithrombin requires that the patient not be receiving heparin. The measurement is performed by collecting blood via venipuncture into a special vial.

At the haematology department of AEGEAN Medical.

Protein C (PC) is vitamin K-dependent, produced exclusively in liver cells, and is one of the most important natural anticoagulants. Activated protein C acts proteolytically, inactivating factors Va and VIIIa, thereby preventing the conversion of prothrombin to thrombin. A decrease in PC, therefore, causes increased activity of Va and VIIIa, thereby activating the coagulation mechanism and leading to thrombosis. As a rule, protein C deficiency causes venous thrombosis. This deficiency can be acquired or inherited. Since it is vitamin K-dependent, its measurement requires that the patient not be taking coumarins. The measurement is performed by collecting blood via venipuncture into a special vial.

Protein S (PS) is vitamin K-dependent and is produced in various cells of the body. It acts as a cofactor for PC, enhancing the anticoagulant activity of activated PC, thereby helping to inactivate Va and VIIIa. Protein S and activated PC form a 1:1 complex on the surface of platelets and endothelial cells. In plasma, it exists in two forms: 40% as free PS and 60% as bound PS. The sum of free and bound forms constitutes total PS. Its deficiency typically causes venous thrombosis and is acquired or hereditary. Since this test is vitamin K-dependent, it must be performed after discontinuing the use of coumarin derivatives. The test is performed by collecting blood via venipuncture into a special vial.

The activated form of protein C (APC-Activated PC) is a natural anticoagulant that acts by cleaving the activated factors Va and VIIIa. A mutation in the factor V molecule (replacement of guanine (G) with adenine (A) at position 1691 (G1691A) is called Factor V Leiden; it is inherited in an autosomal dominant manner and is one of the strongest risk factors for venous thrombosis. The V-Leiden factor exhibits increased resistance to activated protein C (APCR—Activated protein C resistance), i.e., resistance to inactivation by APC. The test is performed by collecting blood via venipuncture into a special vial.

LMWHs constitute a heterogeneous group and differ from one another in terms of manufacturing method, molecular weight, anti-Xa activity, and exhibit different pharmacokinetics. Their anticoagulant action is primarily related to their anti-Xa activity. They are administered prophylactically to prevent thromboembolic disease and therapeutically to treat deep vein thrombosis and pulmonary embolism. The highest plasma concentration is reached between the third and fifth hour; for this reason, blood sampling to monitor anticoagulation should be performed 3–4 hours after subcutaneous administration. The exact time of administration, the formulation used and the units administered are also recorded. The test is performed by collecting blood via venipuncture into a special vial.

At the haematology department of AEGEAN Medical.

LMWHs constitute a heterogeneous group and differ from one another in terms of manufacturing method, molecular weight, and anti-Xa activity, and they exhibit different pharmacokinetics. Their anticoagulant action is primarily related to their anti-Xa activity. They are administered prophylactically to prevent thromboembolic disease and therapeutically to treat deep vein thrombosis and pulmonary embolism. The highest plasma concentration is reached between the third and fifth hour; for this reason, blood sampling to monitor anticoagulation should be performed 3–4 hours after subcutaneous administration. The exact time of administration, the formulation used and the units administered are also recorded. The test is performed by collecting blood via venipuncture into a special vial.

Homocysteine is an amino acid produced by the demethylation of the amino acid methionine. This reaction is reversible; that is, homocysteine is converted back to methionine through remethylation. Folic acid, vitamin B12, and vitamin B6 are involved in homocysteine metabolism; consequently, their deficiency leads to mild hyperhomocysteinemia. Homocysteine is harmful to the vascular wall, so elevated levels are associated with arterial and venous thrombosis. A significant increase in homocysteine occurs in individuals who are homozygous for a point mutation in the gene encoding the MTHFR enzyme (primarily C677T, rarely A1289C). Screening for carriers or homozygotes is possible via PCR. Total homocysteine is measured by venipuncture followed by immediate centrifugation and processing of the collected sample.

At the haematology department of AEGEAN Medical.

Lp(a) is believed to contribute to the processes of atherosclerosis and thrombosis. Elevated Lp(a) levels are inherited through the autosomal dominant pattern. Elevated levels are responsible for the occurrence of premature myocardial infarction and recurrent first-trimester miscarriages. A plasma concentration of 30 mg/dL is a critical threshold; above this level, Lp(a) constitutes a risk factor for thromboembolic disease. Its levels are not affected by gender, age, diet, physical activity, or most lipid-lowering medications. The measurement is performed, following venipuncture and centrifugation of the sample, on an automated biochemical analyser. At the haematology department of AEGEAN Medical.