Risks of thromboembolic complications in pregnant women with hereditary thrombophilia based on the results of platelet aggregation function study

Мұқаба

Дәйексөз келтіру

Толық мәтін

Ашық рұқсат Ашық рұқсат
Рұқсат жабық Рұқсат берілді
Рұқсат жабық Рұқсат ақылы немесе тек жазылушылар үшін

Аннотация

Background. Hereditary thrombophilia significantly increases the risk of thromboembolic complications and obstetric pathology (miscarriage, preeclampsia, placental insufficiency) in pregnant women. Physiological hypercoagulation during gestation aggravates prothrombotic conditions, which requires timely diagnosis and medical prevention. The study of platelet aggregation function allows to evaluate the cellular mechanisms of thrombus formation, which is especially important for pregnant women with genetic forms of thrombophilia.

Objective. Determination of the functional activity of platelets in pregnant women with hereditary thrombophilia and identification of risk factors for thromboembolic complications.

Materials and methods. The study included 253 women in the third trimester of pregnancy, divided into three groups: 63 with hereditary thrombophilia (group 1), 144 with threatening premature birth (group 2), 46 with physiologically proceeding pregnancy (group 3). The aggregation function of platelets was assessed by an optical method (aggregatometry) with inducers: ADP (0.5 and 1.5 μmol/l), adrenaline (5.0 μmol/l), collagen (20 μmol/l). The rate, degree and time of aggregation were analyzed. Statistical analysis was carried out using nonparametric criteria.

Results. In women of group 1, platelet hyperactivation was detected: increased rate and degree of spontaneous aggregation (5.2% compared to 2.5% in group 3, p<0.001); hyperaggregation with ADP 0.5 μmol/l: rate – 49.0%/min compared to 20.2%/min in group 3 (p<0.001), degree – 71.6% compared to 26.6% in group 3 (p<0.001); hyperaggregation with collagen 20.0 μmol/l: rate – 20.8%/min compared to 5.3%/min in group 3 (p<0.001), degree – 92.2% compared to 80.0% in group 3 (p<0.001); adrenaline-induced aggregation: rate – 17.2%/min compared to 10.7%/min in group 3 (p<0.001).

Conclusion. Aggregatometry reveals platelet hyperactivity in pregnant women with hereditary thrombophilia, which correlates with a high risk of thromboembolism. Aggregatometry monitoring allows personalizing medical prevention and improving perinatal outcomes.

Толық мәтін

Рұқсат жабық

Авторлар туралы

Ivan Kurlovich

Republican Scientific and Practical Center “Mother and Child” of the Ministry of Health of the Republic of Belarus

Хат алмасуға жауапты Автор.
Email: ivan.kurlovich@gmail.com
ORCID iD: 0009-0009-7384-8460

Cand. Sci. (Med.), Associate Professor, Deputy Director for Research

Белоруссия, Minsk

Elena Zubovskaya

Republican Scientific and Practical Center “Mother and Child” of the Ministry of Health of the Republic of Belarus

Email: laigp@medcenter.by
ORCID iD: 0009-0002-4781-7854

Cand. Sci. (Med.), Associate Professor, Senior Researcher, Laboratory of Obstetric and Gynecological Pathology

Белоруссия, Minsk

Olga Peresada

Belarusian State Medical University

Email: dr-olga@yandex.by
ORCID iD: 0009-0009-5219-3784

Dr. Sci. (Med.), Professor, Professor, Department of Obstetrics and Gynecology, Institute for Advanced Training and Retraining of Healthcare Personnel

Белоруссия, Minsk

Svetlana Viktor

Republican Scientific and Practical Center “Mother and Child” of the Ministry of Health of the Republic of Belarus

Email: laigp@medcenter.by
ORCID iD: 0009-0002-2932-5514

Cand. Sci. (Med.), Head of the Laboratory of Obstetric and Gynecological Pathology

Белоруссия, Minsk

Tatyana Vashchilina

Republican Scientific and Practical Center “Mother and Child” of the Ministry of Health of the Republic of Belarus

Email: lrz@medcenter.by
ORCID iD: 0009-0009-4964-8071

Cand. Sci. (Med.), Associate Professor, Head of the Laboratory of Reproductive Health

Белоруссия, Minsk

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2. Figure. 1. Aggregatograms in the normal condition: spontaneous and with inducers (1 — spontaneous aggregation, 2 — adrena­line 5.0 µmol/l, 3 — collagen 20 µmol/l, 4 — ADP 0.5 µmol/l, 5-1.5 µmol/l)

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3. Figure. 2. Aggregatograms (platelet hyperaggregation) in Leiden mutation (1 − 0.5 µmol/l ADP, 2 − 1.5 µmol/l ADP, 3 − adrenaline 5.0 µmol/l, 4 − collagen 20 µmol/l, 5 − spontaneous aggregation)

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4. Figure 3. Aggregatogram (platelet hyperaggregation) in AT III deficiency (1 − 0.5 µmol/l ADP, 2 − 1.5 µmol/l ADP, 3 − adrenaline 5.0 µmol/l, 4 − collagen 20 µmol/l, 5 − spontaneous aggregation)

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5. Figure 4. Aggregatogram (platelet hyperaggregation) in protein S deficiency (1 − 0.5 µmol/l ADP, 2− 1.5 µmol/l ADP, 3 − adrenaline 5.0 µmol/l, 4 − collagen 20 µmol/l, 5 − spontaneous aggregation)

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