Abstract
Preeclampsia is an obstetric complication that is becoming a major cause of maternal and perinatal morbidity and mortality. The rate of preeclampsia in diabetes mellitus is 3 to 5-fold higher than in the population. Heparin is used for prevention of preeclampsia due to its experimentally shown important role in the trophoblast invasion and differentiation, as well as its influence on the production of proangiogenic factors. The paper gives a clinical case report that broadens our understanding on the preeclampsia pathophysiology and possibilities of its prevention. A 30-year old patient with no past history of serious physical illnesses had her two previous pregnancies with severe preeclampsia of early onset (arterial hypertension, massive proteinuria, thrombocytopenia, renal and hepatic insufficiency). Both babies were born extremely preterm (24 to 25 weeks of gestation) and died. Her hereditary background included type 2 diabetes in her maternal grandmother. At early terms of both pregnancies she had her fasting venous plasma glucose of 3.8 to 4.6 mmol/L (normal, < 5.1 mmol/L). Oral glucose tolerance test which had to be performed at 24 to 28 weeks of gestation, according to the protocol, was not performed. While planning for the third pregnancy, her body mass index was 29 kg/m 2 , with normal values of the blood pressure and renal function, no proteinuria and no evidence of the anti-phospholipid syndrome. In the 1 st trimester, she had her fasting venous plasma glucose of 4.4 mmol/L. From the early term of her pregnancy, the patient was administered low molecular weight heparin; from the week 15, she was started with antihypertensive medications due to gestational arterial hypertension. Manifest diabetes was diagnosed at week 24 to 25 based on the results of the oral glucose tolerance test (4.96–10.42–11.46 mmol/L). With diet treatment, she had her postprandial glycaemia of up to 8.9 mmol/L, causing the initiation of basal-bolus insulin therapy from week 25 of gestation (0.4 U/kg), with achievement of good glucose control. At week 16, she had her sFlt1/PlGF level of 44 (high risk of preeclampsia). Molecular genetic assessment identified a HNF4A gene mutation, associated with MODY1. From week 34, she had moderate preeclampsia and fetal growth delay. An elective cesarean section was performed at week 38, with a healthy boy of 2300 g and 48 cm. After delivery, her diabetes was controlled by diet. The baby had an identical mutation. Thus, one cannot exclude a genetically determined link between complications of previous pregnancies and manifest diabetes diagnosed during the current pregnancy. Diagnosis of MODY1 in a pregnant patient would require the earliest initiation insulin treatment to prevent fetal macrosomia and neonatal hypoglycemia, as well as to prevent preeclampsia. The reason of successful outcome of this pregnancy could be related to heparin administration at the early terms of pregnancy that allowed for appropriate implantation and placenta formation, as well as for timely good glucose control.
Highlights
Клиническое наблюдениеПреэклампсия – акушерское осложнение, которое становится одной из важнейших причин материнской и перинатальной заболеваемости и смертности
Преэклампсия – акушерское осложнение, которое развивается во второй половине беременности и проявляется артериальной гипертензией и протеинурией
Синдром рассматривается как вариант преэклампсии, может развиваться сам по себе или в сочетании с преэклампсией
Summary
Преэклампсия – акушерское осложнение, которое становится одной из важнейших причин материнской и перинатальной заболеваемости и смертности. Глюкоза венозной плазмы натощак в ранние сроки обеих беременностей составила 3,8–4,6 ммоль/л (норма < 5,1 ммоль/л). С ранних сроков беременности получала низкомолекулярный гепарин, с 15 недель начата гипотензивная терапия по поводу гестационной артериальной гипертензии. На фоне диеты постпрандиальная гликемия до 8,9 ммоль/л, в связи с чем с 25 недель гестации начата базис-болюсная инсулинотерапия (0,4 ЕД/кг), достигнута компенсация диабета. Обнаружение у беременной MODY1 требует максимально ранней инициации инсулинотерапии для предотвращения макросомии плода и неонатальных гипогликемических состояний, а также профилактики преэклампсии. Тяжелая преэклампсия и мутация в гене HNF4A (MODY1): клиническое описание. Тяжелые формы преэклампсии характеризуются выраженным страданием плода и быстрым развитием полиорганной недостаточности у матери, вследствие чего служат одной из важнейших причин материнской и перинатальной заболеваемости и смертности в современном акушерстве.
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