Placental dysfunction on the background of endocrine pathology

Protection of maternal and child health is one of the urgent tasks of modern science and practice. The stable tendency towards deterioration of the population's health status that has formed in recent years against the background of a decrease in the birth rate and an increase in perinatal morbidity and mortality makes it especially important to study the mechanisms of occurrence of pathology in pregnant women and children in modern environmental conditions.

Currently, the key problem of modern obstetrics and perinatology has become placental dysfunction, which is the main cause of antenatal fetal death.

Placental dysfunction is a clinical syndrome caused by morphological and functional changes in the placenta and manifested by impaired growth and development of the fetus, its hypoxia, which occur as a result of the combined reaction of the fetus and placenta to various disorders of the pregnant woman's condition. This syndrome is based on pathological changes in the fetal and/or uteroplacental complexes with a violation of compensatory-adaptive mechanisms at the molecular, cellular and tissue levels. In this case, the transport, trophic, endocrine, metabolic, antitoxic functions of the placenta are disrupted, which underlie the occurrence of pathology in the fetus and newborn.

A fundamentally important issue is the attitude to placental dysfunction as an independent clinical syndrome or symptom complex that accompanies the underlying pathological condition, since literature analysis shows that placental dysfunction is often considered separately from etiological factors - the causes and conditions of its occurrence and development. In this case, as a rule, a violation of blood circulation in the vessels of the fetoplacental complex is noted due to hypovolemia, thrombosis, increased vascular resistance, and a conclusion is made about insufficient oxygen supply to the fetus, the presence of trophic insufficiency, after which recommendations are given to improve microcirculation and oxygen delivery. At the same time, the causes that caused placental dysfunction remain in the shadows, and the treatment of the underlying disease is not always associated with its prevention and treatment.

The causes of placental dysfunction may be changes in the formation and maturation of the placenta in women with hypothalamic-pituitary-ovarian and pituitary-adrenal disorders or with uterine pathology; infection; vascular disorders (both idiopathic and with concomitant pathology); complications of pregnancy (gestosis, sensitization, threat of miscarriage, post-term pregnancy) and extragenital pathology (endocrine, hematological disorders, diseases of the cardiovascular and genitourinary systems, intoxication, etc.).

The polyetiological nature of placental dysfunction is also evidenced by the large number of described risk factors for its development: maternal age - up to 17 and over 35 years, bad habits (smoking, alcohol, drugs), unfavorable social and living conditions, harmful effects of physical or chemical factors in the early stages of the gestational period, the presence of foci of latent infection, a burdened obstetric and gynecological history.

Many studies in recent years have been devoted to assessing the risk of placental dysfunction in the presence of endocrine pathology: it has been shown that the frequency of its development is 24-45%. Thus, thyroid diseases in pregnant women with placental dysfunction are observed in 10.5%, and carbohydrate metabolism disorders - in 22.4%.

During in-depth examination, together with an endocrinologist, more than half of pregnant women with placental dysfunction are found to have various autoimmune disorders - hyperandrogenism, thyroid pathology, diabetes mellitus, etc. Meanwhile, in the population today there is a fairly high level of sick women who have several endocrine diseases. Thus, the most common combination is diabetes mellitus and autoimmune thyroiditis. Antibodies to thyroid globulin and thyroid peroxidase are found in almost 40% of patients with diabetes mellitus, which is significantly higher than in healthy people - 5-14%.

The frequency of the combination of these diseases largely determines the autoimmune genesis of development, as evidenced by the lymphoid infiltration of the islets of Langerhans in patients, the presence of autoantibodies to insulin, thyroid peroxidase, the lymphocytic nature of changes in the thyroid gland as a consequence of autoimmune thyroiditis with an outcome in hypothyroidism.

A significant contribution to the development of placental dysfunction is made by hyperprolactinemia, both independently and in combination with diabetes mellitus, hypothyroidism, and hyperandrogenism, which significantly enhances fetoplacental relationships.

In diabetes mellitus, as is known, there is a combination of hormonal imbalance with obvious disorders of the immune status, which is accompanied by the development of trophic, vascular and neurological complications. The results of morphological studies of placentas in diabetes mellitus indicate changes in the form of blood flow disorders, alteration, edema and sclerosis at all structural levels, including terminal villi (with fetal hypotrophy being 35.5%).

Against the background of both isolated and combined endocrine pathology, pregnancy is complicated by primary (early) placental dysfunction (up to 16 weeks of pregnancy). It is formed during the period of implantation, early embryogenesis and placentation under the influence of genetic, endocrine and other factors. Primary placental dysfunction contributes to the development of congenital defects in the fetus and frozen pregnancy. Clinically, it is manifested by a picture of the threat of termination of pregnancy and spontaneous abortion in the early stages. In some cases, primary placental dysfunction turns into secondary, which appears against the background of a formed placenta after the 16th week of pregnancy under the influence of unfavorable factors.

Most patients with placental dysfunction experience complications during pregnancy, primarily the threat of miscarriage. It has been established that the threat of miscarriage is registered in 91% of women with placental dysfunction, including partial detachment of the ovum in the first trimester occurs in 16% of women, the threat of premature birth - in 25.5%. Severe early gestosis, implantation of the ovum in the lower parts of the uterus, and features of the localization of the placenta are also characteristic. Thus, during an ultrasound examination, 58% of women have a large placenta, which passes from the anterior or posterior wall to the bottom and lower parts of the uterus.

The main clinical manifestations of placental dysfunction are fetal growth retardation (hypotrophy) and intrauterine hypoxia.

A distinction is made between symmetrical fetal hypotrophy (harmonious type), in which there is a proportional lag in body weight and length of the fetus, and asymmetrical hypotrophy (disharmonious type), in which body weight lags with normal fetal length. With asymmetrical hypotrophy, uneven development of individual organs and systems of the fetus is possible. There is a lag in the development of the abdomen and chest with normal head sizes, the growth retardation of which occurs later. This is due to hemodynamic adaptive reactions in the fetus, which prevent disturbances in the rate of brain growth. Asymmetrical hypotrophy carries the risk of giving birth to a child with an incompletely developed central nervous system, less capable of rehabilitation.

In conditions of placental dysfunction in endocrine pathology in pregnant women, both types of hypotrophy are observed, but the most common is the disharmonious type.

Diagnosis of placental dysfunction is based on a comprehensive clinical examination of pregnant women, the results of laboratory research methods and includes: determination of the level of hormones, specific pregnancy proteins in dynamics; assessment of the state of metabolism and hemostasis in the body of the pregnant woman; assessment of fetal growth and development by measuring the height of the uterine fundus taking into account the abdominal circumference and body weight of the pregnant woman; ultrasound biometry of the fetus; assessment of the condition of the fetus (cardiotocography, echocardiography, biophysical profile of the fetus, cordocentesis); ultrasound assessment of the condition of the placenta (localization, thickness, area); volume of the maternal surface, degree of maturity, presence of cysts, calcification; study of placental circulation, blood flow in the vessels of the umbilical cord and large vessels of the fetus (Dopplerometry, radioisotope placentometry); amnioscopy.

All of the above methods register the presence of a defect in one or more functions of the placenta in a pregnant woman, and therefore, when diagnosing placental dysfunction, preventive and therapeutic measures, for objective reasons, begin late and are therefore not always effective.

Diagnosis of placental dysfunction should be performed in the form of screening for all women at high risk of perinatal complications.

Recently, the issue of studying the initial intracellular mechanisms of placental damage and developing methods for their preventive correction has become particularly acute. It has been revealed that placental dysfunction is caused by a breakdown of compensatory-adaptive mechanisms at the tissue level. In its pathogenesis, the decisive role belongs to molecular and cellular changes with a violation of the regulation of adaptive homeostatic reactions of placental cells.

Early stages of compensatory mechanism disorders are probably associated with changes in the membrane structures of cells and determine the essence of the preclinical period of the disease. Damage at the tissue level is already absolute placental insufficiency with a decrease in vascularization and the development of involutional-dystrophic changes in the placenta.

The main metabolic syndrome that leads to pathological morphofunctional changes in cells are disorders of oxygen-dependent processes and oxidation-reduction reactions. Biochemical and ultrastructural changes in cells in placental dysfunction or endocrine pathology are identical.

Management of pregnant women with combined and isolated endocrine pathology requires joint observation by obstetricians-gynecologists and endocrinologists, since the development of gestational complications is determined by the degree of compensation of the concomitant endocrine pathology.

A feature of the course of placental dysfunction against the background of endocrinopathies is its early onset and the correlation of the degree of pathological manifestations and the severity of endocrine pathology. In most cases, when severe forms of endocrine diseases are combined with placental dysfunction, there are indications for early termination of pregnancy.

Taking into account the above, the main link for preventing the development and treatment of placental dysfunction is the influence aimed at improving the uteroplacental blood flow and microcirculation, normalizing gas exchange in the mother-placenta-fetus system, improving the metabolic function of the placenta, and restoring the functions of cell membranes.

For therapeutic purposes in placental dysfunction, drugs are currently used that improve gas exchange (oxygen therapy), micro- and macrocirculation (antispasmodics, cardiotonic drugs, tocolytics, antiplatelet agents), normalize acid-base and electrolyte balance, affect cellular metabolism, and etiotropic therapy is also used.

Thus, pregnancy management against the background of endocrine pathology requires a scientific approach and further study. Identification of etiological factors of placental dysfunction formation allows a differentiated approach to its treatment, which subsequently leads to a decrease in the frequency of gestational and perinatal complications and helps to maintain the health of the mother and child.

Measures to prevent maternal and perinatal complications in women with endocrine pathology must begin before pregnancy, and they should consist not only of normalizing hormonal levels, but also of eliminating all associated disorders in the reproductive system.

Prof. A. Yu. Shcherbakov, Assoc. Prof. I. A. Tikhaya, Prof. V. Yu. Shcherbakov, Assoc. Prof. E. A. Novikova. Placental dysfunction against the background of endocrine pathology // International Medical Journal - No. 3 - 2012

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