Placental dysfunction in the background of endocrine pathology

Maternal and child health is one of the urgent tasks of modern science and practice. The steady tendency towards deteriorating the state of health of the population in the recent years against the background of a decline in the birth rate and an increase in the perinatal morbidity and mortality makes studying mechanisms of the emergence of pathology in pregnant women and children in modern environmental conditions especially relevant.

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 a violation of the growth and development of the fetus, its hypoxia, which arise as a result of the combined reaction of the fetus and placenta to various violations of the condition of the pregnant woman. This syndrome is based on pathological changes in the fruit and / or utero-placental complexes with the violation of compensatory-adaptive mechanisms at the molecular, cellular and tissue levels. This disrupts the transport, trophic, endocrine, metabolic, antitoxic functions of the placenta, which are the basis of the origin of pathology in the fetus and the newborn.

A fundamentally important issue is the attitude towards placental dysfunction as an independent clinical syndrome or symptom complex that accompanies the main pathological state, since literature analysis shows that placental dysfunction is often considered separately from etiological factors - the causes and conditions of its onset and development. In this case, as a rule, there is a violation of blood circulation in the vessels of the fetoplacental complex due to hypovolemia, thrombosis, increased vascular resistance and concludes that the fetus is insufficiently supplied with oxygen, the presence of trophic insufficiency, after which recommendations are given for improving microcirculation and oxygen delivery. At the same time, the causes that caused placental dysfunction remain in the shade, 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 the course of pregnancy (gestosis, sensitization, threat of interruption, repetition) and extragenital pathology (endocrine, hematological disorders, diseases of the cardiovascular and genitourinary systems, intoxication, etc.).

A large number of described risk factors for the development of placental dysfunction testifies to the polyethiologic nature of placental dysfunction: the age of the mother is up to 17 and over 35 years, bad habits (smoking, alcohol, drugs), unfavorable social conditions, the harmful effects of physical or chemical factors at early gestational age period, the presence of foci of latent infection, burdened obstetric-gynecological anamnesis.

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

With in-depth, together with the endocrinologist, more than half of pregnant women with placental dysfunction are diagnosed with various autoimmune disorders - hyperandrogenism, thyroid gland pathology, diabetes mellitus, etc. Meanwhile, in the population there is a sufficiently high level of sick women who have several endocrine diseases. So, the most common combination of diabetes and autoimmune thyroiditis. Antibodies to thyroid globulin and to thyroid peroxidase are detected in almost 40% of patients with diabetes mellitus, which is significantly higher than in healthy globulins, 5-14%.

The frequency of combination of these diseases to a greater extent determines the autoimmune genesis of development, as evidenced by 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 outcome in hypothyroidism.

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

In diabetes, as we know, there is a combination of hormonal imbalance with obvious violations of the immune status, which is accompanied by the development of trophic, vascular and neurological complications. The results of the morphological study of the placenta in diabetes mellitus testify to changes in the form of disorders of blood flow, alteration, edema and sclerosis at all structural levels, including terminal villi (with fetal malnutrition of 35.5%).

Against the background of both isolated and combined endocrine pathology, pregnancy is complicated by primary (early) placental dysfunction (up to 16 weeks gestation). 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 malformations in the fetus and frozen pregnancy. Clinically, it manifests itself as a picture of the threat of abortion and spontaneous abortion in the early period. In some cases, the primary placental dysfunction passes into the secondary, which appears against the background of the formed placenta after the 16th week of pregnancy under the influence of unfavorable factors.

The majority of patients with placental dysfunction experience complications of the course of pregnancy, and first of all it is the threat of interruption. It is established that the threat of miscarriage is registered in 91% of women with placental dysfunction, including a partial detachment of the fetal egg in the first trimester occurs in 16% of women, the threat of premature birth - in 25.5%. Characteristic are also severe course of early gestosis, implantation of the fetal egg in the lower parts of the uterus, features of the localization of the placenta. Thus, in ultrasound, 58% of women have a large placenta that crosses from the anterior or posterior wall to the bottom and into the lower regions of the uterus.

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

There are symmetrical fetal hypotrophy (in harmonious type), at which a proportional lag of the body weight and length of the fetus is observed, and asymmetric hypotrophy (according to the disharmonious type) is the lag of the body weight at the normal length of the fetus. With asymmetric hypotrophy, uneven development of individual organs and fetal systems is possible. There is a lag in the development of the abdomen and thorax at normal head sizes, delayed growth occurs later. This is due to hemodynamic adaptation reactions in the fetus, which prevent the violation of the growth rate of the brain. Asymmetric hypotrophy carries the threat of a child with an inferior development of the central nervous system, less capable of rehabilitation.

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

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

By all the above methods, the presence of one or more placental functions in a pregnant defect is documented, therefore, in the diagnosis of placental dysfunction, preventive and curative interventions for objective reasons start late and are therefore not always effective.

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

Recently, the question of studying the initial intracellular mechanisms of placental damages and the development of methods for their preventive correction arises with particular acuity. It was revealed that placental dysfunction is caused by failure of compensatory-adaptive mechanisms at the tissue level. In the pathogenesis of its decisive role belongs to molecular and cellular changes with a violation of the regulation of adaptive homeostatic reactions of placenta cells.

The early stages of the disorders of the compensatory mechanisms are probably related to changes in the membrane structures of cells and cause the essence of the preclinical period of the disease. Damage at the tissue level is an absolute placental insufficiency with a decrease in vascularization and the development of involute-dystrophic changes in the placenta.

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

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

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

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

With a therapeutic purpose for placental dysfunction currently used drugs that improve gas exchange (oxygen therapy), micro- and macrocirculation (antispasmodics, cardiotonic drugs, tocolytics, disaggregants), normalizing the acid-base and electrolyte balance, affecting the cellular metabolism, also applies etiotropic therapy .

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

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

Prof. A. Yu. Shcherbakov, Assoc. IA Tikhaya, prof. V. Yu. Scherbakov, Assoc. E. A. Novikova. Placental dysfunction with endocrine pathology // International Medical Journal - №3 - 2012
 

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