Placental lactogen (HPL)

Why this test?

For the diagnosis of placental insufficiency and delay in intrauterine development of the fetus. 

For the diagnosis of gestational diabetes. 

For the differential diagnosis of trophoblast diseases: cystic drift, invasive cystic drift, choriocarcinoma and trophoblastic tumor of the placental site. 

To control the treatment of trophoblastic tumor of the placenta after hysterectomy.

In what cases is it prescribed? 

In the presence of risk factors for placental insufficiency, arterial hypertension, heart disease, smoking and use of narcotic substances and alcohol, autoimmune diseases and blood diseases, anatomical anomalies of the uterus and placenta, multiple pregnancy (at the 15-20th week of pregnancy).

 In the presence of risk factors for gestational diabetes: age over 35 years, obesity, large fetus, polycystic ovary syndrome, hereditary history of type 2 diabetes (on the 24th-28th week of pregnancy). 

With uterine bleeding or amenorrhea in the postpartum period of a normal, ectopic, molar pregnancy or after spontaneous termination of pregnancy. 

With a stable low concentration of beta-hCG in the patient in the absence of a normal pregnancy and the presence of a normal, ectopic, molar pregnancy or spontaneous termination of pregnancy in the past. 

At the stage of monitoring the treatment of trophoblastic tumor of the placenta after hysterectomy.

Test Information 

Placental lactogen (PL) is a polypeptide hormone produced by syncytiotrophoblast cells and is necessary for the regulation of maternal and fetal metabolism. It appears in the blood from the 6th week of pregnancy, and its level increases in parallel with the increase in the weight of the placenta until the 34th week of pregnancy, when the increase in the placenta stops. 

Thanks to this, the concentration of PL can be used to assess the weight and function of the placenta and diagnose placental insufficiency. A mature placenta produces about 1 g of placental lactogen per day, no other hormone is produced in such a quantity in the human body. A small part of PL enters the bloodstream of the fetus. 

Placental insufficiency is a pathology of pregnancy in which the main function of the placenta is disturbed - the delivery of nutrients and oxygen to the body of the fetus. The frequency of this pathology ranges from 3% in the group of healthy mothers to 25% in the group of women with risk factors for placental insufficiency.

 This is the main reason for the delay in intrauterine development of the fetus. ZVUR is characterized by a high risk of perinatal pathology (respiratory distress syndrome of newborns, intracranial hemorrhage, necrotizing enterocolitis) and mortality. 

The risk factors for the development of placental insufficiency and ZVUR include: arterial hypertension, smoking and use of alcohol and drugs, uterine abnormalities, autoimmune diseases and blood diseases, multiple pregnancy and others. It has been shown that the concentration of PL reflects the mass of the placenta and is related to the gestational age of the fetus, so the analysis of PL can be used to detect placental insufficiency and ZVUR. PL has a structural similarity with the hormones of the adenohypophysis, somatotropin and prolactin. 

So it is not surprising that PL has similar properties of these hormones. PL is 100 times less powerful than growth hormone, however, given the amount of PL synthesized by the placenta, it can be argued that PL significantly affects anabolic processes in the mother's body. Just like growth hormone, PL is an insulin antagonist. It disrupts the utilization of glucose by the peripheral tissues of a pregnant woman and leads to physiological insulin resistance. 

As a result, the mother's metabolism is restructured: peripheral tissues begin to use triglycerides as an energy source, and excess glucose can be used by the growing fetus. Thus, together with other placental hormones, PL ensures adaptation of the mother's body to the needs of the fetus. 

However, in some women, these metabolic changes during pregnancy provoke serious disturbances in glucose metabolism, which leads to gestational diabetes (GDM) - diabetes of pregnant women. Gestational diabetes develops in genetically predisposed women and occurs with a frequency of 3-10%. Risk factors for the disease are age over 35 years, obesity, gestational diabetes or a large fetus in the obstetric history, polycystic ovary syndrome, hereditary history of type 2 diabetes. Women with gestational diabetes have an increased risk of early gestation, spontaneous abortion, and type 2 diabetes. Children born to mothers with gestational diabetes are prone to respiratory distress syndrome of newborns, macrosomia, birth injuries, polycythemia and CNS damage.

 To detect gestational diabetes, a glucose tolerance test is used, the informativeness of which increases with the PL test. Pathologies of pregnancy include a group of benign and malignant diseases of the placenta, united under the general name - trophoblastic disease: cystic drift, invasive cystic drift, choriocarcinoma and trophoblastic tumor of the placental site. Toppa is a relatively rare malignant tumor that is formed from intermediate trophoblast cells. 

It can occur in the postpartum period of a normal, ectopic or molar pregnancy and after spontaneous abortions (more often in women of childbearing age, but cases of the disease have also been described in postmenopause). Frequent manifestations of toppa are uterine bleeding and amenorrhea. 

The tumor is characterized by invasion of the myometrial tissue and most often does not spread beyond the uterus. Toppa rarely metastasizes (mainly in the lungs and brain) and generally has a favorable prognosis. Trophoblastic disease can be assumed when the patient has a consistently low concentration of beta-hCG in the absence of a normal pregnancy, in the presence of an ectopic, molar pregnancy or spontaneous abortion in the past.