pre-eclampsia

from Wikipedia, the free encyclopedia
Classification according to ICD-10
O14.- Gestational hypertension [pregnancy-induced] with significant proteinuria
O14.0 Moderate preeclampsia
O14.1 Severe preeclampsia
O14.9 Preeclampsia, unspecified
ICD-10 online (WHO version 2019)

The preeclampsia (old name: EPH- toxemia , Spätgestose , Schwangerschaftsintoxikation , eclampsia , eclampsia ) refers to a hypertensive condition that the pregnancy ( gestational hypertension ) and the postpartum period can complicate. In rare cases, it does not appear until 14 days after delivery. Preeclampsia is traditionally characterized by the leading prognostic symptoms of hypertension (increased blood pressure ) and proteinuria (protein in the urine ). Edema (water retention) alone does not affect the prognosis for mother and child. From the earlier triad of key symptoms, the less common today name derives preeclampsia from: E dema ( English ) for edema, P roteinurie and H ypertension for hypertension.

Symptoms

In addition to the main symptoms mentioned (high blood pressure, proteinuria and edema), those affected report dizziness and headaches , drowsiness, visual disturbances such as flickering eyes as well as nausea and vomiting . The doctor can determine hyperreflexia (increased reflexes).

In addition, in 20% of cases there is liver involvement and thus an increase in liver values ( transaminases , alkaline phosphatases and bilirubin ), which can be demonstrated in a laboratory .

Epidemiology

High blood pressure during pregnancy (hypertensive pregnancy disease) develops in around 5 to 7 percent of all pregnancies in Western Europe. In 70% of these cases there is preeclampsia, in 30% a previously passed, undiagnosed high blood pressure. Primiparous women and women over 35 years of age are more frequently affected. Other risk factors include preeclampsia in a previous pregnancy, multiple pregnancies , pre-existing high blood pressure, obesity and diabetes mellitus . Several studies suggest that periodontal disease can increase the risk of severe preeclampsia. Autoimmune diseases significantly increase the risk of preeclampsia; The antiphospholipid syndrome (APS), which is the most serious of all risk factors, promotes the occurrence of preeclampsia or eclampsia by a factor of nine.

etiology

The causes of preeclampsia are not clearly understood. A disturbed implantation of the trophoblast is discussed , with the result that the blood vessels in the decidua are not remodeled and expanded in the way that is actually necessary during pregnancy. An indication of this hypothesis is that the diamine oxidase released into the mother's bloodstream by extravillous trophoblasts is significantly reduced in early pregnancy in those women who were later diagnosed with preeclampsia. Disturbances in prostaglandin metabolism also seem to play a role. A bacterial or viral origin, however, is unlikely. A study by the University of Pittsburgh shows that vitamin D deficiency in early pregnancy promotes the development of the disease. A number of more recent studies, however, suggest a central involvement of blood pressure-regulating (endothelial) substances as the most likely.

In a study on mice, preeclampsia symptoms could be simulated by inducing a deficiency in catechol-O-methyltransferase (COMT).

Changes in the kidney

Signal molecules released by the changed placenta reach the kidney via the bloodstream and lead to characteristic changes in the kidney corpuscle , which are responsible for the main symptoms of gestosis.

The glomeruli (glomeruli) are increased, the lumens of the capillary loops are closed due to swelling of the endothelium - and mesangial - cells . The swelling of the endothelial cells is also known as endotheliosis . The number of endothelial cells is not increased. Only the specific fenestrated endothelium of the kidney corpuscle is affected; the endothelial cells of the arterioles are not changed. The cause of the eclampsia is probably a local vascular constriction of the arteries of medium caliber up to the capillaries (stasis, edema). Deposits of fibrin are detectable in the immunofluorescence , immune complexes are missing. This can lead to thrombosis of the kidney vessels ( thrombotic microangiopathy ). In the electron missing window of endothelial cells. Endothelial cells and mesangium cells are so swollen by the accumulation of fluid and lipids that the capillary clearances have disappeared. The capillary cover cells (podocytes) , however, are not changed (images below).

The closure of the capillary clearings leads to a decrease in the glomerular filtration rate and thus to deterioration in kidney function, water retention and high blood pressure. The cause of proteinuria is not yet clear. In other kidney diseases, proteinuria is usually due to changes in the podocytes, while in gestosis the podocytes do not appear changed.

In the healthy kidney, the podocytes continuously produce the growth factor Vascular Endothelial Growth Factor (VEGF). This growth factor is a prerequisite for proper functioning of the endothelial cells, especially for the formation of the characteristic windows. In the absence of VEGF, the endothelial cells of the kidney corpuscle lose their windows and swell. In the blood of patients with gestosis, high concentrations of a soluble VEGF receptor known as sVEGFR1 or soluble fms-like tyrosine kinase (sFlt1) can be detected even before symptoms appear . sFlt1 is formed in the placenta, reaches the kidney with the bloodstream, binds to VEGF in the kidney corpuscle and thus inhibits its effect.

Endoglin , another protein that is elevated in preeclampsia, also causes endothelial swelling , but does not cause proteinuria. In animal experiments, the simultaneous administration of Endoglin and sFlt1 leads to particularly serious clinical pictures.

Diagnosis

If preeclampsia is suspected - the pregnant woman reports dizziness and headaches, drowsiness, visual disturbances, nausea and vomiting - the person concerned must be admitted to hospital. For diagnosis, several blood pressure measurements should first be taken. The excretion of proteins in the urine ( proteinuria ) should be measured; this should not be carried out using urine test strips for diagnosis , since pregnant women also excrete more proteins physiologically, but rather with a 24-hour urine collection. The urine test strips can be used to monitor the progress. Although the edema has lost its diagnostic significance, it can be used for a rough follow-up using weight measurements.

Preeclampsia is when a new blood pressure during pregnancy of more than 140/90 (or an increase of more than 30/15) and thus pregnancy-induced hypertension is present and more than 300 in the urine in the last 24 hours mg protein per day and thus proteinuria is confirmed.

According to a report by the National Institute of Child Health and Human Development in the USA, a research team led by Richard Levine in Bethesda has now found a test method for the early detection of preeclampsia. The researchers had taken the blood samples of the participants in the "Calcium for Preeclampsia Prevention" study again . There, the preventive effect of calcium had previously been shown to be not significantly effective. During the renewed analysis, they noticed that the endoglin value was already rising two to three months before the clinical occurrence of preeclampsia. They then published a case-control study in the New England Journal of Medicine, which shows that an increase in certain proteins can be detected in the blood of pregnant women weeks before the first symptoms. This allows preeclampsia to be diagnosed using serum markers. In women with preeclampsia, changes in serum levels for PlGF (placental growth factor) and sFlt-1 (soluble fms-like tyrosine kinase-1, also VEGF receptor-1) are found. In addition, by detecting the PlGF and / or sFlt-1 concentrations in the blood, a normal pregnancy can be differentiated from a pregnancy associated with preeclampsia before the onset of clinical symptoms. In a normal pregnancy, the pro-angiogenic factor PlGF increases during the first two trimesters and decreases towards the end of the pregnancy. In contrast, the anti-angiogenic factor sFlt-1 remains the same during the early and middle stages of pregnancy and then shows a steady increase until the end of pregnancy. In women who develop preeclampsia, higher sFlt-1 concentrations and lower PlGF concentrations were found than in normal pregnancies. New studies showed that the determination of PlGF had a higher sensitivity than the quotient of sFlt1 / PlGF. In addition, in preeclampsia, placental endoglin, a member of the TGF-β family, is upregulated and released into the mother's bloodstream as soluble endoglin. In severe cases of preeclampsia, an increased concentration of soluble endoglin was found.

In summary, it can be said that the possibilities for diagnosing preeclampsia, which were previously based on clinical symptoms, proteinuria determination (at least 24 hours) and uterine artery Doppler sonography, through the rapid immunological determination of PlGF and sFlt-1 concentrations can be significantly improved in the mother's blood. The SFlt-1 / PlGF quotient can rule out the development of preeclampsia for one week with a high degree of certainty and predict its occurrence within the next 4 weeks.

therapy

The only causal therapy is premature termination of pregnancy. After giving birth, the mother's condition usually improves quickly. However, as an older woman, she is at a very high risk of developing high blood pressure again.

Since the cause of the disease is still unclear, one should be careful with treating the symptoms . In particular, the attempt to combat edema with a low-salt diet or even dehydration cures usually leads to a deterioration in the state of health of the pregnant woman and a threatening condition of the fetus, which can often only be saved by an immediate emergency caesarean section . Children who are born weeks to months prematurely often struggle with cerebral haemorrhage, respiratory distress syndrome, kidney failure or eye damage, and their development may be impaired for life.

Uncontrolled drug lowering blood pressure can lead to a deficiency of the fetus and should therefore only be - carried out at constant values above 170/110 mmHg - to protect pregnant women. However, the blood pressure should not be lowered below 140/90 mmHg in order not to lower the child's “high pressure requirements ” too much and thus not endanger the child. With special preparations, however - by widening the uterine vessels - on the one hand an effective lowering of blood pressure necessary for the mother can be achieved and at the same time the child's care can be ensured. Due to the loss of protein due to proteinuria, sufficient protein must be supplied through the diet .

In severe cases, seizures must be expected (→ eclampsia ).

Regular monitoring of the child's heart activity with a cardiotocogram (CTG) as well as regular growth and, if necessary, Doppler controls of the child are mandatory in order to diagnose chronic placental insufficiency in good time. In extreme cases, premature termination of the pregnancy is essential to prevent eclampsia, which can be life-threatening for both the child and the mother.

Preventive measures

According to an American study that was carried out on 2291 pregnant women from 1996 to 2000, the consumption of chocolate can reduce the risk of preeclampsia in pregnant women. The number of women with corresponding symptoms was directly and negatively dependent on the level of the theobromine contained in the chocolate in the serum.

course

The course of preeclampsia is progressive and difficult to predict. Any diagnosed preeclampsia requires hospitalization and close medical supervision. Eclampsia or HELLP syndrome can occur as severe complications of preeclampsia . Basically, the risk must be carefully weighed up, taking into account the risk to mother and the unborn child. Worsening cannot be prevented by lowering blood pressure alone.

forecast

The risk of premature birth and life-threatening blood pressure derailment of the mother increases with the severity of preeclampsia. That is why the control and possible adjustment of the blood pressure as well as the measurement of the excreted protein in the urine is very important as part of prenatal care. Early detection of preeclampsia has been possible since 2009 using a blood test (determination of PlGF and sFlt-1 concentration).

The symptoms recede after delivery (whether this occurs spontaneously or forcefully). Long-term damage to children has become rare these days.

literature

  • Adverse perinatal outcomes are significantly higher in severe gestational hypertension than in mild preeclampsia. In: Am J Obstet Gynecol. Volume 186, No. 1, Jan 2002, pp. 66-71. PMID 11810087
  • Hypertensive disorders in pregnancy: a population-based study. In: Med J Aust. Volume 182, No. 7, Apr. 4, 2005, pp. 332-335. PMID 15804223
  • Periodontal disease increases the risk of severe pre-eclampsia among pregnant women. In: Journal of Clinical Periodontology . Volume 34, No. 8, 2007, pp. 639-645. doi: 10.1111 / j.1600-051X.2007.01105.x

Web links

Individual evidence

  1. ^ Heinrich Buess : The doctrine of the late gestosis (eclampsia) in the mirror of general medical history. In: Medical History Journal. Volume 6, 1971, pp. 175-188.
  2. ^ A b W. Rath: Preeclampsia: current management. In: The midwife. Volume 21, No. 2, 2008, pp. 84-89.
  3. ^ Preeclampsia and infections threaten mother and child . In: Pharmaceutical newspaper . No. 31, 2006.
  4. ↑ P. Velicky, K. Windsperger, K. Petroczi, S. Pils, B. Reiter, T. Weiss, S. Vondra, R. Ristl, S. Dekan, C. Fiala, DE Cantonwine, TF McElrath, B. Jilma , M. Knöfler, T. Boehm, J. Pollheimer: Pregnancy-associated diamine oxidase originates from extravillous trophoblasts and is decreased in early-onset preeclampsia . In: Scientific Reports . tape 8 , no. 1 , April 20, 2018, ISSN  2045-2322 , doi : 10.1038 / s41598-018-24652-0 ( nature.com [accessed April 27, 2018]).
  5. ↑ eurekalert.org
  6. ↑ a b Circulatory soluble endoglin and its predictive value for preeclampsia in second-trimester pregnancies with abnormal uterine perfusion. In: Am J Obstet Gynecol. Volume 198, No. 2, Feb 2008, pp. 175.e1-6. PMID 18226617
  7. ↑ K. Kanasaki, K. Palmsten, H. Sugimoto and others: Deficiency in catechol-O-methyltransferase and 2-methoxyoestradiol is associated with pre-eclampsia . In: Nature . tape 453 , no. 7198 , June 2008, p. 1117-1121 , doi : 10.1038 / nature06951 , PMID 18469803 .
  8. ^ Agnes Fogo: Atlas of Renal Pathology - Pre-eclampsia / Eclampsia . In: Am J Kidney Dis . tape 38 , no. 2 , 2001, p. E4 . elsevierhealth.com ( Memento from December 2, 2008 in the Internet Archive )
  9. ↑ Isaac E. Stillman, S. Ananth Karumanchi: The Glomerular Injury of Preeclampsia . In: J Am Soc Nephrol . No. 18 , 2007, p. 2281-2284 , PMID 17634433 .
  10. ^ S. Venkatesha et al.: Soluble endoglin contributes to the pathogenesis of preeclampsia . In: Nat Med . No. 12 , 2006, p. 642-649 , PMID 16751767 .
  11. ↑ NEJM . Volume 355, 2006, pp. 992-1005.
  12. ↑ endoglin, PlGF and sFlt-1 as markers for Predicting pre-eclampsia. In: Acta Obstet Gynecol Scand. Volume 87, No. 8, 2008, pp. 837-842. PMID 18607829 .
  13. ↑ Effective prediction of preeclampsia by a combined ratio of angiogenesis-related factors. In: Obstet Gynecol. Volume 111, No. 6, Jun 2008, pp. 1403-1409. PMID 18515525 .
  14. ↑ alteration of serum soluble endoglin levels after the onset of preeclampsia is more pronounced in women with early-onset. In: Hypertens Res. Volume 31, No. 8, Aug 2008, pp. 1541-1548. PMID 18971528 .
  15. ↑ serum sFlt1: PlGF ratio, PlGF, and Soluble endoglin levels in Gestational proteinuria
  16. ^ SJ Benton, Y. Hu, F. Xie et al.: Angiogenic factors as diagnostic tests for preeclampsia: a performance comparison between two commercial immunoassays. In: Am J Obstet Gynecol. Volume 205, 2011, pp. 469.e1-8.
  17. ↑ Are we getting closer to a Nobel prize for unraveling preeclampsia? In: Curr Cardiol Rep. Volume 10, No. 6, Nov 2008, pp. 440-447. PMID 18950552 .
  18. ↑ LADR informs : Preeclampsia - sFlt-1 / PlGF-Quotient helps with prediction , issue 242, 09/2019
  19. ↑ a b Warning of the seizure. In: Süddeutsche Zeitung. April 2, 2012.
  20. ↑ Information Group Oral Hygiene and Eating Behavior, Press Service No. 06, June 2008.
  21. ↑ EW Triche, LM Grosso, K. Belanger, AS Darefsky, NL Benowitz, MB Bracken: Chocolate Consumption in Pregnancy and Reduced likelihood of preeclampsia . In: Epidemiology. Vol. 19, No. 3, May 2008, pp. 459-464, doi: 10.1097 / EDE.0b013e31816a1d17
  22. ↑ Preeclampsia blood test facilitates diagnosis . In: the standard .