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Prostaglandins & Bladder Infection

Premature births account for 70 percent of all neonatal deaths and 50 percent of long-term neurological disabilities in newborns. Maternal and placental prostaglandins play a role in premature birth and fetal death. Bladder infections occur during pregnancy when the uterus on top of the bladder restricts it from emptying. Prostaglandins are involved in the control of the bacterial inflammation of the urinary tract, contraction of smooth muscle and body temperature.

  1. Prostaglandins in Pregnancy

    • Normal pregnancy increases maternal prostaglandins (PGE). Pregnant women with hypertension or toxemia have lower placental PGE levels. Urinary PGE levels in toxemic pregnant women are much lower than the urinary PGE levels of normal pregnant women and patients with chronic hypertension, but similar to PGE levels of non-pregnant women. Fetal death attributed to chronic hypertension or eclampsia is associated with maternal urinary PGE.

    Aspirin and Anti-inflammatory Drugs

    • Physicians agree that urinary tract infections during pregnancy can be treated easily if detected early, but the same physicians disagree on methods to identify and treat urinary infections in pregnant women. Prostaglandins are like hormones. Aspirin and anti-inflammatory drugs block the production of prostaglandins and divert fetal blood flow to the uterus, which is fatal to the baby.

    Antibiotics

    • Investigators at Brown University in Providence, Rhode Island compared the effects of single-dose and multi-dose antibiotics for bladder infections on pregnant women and found no difference in the effects of either course of treatment. Antibiotics are safe to the mother and the fetus if the urinary infection is diagnosed early.

    Infection Spreads to Kidneys

    • The fetus receives oxygen through the placenta. If the bacterial infection spreads from the bladder to the kidneys, nausea and vomiting, back pain, chills and fever result. Kidney infections can induce early labor with corresponding low birth weight. As the baby leaves the birth canal, the baby's prostaglandin levels drop drastically, causing blood to rush to the baby's lungs.

    Urinary Trypsin Inhibitor

    • The Japanese Hamamatsu School of Medicine determined that urinary trypsin inhibitor (UTI) is essential in the maintenance of pregnancy. UTI is low in premature deliveries and high in normal deliveries. UTI has an important role in amniotic fluid, fetal membranes, the placenta and uterine muscles. UTI protects the fetal membrane from bacterial infections. Prostaglandin F2 alpha (PGF2 alpha) can induce uterine contraction, but UTI can inhibit the uterine contractions.

    Prostaglandins Initiate or Inhibit Labor

    • The study of prostaglandins and their role in the initiation of labor led to prostaglandin synthetase inhibitors for treatment of preterm labor. Indomethacin is a prostaglandin synthetase inhibitor created to prolong pregnancy, but it has had some adverse effects on fetuses. The discovery that labor is accompanied by increased oxytocin receptors led to the creation of atosiban, an oxytocin antagonist. Atosiban is specific in its inhibition of smooth muscles of the uterus, and little atosiban passes through the placenta to the fetus. However, no difference in length of labor or increase in fetal defects has resulted.

    Misconceptions

    • Multiple studies have failed to show benefits of these inhibitors to prevent premature delivery. Physicians want to prevent preterm labor because of the high neonatal mortality, but the American College of Obstetricians and Gynecologists report most interventions fail.

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