Fetal Research and Applications A Conference Summary (1994) / Chapter Skim
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Session III: Fetal Research
Session III: Fetal Research
Pages 26-43
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From page 26... ...
Before effective therapy was developed, the mortality rate was 50 percent. The first leaps forward in the treatment of Rh disease came in the 1950s with exchange blood transfusion of the baby immediately after birth, or preterm delivery, when the mother's Rh history was known.
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From page 27... ...
In addition to Rh disease, ultrasound detects life-threatening obstructions in the urinary tract, chest, and skull; diaphragmatic hernias; and cardiac dysrhythmias. Intrauterine intravascular intervention can reverse nonimmune hydrops, a fetal edema unrelated to Rh hydrops.
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From page 28... ...
In addition to toxoplasmosis, Rh disease, and nonimmune hydrops, PUBS has been used to diagnose fetal thrombocytopenia, a hemorrhaging condition caused by maternal autoimmune antibodies to platelets that cross the placenta, and to monitor drug levels and hyperthyroidism. Therapeutically, PUBS has been indispensable in reversing hydrops in Rh disease.
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From page 29... ...
Embryoscopy and New Advances in Fetal Diagnosis and Treatment E ALBERT REECE Temple University, Philadelphia, Pennsylvania Although great shades have been made in fetal medicine, current diagnostic and therapeutic techniques have, for the most part, been limited to the second and third trimesters of pregnancy.
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From page 30... ...
Regarding the applicability of embryoscopy to gene therapy, a participant wondered whether sufficient blood could be drawn to retrieve enough cells into which altered genes could be inserted. Blood sampling in early embryos is difficult, and the maximum amount that can be taken has not been determined.
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From page 31... ...
In addition, impaired fetal islet-cell developmPnt had horn Inky to biro.- or no~tnnta1 growth deficiency, in particular, secA$.~.~ ^~ - ~__.^ ,.._ - _ ~ _ ~ ~ ~ ~ in, ondary to protein deficiency in infancy. The propensity to obesity and impaired glucose tolerance in the offspring of diabetic mothers establishes a setting in which these conditions may be perpetuated congenitally from generation to generation.
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From page 32... ...
Recent experiments have shown that the absence of IGF-1 leads to significant fetal growth failure. This suggests that in the fetus, something other than pituitary growth hormone is driving IGF production.
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From page 33... ...
In fetal tissues, placental lactogen directly stimulates IGF production, uptake of amino acids, and the activity of an enzyme important in protein and carbohydrate synthesis. Contrary to expectation, the release of hPL is not regulated by the factors that regulate growth hormone or prolactin, but by high-density lipoproteins (HDLs)
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From page 34... ...
Certain placental pathologies were typical of this condition and underscore the importance of examining the placenta in cases of fetal loss. The fetal findings in maternal "immune rejection" included growth retardation and hydrops.
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From page 35... ...
Drugs or vitamins that cross the placenta have been used to accelerate fetal lung maturation, reduce the risk of neural tube defects, and manage cardiac arrhythmias. Among invasive therapies, percutaneous umbilical blood sampling, which provides direct entry into the fetal blood circulation, enables diagnosis, intravenous transfusions, and drug delivery.
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From page 36... ...
As a result, the investigators recommended obtaining measurement of the platelet concentration before removing the needle from the umbilical blood vessel and, if the concentration was less than SO,000/ml3, transfusing previously prepared antigen-negative packed platelets into the fetus prior to removal of the needle. No fetal losses have occurred after adoption of this regimen.
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From page 37... ...
Even so, the investigators wonder whether such couples can really appreciate the enormity of the burdens and concomitant risks of kidney transplants in the absence of experiential knowledge and in the face of trying to save their fetus. Diaphragmatic hernia surgery was attempted next.
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From page 38... ...
It is possible to transplant these stem cells to replace defective marrow cells, but in an immunologically competent adult, all of the patient's own marrow cells must be destroyed and the marrow repopulated with donor cells. Because the number of donors with compatible cell types is limited, there is the danger of graft rejection and the resulting need for sustained immunosuppressant therapy.
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From page 39... ...
Human victims of Hurler's disease, which is due to an enzymatic deficiency that causes accumulation of mucopolysaccharides in many organs, usually die before the age of 10 from respiratory infection and heart failure. In 1990 a fetus diagnosed with Hurler's was given fetal HSC transplants, injected into the peritoneal cavity.
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From page 40... ...
One point made was that given the difficulties encountered in surgical trials for diaphragmatic hernia, it was best that the trials were limited to one institution rather than being conducted by different centers using different protocols. In the view of one of the speakers, as more is learned about molecular and cellular factors controlling fetal growth and development, new approaches, such as stem-cell transplantation and gene therapy, stand to help many more patients than fetal surgery.
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From page 41... ...
Applications of Molecular Biology and Genetics to Developmental Toxicology DANIEL NEBERT University of Cincinnati Medical Center, Cincinnati, Ohio The role of environmental substances in causing infertility, in utero toxicity, and birth defects is an important public health issue. Studies of the genetic mechanisms that control metabolic pathways have begun to clarify the ways in which toxic substances induce abnormalities in the developing fetus.
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From page 42... ...
Recent experiments have been aimed at pinpointing the specific function of P~450, an extensively studied specific P450, in normal fetal development. By using a variant of the very sensitive technique of polymerase chain reaction, which provides a large amount of a particular gene for study, a striking increase in the expression of a gene encoding P450 was discovered in the fertilized egg before the two-cell stage expression that decreases in later stages of embryonic development.
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From page 43... ...
Transgenic mice can be bred to be simultaneously deficient for more than one gene. As the pharmacogenetic variations at P450 genes in humans become wellcharacterized, test tube assays can be set up to determine which women should or should not receive certain prescribed drugs on the basis of individual Phase I and Phase II cytochrome P450 alleles.
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