Читать книгу Genetic Disorders and the Fetus - Группа авторов - Страница 92

Much of the evidence that AF is derived largely (but not only) from maternal sources comes from the study of constituent proteins in the fluid.⁵¹ To some extent at least, the AF in early gestation is probably a dialysate of maternal serum, the total solute concentration being similar.⁶ It is likely that the relative contributions from maternal and fetal sources change as pregnancy progresses. Although urine is present in the fetal bladder at least as early as 12 weeks of gestation, its contribution to AFV is likely to be significant only later.²⁸

Sutcliffe and Brock⁵² observed that the maternal serum protein group‐specific component (Gc) is present in AF early in gestation, suggesting that this protein enters the AF through the placenta or the fetal membranes. For this reason, they cautioned against attempts at prenatal genetic diagnosis by examination of serum proteins or by linkage analysis using serum protein polymorphisms. Most of the albumin in AF, at least near term, is of maternal origin.⁵³ Nevertheless, some AF albumin probably derives from the fetus because its concentration in fetal serum is greater than in maternal serum. In addition, at least after 30 weeks of gestation, most of the AF antitrypsin, ceruloplasmin, Gc, orosomucoid, and transferrin are of maternal origin.⁵¹

Cholesterol and its precursors derive from the mother, likely until at least the 15th gestational week.⁵⁴ Hemopexin, a β‐glycoprotein, in AF⁵⁵ is believed to be of maternal origin.⁵⁶ β₁‐Glycoprotein (SP₁), produced by the syncytiotrophoblast, is elevated in AF in Meckel syndrome, but not in open NTDs and several other fetal disorders.⁵⁷ Another glycoprotein, β₂‐microglobulin, has been noted to have concentrations in the AF in excess of those in maternal serum,⁵¹ although the exact tissue(s) of origin is unknown. Because synthesis of β₂‐microglobulin has been shown in lymphocytes, and other glycoproteins are found on the surface of most cells, adjacent maternal tissues may be the most important source of AF β₂‐microglobulin.

Brace¹⁶ suggested that the fetus may have a substantial volume of fluid of salivary origin. A significant fraction of the secreted lung fluid seems to enter the AF. The phospholipids measured in AF, when lecithin/sphingomyelin (L/S) ratios are determined, are of pulmonary origin and are not passed in significant quantities through the urine.

α‐Fetoprotein (AFP) is feto‐specific, and acetylcholinesterase (AChE) is an extracellular component found in high concentration in the fetal brain (see discussion later). Other neuronal proteins found in the AF of fetuses with NTDs include D2‐protein,⁵⁸ an “S‐100 protein,”⁵⁹ and neuron‐specific enolase.⁶⁰

Gogiel et al.⁶¹ studied the degradation products of collagen in AF. They suggested that nondialyzable collagenous polypeptides may be the products of the proteolytic conversion of procollagen into the monomeric form of this protein.