PubMed · 5773841
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J Samachson. 1969-03-29. Basic requirements for calcification.. https://doi.org/10.1038/2211247a0
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To identify fetal histologic features characteristic of specific chromosomal anomalies, we reviewed histologic slides of 415 cases, including therapeutic and spontaneous abortuses, stillbirths, and perinatal deaths. These included 126 cases (30%) with karyotypically confirmed trisomy 21 and 23 cases (5.5%) with trisomy 13. Two histologic abnormalities of the fetal heart were identified that correlated with specific karyotypic abnormalities: (1) a discrete central papillary muscle calcification was present in 14 of 85 (16%) cases with trisomy 21, in seven of 18 (39%) cases with trisomy 13, and in six of 255 (2%) controls (P less than .001); and (2) a focal ventricular epicardial lymphocytic infiltrate was present in 22 of 93 (24%) cases with trisomy 21 versus nine of 284 (3%) controls (P less than .001). When both histologic abnormalities coexisted, trisomy 21 was present in five of six cases (83%). Neither histologic finding was significantly associated with fetal or maternal infection or congenital heart defects. In a restricted prospective study of the hearts of fetuses with trisomy 21, papillary muscle calcification was demonstrated by specimen radiographs in four of six (67%) cases; one case was studied by specimen ultrasonogram, which identified a papillary muscle echodensity. We conclude that (1) a focal ventricular epicardial lymphocytic infiltrate is characteristic of trisomy 21, (2) papillary muscle microcalcifications are characteristic of trisomies 13 and 21, and (3) further studies are needed to determine whether papillary muscle calcification might be useful in antenatal ultrasonographic screening for chromosomal anomalies.
The present study examined calcium phosphate precipitation in aqueous suspensions of artificial liposomes which closely resembled matrix vesicles (MV) in membrane lipid composition. At 22 degrees C, the liposomes per se did not initiate precipitation in the suspending medium for up to 120 h when the latter was made supersaturated with respect to hydroxyapatite (2.25 mM Ca2+, 1.5 mM PO4, 240 mosmol, pH 7.4). Likewise, the suspending medium remained stable for up to 72 h when precipitation was induced within the aqueous interiors of the liposomes by encapsulating pH 7.4-buffered 50 mM PO4 solutions in the interior spaces and making the enclosing membranes permeable to external solution Ca2+ ions with the ionophore X-537A. However, extraliposomal precipitation readily occurred under these latter conditions when phosphatidylserine (PS) and sphingomyelin (Sph) were deleted from the MV-like lipid formulation used to prepare the liposomes. These results suggest that lipidic membrane constituents such as PS and Sph may have a controlling influence on MV-mediated calcification in vivo by affecting the release of intravesicularly formed mineral crystals into the extracellular matrix space where they can subsequently grow and proliferate.
OBJECTIVES: The hypothesis of this study is that calcium homeostasis and bone mineralization are altered in pregnant women receiving long-term therapy with magnesium sulfate as compared with similar women not receiving magnesium sulfate to control preterm labor. STUDY DESIGN: Thirty-nine women between 24 and 32 weeks' gestation, matched for age, race, and duration of bed rest, were enrolled. Indices of calcium homeostasis in serum and urine were measured serially, and bone mineralization of the distal radius was measured at 1 and 11 weeks post partum. RESULTS: Magnesium therapy was administered for a mean duration of 26 +/- 14 days and a cumulative dose of 1405 +/- 963 gm. Serum concentrations of magnesium, phosphorus, and parathyroid hormone increased and those of calcium decreased from baseline values in the magnesium sulfate group and remained uniform throughout the 3-week investigation. The serum magnesium, phosphorus, parathyroid hormone, and calcium concentrations in the control group were unchanged during the study and differed significantly from those in the magnesium sulfate group (p < 0.001). Urinary output of magnesium, calcium, and copper was significantly greater in the magnesium sulfate group than in the control group throughout the study. Urinary losses of calcium in the magnesium sulfate group, approximately 800 to 900 mg/day, were substantial. Although radius bone density 1 week post partum did not differ between groups, the change in bone density from 1 to 11 weeks post partum was significantly lower in the magnesium sulfate group than in controls. CONCLUSIONS: These data suggest that calcium homeostasis is altered during and after long-term magnesium sulfate therapy. The marked, prolonged urinary calcium losses may affect maternal bone mineralization.