PubMed · 6118482
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1981-11-07. Mini-necropsy.. https://pubmed.ncbi.nlm.nih.gov/6118482/
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OBJECTIVE: To evaluate the influence of maternal age on pregnancy loss rates after early documentation of fetal cardiac activity by transvaginal ultrasound (US) in previously infertile women. DESIGN: Retrospective, observational study. SETTING: Tertiary fertility center. PATIENTS: One hundred eighty-six previously infertile women 20 to 43 years of age undergoing ovulation induction. MAIN OUTCOME MEASURE: We analyzed 201 clinical pregnancies in which cardiac activity had been documented by transvaginal US 35 to 42 days after ovulation in a previously infertile population treated at a tertiary fertility center. Patient age, infertility diagnosis, ovulation induction protocol, and mode of insemination were analyzed by chi 2, Fisher's exact test and logistic regression analyses. RESULTS: A profound increase in spontaneous abortion rates occurred as a function of maternal age in this population (chi 2 for trend = 15.1). A spontaneous abortion rate of 2.1% was observed for maternal ages < or = 35 years but this rate increased to 16.1% for patients > or = 36 years (odds ratio, 8.72; 95 percent confidence interval 2.3 to 32.9). A fivefold increase in spontaneous abortion rate was observed in women > or = 40 years compared with women 31 to 35 years (3.8% versus 20.0%. Infertility diagnosis, mode of insemination, and ovulation induction protocol were not associated with an increased risk of spontaneous abortion. CONCLUSIONS: The incidence of pregnancy loss after confirmation of early fetal cardiac activity by transvaginal US is substantially greater in infertile patients than previously reported, when considered as a function of maternal age. In particular, patients > or = 36 years should be counseled that their risk of spontaneous abortion is significant even after fetal heart motion is present on transvaginal US. Cautious optimism and greater surveillance may be required during the first trimester of pregnancy in these women.
OBJECTIVE: To determine whether chronic menstrual irregularity with elevated LH levels has a role in spontaneous abortion. DESIGN: In 41 consecutively examined women with spontaneous abortions occurring within 11 complete gestational weeks, fetal chromosomal analyses were performed. The differences of endocrinologic background in relation to the result of fetal chromosomal analyses were investigated. MAIN OUTCOME MEASURES: Endocrinologic profiles, including menstrual history, basal hormone levels (LH, FSH, and PRL), ovarian morphology on ultrasound, and fetal chromosomal karyotypes. RESULTS: The women with normal fetal karyotypes compared with those with abnormal fetal karyotypes showed higher frequency of menstrual irregularity (47.1% versus 8.3%), elevated basal LH levels (7.42 +/- 5.12 versus 4.41 +/- 1.39 mIU/mL; conversion factor to SI unit, 1.00), and higher frequency of polycystic ovary (41.2% versus 8.3%). CONCLUSION: Elevated LH-polycystic ovary may be involved in the genesis of spontaneous abortions that are not explainable by fetal chromosomal abnormality.
Certain genetic disorders are rare in the general population but more common in individuals with specific trisomies, which suggests that the genes involved in the etiology of these disorders may be located on the trisomic chromosome. As with all aneuploid syndromes, however, a considerable degree of variation exists within each phenotype so that any given trait is present only among a subset of the trisomic population. We have previously presented a simple gene-dosage model to explain this phenotypic variation and developed a strategy to map genes for such traits. The mapping strategy does not depend on the simple model but works in theory under any model that predicts that affected individuals have an increased likelihood of disomic homozygosity at the trait locus. This paper explores the robustness of our mapping method by investigating what kinds of models give an expected increase in disomic homozygosity. We describe a number of basic statistical models for trisomic phenotypes. Some of these are logical extensions of standard models for disomic phenotypes, and some are more specific to trisomy. Where possible, we discuss genetic mechanisms applicable to each model. We investigate which models and which parameter values give an expected increase in disomic homozygosity in individuals with the trait. Finally, we determine the sample sizes required to identify the increased disomic homozygosity under each model. Most of the models we explore yield detectable increases in disomic homozygosity for some reasonable range of parameter values, usually corresponding to smaller trait frequencies. It therefore appears that our mapping method should be effective for a wide variety of moderately infrequent traits, even though the exact mode of inheritance is unlikely to be known.