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Query: UMLS:C0027960 (mole)
 21,279 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of this study was to investigate the role of ultrasound in the differential diagnosis and management of early pregnancies presenting with placental molar changes. Placental features were recorded over a 10-month period in women undergoing ultrasound examination at 10-14 weeks of gestation. In cases of a molar pregnancy, the fetal karyotype was obtained in utero and, if the pregnancy continued, the maternal concentration of human chorionic gonadotropin (hCG) and uterine artery resistance to flow were measured serially. A histopathological examination of the placenta was performed in all cases after delivery. During the study period, 9425 women had an early scan and 11 molar pregnancies were identified including one classical mole, four hydatidiform moles coexisting with a normal pregnancy, three partial triploid moles and three partial moles associated in one case with a fetus presenting congenitial anomalies diagnostic of Beckwith-Wiedemann syndrome. The hCG levels were high in all cases except one case of triploidy and remained high during the rest of the pregnancy in cases of hydatidiform moles coexisting with a fetus. In these cases, the uterine artery resistance was normal. The present data indicate that placental ultrasound examination can correctly identify molar changes in early pregnancy and together with hCG level and uterine Doppler measurements can establish the differential diagnosis in utero of the various forms of placental molar transformations.
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PMID:Early ultrasound diagnosis and follow-up of molar pregnancies. 933 34

The authors developed a method for obtaining highly specific polyclonal antibodies reacting with different sites of human chorionic gonadotropin (HCG) and an immunometrical method for measuring HCG in human biological fluids, based on the use of these antibodies. The sensitivity of the method is 10-15 IU/liter HCG, specificity 100%, no cross reactions with LH or FSH were observed. The method was tried in testing urine samples for HCG in women at 1-2 to 34 weeks of gestations and in one cancer patient with the diagnosis of vesical mole.
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PMID:[Immunoenzyme method of the determination of human chorionic gonadotropin using polyclonal antibodies]. 909 Nov 36

Non-trophoblastic neoplasms are the most frequent, benign tumors of the placenta, occurring in approximately 1% of all placentas examined. A case is described of a 24-year-old woman who presented with severe, early-onset pre-eclampsia, high human chorionic gonadotropin (hCG) levels, and a triploid fetus and who was found to have a small choriohemangioma. The woman, gravida 2 para 1, was referred to our hospital for perinatal evaluation. The fetus, gestational age 18 weeks 3 days, had fetal growth restriction with multiple congenital anomalies. The fetal karyotype was 69,XXY. Compared with the normal range for this gestational age, the beta-hCG level was significantly elevated (1,054,000 mIU/ml) as was the maternal serum alpha-feto-protein measurement (539.1 ng/ml). Sonographically, the placenta appeared hydropic, irregularly shaped, and gelatinous. A suction dilatation and evacuation under sonographic guidance was performed. Histological examination of placental tissue revealed hydropic degeneration of the chorionic villi. The specific histological features of a partial molar pregnancy were not present. However, there were changes consistent with a choriohemangioma. Flow cytometric DNA analysis performed on formalin-fixed, paraffin-embedded tissue blocks of placenta showed triploidy. Immunohistochemical staining with human placental alkaline phosphatase was consistent with a hydropic degeneration pattern. We conclude, first, that triploidy does not always imply the presence of a partial mole. Second, the dictum, that pre-eclampsia, if it occurs under 20 weeks' gestation, must be associated with a molar pregnancy, may not hold when placental aneuploidy is present. Although the findings in this pregnancy could have been incidental, there may be an association between a choriohemangioma and polyploidy.
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PMID:A non-trophoblastic tumor co-existing with a triploid fetus. 936 38

The majority of second-trimester partial moles are found in association with triploidy. Rarely are they associated with tetraploidy or other aneuploidies and, to our knowledge, this is the first reported case of the prenatal diagnosis of partial mole in a pregnancy presenting with trisomy. The patient was referred at 21 weeks of gestation after a routine ultrasound examination had shown fetal and placental features suggesting a partial mole triploidy. Owing to the severe structural malformations and poor prognosis, the parents requested termination. Prenatal and postnatal cytogenetic investigations demonstrated an additional chromosome 13. Histopathological examination of the placenta showed focal areas of villous edema but no evidence of trophoblastic dysplasia. The maternal serum human chorionic gonadotropin level was within the normal range at all times. This case shows that trisomy can resemble a triploid partial mole in utero without the potential long-term risk to the mother of persisting trophoblastic disease, as villous molar changes can obviously develop without trophoblastic dysplasia.
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PMID:A case of partial mole associated with trisomy 13. 951 Nov 99

The partial hydatidiform mole is a histopathologic entity characterized by focal trophoblastic hyperplasia with villous hydrops together with identifiable fetal tissue which was first described by Szulman and Surti in 1978. Since then major advances in molecular biology have shown that more than 90 per cent of partial moles are secondary to diandric triploidy and that this condition accounts for most cases of persistent trophoblastic disease after partial mole. Case series describing the prenatal diagnosis of triploid partial mole were reviewed and outcomes were analysed for all pregnancies, and compared to those of non-molar triploidy using the chi-square test. In more than 90 per cent of both types of triploidy, the fetus shows growth restriction and multiple structural anomalies. Oligohydramnios and abnormal placental Doppler indices are common in both types. In triploid partial mole, 82.1 per cent of fetuses present with symmetrical growth restriction, the maternal serum human chorionic gonadotropin (MShCG) level is increased in 80.8 per cent of the cases and 41.9 per cent of the women are at risk of pre-eclampsia. The triploid partial mole is a lethal fetal condition which is linked with gestational trophoblastic disorders. The typical placental molar features are not always pathognomonic of triploid partial mole and are less likely to be apparent on ultrasound in early pregnancy. The perinatal diagnosis of this condition relies upon mainly on MShCG level and cytogenetic results which have to be correlated with the histopathologic diagnosis. Women with this pregnancy complication should be offered immediate termination and a specific follow-up.
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PMID:Partial moles: from postnatal to prenatal diagnosis. 1041 2

There is abundant evidence that human chorionic gonadotropin (hCG) is a weak thyrotropin (TSH) agonist. In FRTL-5 rat thyroid cells, hCG increases cyclic adenosine monophosphate (cAMP), iodide transport, and cell growth. hCG has thyroid-stimulating activity in bioassays in mice and in clinical studies in man. In cultured cells transfected with the human TSH receptor, hCG increases generation of cAMP. Molecular variants of hCG with increased thyrotropic potency include basic molecules with reduced sialic acid content, truncated molecules lacking the C-terminal tail, or molecules in which the 47-48 peptide bond in the beta-subunit loop is nicked. In normal pregnancy, when hCG levels are highest at 10 to 12 weeks gestation, there is suppression of serum TSH levels, presumably due to slight increases in free thyroxine (T4) concentration. In twin pregnancies, hCG levels tend to be higher and suppressed TSH levels are more frequent. Hyperemesis gravidarum, defined as severe vomiting in early pregnancy that causes 5% weight loss and ketonuria, is usually associated with increased hCG concentration. A high proportion of patients with hyperemesis gravidarum, about one-third to two-thirds in different series, have evidence of increased thyroid function. Only a small proportion of these patients have clinical hyperthyroidism, termed gestational thyrotoxicosis. These patients probably secrete a variant of hCG with increased thyroid-stimulating activity. Trophoblastic tumors, hydatidiform mole, and choriocarcinoma often cause hyperthyroidism because they secrete very large amounts of hCG. When the serum hCG exceeds about 200 IU/mL, hyperthyroidism is likely to be found. There is a correlation between the biochemical severity of hyperthyroidism and the serum hCG in these patients. Removal of the mole or effective chemotherapy of the choriocarcinoma cures the hyperthyroidism. In conclusion, hCG has thyroid-stimulating activity that influences thyroid function early in pregnancy when hCG levels are high. Excessive hCG secretion may cause hyperthyroidism in patients with hyperemesis gravidarum or trophoblastic tumors.
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PMID:Human chorionic gonadotropin and the thyroid: hyperemesis gravidarum and trophoblastic tumors. 1044 9

We evaluated the stimulation of Chinese hamster ovary cells expressing human thyrotropin receptors (CHO-hTSHR cell) by sera of five patients with hydatidiform mole before and after the evacuation of the mole, and compared the results with serum human chorionic gonadotropin (hCG) concentrations and serum free thyroid hormones in these patients. Significantly increased CHO-hTSHR cell stimulating activities were observed in sera from untreated patients, and the activity decreased promptly after the evacuation of the mole, concomitantly with the decrease in serum hCG and free thyroid hormones. CHO-hTSHR cell stimulating activity of sera of the untreated patients significantly correlated with serum hCG. Moreover, serum hCG stimulated CHO-hTSHR cells in a dose dependent manner similar to the dose-response curve of the stimulation by purified hCG. Sera of the patients and purified hCG did not stimulate nontransfected CHO-K1 cells. However, a significant correlation was not observed between serum-free thyroid hormones and serum hCG or between serum free thyroid hormones and CHO-hTSHR cell stimulating activities in untreated patients. These results indicate that serum hCG from patients with hydatidiform mole stimulates thyroid gland by interacting with TSH receptors, and suggest that the increase in thyroid hormones in patients may depend on both the increased serum hCG and the responsiveness of their thyroid glands to hCG.
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PMID:Stimulation of Chinese hamster ovary cells expressing human thyrotropin receptors by serum human chorionic gonadotropin of patients with hydatidiform mole. 1064 59

The objectives of this study were to determine: 1) whether high proportions of nicked human chorionic gonadotropin (hCG) in serum at the time of mole evacuation and during postmolar surveillance is indicative of trophoblastic malignancy and 2) to investigate whether measurement of nicked hCG provides clinically more useful information in the management of patients with trophoblastic disease than does measurement of total hCG alone. "Tumor marker" total hCG, intact hCG, and nicked hCG were measured in serial samples of serum from our serum bank of patients with representative types of trophoblastic disease. "Tumor marker" hCG has been shown to measure all aspects of the hCG molecule. At the time of presentation of all 45 patients, 83.5% of hCG was intact and 16.5% was nicked. These proportions became reversed as hCG declined either spontaneously after hydatidiform mole evacuation or with chemotherapy in patients with postmolar trophoblastic tumor or with metastatic trophoblastic disease. We conclude that the proportion of nicked hCG compared to intact hCG increases with trophoblastic disease resolution. Measurement of nicked hCG adds no useful clinical information to that provided by reliable measurement of total hCG.
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PMID:Nicked human chorionic gonadotropin in trophoblastic disease. 1124 Jun 95

We attempted to identify the cells expressing alpha and beta subunits of human chorionic gonadotropin (hCG) in the peripheral blood of patients with trophoblastic disease and normal pregnant women by using reverse transcriptase polymerase chain reaction (RT-PCR) and Southern blot. By this method, the mRNAs of hCG alpha and hCG beta were detected in the peripheral blood mononulear cells (PBMNC) from 3 of 7 hydatidiform mole (mole) and 1 of 4 choriocarcinoma patients as well as from normal pregnant women during the first trimester. None of the mRNAs of hCG subunits was detected in the PBMNC from healthy male and nonpregnant healthy women examined. The expression of hCG alpha and hCG beta in patients with trophoblastic disease and normal pregnant women almost correlated with their plasma levels of intact hCG. The present study indicates that the cells expressing hCG alpha and hCG beta, which virtually represent trophoblasts, are circulating in the peripheral blood of patients with trophoblastic disease as well as of normal pregnant women.
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PMID:Trophoblastic cells expressing human chorionic gonadotropin genes in peripheral blood of patients with trophoblastic disease. 1126 89

The present study was undertaken to investigate whether human chorionic gonadotropin (hCG) beta-core fragment (hCG beta cf) was directly produced by gestational trophoblastic tumors. Immunoreactivity of hCG beta cf was demonstrated in the extracts as well as in the culture media of hydatidiform mole tissues. It was also present in the extracts of choriocarcinoma tissues, and its molar concentration exceeded that of intact hCG. The presence of hCG beta cf was then confirmed by gel chromatography and Western blot analysis. Immunohistochemistry showed localization of hCG beta cf immunoreactivity to the syncytiotrophoblasts and scattered cells in the stroma of mole tissue, and to syncytiotrophoblastic cells in choriocarcinoma. Immunoreactivity of hCG beta cf was also detected in the sera of the patients with gestational trophoblastic disease, although the hCG beta cf/hCG ratio was less than one hundredth of that in the tissue extracts. Serial measurement of serum hCG beta cf levels after mole evacuation showed that they declined much more rapidly than those of hCG and became undetectable in the patients with subsequent spontaneous resolution, while hCG beta cf remained or became detectable before the rise of hCG was observed in the patients with subsequent persistent trophoblastic disease. Taken together, these results suggest that hCG beta cf is directly produced by gestational trophoblastic tumors, and monitoring of hCG beta cf in the serum after mole evacuation may be useful for early prediction of subsequent development of postmolar persistent trophoblastic disease.
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PMID:Human chorionic gonadotropin (hCG) beta-core fragment is produced by degradation of hCG or free hCG beta in gestational trophoblastic tumors: a possible marker for early detection of persistent postmolar gestational trophoblastic disease. 1173 9


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