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The International Planned Parenthood Federation (IPPF) new statement on the diagnosis of pregnancy was drawn up in April 1990. A pregnancy diagnosis includes clinical evaluation of the woman's history, symptoms, physical examination, and pregnancy tests. Pregnancy symptoms may include amenorrhea, nausea, vomiting, enlargement and tenderness of the breasts, frequent urination, and changes in appetite and food and drink habits. If biochemical testing is not possible, a reliable clinical diagnosis of pregnancy cannot take place before 6-8 weeks. At this time, the clinician can observe cervical softening and uterine softening and enlargement if a woman is pregnant. If the uterine size does not match the length of amenorrhea, clinicians should suspect the following: earlier or later conception than indicated, ectopic pregnancy, incomplete or missed spontaneous abortion, twin gestation, hydatidiform mole, or other uterine anomaly. They should suspect ectopic pregnancy in women with smaller than expected uterine size when they have been sterilized or are using an IUD or are using low-dose progestogen-only pills or Norplant. They should refer women with smaller than expected uterine size who are experiencing bleeding and/or pain to a more sophisticated clinical facility, where an accurate diagnosis of and adequate treatment for ectopic pregnancy can be done. Biochemical pregnancy tests consist of antibodies that mark human chorionic gonadotropin (hCG) from a urine or serum sample. hCG levels increase beginning about 10 days after fertilization. The most convenient and inexpensive pregnancy test for clinics is the immunoassay test (slide test), which requires a urine or serum sample. It can provide reliable results a few days after the missed menstrual period. Clinicians should provide appropriate counseling regardless of whether the client wishes to continue or terminate the pregnancy.
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PMID:New IPPF statement on the diagnosis of pregnancy. 192 37

Repetitive hydatidiform mole was observed in four pregnancies. The pregnancies presented with heavy bleeding and vomiting, but the post-evacuation courses were uncomplicated, with rapid regression of serum hCG levels. Cytogenetic investigations, analyses of restriction fragment length polymorphisms, and flow cytometry in three pregnancies were consistent with diploid, biparental conception as the origin of fetal tissue and molar and nonmolar villi. In one pregnancy, the analyses of cytogenetic markers suggested the coexistence of two different cell lines of dizygotic, biparental origin, whereas DNA analysis was consistent with a single conception. With incomplete genetic information, a hydatidiform mole with coexistent normal fetus is generally considered to result from dizygous twinning comprising an androgenetic complete mole and a normal conception. In the present gestations, the results based on several techniques applied on numerous samples from different tissues render this possibility unlikely. Some of the contradictions between histologic and cytogenetic classifications of hydatidiform mole may be explained by diploid, biparental partial mole, which seems to constitute a separate subgroup within hydatidiform mole. Following chorionic villus sampling or amniocentesis, continued pregnancy may be considered, depending on prenatal diagnosis including genetic marker analysis.
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PMID:Hydatidiform mole and fetus with normal karyotype: support of a separate entity. 203 Aug 59

Molar pregnancy, which results from an anomaly in the development of the trophoblastic tissue, is now easy to diagnose based on clinical evidence, beta hCG level, and sonography, although it must be histologically confirmed. Treatment remains difficult because of the danger of hemorrhage or trauma during uterine evacuation. Hydatidiform mole was diagnosed in the 1st pregnancy of a 27-year-old woman on the basis of a routine 1st trimester sonogram. Clinical examination revealed a voluminous uterus and a long, closed, very tonic cervix. Sulprostone was administered to aid cervical dilatation. An initial intramuscular injection of sulprostone caused uterine contractions without cervical modifications. 5 hours later an intravenous perfusion of sulprostone was started, during which significant contractions and cervical modifications were observed. An aspiration curettage was performed, in which numerous vesicles typical of the hydatidiform mole were evacuated. There was no need for further cervical dilatation and the curettage was rapid and nonhemorrhagic. The postoperative course was uneventful, and a test of beta hCG levels 6 weeks later was negative. The patient complained of pain during uterine contractions despite use of high doses of pethidine. The frequency of hydatidiform mole varies in different countries. It has been estimated at 1/85 in Indonesia and 1/2000 in the US. The clinical picture of hydatidiform mole includes vomiting often nonresponsive to treatment and metrorrhagia of varying volume, a large uterus for the gestational age, and often bilateral ovarian cysts. A vasculorenal syndrome may also begin at 13-16 weeks of amenorrhea. Beta hCG levels are high for the gestational age. Sonography reveals no embryonic structures. Biopsy shows a complete absence of embryo and amniotic sac. The karyotype is diploid and almost always XX. The mechanism is fertilization of an ovocyte whose nucleus is absent or inactive. The 2 chromosome sets are contributed by the father, a circumstance incompatible with embryonic development. Trophoblastic proliferation occurs without embryonic development. Hydatidiform moles may be transformed to invasive moles or chorioepithelioma. Treatment includes uterine evacuation by aspiration under sonographic control if possible. Many authors recommend oxytocin and antibiotic cover. The use of prostaglandin analogs to facilitate uterine evacuation is controversial, with some authors citing the increased risk of trophoblastic embolism. The mole should be histopathologically and cytogenetically studied, and postmolar follow-up is essential.
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PMID:[Use of sulprostone in the evacuation of molar pregnancies]. 206 88

The use of a synthetic analogue PGE2 (15(S)15 methyl PGE2 methyl ester) in the management of hydatidiform mole was evaluated in 20 affected patients, gestational age ranging from 8 to 20 weeks, parity from 0 to 6. A portex 16 gauge epidural catheter was used to administer a 30 mcg dose of the PG analogue contained in 3 ml of water. A second dose was administered 8 hours later following failed expulsion of molar tissue. Curettage was performed in all patients following expulsion of the hydatidiform mole. Side effects included vomiting, pyrexia, shivering, and diarrhea. The treatment was successful in all patients, with 15 aborting with the single dose and 5 with the 2nd dose 8 hours later. Interval between the 1st dose to expulsion of the hydatidiform mole ranged from 2 3/4 hours to 16 hours with a mean of 9 hours 4 minutes for the 20 patients. This study suggests that the PGE2 analogue is a safe and reliable drug in treating hydatidiform mole.
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PMID:Intrauterine administration of prostaglandin 15 (S) 15 methyl E2 methyl ester in the management of patients with a hydatidiform mole. 441 89

(PGF2alpha) Prostaglandin F2alpha was administered intraamniotically to 16 patients in 3 groups: molar pregnancy (8 cases), fetal death (6 cases), and anencephalic fetus (2 cases). These particular types of situations were selected because the effects of PGs upon the product were unknown. PG was administered in dosages between 3 and 200 mcg after being prepared in an ethanol solution. It appeared to have no effect on uterine contractility. It is best to start contractility stimulation with low doses which should be increased progressively according to uterine response. Tone, intensity, frequency, and uterine activity increased when PG dose was increased. Uterine labor as to maturity and cervical dilatation, was studied in the 3 groups. Blood pressure was registered in 2 patients with molar pregnancy; there were no changes during the 1st hours of the study. However, during the last part, differential pressure increased by systolic increase. In 4 patients with fetal death, cervical dilatation register was taken. Average dilatation time (going from 2-10 cm) was 9.50 hours. There were such side effects as slight nausea, vomiting, and chills. 1 of the patients presented with hypotension upon administration of PGF2alpha 200 mcg. 4 patients suffered complications; 1 with molar pregnancy had a possible pulmonary embolism by trophoblast, another had hemorrhage and hypotension, 1 patient with fetal death had immediate hypotension after administration of 200 mcg, and the other had deciduo-myometritis which cleared with antibiotics and curettage. No other subjects experienced complications. Intraamniotic PG administration produced few side effects. (author's modified)
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PMID:[Effect of prostaglandin F2a on the contractility of the pregnant human uterus]. 441 23

Recent research suggests that the action of prostaglandins on the pregnant uterus is more complex than that of oxytocin. Despite the fact that prostaglandins, like oxytocin, may fall short of the ideal, preliminary work makes it apparent that prostaglandins have attributes for induction of labor that will ultimately rank them as far superior to oxytocin. A 1st sign that prostaglandins might be more than just oxytocic agents came from the discovery of the effectiveness of prostaglandin F2alpha (PGF2alpha) and prostaglandin E2 (PGE2) in inducing mid-trimester abortion. For a long time it has been known that oxytocin seldom causes abortion of a normal pregnancy. Prostaglandins cause rapid dilatation of the cervix and expulsion of the conceptus despite a lesser degree of measurable uterine activity than that induced by oxytocin. Prostaglandins do something more, either to the quality of uterine contractions or to the cervix. A major problem associated with the pharmacological use of prostaglandins has been a high incidence of unpleasant side-effects when given by routes that are associated with substantial systemic uptake. In general, doses of prostaglandins that are oxytocic result in nausea, vomiting and diarrhea when administered by the intravenous, oral or intravaginal routes. The intra-amniotic and extra-ovular routes of administration for induction of mid-trimester abortion, as described by Doctors Karim and Hillier, are examples of the successful application of the principle that prostaglandins can be effective without side-effects when they are delivered close to the site of action. Prostaglandins appear particularly well suited to induction of labor in women with prolonged fetal death, anencephaly or hydatidiform mole.
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PMID:Prostaglandins: current therapeutic status in obstetrics. 443 69

This is report regarding a 28-year-old woman who conceived and delivered a healthy child following treatment for brain metastasis of choriocarcinoma in 1980 and a prolonged postoperative disease-free period. The patient had delivered a hydatidiform mole. Eight months afterwards she was admitted to our hospital with occipital pain, vomiting and stupor, and upon CT examination was found to have a brain tumor. The surgically removed tumor was pathologically diagnosed as choriocarcinoma. Postoperative methotrexate chemotherapy rapidly lowered the preoperative urinary human chorionic gonadotrophin (19 IU/ml), and allowed restoration of the preoperative LH level, consciousness, ambulation, and manifest ovulation. Occasional mild cramps were received by continuous use of anticonvulsants which did not affect her daily life. Four and one-half years postoperatively she conceived, and had a healthy boy weighing 2,294 g at the 39th week of gestation in June 1985. Both mother and baby have been doing well for 7 postpartum years.
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PMID:A case of successful pregnancy and delivery after brain metastasis of choriocarcinoma. 848 64

Hyperthyroidism is second to diabetes mellitus as the most common endocrinopathy in pregnancy. Inappropriate secretion of hCG is the most common cause of hyperthyroidism in the first part of gestation. In addition to hydatidiform mole and hyperemesis gravidarum, nonpathologic-conditions including multiple gestation, mild nausea and vomiting, and even normal pregnancies may present with transient undetectable or suppressed serum TSH values. The syndrome of transient hyperthyroidism of hyperemesis gravidarum is defined as severe nausea and vomiting, dehydration, ketonuria, and weight loss of more than 5% by 6 to 9 weeks of pregnancy. Thyroid tests are in the hyperthyroid range, and the abnormalities are related to the severity of symptoms. Tests normalize with resolution of the vomiting, and ATD therapy is not indicated. The natural history of Graves' disease in pregnancy is characterized by aggravation in the first trimester, amelioration in the second half, and recurrence in the year following delivery. ATD treatment is the therapy of choice in pregnancy. Either PTU or MMI may be used; the goal is to keep the FT4I in the upper limits of normal with the minimum dose of ATD. In approximately 30% of patients, ATDs may be discontinued in the last few weeks of gestation. Maternal, fetal, and neonatal complications are frequent when hyperthyroidism is not under control. Postpartum hyperthyroidism may be caused by an episode of silent thyroiditis or Graves' disease.
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PMID:Hyperthyroidism in pregnancy. 953 33

Nausea and vomiting are common complaints in pregnancy, occurring in more than 50% of pregnant women. Occasionally, the vomiting becomes severe and persistent enough to develop into the syndrome called hyperemesis gravidarum and sometimes requires hospitalization. A 20-year-old woman presented with hyperemesis gravidarum, which was later found to be associated with a molar pregnancy. Hyperemesis gravidarum is reported to occur in as many as 26% of molar pregnancies. Increases in the level of serum beta-human chorionic gonadotropin may be the mechanism of hyperemesis gravidarum in molar pregnancy. Hyperthyroid states linked to molar pregnancy may further exacerbate hyperemesis gravidarum. Physicians should be aware of this possibility of molar pregnancy in all patients with hyperemesis gravidarum and be familiar with the appropriate management to monitor and prevent an often-fatal trophoblastic neoplasm.
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PMID:Molar pregnancy presenting with hyperemesis gravidarum. 1021 11

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


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