Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present report focuses on the two main causes of hyperthyroidism observed in the pregnant state: Graves' disease (GD) and gestational transient thyrotoxicosis. Together, the prevalence of hyperthyroidism may represent 3% to 4% of all pregnancies, and therefore constitutes an important clinical issue. Concerning GD, the variable presentations of the disease (women under treatment, in remission, or considered cured) and specific alterations occurring in pregnancy are discussed: changes in thyrotropin (TSH) receptor antibody titers, the risk of fetal and neonatal thyrotoxicosis, the outcome of pregnancy in relation to the control of hyperthyroidism, and the treatment of active GD during and after pregnancy with antithyroid drugs. Gestational transient thyrotoxicosis is associated with a direct stimulation of the maternal thyroid gland by human chorionic gonadotropin (hCG), and has been shown to be directly related to both the amplitude and duration of peak hCG values. The syndrome is usually transient, observed at the end of the first trimester, and is frequently associated with emesis. Finally, we propose a global strategy for the systematic screening of hyperthyroidism during pregnancy, based on an algorithm that allows for the diagnosis of both autoimmune and nonautoimmune forms of hyperthyroidism in the pregnant state.
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PMID:Thyroid hyperfunction during pregnancy. 977 58

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

Fetal and neonatal hyperthyroidism are usually produced by transplacental passage of thyroid-stimulating immunoglobulins. Most commonly, the thyroid-stimulating immunoglobulins are a component of active maternal Graves' disease. However, such antibodies may continue to be produced after ablation of the thyroid by surgery, radioiodine, or by the immune mechanisms of Hashimoto's thyroiditis. Other mechanisms that have produced fetal and neonatal hyperthyroidism include activating mutations of the stimulatory G protein in McCune-Albright syndrome and activating mutations of the thyrotropin (TSH) receptor. Fetal hyperthyroidism may be associated with intrauterine growth retardation, nonimmune fetal hydrops, craniosynostosis, and intrauterine death. Features of this condition in the neonate include hyperkinesis, diarrhea, poor weight gain, vomiting, ophthalmopathy, cardiac failure and arrhythmias, systemic and pulmonary hypertension, hepatosplenomegaly, jaundice, hyperviscosity syndrome, thrombocytopenia, and craniosynostosis. The time course of thyrotoxicosis depends on etiology. Remission by 20 weeks is most common in neonatal Graves' disease; remission by 48 weeks is nearly always seen. A subset of these patients may have persistent disease when there is a strong family history of Graves' diseases. Disease persistence is characteristic of patients with activating mutations of the TSH receptor. Treatment of fetal hyperthyroidism comprises administration of antithyroid drugs to the mother. Fetal heart rate and fetal growth should be monitored. Ultrasonography may reveal changes in thyroid size. At times, cordocentesis may be useful for monitoring fetal thyroid function. Hyperthyroid neonates may be treated with antithyroid drugs, beta-adrenergic receptor blocking agents, iodine, or iodinated contrast agents, and at times, with glucocorticoids and digoxin. Nonremitting causes of neonatal hyperthyroidism require ablative treatments such as thyroidectomy.
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PMID:Fetal and neonatal hyperthyroidism. 1044 21

A 35-year-old hyperthyroid woman who developed nausea, vomiting, tachycardia, nystagmus and mental disturbance, was referred to our hospital with a suspected diagnosis of thyroid storm. However, the thyroid gland was only slightly palpable, bruits were not audible, and exophthalmos was not present. Serum levels of thyroid hormone were increased, but TSH receptor antibodies were negative. Echography and color flow doppler ultrasonography revealed a slightly enlarged thyroid gland and a slightly increased blood flow, both of which were much less milder than those expected for severe hyperthyroid Graves' disease. Under the diagnosis of hyperthyroidism due to gestational thyrotoxicosis associated with Wernicke encephalopathy, vitamin B1 was administered on the first day of admission. Her consciousness became nearly normal on the second day except for slight amnesia. Her right abducent nerve palsy rapidly improved, but horizontal and vertical nystagmus, diminished deep tendon reflexes and gait ataxia improved only gradually. MRI findings of the brain were compatible with acute Wernicke encephalopathy. We concluded that history taking and physical findings are important to make a differential diagnosis of gestational thyrotoxicosis with acute Wernicke encephalopathy from Graves' thyroid storm, and that Wernicke encephalopathy should be treated as soon as possible to improve the prognosis.
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PMID:Gestational thyrotoxicosis with acute Wernicke encephalopathy: a case report. 1072 54

A cat was presented for anorexia and vomiting. Hyperthyroidism and primary hyperparathyroidism were diagnosed. A thyroid adenoma and parathyroid adenoma, respectively, were responsible for these conditions. Unilateral thyroidectomy and parathyroidectomy successfully resolved both disorders.
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PMID:Primary hyperparathyroidism and concurrent hyperthyroidism in a cat. 1184 93

The Indian Contraceptive Testing Unit started making field trials with oral contraceptives in 1964. By June 1968, 958 women were taking oral contraceptives. Combination tablets used contained a minimum amount of progestogen (.5-3 mg) and a suitable amount of estrogen. The 21-tablet pack was found mot suitable. It was found that if a woman missed taking the tablets in the latter half of the cycle usually no harm resulted, but if she missed them at the beginning of the cycle pregnancy might follow as ovulation would not be inhibited. Main contraindications are liver damage, toxic hyperthyroidism, thromboembolic disease, and cancer of the genital tract or breast. Caution is advised for persons with chronic nephritis, a history of eclampsia, hypertension, varicose veins, ophthalmological disorders, or psychic depressive states. Side effects have been less with the smaller doses. The most serious side effect is thromboembolism. Those reported have been leg pain, giddiness, headache, breakthrough bleeding, nausea, vomiting, amenorrhea, abdominal pain, weakness, increased blood pressure, and skin rashes. Others have reported ocular disease and cranial nerve palsy. Sequential therapy has been reported to have a lower incidence of side effects but a higher rate of pregnancy. Low-dose progestogen therapy, the "minipill," does not inhibit ovulation but is effective by causing changes in the endometrium and in the mucus. The chlormadinone in the minipill does not affect lactation. However, the incidence of pregnancy is similar to that with an IUD (Lippes loop) which is 2.6/100 cases. Laboratory tests have been normal, except an increase in the thymol turbidity test. Vaginal cytology has revealed no case of malignancy. Results show that oral contraceptives are suitable for use on a mass scale as a method of population control.
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PMID:Experience with oral contraceptives. 1225 72

Radiographic contrast media (CM) are necessary to provide x-ray absorption of the bloodstream; all other observed effects need to be regarded as adverse. Four types of CM are currently used in diagnostic and interventional cardiology: ionic high-osmolar CM (HOCM), either ionic or non-ionic low-osmolar CM (LOCM), and non-ionic iso-osmolar CM (IOCM). Focusing on the potential cardiovascular effects caused by the CM, there is a clear difference between HOCM and the LOCM or IOCM. HOCM have a poorer profile due to a higher incidence of hypotension and electrophysiological effects. To prevent contrast-induced nephropathy, HOCM should be avoided and patients should receive the minimal dose of LOCM or IOCM with intravenous hydration before and after the procedure. Clinical hyperthyroidism has been detected after CM use, but the condition appears, ultimately, to be self-limited and to occur mainly in elderly patients. When assessing the need for a CM in terms of improved patient safety, preventing serious complications should be the major factor determining the choice. CM should not be selected on the basis of minor adverse effects since these are, ultimately, of low clinical relevance. Thrombotic events, in contrast, carry a high clinical relevance and we consider that these should be the main issue governing current choice. Ionic LOCM appear to have better profile than other CM with respect to interaction with platelet function and coagulation. In relation to thrombotic events in randomised clinical studies, ionic CM have been associated, mainly, with favourable and some neutral results compared with non-ionic agents. Only one trial indicated a more pronounced antithrombotic effect of the non-ionic IOCM relative to the ionic LOCM. The antithrombotic advantages of ionic over non-ionic LOCM are, in part, balanced by a greater frequency of minor adverse effects such as nausea, vomiting or cutaneous rashes. A matter of concern is the delayed adverse effects observed with non-ionic IOCM. However, severe and life-threatening reactions are exceptional and there are probably no significant differences between IOCM and LOCM whether ionic or non-ionic. However, in patients with known allergies, non-ionic CM are to be recommended. On the basis of the available pre-clinical and clinical data, the ionic LOCM or the non-ionic IOCM are the agents to be recommended in percutaneous coronary interventions because of their antithrombotic advantages over non-ionic LOCM.
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PMID:Comparative tolerability of contrast media used for coronary interventions. 1245 33

Hyperthyroidism can occur secondary to gestational trophoblastic disease. The clinical and biochemical data of four women who had hyperthyroidism secondary to gestational trophoblastic disease was analyzed. The parity ranged from primi to gravida four and the period of amenorrhoea from six weeks to sixteen weeks. Three women had vomiting, two had bleeding per vaginum and two had tachycardia and minimal thyromegaly. The betahCG was more than 5,00,000 mlu/ml in all the cases. Three women required treatment for the hypermetabolic status and one woman had biochemical hyperthyroidism. Two of them had molar pregnancy, one had partial mole and one had persistent trophoblastic disease.
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PMID:Trophoblastic hyperthyroidism. 1471 95

A 16-year-old girl had symptoms of vomiting, malaise and weight loss for two months. Blood tests revealed an elevated activity of liver enzymes and hyperthyroidism. Although the patient at first denied the possibility of pregnancy, a pregnancy was subsequently confirmed. Hyperemesis gravidarum was diagnosed based on the combination of the clinical symptoms, pregnancy and increased serum human chorionic gonadotrophin and oestradiol. Hyperemesis gravidarum also explained the demonstrated biochemical hyperthyroidism and elevated liver enzyme levels. Rapid alleviation of all the clinical symptoms was seen after termination of this unwanted pregnancy. Although vomiting, malaise and weight loss in children can have many different causes, in girls at a sexually mature age a pregnancy with possible hyperemesis gravidarum should certainly also be considered and a gynaecological examination performed.
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PMID:[A teenager presenting with vomiting, general malaise and weight loss]. 1518 43

Human chorionic gonadotropin (hCG) is a glycoprotein hormone that has structural similarity to TSH. At the time of the peak hCG levels in normal pregnancy, serum TSH levels fall and bear a mirror image to the hCG peak. This reduction in TSH suggests that hCG causes an increased secretion of T4 and T3. Women with hyperemisis gravidarum often have high hCG levels that cause transient hyperthyroidsm. In the vast majority of such patients, there will be spontaneous remission of the increased thyroid function when the vomiting stops in several weeks. When there are clinical features of hyperthyroidism, it is be reasonable to treat with antithyroid drugs or a beta-adrenergic blocker, but treatment is rarely required beyond 22 weeks of gestation. Hyperthyroidism or increased thyroid function has been reported in many patients with trophoblastic tumors, either hydatiditform mole or choriocarcinoma. The diagnosis of hydatidiform mole is made by ultrasonography that shows a 'snowstorm' appearance without a fetus. Hydatidiform moles secrete large amounts of hCG proportional to the mass of the tumor. The development of hyperthyroidism requires hCG levels of >200 U/ml that are sustained for several weeks. Removal of the mole cures the hyperthyroidism. There have been many case reports of hyperthyroidism in women with choriocarcinoma and high hCG levels. The principal therapy is chemotherapy, usually given at a specialized center. With effective chemotherapy, long-term survival exceeds 95%. A unique family with recurrent gestational hyperthyroidism associated with hyperemesis gravidarum was found to have a mutation in the extracellular domain of the TSH receptor that made it responsive to normal levels of hCG.
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PMID:Physiological and pathological aspects of the effect of human chorionic gonadotropin on the thyroid. 1515 39


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