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

MOST IMPORTANT OBSERVATIONS: (FROM COUNTRY-WIDE POPULATION STUDIES) 1. In some voivodships localized in south-east and north-east parts of Poland thyroids of young children would, without protective measures, accumulate more then 60 MsV of radioiodine, thus exceeding intervention level settled for the country. 2. Thyroid function of newborns exposed to radioiodine during neonatal life was normal and frequency of neonatal hypothyroidism similar to that seen in years before Czernobyl accident. 3. Potassium iodide administrated to newborns in some of them profuced transient rise of TSH (Wolff-Chaikoff phenomenon), thus suggesting, that ki dose settled for newborns could be to high. 4. Thyroid radioiodine dose accumulated in thyroids of older children, teenagers and adults was in majority of regions well below the dose of 50 MsV. 5. The frequency of non-toxic diffuse goiter, especially in traditional endemic goiter area was found to be high, but is also relatively high in others regions of Poland and seems to depend on iodine deficiency or relative iodine deficiency. 6. The frequency of other thyroid disorders is within the limit reported in countries with relative iodine deficiency. 7. More than 95% of children and teenagers took protective, single dose of potassium iodide (about 10 millions). 8. Approximately 27% of adults took protective dose of potassium iodide (about 7 millions). 9. Organization of protective action in 11 north-east and south-east voivodoships was good about 75% of all obtain ki solution within 24 hours. In the rest of the country where protective action was ordered april 30, in afternoon hrs only about 25% obtained ki the same day and the rest during next 48-72 hrs. 10. The fact that prior to the protective action limited number of children was given iodine alcohol solution permitted for external use speaks about the fear and panic observed in Poland in first days after Czernobyl accident. 11. Extrathyroidal side-effects after ki administration appeared in about 5% were usually light or moderate and in majority of cases disappearing without medical assistance. Vomiting was most commonly seen side-effect in young children, thus suggesting that either dose, or the chemical form of the drug for this group of age was unproper. 12. Intrathyroidal side-effects of single dose of ki was rare phenomenon seen mostly in newborns, very young children and some adults with history of thyroid disease in the past. 13. Its possible that even small dose of radioiodine accumulated in thyroid produce immunological response leading to the appearance of thyroid antibodies in blood serum.
 ...
PMID:[Results of studies performed with the MZ-XVII program on a national scale; summary and conclusions]. 136 84

Thyroid function was evaluated in 41 consecutive women with hyperemesis gravidarum (HG). In 11, increased free thyroxin concentrations (FT4) were measured. After one week of conservative therapy, 4 patients with persistent emesis were treated with antithyroid agents. Three of these 4 displayed other signs of hyperthyroidism. Emesis resolved in the other 7 patients within a week of conservative therapy. FT4 levels also returned to normal in these 7 patients within several weeks. Thyrotropin-releasing hormone (TRH) was administered to 10 of the 11 patients. Abnormal TSH responses, suggesting varying degrees of autonomous thyroid function were noted in all 4 patients treated with antithyroid drugs and in 3 of the untreated patients. Underlying clinical signs and symptoms of hyperthyroidism should be sought in patients with HG. In the presence of persistent emesis, despite conservative therapy of at least one week's duration and the presence of abnormal thyroid function studies, the use of antithyroid agents should be considered.
 ...
PMID:Abnormal thyroid function in hyperemesis gravidarum. 248 11

The clinical course of a 29-month-old girl who was referred for evaluation after ingesting ninety 0.2-mg tablets of levothyroxine is reported. Despite an initial thyroxine (T4) level of 282 micrograms/dl and a triiodothyronine (T3) level of 1,837 ng/dl at 48 hours postingestion, her symptoms were mild and included irritability, vomiting, tremor, and tachycardia. Treatment was limited to activated charcoal and propranolol. Thyroid hormone levels fell to normal by 13 days postingestion. The child's clinical course was benign. Even after massive acute ingestions of levothyroxine, children's symptoms are usually mild and may be controlled with propranolol. This conservative approach should be considered before expensive and potentially dangerous therapies are undertaken.
 ...
PMID:Massive levothyroxine ingestion. Conservative management. 275 19

Thyroid function in early normal pregnancy was evaluated with reference to morning sickness using a newly developed free thyroxine (T4) radioimmunoassay and a highly sensitive TSH immunoradiometric assay. A significant increase in serum free T4 and a decrease in serum TSH were observed in early pregnancy relative to the levels in nonpregnant controls. The increased free T4 and hCG and decreased TSH correlated with the severity of morning sickness, and these changes were especially marked in subjects with nausea and vomiting. The individual serum levels of hCG in the pregnant group correlated significantly, directly with the levels of free T4 and inversely with those of TSH. The increased free T4 and decreased TSH in subjects with emesis returned to the normal ranges of nonpregnant controls after improvement of emesis. These data indicate that the thyroid gland is physiologically activated in early pregnancy, possibly by hCG or a related substance, which may induce gestational emesis. On the other hand, an increased level of free T4 and a reduced level of TSH in early normal pregnancy are not indications of thyrotoxicosis and may not necessitate antithyroid drug treatment.
 ...
PMID:Morning sickness and thyroid function in normal pregnancy. 340 51

Hyperthyroidism was diagnosed in 131 cats during a 3 1/2-year period. The cats ranged in age from 6 to 20 years; there was no breed or sex predilection. The most frequent clinical signs included weight loss, polyphagia, increased activity, polydipsia, polyuria, and vomiting. Common serum biochemical abnormalities included high values for alkaline phosphatase activity (75%), lactate dehydrogenase activity (66%), aspartate transaminase activity (66%), and alanine transaminase activity (54%). Electrocardiographic changes included tachycardia (greater than or equal to 240 beats/min) and increased R-wave amplitude in lead II (greater than or equal to 0.9 mV) in 66% and 29% of the 131 cats, respectively. Thoracic radiography in 82 cats revealed cardiomegaly in 40 (49%) of these cats; 16 cats with congestive heart failure also had pulmonary edema or pleural effusion. In 5 cats with markedly increased fecal volume, mean 48-hour fecal fat content was significantly greater than normal, with daily fat excretion 2 to 15 times the upper limit of normal. Base-line serum thyroxine concentrations were increased above normal range in all cats, whereas triiodothyronine concentrations were increased in 127 (97%) of the 131 cats. In 11 cats tested, mean thyroxine concentration did not increase significantly after thyroid-stimulating hormone administration. Mean 24-hour percentage of thyroid radioiodine uptake in 32 hyperthyroid cats was significantly higher (39.1%) than normal (9.2%). Thyroid scans, performed on 126 cats, showed enlargement and increased radionuclide accumulation in 1 thyroid lobe in 36 (29%) and both lobes in 90 (71%) of the cats.
 ...
PMID:Feline hyperthyroidism: pretreatment clinical and laboratory evaluation of 131 cases. 687 10

Hyperthyroidism or increased thyroid function has been reported in many patients with trophoblastic tumors. In these cases, greatly increased human chorionic gonadotropin (hCG) levels and suppressed TSH levels suggest that hCG has thyrotropic activity. Recent investigations have clarified the structural homology not only in the hCG and TSH molecules but also in their receptors, and this homology suggests the basis for the reactivity of hCG with the TSH receptor. The clinical significance of the thyrotropic action of hCG is now also recognized in normal pregnancy and hyperemesis gravidarum. Highly purified hLH binds to recombinant hTSH receptor and is about 10 times as potent as purified hCG in increasing cAMP. The beta-subunits of hCG and hLH share 85% sequence identity in their first 114 amino acids but differ in the carboxy-terminal peptide because hCG beta contains a 31-amino acid extension (beta-CTP). A recombinant mutant hCG that lacks beta-CTP showed almost identical potency to LH on stimulation of recombinant hTSH receptor. If intact hCG were as potent as hLH in regard to its thyrotropic activity, most pregnant women would become thyrotoxic. One of the roles of the beta-CTP may be to prevent overt hyperthyroidism in the first trimester of pregnancy when a large amount of hCG is produced by the placenta. Nicked hCG preparations, obtained from patients with trophoblastic disease or by enzymatic digestion of intact hCG, showed approximately 1.5- to 2-fold stimulation of recombinant hTSH receptor compared with intact hCG. This suggests that the thyrotropic activity of hCG may be influenced by the metabolism of the hCG molecule itself. Deglycosylation and/or desialylation of hCG enhances its thyrotropic potency. Basic hCG isoforms with lower sialic acid content extracted from hydatidiform moles were more potent in activating adenylate cyclase, and showed high bioactivity/immunoactivity (B/I) ratio in CHO cells expressing human TSH receptors. This is consistent with the finding that the beta-CTP truncated hCG with higher thyrotropic potency is substantially deglycosylated and desialylated in the beta-subunit relative to intact hCG because all four O-linked glycosylation sites occur within the missing C-terminal extension. The desialylated hCG variant also interacts directly with recombinant hTSH receptors transfected into human thyroid cancer cells. There is thyroid-stimulating activity in sera of normal pregnant women, and this correlates with serum hCG levels. The thyroid gland of normal pregnant women may be stimulated by hCG to secrete slightly excessive quantities of T4 and induce a slight suppression of TSH, perhaps being about 1 mU/L less than nongravid levels, but not high enough to induce overt hyperthyroidism. Maternal thyroid glands may secrete more thyroid hormone during early pregnancy in response to the thyrotropic activity of hCG that overrides the normal operation of the hypothalamic-pituitary-thyroid feedback system. Biochemical hyperthyroidism associated with hyperemesis gravidarum has been attributed to hCG. In patients with hyperemesis gravidarum, thyrotropic in serum correlated with hCG immunoreactivity, and the severity of vomiting as indicated by clinical and biochemical parameters correlated with the degree of thyroid stimulation. To understand the thyrotropic action of hCG, it is necessary to know whether hCG activates the same domain of the TSH receptor as does TSH. The identification of the molecular structure of the hCG isoform with the highest thyrotropic potency will resolve the enigma of gestational thyrotoxicosis and the hyperthyroidism associated with trophoblastic disease and hCG-producing tumors.
Thyroid 1995 Oct
PMID:Thyrotropic action of human chorionic gonadotropin. 856 83

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.
 ...
PMID:Hyperthyroidism in pregnancy. 953 33

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.
Thyroid 1998 Sep
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.
Thyroid 1999 Jul
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.
Thyroid 1999 Jul
PMID:Fetal and neonatal hyperthyroidism. 1044 21


1 2 3 4 Next >>