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)

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.
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PMID:Feline hyperthyroidism: pretreatment clinical and laboratory evaluation of 131 cases. 687 10

Untreated hyperthyroidism during pregnancy is associated with increased maternal and perinatal morbidity. Some features of this disease simulate preeclampsia, which may encourage delivery of the fetus. We report a case of poorly controlled hyperthyroidism associated with generalized seizures, where patient management was directed at a diagnosis of preeclampsia-eclampsia. Although the presence of eclampsia and marked hyperthyroidism is very rare, this case illustrates the importance of aggressive medical management of hyperthyroidism. A 17-year-old gravida was diagnosed with hyperthyroidism at 15 weeks' gestation. At 26 weeks' gestation, she was admitted to the hospital after noting edema of the upper and lower extremities, nausea, vomiting, shortness of breath, and a cough. At admission, she was hypertensive, tachycardic, and dyspneic. The patient was believed to have preeclampsia with pulmonary edema complicated by hyperthyroidism. We initiated magnesium sulfate therapy and administered several bolus doses of hydralazine, with little effect on blood pressure. Oliguria was noted, and a pulmonary artery catheter was inserted. Hours later, generalized seizure activity occurred, and a decision was made for abdominal delivery. Postoperatively, cardiovascular function stabilized. On postoperative day 3, we received the results of the thyroid function tests obtained at admission, which suggested a markedly hyperthyroid condition. Untreated or poorly treated hyperthyroidism may present a clinical picture similar to preeclampsia. In our case, both disease processes coexisted in their severest forms. It is possible, although completely unproven, that a relationship exists between poorly controlled hyperthyroidism and preeclampsia-eclampsia. More importantly, accurate diagnosis of hyperthyroidism should lead to prompt medical or surgical management, thereby decreasing maternal and perinatal morbidity.
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PMID:Hyperthyroidism and seizures during pregnancy. 761 94

We report two cases of hyperemesis gravidarum with hyperthyroidism and jaundice. The cessation of vomiting associated with supportive care was followed by complete recovery in 5 weeks. Hyperthyroidism occurs in 60% of hyperemesis gravidarum, but jaundice is uncommon. The association of jaundice and hyperthyroidism suggests that hyperthyroidism is a possible factor of cholestasis in patients with hyperemesis gravidarum.
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PMID:[Hyperthyroidism: a possible factor of cholestasis associated with hyperemesis gravidarum of prolonged evolution]. 795 55

A 24-year-old man with anorexia, repeated bouts of vomiting, and wasting was found to have florid thyrotoxicosis and hypercalcaemia. Pamidronate promptly reduced the serum calcium concentration to normal, and simultaneously abated the abdominal symptoms, which did not recur in spite of continuing severe hyperthyroidism, which was eventually controlled by radioactive iodine ablation of thyroid activity.
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PMID:Abdominal symptoms, hypercalcaemia and apathetic hyperthyroidism: treatment with pamidronate. 774 97

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.
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PMID:Thyrotropic action of human chorionic gonadotropin. 856 83

At the Institutes of Gynecology and Obstetrics of the University of Rome (La Sapienza), Italy, serum levels of free thyroxine (FT4), FT3, thyroid stimulating hormone (TSH), and the beta subunit of human chorionic gonadotropin (hCG-beta) were compared before and 7-10 days after induced abortion in 19 normal women in their first trimester of pregnancy. The women were divided into those with nausea and vomiting (7) and those without these symptoms (12). The aim was to distinguish slight transient hyperthyroidism associated with nausea and vomiting in normal early pregnancy with pre-existing thyrotoxicosis or hyperemesis gravidarum. In both groups of women, serum hCG-beta levels were significantly lower 7-10 days after the induced abortion than before (p 0.01) while serum TSH levels were significantly higher (p 0.02). The serum levels of FT4 were higher before than after abortion in both groups of women, but were significantly so in women with nausea and vomiting (p 0.001). After induced abortion, serum levels of FT4 and TSH returned to normal levels. Earlier research found that hCG peaks at 10-13 weeks gestation and decreases to a stable level by 20 weeks gestation and that hCG is associated with thyroid hormone levels. This study's findings support those of earlier research since women in the nausea and vomiting group had higher levels of FT4 and hCG-beta and lower levels of TSH before the induced abortion than after it. Perhaps, hCG physiologically activates the thyroid gland in early pregnancy, which may in turn induce vomiting during early pregnancy.
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PMID:Nausea, vomiting and thyroid function before and after induced abortion in normal pregnancy. 865 28

A 50-year-old woman was transported to a hospital complaining of marked general malaise and epigastralgia with diarrhea and vomiting. Her electrocardiogram showed sinus arrest with a duration of nearly 8 sec. Atrial pacing with an external pacemaker improved her symptoms promptly. Following transfer to our hospital 3 days later, bradyarrhythmia was not detected despite the removal of the external pacemaker. Transient atrial fibrillation was found in our hospital, and she was diagnosed as hyperthyroidism based on findings of finger tremor, exophthalmos, diffuse goiter and an abnormally high level of thyroid hormone. On cardiac catheterization, left ventriculography showed anterior wall hypokinesis and mild mitral regurgitation. Coronary arteriography showed the absence of organic stenosis. Right ventricular endomyocardial biopsy showed myocardial hypertrophy and partial disarray, but no findings of myocarditis. Electrophysiological study showed the normal upper range of AH-time (120 msec) and HV-time (50 msec), and prolongation of corrected sinus recovery time (CSRT, 955 msec). After a euthyroid state was successively induced for about 10 days by methylmercaptoimidazole therapy, AH-time, HV-time and CSRT were shortened to 85, 35 and 290 msec respectively. Her complaints and sick sinus syndrome disappeared after the treatment of hyperthyroidism without a pacemaker.
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PMID:Hyperthyroidism complicated with sick sinus syndrome. 878 74

A twelve year old boy presented with a sudden onset of recurrent nausea and vomiting. During the past six weeks he had a weight loss of 13 kg. While he was in the hospital, persistent tachycardia and a slightly elevated blood pressure were noted. The gastroenterologic, cardiologic and neuropediatric examinations were normal. To exclude the differential diagnosis of hyperthyroidism, thyroid hormones were checked. They showed clearly elevated levels of tri-iodothyronine and thyroxine, while thyrotropin was suppressed. The boy did not have a goiter. Under thyrostatic therapy his clinical condition improved quickly. Among our 20 patients with hyperthyroidism he was the only one whose main symptom was severe vomiting.
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PMID:[Vomiting as main symptom: unusual presentation of a hyperthyroidism in a 12-year-old boy]. 924 23

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 both common in early pregnancy. Most cases are mild and do not require treatment. However, persistent vomiting and severe nausea can progress to hyperemesis if the woman is unable to maintain adequate hydration, and fluid and electrolyte as well as nutritional status are jeopardised. Hyperemesis gravidarum is a diagnosis of exclusion, characterised by prolonged and severe nausea and vomiting, dehydration, ketosis and bodyweight loss. Investigation may show hyponatraemia, hypokalaemia, a low serum urea level, metabolic hypochloraemic alkalosis and ketonuria. The haematocrit is raised and the specific gravity of the urine is increased. There may be associated liver function test abnormalities and abnormal thyroid function tests, with biochemical thyrotoxicosis with raised free thyroxine levels and/or suppressed thyroid-stimulating hormone levels. The pathophysiology of hyperemesis is poorly understood. Various hormonal, mechanical and psychological factors have been implicated. Studies have demonstrated a direct relationship between the severity of hyperemesis, the degree of biochemical hyperthyroidism and the levels of human chorionic gonadotrophin (hCG). Management of hyperemesis should include hospitalisation, intravenous fluid and electrolyte replacement, thiamine (vitamin B1) supplementation, use of conventional antiemetics and psychological support. Most patients improve spontaneously with the help of the above measures without long term sequelae. Conventionally, antiemetics are not usually prescribed, especially before 12 weeks gestation, except for women with hyperemesis. This reluctance relates to fears which are often unfounded concerning the teratogenic effects of antiemetics. Severe hyperemesis, refractory to conventional management with intravenous fluids and antiemetics is a rare, miserable and disabling condition, associated with multiple hospital admissions, time away from work and the family, and psychological morbidity. If inadequately or inappropriately treated, it may cause Wernicke's encephalopathy, central pontine myelinolysis and death. In extreme cases, women may request, or their obstetricians recommend, termination of the pregnancy. There are uncontrolled data supporting a beneficial effect of corticosteroids in these women, and a randomised placebo-controlled trial is currently in progress.
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PMID:Treatment of nausea and vomiting in pregnancy. When should it be treated and what can be safely taken? 970 51


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