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)

A particularly high hypercalcemia (141 mg/ml) was observed in a man with Graves' disease. An intense muscle asthenia, with lack of dynamism and vomiting which may cause dehydration, are the most suggestive signs of hypercalcemia. Bone biopsy and above all parathormone estimations permit one to eliminate associated hyperparathyroidism. The efficacy of mithramycin used alone, without any other hypocalcemic drug, was remarkable. The direct responsibility of thyrotoxicosis as a cause of the calcium disorder seems undoubted but the precise mechanism of the hypercalcemia remains unexplained.
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PMID:[Severe hypercalcemia during hyperthyroidism]. 19 81

In seven patients vomiting played an important part in the presentation of thyrotoxicosis. Vomiting does not always indicate severe thyroid disease, and the diagnosis in patients presenting with this symptom may be long delayed.
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PMID:Thyrotoxic vomiting. 97 94

A male patient with hyperemesis as a result of hyperthyroidism was presented. Investigations for causes were negative except for hyperthyroxinaemia. Treatment with antithyroid drug relieved the symptom. Hyperemesis associated with hyperthyroidism occurs predominantly in females. A likely emetic factor oestrogen. Hyperthyroidism could have potentiated this effect. Levels of oestrogens are raised in thyrotoxicosis. The hyperthyroidism, the raised oestrogens and a low emetic threshold conspired to hyperemesis in this patient, a situation not unlike hyperemesis gravidarum. Thyrotoxic vomiting once recognised is readily by antithyroid treatment.
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PMID:Thyrotoxic hyperemesis: a case report. 261 5

The prevalence of symptoms in thyrotoxicosis at the time of diagnosis has received little attention in studies of this condition. Vomiting, nausea, and abdominal pain have not been included as common presenting symptoms for thyrotoxicosis in standard textbooks of medicine and endocrinology. Some reports in the medical literature, however, indicate that these abdominal symptoms may be important manifestations of this condition. A retrospective chart review was undertaken to determine the prevalence of vomiting, nausea, and abdominal pain in patients hospitalized for thyrotoxicosis at Louisiana State University Medical Center, Shreveport, from 1982 through 1986. Of 25 thyrotoxic patients who had thyrotoxicosis diagnosed during or immediately prior to admission, 44% reported vomiting, 28% reported nausea, and 20% complained of abdominal pain. One or more of these abdominal symptoms were included as a chief complaint in 36% of cases reviewed. Further study of the clinical presentation of thyrotoxicosis in the outpatient setting is needed to improve the timeliness and cost effectiveness of the clinical diagnosis of this condition.
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PMID:Vomiting, nausea, and abdominal pain: unrecognized symptoms of thyrotoxicosis. 279 86

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.
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PMID:Morning sickness and thyroid function in normal pregnancy. 340 51

In three patients with thyrotoxicosis and with symptomatic hypercalcaemia antithyroid therapy restored the plasma calcium concentration to normal, though initially in one case intravenous and oral neutral phosphate solution were required to curtail intractable vomiting.Nine cases have been recorded in which the plasma calcium concentration returned to normal after antithyroid treatment was started; all but one became normocalcaemic within eight weeks. It is suggested that in hypercalcaemic thyrotoxicosis a second pathological condition should be considered only if the plasma calcium concentration fails to return to normal within eight weeks.
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PMID:Symptomatic hypercalcaemia in thyrotoxicosis. 542 53

Vomiting is a poorly recognized manifestation of hyperthyroidism. During pregnancy, this appearance can be indistinguishable from hyperemesis gravidarum. Two patients with intractable hyperemesis gravidarum were found to have hyperthyroidism. Their symptoms resolved when thyroid functions returned to normal. Given the ease of laboratory confirmation, excellent therapy, and the seriousness of delay in diagnosis, thyrotoxicosis should be considered in patients with unusual or severe hyperemesis gravidarum.
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PMID:Hyperthyroidism appearing as hyperemesis gravidarum. 668 67

A case of hyperemesis gravidarum at 9 weeks' gestation is described for which no cause could initially be found. Intravenous feeding was needed as a life preserving measure and following improvement on this regime the patient went into a thyrotoxic crisis which was successfully diagnosed and treated. The continuing pregnancy and its outcome is described. The need for practitioners to remember vomiting as a presenting sign of thyrotoxicosis is stressed.
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PMID:Hyperemesis gravidarum due to thyrotoxicosis. 678 10

The main objective of the present study was to present additional evidence of the potentially important thyrotropic role of hCG to regulate the maternal thyroid gland during normal pregnancy. Sequential determinations (first and last trimesters) of intact hCG, free alpha and beta-hCG subunits concentrations (using monoclonal IRMAs), and assessment of parameters of thyroid function and thyroid volume were carried out in 62 pregnant women who exhibited during the first trimester of gestation low TSH levels (< or = 0.20 mU/L), and compared to 276 pregnant women with normal TSH levels. The prevalence of having low serum TSH represented 18% of all pregnancies, with almost one half of cases who transiently had undetectable TSH levels. Lowering of TSH was associated with high hCG levels, and occurred primarily during the first trimester. About 10% of women with low TSH presented transient gestational thyrotoxicosis, frequently associated with vomiting. In comparison to control subjects, women with a suppressed serum TSH had significantly and markedly higher intact hCG and free beta-hCG subunit concentrations. The results suggest that TSH reduction may result from a relative oversecretion of both intact hCG and free beta-hCG subunits, compatible with three hypotheses: a) transient overexpression of the beta-hCG gene, leading to enhanced production of hCG heterodimer; b) increased glycosylation of circulating hCG, with in turn a prolonged half life; c) larger syncytiotrophoblast mass with increased hCG production.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum levels of intact human chorionic gonadotropin (HCG) and its free alpha and beta subunits, in relation to maternal thyroid stimulation during normal pregnancy. 751 22

We reported that gestational thyrotoxicosis is induced by thyroid-stimulating activity (TSA) of circulating hCG. However, the serum immunological hCG concentration did not correlate to TSA. To elucidate this, we examined the relation of carbohydrate moieties of hCG to bioactivity in 79 early pregnant women, divided into 4 groups: no emesis, mild emesis, hyperemesis, and gestational thyrotoxicosis with hyperemesis. Serum free T4 (FT4) and free T3 (FT3) levels were significantly higher and TSH was lower in the hyperemesis (FT4, 23.42 +/- 5.02 pmol/L; FT3, 6.26 +/- 1.80 pmol/L; TSH, 0.30 +/- 0.44 mU/L) and in gestational thyrotoxicosis (FT4, 48.65 +/- 14.80 pmol/L; FT3, 14.71 +/- 3.47 pmol/L; TSH, < 0.04 mU/L) groups than in the no emesis group (FT4, 16.99 +/- 2.48 pmol/L; FT3, 5.51 +/- 0.75 pmol/L; TSH, 1.37 +/- 1.23 mU/L; P < 0.0005). TSA was also significantly higher in the hyperemesis (566 +/- 187%) and gestational thyrotoxicosis (832 +/- 168%) groups than in the no emesis group (321 +/- 135%). We found no significant difference among serum hCG concentrations measured by immunoassay in the four groups. To characterize the carbohydrate chains, serum hCG was fractionated by Concanavalin-A and ricin lectin affinity chromatography. The fraction firmly bound to Con-canavalin-A, which contains hCG with high mannose and hybrid-type carbohydrate chains, was significantly higher in the hyperemesis group (91.07 +/- 2.06%; n = 15) than in the no emesis group (89.61 +/- 2.38%; n = 24; P < 0.04). The fraction firmly bound to ricin column, which contains hCG with asialo-carbohydrate chains, was significantly increased in the gestational thyrotoxicosis group (3.44 +/- 1.70%; n = 5) compared with that in the no emesis group (1.77 +/- 0.49%; n = 24; P < 0.03). Serum FT4 positively correlated to the hCG fraction firmly bound to ricin column (r = 0.61; P < 0.001). We conclude that thyrotoxicosis with hyperemesis may be caused by circulating asialo-hCG with higher thyrotropic bioactivity.
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PMID:Pathogenic role of asialo human chorionic gonadotropin in gestational thyrotoxicosis. 785 89


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