Thyroid volume measured by ultrasonography and CT.

PURPOSE: To evaluate measurements of thyroid volume by two different US methods and CT in a blinded design. MATERIAL AND METHODS: Four observers evaluated 27 patients. Observer 1 used US and calculated thyroid volume based on recordings of cross-sections through the gland. Observer 2 used US and calculated the volume of each lobe as a rotation ellipsoid. Observers A and B used CT images and calculated thyroid volume based on recordings of cross-sections through the gland. All measurements were made twice. RESULTS: The median thyroid volume was 81 ml (range 7-470 ml) evaluated by CT. All three methods had fair reproducibility. When correlating the two different methods using US, an r of 0.837 was found. When correlating data from patients without intrathoracic goitre evaluated by US (Observer 1) and CT, r = 0.945. The method based on a rotation ellipsoid systematically produced smaller thyroid volumes than those of the cross-sectional method. Evaluation by US systematically produced smaller thyroid volumes than CT. CONCLUSION: Calculation of thyroid volume based on US recordings of cross-sectional areas is a reproducible method in patients without substernal goitre extension. The US method calculating thyroid volume as a rotation ellipsoid is less reproducible, especially in large goitres. Measurement of thyroid volume using CT should be preferred in goitres with substernal extension.

Stress-induced release of anterior pituitary hormones: effect of H3 receptor-mediated inhibition of histaminergic activity or posterior hypothalamic lesion.

The effect of stress- or lipopolysaccharide (LPS) endotoxin-induced release of ACTH, beta-endorphin (beta-END) and prolactin (PRL) was investigated in two groups of conscious male rats: (1) Rats pretreated with different H3 receptor agonists, which inhibit neuronal histamine (HA) synthesis and release, and (2) rats with bilateral posterior hypothalamic lesion, which destroys the histaminergic perikarya exclusively localized in the mammillary nuclei. The H3 receptor agonists R(alpha)methyl-HA, BP 2-94 or imetit injected intraperitoneally (ip) had no effect on basal secretion of ACTH or PRL but inhibited the ACTH and PRL responses to restraint stress and the ACTH response to LPS endotoxin. LPS had no effect on PRL secretion. The inhibitory effect of the agonists was prevented by prior ip administration of the H3 receptor antagonist thioperamide. Bilateral lesion of the posterior hypothalamus inhibited the ACTH, beta-END and PRL responses to restraint stress, ether stress and LPS endotoxin, whereas sham operation had no effect compared to nonoperated control rats. In addition, posterior hypothalamic lesion inhibited the PRL response but not the ACTH and beta-END responses to activation of serotonergic neurons induced by ip administration of the 5-HT precusor 5-hydroxytryptophan in combination with the 5-HT re-uptake inhibitor fluoxetine. Thus, serotonergic pathways were not damaged by the lesions. The present results support our previous findings that inhibition of neuronal HA synthesis by alpha-fluoromethylhistidine as well as blockade of H1 or H2 receptors inhibit the ACTH, beta-END and PRL responses to stress and LPS endotoxin and further substantiate an important role of histaminergic neurons in the mediation of the stress-induced release of pituitary stress hormones. Furthermore, in accordance with our previous findings, the lesion experiments indicated the existence of an interaction between the histaminergic and serotonergic system in regulation of the stress- and LPS-induced PRL release.

Iohexol: effects on uptake of radioactive iodine in the thyroid and on thyroid function.

RATIONALE AND OBJECTIVES: The authors attempted to determine whether the use of nonionic contrast media causes uptake of iodine by the thyroid to be blocked and whether use of these agents could cause iodine-induced hyperthyroidism. MATERIALS AND METHODS: Twenty-eight persons, including 22 with thyroid disease, were included in the study. Subjects underwent computed tomography (CT) of the thyroid after injection of 100 mL of iohexol. Thyroid function variables were measured before CT scanning and 1 week and 1 month later. In 16 subjects, uptake of iodine-131 by the thyroid was measured before and 1 week after CT. RESULTS: I-131 uptake was reduced to 53.4% at 1 week after the injection of iohexol but became normal within a few weeks (followed up in one patient). An accelerated escape of I-131 from the thyroid was seen during the 1st days after the iohexol administration. Eight of 22 patients with an underlying thyroid disease had a temporary change in thyroid function. In four patients, the serum thyrotropin level was increased 1 week after the iohexol administration. In four other patients, temporary hyperthyroidism developed during the following months. CONCLUSION: Iohexol can be used in patients with an underlying thyroid disease, but close monitoring in the following months is necessary.

Influence of compensated radioiodine therapy on thyroid volume and incidence of hypothyroidism in Graves' disease.

OBJECTIVES: To investigate the long-term effect of radioactive iodine (131I) on thyroid function and size in patients with Graves' disease. SETTING: Out-patient clinic in Herlev Hospital. SUBJECTS: One hundred and seventeen consecutive patients (104 women) with Graves' disease selected for 131I treatment and followed for a minimum of 12 months (range 1-10 years, median 5 years). INTERVENTIONS: 131I dose was calculated based on thyroid volume and 24-h 131I uptake. MAIN OUTCOME MEASURES: Standard thyroid function variables and ultrasonically determined thyroid volume before treatment as well as 0.75, 1.5, 3, 6 and 12 months after treatment, and then once a year were investigated. RESULTS: Seventy-eight patients were cured by one 131I dose and 30 by two doses, while the remaining nine patients received additional doses (range one to five doses, median one dose). Within one year, 25% developed hypothyroidism, and hereafter, hypothyroidism developed at a constant rate of 3% per year independent of antithyroid pretreatment. The cumulative 10-year risk of hypothyroidism was 60%. Initial median thyroid volume was 33 mL (range 9-106 mL). At 12 months after the last 131I dose, median thyroid volume was reduced to 14 mL (range 6-36 mL) (P < 0.00001). The median reduction being 58% (range 0-80%), hereafter no further reduction occurred. A significant reduction in thyroid volume was also noted in patients needing subsequent 131I doses and in those developing hypothyroidism within the first year. CONCLUSIONS: 131I normalizes thyroid volume in patients with Graves' disease. Hypothyroidism seems an inevitable end result of this treatment. The present study suggests that it will be impossible to modify 131I therapy in a way to achieve both early control of hyperthyroidism and a low incidence of hypothyroidism.

[Long-term effect of 131I therapy of multinodular non-toxic goiter]. / Langtidseffekten af 131I-behandling ved multinodøs atoksisk struma.

The aim of this study was to investigate the long term effect of 131I treatment on thyroid function and size in patients with non-toxic multinodular goitre. The subjects were 69 consecutive patients with multinodular non-toxic goitre selected for 131I treatment and followed for a minimum of 12 months. Outcome measures were standard thyroid function variables and ultrasonically determined thyroid volume before and after treatment. Fifty-nine patients were treated with a single dose of 131I, 12 with two doses, and one with four doses. In 45 patients treated with one dose who remained euthyroid the median thyroid volume was reduced from 73 (interquartile range 50-106) ml to 29 (interquartile range 23-48) ml at 24 months. The median reduction was 40 (22-48) ml, half of which occurred within three months. Patients treated with two doses as well as those developing hypo- or hyper-thyroidism also had a significant reduction in thyroid volume. Eleven patients developed hypothyroidism (cumulative five year risk 22%). Side effects were few. In conclusion we find that 131I treatment of multinodular non-toxic goitre is an attractive alternative to surgery.

Radioiodine treatment of multinodular non-toxic goitre.

OBJECTIVE: To investigate the long term effect of radioactive iodine on thyroid function and size in patients with non-toxic multinodular goitre. DESIGN: Consecutive patients with multinodular non-toxic goitre selected for radioactive iodine treatment and followed for a minimum of 12 months (median 48 months) after an intended dose of 3.7 MBq/g thyroid tissue corrected to a 100% uptake of iodine-131 in 24 hours. PATIENTS: 69 patients with a growing multinodular non-toxic goitre causing local compression symptoms or cosmetic inconveniences. The treatment was chosen because of a high operative risk, previous thyroidectomy, or refusal to be operated on. MAIN OUTCOME MEASUREMENTS: Standard thyroid function variables and ultrasonically determined thyroid volume before treatment as well as 1, 2, 3, 6, and 12 months after treatment and then once a year. RESULTS: 56 patients were treated with a single dose of 131I, 12 with two doses, and one with four doses. In 45 patients treated with one dose and remaining euthyroid the median thyroid volume was reduced from 73 (interquartile range 50-106) ml to 29 (23-48) ml at 24 months in the 39 patients in whom this was measured during follow up. The median reduction was 40 (22-48) ml (60% reduction, p < 0.0001), half of which occurred within three months. Patients treated with two doses as well as those developing hypothyroidism and hyperthyroidism had a significant reduction in thyroid volume. Eleven patients developed hypothyroidism (cumulative five year risk 22%, 95% confidence interval 4.8% to 38.4%). Side effects were few: three cases of hyperthyroidism and two cases of radiation thyroiditis. Only one patient was dissatisfied with the result; she was referred for operation six months after treatment. CONCLUSIONS: A substantial reduction in thyroid volume accompanied by a low incidence of hypothyroidism and few side effects makes the use of radioactive iodine an attractive alternative to surgery in selected cases of non-toxic multinodular goitre.

Insulin/hypoglycemia-induced adrenocorticotropin and beta-endorphin release: involvement of hypothalamic histaminergic neurons.

We have previously found that histamine (HA) is involved in the mediation of restraint- and ether stress-induced release of the POMC-derived peptides ACTH and beta-endorphin (beta-END). In the present study we investigated the possible involvement of hypothalamic histaminergic neurons in the mediation of insulin/hypoglycemia-induced release of ACTH and beta-END in conscious male rats. To do so, hypoglycemia stress was performed during 1) inhibition of HA synthesis, 2) activation of inhibitory presynaptic HA H3-auto-receptors, or 3) blockade of postsynaptic HA H1- or H2-receptors. Hypoglycemia (plasma glucose, 2.2 +/- 0.3 nmol) induced by insulin (3 IU/kg, ip) caused a 3- to 5-fold increase in the plasma concentrations of ACTH and beta-END. A negative exponential correlation was found between the plasma glucose concentration and the ACTH and beta-END levels. Pretreatment of the animals with the HA synthesis inhibitor alpha-fluoromethylhistidine (1.0 mumol) intracerebroventricularly (icv) in a lateral ventricle, inhibited the ACTH and beta-END responses to insulin/hypoglycemia by 60%. When administered ip (100 mumol/kg), the synthesis inhibitor decreased the beta-END response 50%, but did not affect ACTH secretion significantly. Pretreatment of the rats with the H3-receptor agonist R(alpha)methylhistamine (50 mumol/kg, ip, twice) inhibited the secretory responses of ACTH and beta-END to insulin/hypoglycemia by 60-80%. This inhibitory effect of R(alpha)methylhistamine was reversed by prior administration of the specific H3-receptor antagonist thioperamide. Administration of the H1-antagonists mepyramine and cetirizine dose-dependently inhibited the ACTH and beta-END responses to insulin/hypoglycemia, with the highest dose (mepyramine, 350 nmol, icv; cetirizine, 40 mumol/kg, ip) inhibiting the response by 80-100%. The H1-antagonist SKF-93944 (226 nmol, icv) inhibited the ACTH response, but had no effect on the beta-END response. Administration of the H2-antagonists cimetidine (400 nmol, icv) and ranitidine (400 nmol, icv) inhibited the ACTH and beta-END responses to insulin/hypoglycemia by 50-80%. We conclude that histaminergic neurons are involved in the mediation of the insulin/hypoglycemia-induced release of ACTH and beta-END and that the effect is mediated via activation of primarily postsynaptic H1-receptors and, to a lesser extent, H2-receptors.

Responses of anterior pituitary hormones and hypothalamic histamine to blockade of histamine synthesis and to selective activation or inactivation of presynaptic histamine H3 receptors in stressed rats.

The stress-induced release of anterior pituitary hormones and changes in hypothalamic content of histamine (HA) and its metabolite tele-methylHA (t-meHA) were studied in male rats during inhibition of HA synthesis or activation or blockade of HA H3 receptors. Pretreatment with the HA synthesis inhibitor alpha-fluoromethylhistidine (alpha-FMH; 200 micrograms intracerebroventricularly (icv) at -120 min) or the specific H3 receptor agonist R(alpha)methylhistamine (RmHA; 10 mg/kg intraperitoneally (ip) at -180 and -60 min) inhibited by 30-80% the responses of prolactin (PRL), corticotropin (ACTH) and beta-endorphin (beta-END) immunoreactivity to 1, 2.5 or 5 min of restraint stress (p < 0.05-0.01), but had no effect on basal secretion of the hormones. The inhibitory effect of the H3 receptor agonist RmHA (10 mg/kg x 2) on the hormone response to 5 min of restraint stress was prevented by simultaneous ip administration of the H3 receptor antagonist thioperamide. alpha-FMH reduced the hypothalamic content of HA 60% and that of t-meHA 30%, while RmHA had no effect on the HA content. Restraint stress for 5 min did not affect the HA and t-meHA contents, which may be due to the short duration of stress exposure. Pretreatment with the H3 receptor antagonist thioperamide (5 or 10 mg/kg ip at -120 min) had no effect on basal or restraint stress-induced release of PRL, ACTH or beta-END, although the compound increased the hypothalamic content of t-meHA 2-fold.(ABSTRACT TRUNCATED AT 250 WORDS)