Thyroid-stimulating hormone (TSH) suppression in differentiated thyroid carcinoma: combined treatment with triiodothyronine and thyroxine.
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Depression, Chemical↗
Biomedical subjects
R Sciuto
Publications and source records attributed to R Sciuto.
Thallium-201 scintigraphy and chemotherapeutic response in rhabdomyosarcoma.
Thallium-201 scintigraphy was used to evaluate chemotherapeutic response in a case of rhabdomyosarcoma treated with epirubicin. A scintigraphic semiquantitative index of tumor viability was correlated with MRI and clinical assessment. Both imaging studies were performed before therapy and after treatment involving a cumulative dose of 640 mg/m2 of epirubicin. A very good inverse correlation was observed between Tl-201 uptake and tumor necrosis evaluated by MRI, leading to the conclusion that sequential Tl-201 scintigraphy may have a role not only in delineating the extent of the tumor, but in objectively assessing tumor response to therapeutic interventions. The proposed scintigraphic method is much simpler to perform and less expensive than MRI-derived semiquantitative measurement of tumor necrosis.
Adult↗
TSH suppression by octreotide in differentiated thyroid carcinoma.
OBJECTIVE: This study evaluates the addition of octreotide and L-thyroxine to shorten the period of exposure to unduly elevated TSH levels in patients with differentiated thyroid carcinoma undergoing total body scan with 131I. DESIGN: Fourteen thyroidectomized patients were studied after total body scan and the restarting of different doses of thyroxine. After one year a second total body scan and a schedule of the same dose of thyroxine combined with octreotide were performed in each subject. PATIENTS: Patients were divided into four groups according to the treatment: seven patients received initially 100 micrograms of L-thyroxine (Group 1) and after 1 year 100 micrograms of L-thyroxine plus 300 micrograms of octreotide/day (Group 3); the other seven received initially 150 micrograms of L-thyroxine (Group 2) and then 150 micrograms of L-thyroxine plus 300 micrograms of octreotide/day (Group 4). MEASUREMENTS: Serum TSH, T3 and T4 were measured on the day of radioiodine administration (day 0) and after 14, 21, 30, 45, 60 and 90 days. RESULTS: Mean basal TSH levels were elevated in all four groups ranging from 104 to 91 mU/I without significant differences. The patterns of TSH inhibition were however different in the four groups studied. TSH remained very elevated for a long time in Group 1 patients: at day 90 the TSH value was still 2.1 +/- 1.2 mU/I (mean +/- SEM). Patients in Groups 2 and 3 showed a similar pattern: TSH was suppressed in 45 days. The most rapid TSH inhibition was observed in Group 4 patients with a mean decrease of 88% in 14 days and complete suppression in 30 days. CONCLUSIONS: TSH suppression by L-thyroxine is very slow and it can be significantly enhanced by combined octreotide administration. Combined therapy is safe and offers an alternative choice when high dosages of L-thyroxine are inappropriate or in conditions of advanced illness.
Adolescent↗
Delayed thyroid-stimulating hormone suppression by L-thyroxine in the management of differentiated thyroid carcinoma.
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Dose-Response Relationship, Drug↗
Somatostatin receptor imaging in small cell lung cancer using 111In-DTPA-octreotide: a preliminary study.
Small cell lung cancer is a common and aggressive disease. Combined multiagent chemotherapy and radiotherapy can improve short-term prognosis, but long-term prognosis remains dim. Somatostatin receptors have been identified on the cellular surface of subsets of this cancer and may be associated with less aggressive evolution. Moreover, medical therapy with somatostatin analogues holds promise for neoplastic growth control. Planar scintigraphy has been performed in 15 patients with histologically proven small cell lung cancer at 4 and 24 h after the intravenous (i.v.) injection of 185 MBq 111In-octreotide (Octreoscan, BYK-Gulden). No short-term adverse effects were recorded; tumour uptake of the radiopharmaceutical was observed in 13 patients at 4 h and in 12 patients at 24 h suggesting more extensive disease than apparent by computed tomography (CT). It is highly likely that the 24 h uptake reflects the presence of somatostatin receptors on the tumour. Previous chemotherapy does not seem to play a key role in tumour visualization. 111In-octreotide is a suitable radiopharmaceutical for in vivo evaluation of somatostatin receptor status of small cell lung cancer. Quantitative scintigraphic methods are needed to investigate nonspecific binding and receptor kinetics.
Aged↗
Somatostatin receptors in meningiomas: a scintigraphic study using 111In-DTPA-D-Phe-1-octreotide.
111In-octreotide (Octreoscan) planar scintigraphy was performed in 12 patients with suspected meningioma. The scan was positive in 10 patients with meningioma and negative in two patients with acoustic neurinoma assisting in the differential diagnosis. Good quality images were obtained as early as 2 h after injection and there was no increase in diagnostic quality at 24 h. No adverse effects were observed to radiopharmaceutical administration. The following conclusions are drawn: 111In-octreotide is a safe and fast test which can increase the specificity of traditional neuroimaging procedures.
Adolescent↗
Corticotropin-releasing hormone inhibition of paradoxical growth hormone response to thyrotropin-releasing hormone in insulin-dependent diabetics.
A paradoxical growth hormone (GH) response to thyrotropin-releasing hormone (TRH) has been observed in type 1 diabetic patients and was hypothetically attributed to a reduced hypothalamic somatostatin tone. We have previously reported that corticotropin-releasing hormone (CRH) inhibits GH response to growth hormone-releasing hormone (GHRH) in normal subjects, possibly by an increased release of somatostatin. To study the effect of CRH on anomalous GH response to TRH, we tested with TRH (200 micrograms intravenously [IV]) and CRH (100 micrograms IV) + TRH (200 micrograms IV) 13 patients (six males and seven women) affected by insulin-dependent diabetes mellitus. A paradoxical GH response to TRH was observed in seven of 13 patients, one man and six women. In these subjects, the simultaneous administration of CRH and TRH significantly reduced the GH response to TRH, as assessed by both the maximal GH mean peak +/- SE (2.18 +/- 0.67 v 9.2 +/- 1.26 micrograms/L, P less than 0.005) and the area under the curve (AUC) +/- SE (187 +/- 32 v 567 +/- 35 micrograms.min/L, P less than .001). CRH had no effect on TRH-induced thyroid-stimulating hormone (TSH) release. Our data demonstrate that the paradoxical GH response to TRH in patients with type 1 diabetes mellitus is blocked by CRH administration. This CRH action may be due to an enhanced somatostatin release. Our data also show that exogenous CRH has no effect on TSH response to TRH, thus suggesting the existence of separate pathways in the neuroregulation of GH and TSH secretion.
Adult↗
Effects of sex and age on pyridostigmine potentiation of growth hormone-releasing hormone-induced growth hormone release.
Previous studies have shown that pyridostigmine (PD) is capable of increasing the growth hormone (GH) response to GH-releasing hormone (GHRH) in young healthy subjects. In order to investigate the influence of age and sex on the PD potentiation of GHRH-induced GH release, we have studied the GH response to GHRH (50 micrograms i.v.) 1 h after oral administration of placebo or PD (60 mg) in 8 young healthy men (aged 19-28 years) and 8 age-matched young women (aged 18-25 years) during the follicular phase of the menstrual cycle, as well as in 8 postmenopausal women (aged 57-62 years) and 8 age-matched elderly men (aged 56-64 years). In the same subjects the effect of PD alone (60 mg p.o.) was also studied. Furthermore, in 6 postmenopausal women and 6 elderly men, the effect of a 30-mg PD oral dose on GH secretion and GH response to GHRH was evaluated with a similar protocol. The GH responses (mean +/- SE) to GHRH + placebo were similar in young men (peak 20.1 +/- 2 ng/ml, AUC 1,250 +/- 113 ng/ml/min) and women (peak 29.3 +/- 2.3 ng/ml, AUC 1,769 +/- 305 ng/ml/min). PD 60 mg was capable of significantly increasing the GH response to GHRH in young men (peak 43.5 +/- 5.1 ng/ml, AUC 3,734 +/- 472 ng/ml/min, p less than 0.005) but not in women (peak 39 +/- 2.3 ng/ml, AUC 2,479 +/- 205 ng/ml/min).(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Activation of cholinergic tone by pyridostigmine reverses the inhibitory effect of corticotropin-releasing hormone on the growth hormone-releasing hormone-induced growth hormone secretion.
Previous studies have shown that corticotropin-releasing hormone (CRH) is capable of inhibiting growth hormone (GH) secretion in response to GH-releasing hormone (GHRH). In an attempt to clarify the mechanism of the CRH action, we have studied the effect of enhanced cholinergic tone induced by pyridostigmine on the CRH inhibition of the GH response to GHRH in a group of six normal men and six normal women. All subjects presented a normal GH response to 50 micrograms i.v. GHRH administration (mean peak +/- SEM plasma GH levels 20 +/- 2.9 micrograms/l in men and 28.9 +/- 2.9 micrograms/l in women) with a further significant increase after pyridostigmine pretreatment (60 mg orally given 60 min before GHRH) in men (GH peaks 43.1 +/- 6.9 micrograms/l, p less than 0.005) but not in women (GH peaks 39.2 +/- 3.0 micrograms/l). In the same subjects, peripherally injected CRH (100 micrograms) significantly inhibited the GH response to GHRH (GH peaks 8.1 +/- 0.6 micrograms/l in men, p less than 0.005 and 9.9 +/- 0.7 micrograms/l in women, p less than 0.005). Pyridostigmine (60 mg) given orally at the same time of CRH administration (60 min before GHRH) reversed the CRH inhibition of GHRH-induced GH secretion (GH peaks 35.3 +/- 8.2 micrograms/l in men and 35 +/- 3.3 micrograms/l in women) with a response not significantly different to that seen in the pyridostigmine plus GHRH test. Our data confirm that pyridostigmine is capable of potentiating the GHRH-induced GH release in normal male but not female subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Evaluation of dopaminergic tone in postmenopausal women: effects of piribedil on anterior pituitary hormones.
In order to evaluate the relationships between gonadal steroid hormones and central dopaminergic (DA) tone, we have administered a "weak" dopamine agonist drug (piribedil) in 12 normal women, who were postmenopausal for at least 5 yrs, and we have studied the effects on anterior pituitary hormone release. We observed a decrease of plasma PRL levels and an increase of plasma GH values with all doses (40, 60, 100 mg p.o.) of the drug employed. No consistent changes in plasma FSH, LH, ACTH and TSH were observed and no side effects were reported. These results were greatly different from those previously described in premenopausal women in whom dose-related effects were observed and were similar to those observed in normal male subjects. The differences in the response to piribedil observed in women before and after the menopause could be due to a different sexual steroid environment.
Adrenocorticotropic Hormone↗
Sexual dimorphism of pyridostigmine potentiation of growth hormone (GH)-releasing hormone-induced GH release in humans.
Sex differences in the neuroregulation of GH secretion are not now known in humans. To investigate whether activation of cholinergic tone by pyridostigmine could cause a sex-related difference in the pituitary responsiveness to GH-releasing hormone (GHRH), we have studied the GH response to GHRH in 16 normal subjects (8 men and 8 women) tested after oral placebo or different doses of pyridostigmine (30, 60, and 120 mg). Each subject presented a normal response after iv administration of 50 micrograms GHRH and placebo. In men each dose of pyridostigmine induced a significant increase in the GH response to GHRH, as assessed by both the maximal GH peak and the area under GH curve. In women, on the contrary, the GH response to GHRH was not potentiated by pretreatment with pyridostigmine at any given dose. Only five female subjects were tested with 120 mg pyridostigmine because of the severe side-effects of the drug at this dosage. Our present data strongly suggest that in humans there is a sex-related difference in the neuroregulation of GH secretion and this is probably expressed through a different cholinergic tone.
Adult↗
Corticotropin-releasing hormone inhibition of growth hormone-releasing hormone-induced growth hormone release in man.
Recent studies in the rat have shown that intracerebroventricular administration of CRH inhibited spontaneous pulsatile GH secretion and prevented GH-releasing hormone (GHRH)-induced GH release. We have studied the effect of CRH on GHRH-induced GH release in man. In the first study, CRH was injected iv at three different doses (100, 50, or 25 micrograms) at 0800 h together with 50 micrograms GHRH in six men and six women. In a second study, 100 micrograms CRH were given iv at 0800 h, 1 h before the administration of 50 micrograms GHRH in five men and five women. Each subject demonstrated a normal GH response after the administration of 50 micrograms GHRH plus saline. All doses of CRH administered simultaneously with GHRH significantly inhibited GHRH-induced GH release in women [peak value +/- SE after GHRH plus saline, 28.9 +/- 2.9 micrograms/L; after GHRH plus 100 micrograms CRH, 9.9 +/- 0.7 micrograms/L (P less than 0.001); after GHRH plus 50 micrograms CRH, 8.7 +/- 0.8 micrograms/L (P less than 0.001); after GHRH plus 25 microgram CRH, 9.5 +/- 1.6 microgram/L (P less than 0.001]). In contrast, in men, while a dose of 100 micrograms CRH was capable of suppressing GHRH-induced GH secretion (peak value +/- SE, 8.1 +/- 0.6 vs. 20 +/- 2.9 micrograms/L; P less than 0.001), no inhibition was observed after 50- and 25-micrograms doses. When 100 micrograms CRH were injected 1 h before the administration of 50 micrograms GHRH, it strongly inhibited GHRH-induced GH secretion in both men (peak value +/- SE, 6.2 +/- 2.8 vs. 24.6 +/- 5.9 micrograms/L; P less than 0.02) and women (peak value +/- SE, 14.2 +/- 4.5 vs. 37.8 +/- 6.7 micrograms/L; P less than 0.005), and this inhibition lasted up to 2 h post-CRH administration. These results demonstrate that CRH is capable of inhibiting GHRH-induced GH release in both men and women. Furthermore, the findings suggest that a sexual dimorphism in the neuroregulation of GH secretion may be present in man. In view of the inhibitory action of CRH on GH secretion, simultaneous administration of CRH and GHRH for testing should be avoided in clinical practice.
Adult↗
[The role of autoimmune mechanisms in the hyperthyroidism-viral hepatitis syndrome: a possible noncausal association. A review of the literature and the authors' own cases].
Several patients with both Basedow-Graves' hyperthyroidism and viral hepatitis were observed and it was hypothesised that this association could be explained by the individual genetic pattern in which an immunological fragility conditioned a predisposition to autoimmune diseases. This paper reports on the cases observed, the patients' histocompatibility antigen profile and the experimental data found in the literature on autoimmune involvement in the two diseases, whose association may not be coincidental.
Antibody Formation↗
Evaluation of metabolic status in amiodarone-induced thyroid disorders: plasma coenzyme Q10 determination.
In previous works we have demonstrated that Coenzyme Q10 (CoQ10) levels have a significant inverse correlation with thyroid hormone concentration in patients with spontaneous hyper- or hypothyroidism. In order to verify whether this correlation is maintained in patients on long-term amiodarone therapy, in whom thyroid metabolism is altered by the iodine contained in the drug, we have studied 30 patients with thyroid dysfunction induced by chronic amiodarone treatment. We have distinguished four groups of patients: group A (n = 8): patients with true hyperthyroidism induced by drug administration; group B (n = 11): patients with mild hyperthyroid symptoms, but isolated thyroxine increase or dissociation between different indexes of thyroid function; group C (n = 5): patients with normal thyroid hormone levels, but increased TSH levels; group D (n = 6): patients who appeared really clinically euthyroid, with normal thyroid hormone levels and normal TSH response to TRH. In group A patients, plasma CoQ10 levels averaged 0.49 +/- 0.03 micrograms/ml, significantly lower than those in normal subjects and similar to those observed in spontaneous hyperthyroid patients. In group B patients, CoQ10 levels were in the normal range (0.88 +/- 0.10 microgram/ml). In group C patients, CoQ10 levels were lower than those in normal subjects and similar to those of group A patients (0.49 +/- 0.04 microgram/ml); they differed, in regards to CoQ10 values, in comparison with spontaneous primary hypothyroid patients, who had very high levels of plasma CoQ10. Finally, in group D patients, CoQ10 levels were in the normal range (0.77 +/- 0.04 microgram/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Naloxone inhibition of postprandial growth hormone releasing hormone-induced growth hormone release in obesity.
The effects of opiate receptor antagonist naloxone on growth hormone (GH) release after growth hormone-releasing hormone (GHRH) administration were investigated, before or after feeding, at 13.00 h, in 20 obese women and in 10 normal women. When GHRH was administered to obese women before a meal at lunch time, the mean peak plasma GH levels were very low, while plasma GH responses significantly increased after feeding. Naloxone, infused at a rate of 1.6 mg/h starting 1 h before GHRH administration (50 micrograms i.v. as a bolus), was capable of inhibiting GH release induced by administration of GHRH after feeding. On the contrary, naloxone did not induce significant variations on the fasting GHRH-induced GH release. In normal women, naloxone did not significantly modify the GH response to GHRH, both before and after lunch. The inhibitory effect of naloxone indicates that in obese women there is an increased opioid activity, which could represent an abnormal response of the gastrointestinal tract to food ingestion.
Adult↗
Corticotropin-releasing hormone inhibition of gonadotropin release and the effect of opioid blockade.
We studied the inhibitory effect of exogenous CRH on pulsatile gonadotropin secretion and the role of endogenous opioid peptides in this phenomenon in normal women. To do so, we infused human CRH (100 micrograms/h for 3 h) into 15 normal women during the midluteal phase of their menstrual cycle and studied its effect on both basal (10 women) and GnRH-stimulated (5 women) plasma gonadotropin levels. CRH infusion induced a significant decrease in plasma LH and FSH levels in all women. The decline in plasma LH (62%) was greater than that in FSH (36%). Plasma LH and FSH concentrations returned to basal levels within 30 min after the end of the CRH infusion. CRH infusion did not alter the gonadotropin response to GnRH. We also infused naloxone plus CRH in the 10 women who had received CRH alone during the midluteal phase of a different cycle. Addition of naloxone to CRH (5 women) reversed the LH and FSH inhibition when naloxone was started 1 h after the start of the CRH infusion. When naloxone was started 1 h before CRH infusion (5 women), plasma LH and FSH concentrations did not change. Plasma cortisol increased similarly during both the CRH and CRH plus naloxone infusions; the mean cortisol levels at the end of the CRH and CRH plus naloxone infusions were 497 +/- 40 (+/- SE) and 484 +/- 41 nmol/L, respectively, compared to 240 +/- 14 nmol/L after saline infusion (P less than 0.001). These results demonstrate that in normal women during the midluteal phase of the menstrual cycle, CRH inhibits the secretion of both LH and FSH. The CRH-induced inhibition of gonadotropin secretion is primarily mediated by endogenous opioid peptides, and this effect is not dependent on glucocorticoid levels. We suggest that the disruptive effect of stress on reproductive function in the women could be, at least in part, dependent on decreased gonadotropin secretion induced by elevated endogenous CRH levels.
Adult↗
[Electroanesthesia. Characteristics and function of a new apparatus for electronarocosis (preliminary note)].
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Electronarcosis↗
Clinical relevance of radionuclide angiography and antimyosin immunoscintigraphy for risk assessment in epirubicin cardiotoxicity.
BACKGROUND: Cardiotoxicity is the major limiting factor in anthracycline chemotherapy of advanced neoplastic disease. Epirubicin shows a more favorable therapeutic index than does doxorubicin, but it is still cardiotoxic. Limited data regarding epirubicin cardiotoxicity are available, and suggested guidelines for doxorubicin with left ventricular ejection fraction (LVEF) measurement may not be empirically useful for epirubicin therapy. This study evaluates the diagnostic role of antimyosin immunoscintigraphy for early identification of patients at risk for late pump dysfunction from cardiotoxicity induced by high-dose administration of epirubicin up to high cumulative dosages. METHODS AND RESULTS: Chemotherapy with epirubicin was administered to 36 patients with cancer at a dosing rate of 160 mg/m2 as a bolus injection every 21 days to a cumulative dosage of 960 mg/m2. Radionuclide angiography (LVEF) and antimyosin immunoscintigraphy with heart-lung ratio (HLR) measurements were performed before chemotherapy, at intermediate cumulative epirubicin dosages, at the end of treatment, and during the follow-up. LVEF decreased significantly at the end of the treatment and after therapy discontinuation. HLR values were significantly increased at intermediate epirubicin dosage levels and continued to increase to the end of the treatment but thereafter remained substantially unmodified for 3 to 6 months after therapy discontinuation. A value of HLR >1.85 at intermediate epirubicin dosage level showed a sensitivity of 95% and a specificity of 57% as a predictor of late LVEF impairment. CONCLUSIONS: LVEF appears more useful at high cumulative dosages and during follow-up to monitor late pump dysfunction, whereas HLR may be effective during the early phase of the therapy in determining which patients are at risk for development of late cardiac dysfunction.
Adolescent↗