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Biomedical subjects

E Roti

Publications and source records attributed to E Roti.

17 recordsLinked to original sources
PubMed1992

Subclinical hypothyroidism, overt thyrotoxicosis and subclinical hypothyroidism: the subsequent phases of thyroid function in a patient chronically treated with amiodarone.

In a patient chronically treated with amiodarone, subclinical iodine-induced hypothyroidism occurred as a result of excess iodine released from the amiodarone molecule. The patient was maintained on amiodarone and developed thyrotoxicosis as a result of a destructive process into the thyroid follicles. Amiodarone was withdrawn and methylprednisolone and methimazole treatment was started with resolution of the thyrotoxic phase. Months later, off therapy, the patient developed subclinical hypothyroidism. This is the first description of hypo- and hyperthyroidism in the same patient caused by amiodarone therapy. This unusual observation suggests that patients treated with amiodarone are at risk to develop hyperthyroidism even if they show laboratory findings consistent with hypothyroidism.

Amiodarone↗
PubMed1992

Sinus node function in hyperthyroid patients.

We have studied the electrophysiology of the sinus node and the role of the autonomic nervous system on sinus node function in 8 thyrotoxic patients of both sexes, 37.5 +/- 4.3 (mean +/- SE) yr old. The resting heart rate (RHR), the sino-atrial conduction time (SACT), and the sinus node recovery time (SNRT) were measured in the untreated condition (basal), after sympathetic blockade with propranolol 0.2 mg/kg body weight (BW) i.v. infusion, and after complete autonomic blockade with the additional administration of atropine 0.04 mg/kg BW i.v. bolus. 1) In the thyrotoxic patients the RHR was higher [117 +/- 6 beats per min (bpm)] than in 20 normal subjects (73 +/- 1 bpm, P less than 0.001), whereas the SACT and SNRT values were not different. 2) After sympathetic blockade with propranolol, the RHR decrement and SACT increase were greater in the hyperthyroid patients than in normal subjects, whereas there was no difference in SNRT values between the two groups. 3) In the thyrotoxic patients the complete autonomic blockade reestablished the electrophysiological parameters to values similar to those observed in basal condition. In conclusion, in thyrotoxic patients the intrinsic activity of the sinus node is increased. It appears that this is a direct consequence of thyroid hormone excess, rather than an effect of extrinsic influences exerted by the autonomic nervous system on sinus node activity.

Adolescent↗
PubMed1992

Iodine-induced subclinical hypothyroidism in euthyroid subjects with a previous episode of amiodarone-induced thyrotoxicosis.

Amiodarone-induced thyrotoxicosis (AIT) occurs most frequently in patients with underlying thyroid disease and is generally believed to be due to the iodine contamination of amiodarone and iodine released by the metabolism of the drug. We and others have suggested that the thyrotoxicosis may also be secondary to amiodarone-induced thyroiditis. To further determine the etiology of AIT, we administered large doses of iodides [10 drops saturated solution of potassium iodide (SSKI) daily] to 10 euthyroid patients long after an episode of AIT believed to be due at least in part to amiodarone-induced thyroiditis. Six of these 10 patients had an abnormal iodide-perchlorate discharge test before SSKI administration, indicating a subtle defect in the thyroidal organification of iodide. During SSKI administration, 6 patients developed marked iodine-induced basal and/or TRH-stimulated serum TSH elevations, 2 had suppressed basal and TRH-stimulated TSH values, and 2 had normal TSH responses compared to SSKI-treated euthyroid subjects with no history of amiodarone ingestion or thyroid disease. Serum T4 and T3 concentrations remained normal and unchanged during SSKI administration in both the AIT patients and control subjects. These results strongly suggest that excess iodine may not be the cause of the hyperthyroidism associated with amiodarone therapy, especially in those patients with probable amiodarone-induced thyroiditis. Furthermore, like patients with a previous history of subacute thyroiditis and postpartum thyroiditis, the present results suggest that some patients with a previous history of AIT may be at risk to develop hypothyroidism when given excess iodine.

Amiodarone↗
PubMed1992

Prevalence of anti-thyroid peroxidase antibodies in serum in the elderly: comparison with other tests for anti-thyroid antibodies.

Autoimmune thyroid disease, especially chronic thyroiditis, is prevalent in elderly women and is probably the major cause of hypothyroidism in this population. The reported prevalence of chronic thyroiditis is variable, depending on the area of residence and the method(s) used to detect the presence of anti-thyroid antibodies. The recent finding that thyroid peroxidase (TPO) is the antigen for the thyroid anti-microsomal antibody (AbM) has resulted in the development of sensitive radioimmunoassays (RIA) to detect the presence of AbTPO. We have determined the prevalence of AbTPO (by RIA) in sera from 342 elderly subjects, 248 women and 94 men (mean age 80 years) residing in Reggio Emilia, Italy, and compared the results with other methods for detecting anti-thyroid antibodies, including anti-thyroglobulin (AbTg) and AbM measured by passive hemagglutination (PH) of tanned erythrocytes, and AbM measured by RIA. The prevalence of positive AbTPO was 2.3% in the men and 10.2% in the women, only slightly higher than the prevalence of AbM. However, in the antibody-positive sera, the mean value for AbTPO was approximately 20-fold greater than the upper limit of the normal range, whereas the mean value for AbM was only threefold greater. The prevalence of positive titers for AbM and AbTg measured by PH was far lower, 1.2% and 3.2%, respectively, and those sera weakly positive for AbM and AbTg by PH were strongly positive for AbTPO by RIA. AbTPO RIA may be more useful than AbM and AbTg hemagglutination and AbM RIA for detecting the presence of autoimmune thyroid disease.

Aged↗
PubMed1991

Postpartum thyroid dysfunction in an Italian population residing in an area of mild iodine deficiency.

We have evaluated the occurrence of postpartum thyroid dysfunction (PPTD) in a group of 372 women residing in area of mild iodine deficiency. Thyroid function and autoimmune status were evaluated by means serum T4, T3, TSH measurement and detecting the presence of positive antithyroglobulin antibodies (AbTg), antimicrosomal antibodies (AbM) and thyroid-peroxidase antibodies (AbTPO) titers in women at parturition, at 1, 3, 6 and 12 months postpartum. New onset transient hypothyroidism occurred in 6.4% of women whereas transient thyrotoxicosis in only 1.8% of women. Transient hypothyroidism was not preceded by thyrotoxicosis as indicated by thyroid function tests and serum Tg concentrations. At parturition, the positivity of AbM and AbTPO titers and the presence of goiter appeared to be a risk factors for the development of PPTD.

Antibodies↗
PubMed1991

Thyroid function evaluation by different commercially available free thyroid hormone measurement kits in term pregnant women and their newborns.

Evaluation of thyroid status by measurement of free thyroid hormone concentrations seems particularly helpful in conditions with altered serum binding proteins. In pregnancy, a condition of increased thyroxine binding globulin, serum free thyroxine (FT4) and free triiodothyronine (FT3) concentrations have been reported to be normal, increased or decreased. In the present study we have measured serum total and free thyroid hormone concentrations in pregnant women, their newborns and nonpregnant women. Serum FT4 and FT3 concentrations have been measured with 10 different commercially available kits and the results obtained have been compared. Serum total thyroid hormone concentrations in pregnant women were significantly higher than in their newborns and in nonpregnant women. Maternal serum FT4 concentrations measured with the different kits were always significantly lower than values in nonpregnant women. Furthermore, with one kit, the mean maternal serum FT4 concentration was below the normal range and with many kits, a large number of maternal serum samples had serum FT4 concentrations below the normal range. With all kits, except two, neonatal serum FT4 concentrations were higher than values in their respective mothers and, in general, lower than values in nonpregnant women. Serum FT3 concentrations in nonpregnant women were in the normal range, except with one kit, in which the mean serum FT3 concentration was below the normal range. Serum FT3 concentrations in newborns resulted markedly lower than in parturient and in non pregnant women. With almost all kits, serum FT3 values were below the normal range in many maternal samples. With one kit, maternal serum FT3 concentrations resulted higher than in nonpregnant women, whereas with the other kits serum FT3 concentrations were lower.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Impaired intrathyroidal iodine organification and iodine-induced hypothyroidism in euthyroid women with a previous episode of postpartum thyroiditis.

Postpartum thyroiditis (PPT) is common and occurs in 1.7 to 16.7% of pregnant women, depending upon the study population. Most of these women develop transient hypothyroidism and thyroid function usually returns to normal. We have studied 11 euthyroid women with a previous history of PPT to determine the incidence of subtle defects in thyroid function measured by iodide-perchlorate (I-ClO4) discharge tests and TRH tests and to determine whether these women would develop iodide-induced hypothyroidism. Seven (64%) had positive I-ClO4 discharge tests and 5 (46%) had an abnormally high TSH response to TRH. Thyroid antimicrosomal and antithyroid peroxidase were positive in 8 women (73%) with a previous episode of PPT. The administration of pharmacological amounts of iodide (10 drops of saturated solution of potassium iodide daily) for 90 days to these 11 women resulted in elevated basal and TRH stimulated serum TSH concentrations in 8 (72.7%) compared to TSH values during iodide administration to women who had never been pregnant. Antimicrosomal and antithyroid peroxidase concentrations did not change during iodide administration. These findings strongly suggest that euthyroid women with a previous episode of PPT have permanent subtle defects in thyroid hormone synthesis and are inordinately prone to develop iodide-induced hypothyroidism, similar to findings previously reported in euthyroid subjects with Hashimoto's thyroiditis, with a previous episode of painful subacute thyroiditis, or previously treated with radioactive iodine or surgery for Graves' disease.

Adult↗
PubMed1990

Serotonergic control of TSH and PRL secretion in obese men.

To evaluate whether the inhibitory control of TSH and the stimulatory control of prolactin (PRL) secretion exerted by endogenous serotonin was altered in obesity, 22 obese men and 10 normal controls were tested with TRH (200 micrograms IV bolus) in the presence (experimental test) and absence (control test) of the serotonergic agonist fenfluramine (60 mg PO 90 min before TRH). Control and experimental tests were also performed in seven male patients with subclinical hypothyroidism and were repeated in the same obese subjects after substantial weight loss. Basal TSH levels were similar in control and obese men. Normal TSH responses to TRH (peak less than or equal to 14 mU/L) were observed in all normal controls (mean peak +/- SE 9.8 +/- 0.6 mU/L). In contrast, obese men were divided into two groups: nine in whom the TRH-induced TSH rise was higher than normal (group I: mean peak = 16.5 +/- 0.5 mU/L) and 13 in whom it was normal (group II: mean peak = 10.6 +/- 0.7 mU/L). The hypothyroid men all had elevated basal and TRH-stimulated TSH levels. Basal PRL concentrations were similar in the normal controls and both groups of obese subjects. The PRL response to TRH was lower in both group I and group II obese men than in normal controls and was similar between group I and group II.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Iodine-induced hypothyroidism in euthyroid subjects with a previous episode of subacute thyroiditis.

The effects of the administration of pharmacological quantities of iodide on thyroid function in 18 euthyroid patients with a previous history of painful subacute thyroiditis (SAT) were evaluated, and the results compared to those of iodide administration to 12 euthyroid patients with a previous history of thyroid surgery (TX) for benign nodular thyroid disease. After baseline thyroid function tests, saturated solution of potassium iodide (SSKI; 10 drops; 300 mg iodide) was administered daily for 120 days, and serum T4, T3, and TSH concentrations were assessed 15, 30, 60, 90, 120 days and 2-4 months after SSKI was discontinued. Iodide perchlorate discharge tests were carried out before SSKI administration, and TRH tests were performed on the last day of iodide administration. Two SAT subjects developed clinical evidence of hypothyroidism with markedly elevated serum TSH concentrations, and SSKI was discontinued on days 60 and 90, respectively. Thirteen of 18 SAT patients had at least 1 abnormal thyroid function test (iodide perchlorate discharge test, elevated serum TSH concentration, and abnormal TSH response to TRH) compared to 2 of 12 TX patients. These findings strongly suggest that euthyroid subjects with a previous history of SAT are prone to develop iodide-induced hypothyroidism, suggesting that subtle abnormalities in the thyroid organification of iodide and subsequent thyroid hormone synthesis persist years after the episode of SAT.

Analysis of Variance↗
PubMed1990

Thyrotropin releasing hormone does not stimulate prolactin release in the preterm human fetus.

Previous studies have suggested that fetal PRL secretion does not respond to stimuli such as TRH, metoclopramide, and cimetidine. It was postulated that the lack of response to TRH could be due to the possibility that, in the term fetus, lactotropes secrete PRL maximally and would be unresponsive to further stimulation. In order to study this hypothesis, 200 micrograms TRH or saline were administered to preterm pregnant women in labor. Maternal blood was obtained before TRH and saline administration. Maternal and cord blood were obtained at parturition. PRL, TSH, T4 and T3 concentrations were measured in all sera. TRH administration induced a significant increase in maternal serum PRL, TSH and T3 concentrations. In the cord blood of newborns whose mothers received TRH, serum TSH, T4 and T3 concentrations were significantly higher than in cord blood of newborns whose mothers received saline. Cord blood serum PRL concentrations were unchanged after TRH administration. This latter finding suggests that fetal lactotropes do not respond to TRH in the preterm fetus. Desensitization of fetal PRL secreting cells to TRH stimulation and/or the inhibitory effect of elevated fetal circulating corticosteroids on TRH-induced PRL secretion may explain the absent PRL response to TRH during fetal life.

Female↗
PubMed1978

"Short" loop feedback regulation of hypothalamic and brain thyrotropin-releasing hormone content in the rat and dwarf mouse.

In order to determine whether T4, TSH, or both affect hypothalamic TRH content, primary or secondary hypothyroidism was induced in the rat by thyroidectomy (Tx) or hypophysectomy (Hx), respectively. Two weeks later, rats were treated with T4, TSH, or both for 14--16 days. Tx or Hx significantly decreased hypothalamic TRH content, and T4 treatment restored hypothalamic TRH to normal in the Tx but not in the Hx rats. When TSH was administered simultaneously with T4 to Hx rats, hypothalamic TRH content was restored to normal. Whole brain TRH content was not affected by Tx, Hx, or by the various treatment regimens. Similar experiments were performed in Snell dwarf (dw/dw) mice. Hypothalamic TRH content was significantly decreased when compared to normal litter mates (dw/+). As in Hx rats, T4 administration to dw/dw mice for 16 days did not restore hypothalamic TRH content to normal. Brain TRH content was similar in both groups and was not altered by T4 treatment. It is concluded that T4 affects hypothalamic TRH content, but that TSH is required for this T4 effect. Whole brain TRH, on the other hand, is unaffected by any of these alterations in thyroid-pituitary function.

Animals↗
PubMedDate not supplied

3,3',5'-Triiodothyronine concentrations in amniotic fluid at different stages of pregnancy.

Since it is feasible to detect reverse T3 (rT3) in amniotic fluid, we investigated the possibility as to whether measurements of amniotic rT3 could be useful in diagnosing fetal hypothyroidism during pregnancy. In 55 amniotic fluid samples, obtained at different stages of pregnancy, we have documented increasing concentrations of this hormone. The results obtained are conflicting with previous reports. The reason for this discrepancy is not clear, however methodological differences in rT3 determination should be taken in account. The large scatter of rT3 values in amniotic fluid suggests that the diagnosis of neonatal hypothyroidism based on measurement of rT3 may require caution.

Amniotic Fluid↗
PubMedDate not supplied

Clinical evaluation of a hemagglutination method for microsomal and thyroglobulin antibodies in autoimmune thyroid disease.

A simple and reproducible hemagglutination technique for detecting microsomal and thyroglobulin antibodies has been evaluated in normal subjects and in patients with thyroid disease. Microsomal antibodies were detected in 89 percent of all patients with autoimmune thyroid disease and in 97 percent of patients with biopsy proven Hashimoto's thyroiditis. In contrast, thyroglobulin antibodies were present in only 55 percent of patients with biopsy proven Hashimoto's thyroiditis and in 44 percent of all patients with suspected autoimmune thyroid disease. It is suggested, therefore, that measurement of microsomal antibodies by a simple hemagglutination techniques be carried out in all patients with suspected thyroid disorders.

Antibodies↗