PubMed Health⌕ Search

Biomedical subjects

E Roti

Publications and source records attributed to E Roti.

At least 37 records · Page 2Linked to original sources
PubMed1997

Effects of excess iodine administration on thyroid function in euthyroid patients with a previous episode of thyroid dysfunction induced by interferon-alpha treatment.

OBJECTIVE: To determine the effects of pharmacological quantities of iodide (SSKI) on thyroid function in euthyroid patients previously treated with recombinant interferon-alpha (rIFN-alpha) for chronic viral hepatitis B and C (HCV), a cytokine which may induce thyroid dysfunction. DESIGN: Thyroid function tests were carried out in 16 euthyroid patients, 8 of whom had previously developed thyroid dysfunction during rIFN-alpha therapy for HCV, before, during and after the administration of 10 drops of saturated solution of potassium iodide (SSKI) (approximately 350 mg iodide). PATIENTS: All 16 patients had been treated in the past with rIFN-alpha for HCV. Eight patients had developed rIFN-alpha induced abnormalities in thyroid function (5 inflammatory thyrotoxicosis, 1 Graves' disease, and 2 impaired thyroid organification of iodide) and 8 had not developed thyroid dysfunction. MEASUREMENTS: After baseline serum free T4 (FT4) and free T3 (FT3) concentrations, basal and TRH stimulated TSH concentrations, and TSH-receptor (TSH-R-Ab) and thyroid peroxidase (TPO-Ab) antibodies were measured, 10 drops saturated solution of potassium iodide (SSKI, approximately 350 mg iodide) were given daily for 60 days and the above parameters assessed during and after SSKI was discontinued. RESULTS: Five of 8 patients with a previous history of rIFN-alpha induced thyroid dysfunction developed mild iodide induced abnormalities of thyroid function (subclinical hypothyroidism (slightly elevated basal and TRH stimulated serum TSH concentrations with normal serum FT4 and FT3 concentrations) or hyperthyroidism) compared with the 8 patients who had no previous evidence of thyroid dysfunction during rIFN-alpha therapy. CONCLUSIONS: In view of the present observations, it is prudent to avoid the administration of excess iodine to euthyroid subjects with a previous episode of thyroid dysfunction during rIFN-alpha therapy, adding a new group of patients susceptible to iodine induced thyroid disease.

Adult↗
PubMed1997

The study of visual evoked potentials in patients with thyroid-associated ophthalmopathy identifies asymptomatic optic nerve involvement.

In the present study we have recorded visual evoked cortical potentials (VECP) in 88 patients affected by autoimmune thyroid disease and thyroid-associated ophthalmopathy (TAO) without clinical signs of optic neuropathy. At the time of ophthalmological examination, 37 of these patients were hyperthyroid, 41 were euthyroid, and 8 were hypothyroid; 2 were not assessed. Twenty-nine normal subjects served as controls. We performed pattern reversal visual stimulation and recorded the amplitude and latency of the cortical electric response at 100 ms (P100 wave). There were no differences in the mean P100 amplitude of TAO patients and normal subjects. The mean P100 latency in patients was 105.6 +/- 0.5 ms, significantly higher than that in normal subjects (102.0 +/- 0.5 ms; P < 0.00003). Latency in euthyroid patients did not differ from that in either hypo- or hyperthyroid patients. The VECP test was positive (latency, > or = 110.0 ms) in 21 (23.8%) TAO patients. In patients with proptosis greater than 21 mm, latency was 106.7 +/- 0.7 ms, significantly higher than that in patients with normal Hertel measurements (104.3 +/- 0.6 ms; P < 0.01). Latency was not increased in patients with acute inflammatory signs compared to those with inactive eye disease and in patients with altered extrinsic motility. In patients with an abnormal visual field study, the mean latency was 110.3 +/- 1.5 ms, significantly higher than that in patients with a normal visual field (104.7 +/- 0.4; by t test, P < 0.000003). In conclusion, we observed a prolongation of the latency of the evoked cortical response in patients with TAO without subjective visual complaints and without optic nerve compression. We believe that the study of VECP in TAO is complementary to the study of the visual field in identifying early optic nerve dysfunction in the absence of decreased visual acuity.

Adolescent↗
PubMed1996

Multiple changes in thyroid function in patients with chronic active HCV hepatitis treated with recombinant interferon-alpha.

OBJECTIVE: Recombinant human interferon-alpha (r-IFN-alpha) is often successfully used in the treatment of patients with chronic viral hepatitis B and C. Thyroid dysfunction has been reported to occur with variable frequency during r-IFN-alpha therapy especially in patients with preexisting thyroid autoimmunity. We have prospectively evaluated the effect of r-IFN-alpha on various aspects of thyroid function in patients with HCV chronic hepatitis. DESIGN: Thirty-two patients with HCV chronic active hepatitis were studied prospectively before and during r-IFN-alpha therapy. Serum TSH, FT4, FT3, and thyroid receptor (TSR) and thyroid peroxidase (TPO) antibodies, and the iodide-perchlorate discharge test (I-C10(4)) to detect subtle defects in the thyroid organification of iodide were carried out during the study. Thyroid radioactive iodine uptakes (RAIU) were obtained in patients who developed thyrotoxicosis. RESULTS: All patients were clinically and biochemically euthyroid prior to r-IFN-alpha therapy with negative I-C10(4) discharge tests. Four patients became thyrotoxic, 3 secondary to destructive or inflammatory thyroiditis with a low thyroid RAIU, and 1 patient developed hypothyroidism. The I-C10(4) discharge test became positive in 7 of the 32 patients studied prospectively; 5 of these patients did not develop other evidence of thyroid dysfunction and did not have positive TPO antibodies. In these 5 patients the test became negative after r-IFN-alpha was discontinued. Appropriate therapy of the patients with thyrotoxicosis (methylprednisolone for 3 patients with destructive thyroiditis and methimazole for 1 patient with hyperthyroidism) or with hypothyroidism (L-thyroxine) was successful. CONCLUSIONS: Thyroid dysfunction, especially destructive or silent thyroiditis resulting in thyrotoxicosis, is not infrequently observed in patients receiving r-IFN-alpha therapy for chronic active hepatitis. Although underlying autoimmune thyroid disease appears to predispose patients to develop thyroid dysfunction, other patients become thyrotoxic or hypothyroid in the absence of baseline positive TPO-Ab. Subtle defects in the thyroidal organification of iodine as determined by the I-C10(4) discharge test, in the absence of autoimmune thyroid disease, was observed in 5 patients who remained euthyroid, suggesting that r-IFN-alpha directly reduces the intrathyroidal organification of iodine.

Adult↗
PubMed1996

Increased serum concentrations of interleukin-6 (IL-6) and soluble IL-6 receptor in patients with Graves' disease.

Increased serum interleukin-6 (IL-6) concentrations have been reported in patients with thyroid destructive processes. In the present study we measured IL-6 and soluble IL-6 receptor (sIL-6R) concentrations in the serum of normal subjects and patients with Graves' disease using a high sensitivity sandwich enzyme-linked immunoassay. We found increased serum IL-6 and sIL-6R concentrations (69.3 fmol/L, and 964 pmol/L, respectively) in 49 hyperthyroid patients with Graves' disease (GD) compared to those in controls [55.8 fmol/L (P = 0.019) and 772 pmol/L (P = 0.007), respectively]. In 31 newly diagnosed GD patients, serum concentrations of IL-6 and sIL-6R during the hyperthyroid phase were elevated, and after therapy with methimazole only, serum sIL-6R concentrations returned to normal (940 vs. 726 pmol/L; P < 0.001) but serum IL-6 did not. Serum sIL-6R concentrations (mean +/- 2 SD) were higher in GD patients with active inflammatory thyroid-associated ophthalmopathy than those in patients with inactive or absent thyroid-associated ophthalmopathy (P < 0.05). In conclusion, we have demonstrated activation of the IL-6 system in GD and, for the first time, have measured and found increased serum sIL-6R concentrations in hyperthyroid GD patients.

Adolescent↗
PubMed1996

Lack of increased serum interleukin-6 and soluble IL-6 receptor concentrations in patients with thyroid diseases following recombinant human interferon alpha therapy.

BACKGROUND: Serum interleukin-6 (IL-6) concentrations are frequently elevated in inflammatory thyroid diseases, such as subacute thyroiditis and amiodarone induced thyroiditis. We and others have recently observed that recombinant interferon-alpha (rIFN-alpha) therapy for chronic, active viral hepatitis and malignant disorders may induce thyroid dysfunction, including thyrotoxicosis secondary to thyroiditis. Serum IL-6 and its soluble receptor (sIL-6R) have been measured for the first time in patients with chronic active hepatitis receiving rIFN-alpha therapy. METHODS: Studies were carried out in 37 patients treated with rIFN-alpha for chronic, active viral hepatitis. Thyroid function tests and serum IL-6 and sIL-6R were measured before and during rIFN-alpha therapy. RESULTS: Six patients developed inflammatory or destructive thyrotoxicosis confirmed by elevated serum free T4 or free T3 concentrations, suppressed serum thyroid-stimulating hormone (TSH) values, and a low thyroid radioactive iodine uptake. Serum IL-6 and sIL-6R concentrations were not elevated in these patients with rIFN-alpha-induced thyroiditis. CONCLUSIONS: These results suggest that serum IL-6 concentrations are not useful in differentiating between inflammatory thyrotoxicosis and hyperthyroidism induced by rIFN-alpha therapy as is the case in amiodarone-induced thyrotoxicosis. It is possible that rIFN-alpha therapy could be associated with an inhibitory effect of rIFN-alpha on the release of IL-6 from damaged thyroid cells and not on the basal secretion of IL-6.

Antigens, CD↗
PubMed1995

Circadian thyrotropin variations are preserved in normal pregnant women.

Serum thyrotropin (TSH) concentration circadian rhythm is abolished in many endocrine and non-endocrine diseases. In the present study we have measured serum TSH concentration over 24 h every 2 h in second and third trimester pregnant women. During the 24-h period, serum free thyroxine and free triiodothyronine concentrations did not change significantly. In contrast, serum TSH concentrations demonstrated significant circadian variations both in the second and third trimester pregnant women (p < 0.02 and p < 0.005, respectively). In summary, second and third trimester pregnancy is associated with a normal circadian TSH rhythm.

Adult↗
PubMed1994

Thyroid ultrasonography in patients with a previous episode of amiodarone induced thyrotoxicosis.

Amiodarone induced thyrotoxicosis (AIT) occurs most frequently in euthyroid patients with nodular goiter or Graves' disease due to release of iodine from this iodine rich drug. However, some cases of AIT have been attributed to an inflammatory process of the thyroid gland due to amiodarone itself. We have studied the echographic pattern of the thyroid in 11 euthyroid patients who had an episode of AIT 32.4 +/- 3.6 months earlier due to amiodarone induced thyroiditis. There was a significant increase in dyshomogeneous echo patterns and hyperechogenecity which suggests fibrotic lesions. These findings were similar to those observed in 10 euthyroid patients who 77 +/- 12 months earlier had an episode of subacute thyroiditis (SAT). Thyroid volumes of control subjects and patients with a history of AIT and SAT were 10.9 +/- 1.4, 8.7 +/- 1.4 and 9.8 +/- 1.7, in the order. These values were not significantly different. These echographic findings, normal serum thyroid hormone and TSH concentrations and the absence of circulating antithyroid peroxidase antibodies suggest that underlying thyroid autonomy and Graves' disease were not the cause of the previous episode of AIT. The presence of hyperechogenic and dyshomogeneous patterns appears the result of the healing of the inflammatory AIT process.

Adult↗
PubMed1994

The iodine perchlorate discharge test before and after one year of methimazole treatment of hyperthyroid Graves' disease.

We have recently reported that many euthyroid patients with a history of Graves' disease treated years earlier with methimazole (MMI) have a positive iodide (500 micrograms)-perchlorate discharge test (I-ClO4 test), suggesting a permanent thyroid iodide organification defect. We now report the results of the I-ClO4 test in patients with hyperthyroid Graves' disease before beginning a 1-yr course of MMI therapy and 40 days after MMI was discontinued. Twenty-nine patients (25 women and 4 men; mean age, 38 +/- 1.7 yr) with their first episode of hyperthyroid Graves' disease were studied. Before MMI therapy, I-ClO4 tests were carried out, and serum T4, T3, and TSH were measured to confirm the diagnosis of hyperthyroidism. A positive I-ClO4 test is defined as more than 15% 131I discharged from the thyroid 1 h after the administration of 1 g KClO4. Patients were then treated with 20 mg MMI for the first 2 months and variable doses thereafter for the next 10 months to maintain euthyroidism. Serum T4, T3, and TSH were measured monthly. Forty days after MMI was discontinued, I-ClO4 tests were repeated, and serum T4, T3, and TSH were measured every 2 months thereafter. Before MMI treatment, the I-ClO4 test was positive in 20 of 29 patients (69%) and negative in 9. The favorable responses (normal serum T4 and T3 values) to MMI therapy were similar in both groups. We have thus far studied 16 patients after MMI was discontinued and 9 of 12 patients (75%) with a negative I-ClO4 test after MMI therapy, and 1 of 4 patients (25%) with a positive test remained in remission for a mean of 7 months. We conclude that the I-ClO4 test is frequently positive in patients with untreated hyperthyroid Graves' disease, suggesting either an inability to organify the increased iodide concentrated by the hyperfunctioning gland or the concomitant presence of Hashimoto's thyroiditis, which almost always is associated with a positive I-ClO4 test. The former hypothesis is more likely, because many patients with a positive I-ClO4 test before MMI therapy had a negative test after MMI was discontinued.

Adult↗
PubMed1994

Echographic diagnosis of pretibial myxedema in patients with autoimmune thyroid disease.

In the present study we have evaluated the use of pretibial ultrasound for the diagnosis of pretibial myxedema (PTM). We studied 76 patients, 58 with Graves' disease, 13 with Hashimoto's thyroiditis and five with idiopathic hypothyroidism. Thirty-two normal subjects were also studied as controls. Sixty-four patients had associated ophthalmopathy. The ultrasound scanner was equipped with 10- and 13-MHz probes. Punch biopsies were carried out in 11 patients and tissue sections examined on a light microscope. On clinical examination 21 patients (28%) had suspected PTM. By ultrasound, we measured the thickness of dermis and subcutaneous tissue (D1) and that including only deeper dermis (D2) in normal subjects to define the echographic parameters of normal pretibial skin. We then found increased skin thickness in 25 patients (33%), with mean D1 and D2 values significantly higher than those measured in controls (p < 0.00001). The echographic study was positive in 20 patients with ophthalmopathy (31%). Ultrasound showed increased skin thickness in 16 of 21 patients (76%) with clinically suspected PTM. Histopathological findings confirmed the presence of PTM in all the patients who underwent pretibial skin biopsy. We believe that the measurement of pretibial skin thickness by ultrasound may be useful for revealing the presence of PTM.

Adult↗
PubMed1993

Thyrotoxicosis followed by hypothyroidism in patients treated with amiodarone. A possible consequence of a destructive process in the thyroid.

Amiodarone is an iodine-rich drug used in the treatment of resistant cardiac arrhythmias. Amiodarone-induced thyrotoxicosis (AIT) is well recognized and is generally believed to be due to the excess iodine released from the metabolism of the drug, although amiodarone-associated thyroiditis has occasionally been observed. We report the clinical, laboratory, and therapeutic course of nine patients with AIT. The thyrotoxic phase was often followed by mild hypothyroidism during and after antithyroid drug or corticosteroid therapy. The thyroid was tender to palpation in two patients and a fine-needle aspiration biopsy of the thyroid revealed changes consistent with thyroiditis in three patients who underwent biopsy. These findings strongly suggest that the etiology of AIT, at least in some patients, is due, in part, to drug-induced inflammatory changes in the thyroid, as has been reported to occur in lung, bone marrow, and testes. Thus, the AIT may be due to excess iodine, drug-induced thyroiditis, or a combination of the two. The favorable response of AIT to corticosteroids in occasional patients previously reported also suggests that acute thyroiditis was probably present.

Adult↗
PubMed1993

Sodium ipodate and methimazole in the long-term treatment of hyperthyroid Graves' disease.

A prospective study was conducted to evaluate the effect of prolonged treatment of hyperthryoid Graves' disease with methimazole (MMI) for 12 months or Na ipodate for only 6.6 +/- 1.1 months, since the drug had to be discontinued because of persistent or recurrent hyperthyroidism during treatment. The eight patients who were treated with MMI alone for 12 months became euthyroid, and seven remained in remission for at least 6 months after MMI was discontinued. In contrast, only two of 10 patients treated with Na ipodate alone became euthyroid and remained so during therapy. No ipodate was discontinued in the eight patients who did not respond, and they were then treated with MMI. One patient had recurrent hyperthyrodism after NA ipodate was discontinued, and she was then treated with MMI. MMI was efficacious in treating these nine patients, and all patients were euthyroid by the third month of MMI administration. Five of these nine patients remained euthyroid for at least 6 months after MMI was discontinued, a remission rate that was not significantly different from that observed in the eight patients treated only and initially with MMI (Fisher's Exact Test). There was no significant change in serum thyroid peroxidase antibodies during treatment with MMI alone, Na ipodate alone, or Na ipodate followed by MMI.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Effects of chronic iodine administration on thyroid status in euthyroid subjects previously treated with antithyroid drugs for Graves' hyperthyroidism.

In view of the adverse effects of the administration of pharmacological quantities of iodine to euthyroid patients with a history of a wide variety of thyroid disorders, it has been suggested that iodine-containing medications and radioopaque dyes containing iodine should be avoided, if possible, in patients with underlying thyroid disease. We have now prospectively studied the effects of pharmacological doses of a saturated solution of potassium iodide (SSKI) on thyroid function in euthyroid patients with a previous history of hyperthyroid Graves' disease successfully treated with antithyroid drugs. Ten euthyroid women (mean age, 56 yr) who had hyperthyroid Graves' disease successfully treated with methimazole 36.4 +/- 4.7 months earlier were evaluated before, during, and after the administration of 10 drops SSKI daily for 90 days. The following thyroid function tests were obtained: serum T4, T3, TSH, TSH receptor antibody (TSH-RAb), and antithyroid peroxidase antibody (AbTPO) concentrations; TRH tests; and iodine perchlorate discharge tests. Serum T4, T3, basal and TRH-stimulated TSH, and TSH-RAb values were normal before SSKI administration, but serum AbTPO levels were markedly positive in 7 and iodine perchlorate discharge tests were positive in 4 of these 10 women. During SSKI administration, basal and TRH-stimulated serum TSH values increased above normal in 2 women with normal serum T4 and T3 concentrations; thyroid hormone values and TRH tests were normal in the other 8 patients and similar to values observed in 4 euthyroid women without a history of thyroid disease given SSKI. Serum AbTPO increased slightly, but significantly, during SSKI administration in the 7 women with positive values at baseline (P < 0.05). TSH-RAb remained undetectable. After SSKI withdrawal, the 10 women were reevaluated 60 and 120 days later. Two women developed a blunted TSH response to TRH, but normal serum T4 and T3 concentrations, and 2 women developed overt hyperthyroidism, with undetectable basal and TRH-stimulated serum TSH and elevated serum T4 and T3 concentrations, requiring methimazole therapy. All values in the remaining 6 women were similar to those present before SSKI administration. These results suggest that some euthyroid patients with a history of antithyroid drug therapy for Graves' disease may develop thyroid dysfunction during and after excess iodine administration. The development of subclinical hypothyroidism during SSKI administration was not clinically important, but the occurrence of overt hyperthyroidism after SSKI was discontinued did require antithyroid drug therapy. It is advisable, therefore, to avoid iodine-containing substances in euthyroid patients with a history of antithyroid drug therapy for Graves' disease.

Antithyroid Agents↗
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↗