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PubMed1975

[Diurnal rhythms of thyroid hormones in rooster chicks (Gallus domesticus). 1. Studies on the colloid epithelium portion, the radioiodine accumulation in the thyroid gland and the plasma radioiodide concentration].

Four and five week old White Leghorn cockerels were investigated concerning diurnal changes of thyroidal activity. They were kept under normal conditions, including the changes in day light (light from 5.00 am to 8.00 pm). In the thyroid maxima of the per cent amount of colloid were found at 3.00 am and at noon. The values differed significantly from the intermediate ones (2P less than 0.001) which reached only 22 per cent of the maxima. The thyroidal uptake of radioiodine had also a maximum at 3.00 am (51 percent and 78 percent resp., 90 min. or 24 hours p.i.). The 24-h uptake at 3.00 am was significant different from the corresponding uptakes between 6.00 am and 6.00 pm (53-61 percent; 2P less than 0.05). The plasma radioiodide increased at afternoon and in the evening. The 9.00 pm concentration differed significantly from the 9.00 am concentration (2P less than 0.001). Since in the afternoon most of the food is ingested the thyroid can take up a greater amount of untracered iodide and therefore the radioiodide concentration of plasma may remain high. The above observations may be explained in the following way: (1) The thyroidal iodine uptake is increased in the afternoon corresponding to the increase in colloid; however these increase is not detectable by measuring the radioiodine uptake because of dilution effects (during the night the increase in colloid coincidences with the increase in iodine uptake); (2) looking at the daily changes of colloid and radioiodine uptake the thyroid may be stimulated in the early morning and in the evening.

Animals↗
PubMed2001

Body, heart, thyroid gland and skeletal muscle weight changes in rats with altered thyroid status.

In the present paper we describe changes of anatomical parameters in inbred Lewis strain rats, namely their body weight, body weight gain per week, absolute and relative heart, thyroid gland and skeletal muscle weights, that are assumed to reflect experimentally altered thyroid status. The hyperthyroid state was induced by DL-thyroxine or Na 3,3',5-triiodo-L-thyronine, while methimazole was employed for inducing hypothyroidism. We have found that when compared to euthyroid rats, hypothyroidism resulted in a significantly lower body weight gain, absolute and relative heart weight and, in contrast, in a significant increase of absolute and relative thyroid gland weight. On the other hand, hyperthyroidism led to a significant increase of absolute and relative heart weight and to a significant reduction of absolute and relative thyroid gland weight. However, the body mass was not significantly altered in hyperthyroidism as compared with euthyroid rats. We conclude that our protocol leads to chronic hyper- or hypothyroidism as demonstrated by body, heart and thyroid gland weight changes. These anatomical data can thus be utilized as supplemental criteria for the assessment of the thyroid state of experimental rats.

Animals↗
PubMed2003

Why are thyroid cancer rates so high in southeast asian women living in the United States? The bay area thyroid cancer study.

The purpose of this study is to understand why thyroid cancer incidence rates are higher among Southeast Asian (SA) women living in the United States than among other United States women. A multiethnic population-based, case-control study of thyroid cancer among women ages 20-74 was conducted in the San Francisco Bay Area. Cases diagnosed between 1992 and 1998 were identified through the area's population-based cancer registry. Controls were identified using random digit dialing and matched to cases on age and ethnicity. Asian women were classified as SA (n = 214) or Northern Asian (n = 196) based on self-reported ethnicity. Relative attributable risks, by age group (<50 and 50+), were calculated to assess what proportion of the difference in incidence rates between these populations could be attributed to the prevalence of specific thyroid cancer risk factors, assuming common relative risks across ethnic groups. Among younger women, a history of goiter or thyroid nodules and lower consumption of isoflavones from soy-based foods account for 66% of the difference in incidence between SA and Northern Asian women. Among older women, these factors, along with recent migration, accounted for 95% of the difference between these groups. When comparing SA with Caucasian women, goiter/nodules and lower consumption of carotenoids explained 67% of the difference in incidence in younger women, whereas goiter/nodules and socioeconomic variables explained 81% of the difference in incidence in older women. A greater prevalence of goiter and thyroid nodules accounts for a substantial portion of the higher thyroid cancer incidence rates among SA women. Dietary patterns also contribute to the rate differences.

Adult↗
PubMed2004

The hypothalamic-pituitary-thyroid axis in subjects with subclinical thyroid diseases: the impact of the negative feedback mechanism.

OBJECTIVE: To evaluate the hypothalamus-pituitary-thyroid (HPT) axis in patients with subclinical thyroid dysfunction recently reported to have either symptoms or organ involvements with potential morbidity, in order to better differentiate these patients with respect to controls. PATIENTS: Sixtythree patients with subclinical hyperthyroidism (HyperT), 178 normal subjects (EuT) and 106 patients with subclinical hypothyroidism (HypoT) were enrolled; the groups presented normal thyroid hormone (FT4, FT3) levels and, respectively, reduced (HyperT), normal (EuT) and increased (HypoT) TSH levels. The negative feedback was simultaneously evaluated by multiple linear regression. RESULTS: The mean TSH, FT4 and FT3 levels were significantly different in the three groups. The negative correlation between thyroid hormones (FT4 and FT3) and TSH secretion was significant (p<0.001 in HyperT; p<0.01 in EuT; p<0.000001 in HypoT group). FT4 mostly contributed to the negative correlation with TSH. The normal ranges of TSH values was accurately defined on the basis of the regression equation in the EuT group, due to the combining influence of both thyroid hormones (FT3 and FT4). No patient of the HyperT or HypoT group fell inside the range of estimated values of the normal group. CONCLUSIONS: The HPT axis in patients with subclinical hyper- and hypo-thyroidism is significantly modified with respect to normal subjects. The status of the axis, as evaluated by the relationship between the three hormones (FT4, FT3, TSH) together considered, is characteristic of the normal or pathologic condition. A reliable method based on the regression analysis is proposed to correctly evaluate the status of the HPT axis.

Adult↗
PubMed2005

Hashimoto's thyroiditis in a patient with non-Hodgkin's thyroid lymphoma of B cell type and originated from mucosa-associated lymphoid tissue (MALT): A case report.

This is a rare case report of Hashimoto's thyroiditis in a patient with MALT thyroid lymphomas. The patient presented with an enlarged neck mass over the past 10 years and had rapidly enlarged neck mass with compressive symptoms for about 2 months. Examination by an endocrinologist found that the size of the thyroid gland was 120 gm with firm consistency and with no tenderness. She had clinical hypothyroidism and no abnormality of neither lymphadenopathy nor any masses. She was diagnosed with Hashimoto's thyroiditis because her thyroids function lest showed primary hypothyroidism [(FT4 = 0.76 ng/dl (0.93-1.71), FT3 = 1.76 pg/ml (1.8-4.6), TSH = 8.24 mIU/L (0.27-4.21)] with antimicrosomal antibody positive titers (> 1:409,600): Diagnosis of primary thyroid lymphoma was diagnosed by FNA and total thyroidectomy was performed. About 1 day after total thyroidectomy, she developed clinical hypocalcemia and the laboratory showed that calcium was = 6.2 ng/dl (8.5-10.1), phosphorus = 6.4 mg/dl (2.5-4.9). After 10% calcium gluconate replacement, her hypocalcemic symptoms didn't appear and she received oral replacement of calcium carbonate and vitamin D before discharge. During OPD follow up, her pathological report from Maha Chakri Sirinthorn Medical Center was a diagnosis of Non Hodgkin's lymphoma, low grade and the latter 1 week immunohistochemically staining of tumor markers indicated B-cell type (CD20) with MALT (AE1/AE3) lymphoma. Staging of the disease was stage IE and she received one course of CHOP (Cyclophosphamide, doxorubicin, vincristin and prednisolone). After one course of CHOP regimen, she was healthy and the hematologist ordered two courses of CHOP and external radiation.

Aged↗
PubMed1991

Mutation of the p53 gene in a differentiated human thyroid carcinoma cell line, but not in primary thyroid tumours.

The p53 gene has been implicated as a tumour suppressor, with mutations occurring in many carcinomas, such as colon, breast and lung. We have sequenced exons 5, 7 and 8 containing conserved gene regions in the only available differentiated thyroid follicular carcinoma cell line and found a mutation at position 273, Arg----His, with no normal allele present. The same mutation was also present in DNA from the tumour of origin. However immunohistochemical analysis of 129 human thyroid tumours using a panel of p53 antibodies was unequivocally negative. Southern blotting in 20 cases failed to demonstrate any deletion or rearrangement, and direct genomic sequencing of 20 carcinomas showed normal DNA sequence for exons 5, 7 and 8. Thus p53 abnormalities may not be important in human thyroid carcinogenesis, in contrast to colon, breast and lung. However, the FTC 133 cell line was only established after 132 unsuccessful attempts with other differentiated thyroid follicular tumours. Since this line and the corresponding tumour of origin have a p53 mutation, we propose that p53 mutation may confer on thyroid follicular tumour cells the ability to grow in culture. This has potential applications for the future development of thyroid carcinoma cell lines.

Antibodies, Monoclonal↗
PubMedDate not supplied

[Functional state of the hypothalamo-hypophyseal-thyroid system in euthyroid hyperplasia of the thyroid gland].

Function of the hypothalamo-hypophyseal-thyroid system was investigated in 51 patients with euthyroid hyperplasia. Basal and TRH-stimulated levels of TSH and STH were investigated. Hyperergic ejection of STH and two pathological types of STH reaction (suggesting dysfunction of the hypothalamohypophyseal-thyroid system in euthyroid hyperplasia) were revealed. A group of patients with a low level of STH in response to TRH-stimulation demonstrated more pronounced changes of the hypothalamo-hypophyseal-thyroid system, characterized by a rise of a TSH level in response to stimulation up to 27.59 +/- 3.7 microU and a slightly reduced level of thyroid hormones. Changes in the level of STH indicated certain interest of growth hormone in the genesis of thyroid hyperplasia and could also serve an additional sign in the evaluation of a severity of disorders of the hypothalamo-hypophyseal-thyroid system.

Adolescent↗
PubMed1991

Difference in the susceptibility of two phenobarbital-inducible forms, P450IIB1 and P450IIB2, to thyroid hormone- and growth hormone-induced suppression in rat liver: phenobarbital-inducible P450IIB2 suppression by thyroid hormone acting directly, but not through the pituitary system.

Suppression of two major phenobarbital-inducible cytochrome P-450s, P450IIB1 and P450IIB2, by thyroid hormone was studied and compared with growth hormone (GH)-induced suppression in rats in vivo and hepatocytes in primary culture in vitro. Treatment of adult male rats with 50 micrograms/kg triiodothyronine (T3) reduced the constitutively expressed amounts of P450IIB1 (up to 1 pmol/mg of protein) and P450IIB2 (2-5 pmol/mg of protein) to 42% and 3% of their levels in nontreated controls. Thyroidectomy increased the hepatic contents of P450IIB2 (to levels of 50-80 pmol/mg of protein) and, to a lesser extent, P450IIB1 (1-5 pmol/mg of protein) in male and female rats. Supplement of T3 to thyroidectomized rats reversed the increased contents to levels similar to those observed in normal rats. Hypophysectomy also increased both P450IIB1 and P450IIB2 protein, and their levels in both sexes were similar to that of P450IIB2 in thyroidectomized rats. Treatment of hypophysectomized rats with T3 as well as human GH suppressed hepatic contents of P450IIB1 and P450IIB2. In a hepatocyte culture including 2 mM phenobarbital, T3 and GH suppressed both P450IIB1 and P450IIB2. Other thyroid hormone derivatives, including thyroxine, D-T3, and reversed T3, also showed suppressive effects, in parallel with the potencies for their stimulatory action that have been reported. These results indicate that thyroid hormone may suppress both P450IIB1 and P450IIB2 by a direct effect on the liver, but not by an indirect effect through the modulation of pituitary GH synthesis. The high susceptibility of hepatic P450IIB2 to thyroid hormone-induced suppression also indicates that constitutive and phenobarbital-induced levels of P450IIB2 are suppressively regulated preferentially by thyroid hormone, in contrast to the high susceptibility to GH of P450IIB1 in rat liver. In addition, a difference in the suppressive mechanisms of thyroid hormone and GH was suggested by the difference in susceptibility to cycloheximide.

Animals↗
PubMed1989

Frequency of thyroiditis and postpartum thyroiditis in a 10-year consecutive hyperthyroid Danish population.

In a retrospective study 716 consecutive newly diagnosed and untreated hyperthyroid patients were examined in regard to the frequency of silent thyroiditis and postpartum thyroiditis. Six patients (0.8%) had possible silent thyroiditis (24-hour radioiodine uptake less than or equal to 5% and hyperthyroidism without anterior neck pain). None occurred within one year postpartum. We conclude that silent thyroiditis is a rare cause of hyperthyroidism in our thyroid clinic. The fact that none occurred postpartum suggests that postpartum thyroiditis is oligosymptomatic and that screening programmes are needed if one wants to diagnose the earliest phases of this condition.

Adolescent↗
PubMed1976

Thyroid-bound Y-chromatin-like fluorescence in the nuclei of thyroid adenomas.

Brilliantly fluorescent supernumerary chromocenters indistinguishable from the Y-chromatin have been often found electively in the thyroid nuclei. The authors compared the occurrence of this Y-chromatin-like fluorescence in 31 thyroid adenomas obtained from 30 autopsy cases (10 males, 20 females) with non-adenomatous thyroid tissues of the same cases. All adenomas had follicular structure but one with papillary structure. The frequency class of Y-chromatin-like fluorescence of adenomas was lower in 15 cases out of 31 than that of the same non-adenomatous thyroid tissue. The Y-chromatin-like fluorescence had a negative count in 13 cases of 31 adenomas but only in 3 cases of normal thyroid tissues from 30 persons. The disappearance of the nuclei with Y-chromatin-like chromocenters is supposedly connected with cellular dedifferentiation of thyroid adenomas.

Adenoma↗
PubMed1980

Lymphocytic thyroiditis with spontaneously resolving hyperthyroidism (silent thyroiditis).

Spontaneously resolving hyperthyroidism (SRH) is a transient form of hyperthyroidism characterized by a painless, nontender, normal-sized or slightly enlarged thyroid gland, elevated levels of thyroxine and triiodothyronine, a depressed thyroid radioactive iodine uptake (RAIU), spontaneous resolution in two to five months, and a focal or diffuse lymphocytic thyroiditis on biopsy. Since 1962, 62 episodes of SRH were found in 56 individuals. Twelve thyroid biopsy specimens showed diffuse or focal lymphocytic thyroiditis. Testing of viral antibodies to a wide range of viruses demonstrated only one patient with notable titer change of 18 tested. Resolution of the hyperthyroidism took two to five months. Four patients were treated inappropriately. Lymphocytic thyroiditis with spontaneously resolving hyperthyroidism appears to be a new syndrome that has dramatically increased in frequency in the past ten years. It is difficult to differentiate from common forms of hyperthyroidism unless RAIU is determined.

Adolescent↗
PubMed1982

Clinical and subclinical thyroid disorders associated with pernicious anemia. Observations on abnormal thyroid-stimulating hormone levels and on a possible association of blood group O with hyperthyroidism.

of 162 patients with pernicious anemia whom we studies, 24.1% had clinical thyroid disease; 11.7% were hypothyroid and 8.6% were hyperthyroid. When abnormal serum thyroid-stimulating hormone (TSH) levels were also considered, thyroid disorders existed in 48.3% of 143 patients. Increased or decreased TSH levels as the sole dysfunction occurred in 14.7% and 6.3% of cases, respectively, and were often associated with thyroid antibodies. The high TSH group fits the picture of subclinical hypothyroidism. The nature of the low TSH group remains to be defined. We conclude that TSH screening in patients with pernicious anemia uncovers frequent abnormalities, which are superimposed on a higher coincidence of overt thyroid disease than previously described. Interestingly, also, eight of nine hyperthyroid patients and all seven patients with low TSH levels had blood type O, contrasting significantly with hypothyroid subjects, who more often had blood type A, and with patients without thyroid disorders.

ABO Blood-Group System↗
PubMed1995

Isolation of thyroid peroxidase and lack of autoantibodies to the enzyme in dogs with autoimmune thyroid disease.

Fifty serum samples from dogs with clinical signs of hypothyroidism and autoantibodies (AA) to thyroglobulin (Tg), thyroxine, or triiodothyronine were screened for AA to thyroid peroxidase (TPO). Thyroid peroxidase is the antigen against which microsomal AA are formed in human beings with lymphocytic thyroiditis. The TPO was isolated from canine thyroid tissue, using a modification of the procedure for purifying porcine TPO. The enzyme was solubilized from the membrane, using a deoxycholate-trypsin solution, followed by ammonium sulfate precipitation and diethylaminoethyl Sephadex chromatography. Activity of TPO was determined, using an iodide oxidation assay and a guaiacol assay. A monoclonal antibody to canine Tg, coupled to an immunoaffinity column, was used to eliminate the contaminating Tg from the TPO preparation. Using the TPO preparation as an antigen, an ELISA was performed on 10 serum samples and immunoblot assays were performed on 50 canine sera. Autoantibodies to TPO were not found in any of the sera. Assays also were performed, using purified porcine and human TPO and evidence of cross-reactivity with canine TPO was not identified. The absence of AA to TPO in dogs suggests a different pathogenesis for autoimmune thyroid disease in dogs than that hypothesized for lymphocytic thyroiditis in human beings.

Animals↗
PubMed1994

Radioiodine therapy for well-differentiated thyroid cancer: a quantitative dosimetric evaluation for remnant thyroid ablation after surgery.

UNLABELLED: The influence of cumulative absorbed dose, initial dose rate and mass of the remnant thyroid tissue on outcome of radioiodine treatment was assessed to determine an optimum value of absorbed dose and initial dose rate predictive of successful ablation. METHODS: In 87 patients with thyroid carcinoma treated with 0.85-9.55 GBq (23-258 mCi) of 131I to ablate residual thyroid tissue, the cumulative absorbed dose and the initial dose rate were calculated. Following therapy, the parameters of radioactive iodine uptake and effective half-life were determined in each patient from the surface neck exposure rates measured using a beta/gamma exposure rate meter. Mass of the thyroid remnant was determined from rectilinear images after scatter correction obtained from phantom studies. RESULTS: Sixty-eight patients showed complete ablation and 19 showed partial ablation of the thyroid remnant after radioiodine therapy. The cumulative absorbed doses delivered to the tissue in completely ablated and partially ablated groups were not significantly different (0.6 > p > 0.5). The initial dose rate delivered to the tissue in both groups, however, showed a significant difference (0.05 > p > 0.02). An initial dose rate of 3 Gy/hr or more completely ablated up to 5 g of tissue in 54 out of 62 patients (87.1%). Dose rate above 3 Gy/hr and cumulative doses above 300 Gy resulted in ablation in 50% of patients with more than 5 g of tissue. CONCLUSION: In patients receiving 131I to ablate thyroid remnant, the initial dose rate and the tissue mass are determinants of successful treatment response.

Combined Modality Therapy↗
PubMed1995

Ha-ras oncogene (codon 12) mutation in thyroid carcinogenesis: analysis of 60 benign and malignant thyroid tumors.

Protooncogene Ha-ras codon 12 mutations are frequently observed in thyroid cancers. However, their role in the initiation and development of this pathology remains to be clarified. Here we present a preliminary study using 60 samples corresponding to different types of cancer. DNA amplification by PCR (polymerase chain reaction) followed by RFLP (restriction fragment length polymorphism) analysis enabled the detection of a point mutation in codon 12 of the Ha-ras oncogene in human thyroid adenomas and carcinomas. Our results confirm the high frequency of codon 12 Ha-ras oncogene mutation in thyroid tumors: adenomas 33%, with a particularly high rate for atypical adenomas 71%, follicular carcinomas 33%, and papillary carcinomas 19% (n = 18, 7, 12, 26, respectively). No mutation was detected in undifferentiated carcinomas (n = 4). The Ha-ras codon 12 gene point mutation can exist at all stages of development of both benign and malignant thyroid tumors. It may be a necessary part of the thyroid tumorigenesis process, but it is not the only carcinogenic factor. Additionally, the association with other molecular anomalies should be sought depending on the thyroid cancer type.

Adenoma↗
PubMed1993

Thyroid neoplasia coexistent with chronic lymphocytic thyroiditis.

During a 6-year period 115 patients presenting with thyroid enlargement had evidence of chronic lymphocytic thyroiditis on fine-needle aspiration cytology. Of 27 patients in whom histological analysis was carried out, 16 had neoplasms (follicular adenoma, four; follicular carcinoma, one; papillary carcinoma, four; lymphoma, seven). Assuming that neoplasia was not overlooked in the absence of histological examination, the overall incidence was 14 per cent and that of malignant disease 10 per cent. All patients with carcinoma had cytological features suspicious of neoplasia on the first or subsequent aspirates in addition to those of thyroiditis. Cytology was suspicious of lymphoma in only two of seven patients but increasing size of the thyroid swelling was a consistent feature. Evidence of chronic lymphocytic thyroiditis may lead to neoplasia being overlooked. Repeated cytological analysis is helpful in identifying coexistent carcinoma but unreliable in excluding lymphoma.

Adenocarcinoma, Follicular↗
PubMed1989

Thyroid growth stimulating activity in highly purified IgG-fractions of patients with nonimmune thyroid diseases.

Two different proliferation assays have been used to measure the proliferative potential of IgG-fractions from 57 patients with nontoxic goiter of an iodine-deficient area: primary human thyroid epithelial cells (TEC) and the thouroughly investigated FRTL-5 cell line. IgG-fractions from patients with nontoxic goiter (n = 30), nontoxic recurrent goiter (n = 8), toxic-nodular goiter (n = 15) and carcinoma of the thyroid (n = 4) were highly purified on DEAE-Sepharose and additionally Protein A-Sepharose in some cases. The two proliferation assays gave contradictory results: primary cultures of human thyroid epithelial cells (TEC) could not be stimulated by any of the patient's IgG-fractions nor by bTSH. The FRTL-5 cells, however, were stimulated with 10 microU/ml bTSH by 326% +/- 96% (range: 222% - 497%, p less than 0.001). In one experimental series, 72% of all patients exceeded mean + 2 SD of normal controls, when the stimulation index was referred to the effect of bTSH (NTG: 77%, Rec. G.: 88%, Tox. G.: 53%, Ca. thyroid: 75%). With a different method of calculation - stimulation index referred to the basal value - the number of patients above mean + 2 SD of normal controls decreased to 30% (NTG: 33%, Rec. G.: 12.5%, Tox. G.: 33%, Ca. thyroid: 25%). Statistical analysis, however, of results of different patient groups compared to the normal control group failed to show any significance.

Adolescent↗
PubMed1980

Postpartum lymphocytic thyroiditis in American women: a spectrum of thyroid dysfunction.

Six episodes of primary hypothyroidism followed pregnancy in five women. Within 6 months post partum, all were clinically hypothyroid, with a diffuse goiter of two or three times normal size, altered thyroid function tests (average thyroxine [T4] = 2.6 micrograms/dl, thyroid-stimulating hormone [TSH] = 58.2 microunits/ml), and elevated antithyroid antibodies. (All had antimicrosomal antibody titers of 1:6,400 or more.) After 5 more months, all patients had a decrease in antibody titer, resolution of symptoms, and recovery of thyroid hormone levels (average T4 = 7.3 micrograms/dl), although two patients had compensated hypothyroidism (their average TSH = 9.3 microunits/ml). Four patients had lymphocytic thyroiditis diagnosed by fine-needle aspiration biopsy. Despite the apparent transience of postpartum hypothyroidism, all five patients have chronic thyroid dysfunction: three women have persistent goiters (all less than twice normal size) and two have compensated hypothyroidism; one patient had previous Graves' hyperthyroidism, and two had recurrent transient hypothyroidism (at 21 months postpartum in one patient, and 5 months after another pregnancy in the other). Three women had transient, painless hyperthyroidism (average T4 = 16.1) before becoming hypothyroid: two patients within 8 weeks post partum, and the third patient at 20 months (preceding an episode of recurrent hypothyroidism). Previous reports of postpartum hypothyroidism have come from scattered locales abroad, and it is unclear whether local environmental factors are pathogenic. Nevertheless, this syndrome may, in general, have gone unrecognized and may be a significant cause of illness in postpartum women.

Adult↗