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Expansion of microsatellite in the thyroid hormone receptor-alpha1 gene linked to increased receptor expression and less aggressive thyroid cancer.

PURPOSE: The purpose of this study was to determine whether the length of the THRA1 microsatellite, which resides in a noncoding portion of the thyroid hormone receptor-alpha1 gene, affects receptor expression and is linked to clinicopathological parameters in thyroid cancer. EXPERIMENTAL DESIGN: In 30 cases of surgically resected sporadic thyroid cancer, the length of the THRA1 microsatellite was determined by DNA sequence analysis, and expression of thyroid hormone receptor-alpha1 was assessed immunohistochemically in thin sections cut from tumor blocks. The length of THRA1 and expression of thyroid hormone receptor-alpha1 were also assessed in seven cancer cell lines. Regression analysis was used to gauge the correlation between the size of THRA1 and receptor expression. Multivariate analysis was used to test for links to the clinical parameters of gender, age, histology, stage, nodal involvement, distant metastasis, extrathyroidal invasion and tumor-node-metastasis (TNM) classification. RESULTS: A statistically significant correlation between the length of THRA1 and thyroid hormone receptor-alpha1 expression was observed in both cell lines and primary thyroid cancers. Thyroid tumors that displayed higher than average thyroid hormone receptor-alpha1 expression had expanded THRA1 microsatellites and were less aggressive as judged by TNM ranking. A statistically significant correlation was also found between low thyroid hormone receptor-alpha1 expression and more aggressive thyroid cancer, as judged by extrathyroidal invasion and nodal involvement. CONCLUSIONS: Less aggressive thyroid cancer was found to be linked to increased thyroid hormone receptor-alpha1 expression and an expanded THRA1 microsatellite.

Adenocarcinoma, Follicular↗

[The effect of thyroid hormone on the growth of thyroid cancer].

Thyroid cancer is well known to be hormone sensitive as well as breast cancer, prostatic cancer, and endometrial cancer of the uterus. Various experimental results suggest that the growth regulation for thyroid cancer, as well as the normal thyroid gland, appears to depend upon the TSH (Thyroid stimulating hormone) receptor on cell membranes. Differentiated thyroid carcinoma cells possess TSH receptor, although anaplastic carcinoma cells do not; therefore suppression therapy of TSH with thyroid hormone is considered to be effective against differentiated thyroid carcinoma. It has been recognized that some recurrent differentiated thyroid cancers cause regression in size in response to treatment with thyroid hormone. But the administration of the thyroid hormone after the operation for the differentiated thyroid carcinoma does not necessarily enhance the survival rate. To analyze the difference in survival rate is very difficult because of the excellent survival rate of thyroid cancer patients after the operation. It is hoped that further clinical study and laboratory investigation about suppression in adjuvant therapy for differentiated thyroid cancer will give us a conclusive answer.

Adolescent↗

Thyroid transplantation developing autoimmune thyroiditis following thymectomy and irradiation.

Post-irradiation transplantation of normal thyroids under the renal capsule of syngenetic thymectomized and irradiated (Tx-X) rats leads to the development of thyroiditis in the ectopic grafted thyroids. A close correlation was observed between the extent of the lesions in the grafted and recipient's own thyroid. The histopathology of both grafted and recipient thyroid was similar and was characterized by infiltration with mononuclear cells together with some plasma cells. Conversely, grafting of affected thyroids from Tx-X rats to normal animals resulted in the regression of the lesion in the graft and no evidence thyroiditis was observed in either the graft or the recipient's thyroid when these were examined 60 days post-grafting. Thyroids derived from normal animals grafted to syngenetic normal rats were found to remain healthy and intact over a 60-day period. In contrast to normal animals, Tx-X rats were unable to reject totally in transplanted allogeneic thyroids by 28 days post-grafting, suggesting that some impairment of cell-mediated immunity follows this treatment. These findings indicate that the pathological change occurring in the thyroid gland of Tx-X rats is not attributable to the local effect of irradiation of the thyroids and adds further support to the concept that the process is immunologically mediated by thyroid-specific circulating components in the absence of normal immune regulatory function.

Animals↗

Thyroid nodules and thyroid cancer: surgical aspects.

Patients with thyroid nodules must be treated selectively because these nodules develop far more frequently than does thyroid cancer. A thorough clinical history, family history and history of radiation, as well as an accurate physical examination, are very important in determining whether surgical treatment is indicated. Thyroid function tests, a radioactive isotope scan, a thyroid echogram and fine-needle biopsy are also useful. Although there is considerable debate concerning the amount of thyroid tissue that should be removed at operation, the minimal procedure for a "cold," solid thyroid nodule is a total thyroid lobectomy and isthmectomy. This is the treatment of choice for patients with occult papillary thyroid carcinoma. Partial lobectomy is to be discouraged. Near total or total thyroidectomy should be considered for all other patients with differentiated thyroid cancer. Many factors influence the prognosis of patients with thyroid cancer including age, sex, type of thyroid cancer, invasion, symptoms, lymph node metastasis, metastasis to distant sites, extent of the surgical procedure, and use of radioactive iodine and thyroid hormone. With adequate treatment, the prognosis for differentiated thyroid carcinoma is excellent.

Adolescent↗

18F-fluorodeoxyglucose uptake in thyroid from positron emission tomogram (PET) for evaluation in cancer patients: high prevalence of malignancy in thyroid PET incidentaloma.

OBJECTIVES: To investigate the prevalence of incidental thyroid F-fluorodeoxyglucose (FDG) uptake in positron emission tomogram (PET) scan for evaluation in cancer patients and the role of standard uptake value (SUV) measurement in differentiation of thyroid malignancy from benign disease. STUDY DESIGN: Retrospective single-center study. METHODS: Four thousand one hundred thirty-six subjects had been given FDG-PET scan for evaluation of known malignancies not associated with thyroid. The maximum SUVs of the thyroid lesions were recorded and reviewed. Fine needle aspiration was performed in patients with definite nodule by palpation or ultrasonography. RESULTS: Ninety-four (2.2%) were identified to have focal (n = 45, 1.1%) or diffuse (n = 45, 1.1%) thyroid FDG uptake. The incidence of focal or diffuse thyroid FDG uptake was higher in women (2.7% or 1.9%) than in men (0.4% or 0.7%). Cytologic diagnosis was available in 32 of 45 focal thyroid FDG uptakes. In 16 (50%) patients, the tumor was found to be malignant; 14 were papillary thyroid carcinoma (surgically confirmed in 7 cases), 2 were metastatic tumor from breast and esophagus. Sixteen were cytologically diagnosed as follicular cell lesions: follicular neoplasm (n = 2), nodular hyperplasia (n = 7), indeterminate follicular lesion (n = 7). There was no significant difference in maximum SUV between benign and malignant nodules. From 45 patients with diffuse thyroid FDG uptake, presumptive diagnosis of chronic thyroiditis was possible in 34 patients by clinical and laboratory findings. CONCLUSION: Our data suggest that a cytologic diagnosis of focal thyroid FDG-PET incidentaloma regardless of SUV is mandatory considering the very high prevalence of thyroid malignancy.

Adolescent↗

Thyroid remnant 131I ablation for papillary and follicular thyroid carcinoma.

Outcome was compared in 1,004 patients with differentiated thyroid carcinoma (DTC) who underwent thyroid remnant ablation with 131I (n = 151) or were either treated with thyroid hormone alone (755) or given no postoperative medical therapy (98). Median follow-up time was 18.7 years for patients treated with thyroid hormone alone, 21.3 years for those given no adjunctive medical therapy, and 14.7 years for those treated with thyroid remnant ablation. End points measured were cancer recurrence, development of distant metastases, and death due to thyroid carcinoma. Tumor recurrence was about threefold lower (p < 0.001) and fewer patients developed distant metastases (p < 0.002) after thyroid remnant ablation than after other forms of postoperative treatment, an effect observed only in patients with primary tumors > or = 1.5 cm in diameter. The doses of 131I were stratified into two groups: 29-50 mCi (mean 47 mCi) in 43% and 51-200 mCi (111 mCi) in 57% of patients. Both groups experienced similar recurrence rates (7% and 9%, respectively, p = 0.7). There were fewer cancer deaths after thyroid remnant ablation than after the other treatment strategies (p < 0.001), differences that occurred only in patients aged 40 years or older at the time of initial treatment and with primary tumors > or = 1.5 cm. The variables that influenced cancer recurrence in a Cox proportional hazards model were absence of cervical lymph node metastases (hazards ratio [HR] 0.8), tumor stage (HR 1.8), and treatment of the thyroid remnant (HR 0.9); those that independently affected cancer-specific death rates were age (HR 13.3), recurrence of cancer (16.6), time to treatment (HR 3.5), thyroid remnant ablation (HR 0.5), and tumor stage (HR 2.3). This study suggests that thyroid remnant ablation is effective in reducing recurrence of DTC in patients of all ages and reduces the risk of death from thyroid carcinoma in patients > age 40 at the time of diagnosis. These effects are not apparent in patients with isolated tumors < 1.5 cm that are not metastatic to regional lymph nodes or invading the thyroid capsule. The optimal dose of 131I necessary to achieve this effect remains uncertain.

Adenocarcinoma, Follicular↗

Effect of adrenal hormones on thyroid secretion and thyroid hormones on adrenal secretion in the sheep.

1. Previous work has shown that after stressful stimuli, sheep initially secrete increased amounts of thyroid hormone, at a time when adrenal secretion is also elevated. 2. This study was designed to evaluate (a) any short-term activation or inhibition of thyroid secretion by exogenous cortisol or ACTH administered in quantities comparable to those secreted after stress in sheep and (b) any short-term effect that exogenous thyroxine or triiodothyronine may have on the concentration of plasma cortisol in the sheep. 3. Thyroid activity was measured by determination of plasma protein bound 125I (PB125I) and total 125I in thyroid vein and mixed venous (jugular) blood. Plasma cortisol and thyroxine concentrations were measured by a competitive protein-binding assay at intervals for up to 5 hr after commencement of the experiment. 4. No evidence of an activation of thyroid secretion was found during cortisol or ACTH infusion, as monitored by thyroid vein PB125I. Similarly there was no evidence of any inhibition of thyroid function, as measured by continued secretion of thyroid hormones into thyroid vein blood. 5. No effect on plasma cortisol concentration due to thyroid hormone treatment was observed. 6. It was concluded that (a) elevated circulating corticosteroids in physiological concentrations have no short-term effects on thyroid activity in the sheep and (b) the short-term alterations in thyroid and adrenal cortical secretion observed during stress in the sheep could not be attributed to direct interaction of elevated thyroid hormone concentrations with adrenal cortical secretion.

Adrenal Glands↗

Thyroid hemiagenesis: prevalence in normal children and effect on thyroid function.

Thyroid hemiagenesis prevalence was studied by neck ultrasound examination in 24,032 unselected 11- to 14-yr-old schoolchildren from southeastern Sicily. Twelve cases of thyroid hemiagenesis were identified, with a prevalence of 0.05%. The female to male ratio was 1:1.4. Thyroid hemiagenesis was always due to the absence (11 cases) or severe hypoplasia (1 case) of the left lobe. The hemiagenetic thyroid volume was within the normal total thyroid volume range normalized to age in 4 of 12 cases, enlarged in 3, and significantly reduced in 5. Thyroid function (thyroid hormones and TSH, both basal and 30 min after administration of 200 micro g TRH, iv) was evaluated in 9 of 12 children and was always within the normal range. However, children with thyroid hemiagenesis had an average serum TSH significantly higher than that of 18 matched controls (2.8 +/- 0.6 vs. 1.9 +/- 0.5 mU/liter; P < 0.001). This study confirms that thyroid hemiagenesis is nearly always due to left lobe defect, and that its prevalence is similar to the cumulative prevalence of thyroid agenesis and ectopia. Compensatory hypertrophy of the residual thyroid lobe occurs in most, but not all, cases and is due to thyroid tissue overstimulation by TSH. The high risk of goiter and hypothyroidism suggests systematic follow-up of all identified cases of thyroid hemiagenesis.

Adolescent↗

Disturbance of the fetal thyroid hormone state has long-term consequences for treatment of thyroidal and central congenital hypothyroidism.

BACKGROUND: During T(4) supplementation of patients with thyroidal (primary) congenital hypothyroidism (CH) TSH concentrations are frequently elevated despite free T(4) (FT(4)) concentrations being well within the reference range. To examine the thyroid's regulatory system, we analyzed thyroid function determinants in children with congenital and acquired thyroid disorders and in controls. METHODS: Retrospectively, plasma FT(4), TSH, and T(3) concentrations were analyzed in T(4)-supplemented children aged 0.5-20.0 yr with thyroidal CH, central (secondary or tertiary) CH, or autoimmune thyroid disease and in control children with type 1 diabetes mellitus. RESULTS: When TSH was within the reference range (0.4-4.0 mU/liter), mean FT(4) in thyroidal CH [1.65 ng/dl; 95% confidence interval (CI), 1.62-1.67] was significantly higher than in autoimmune thyroid disease (1.15 ng/dl; 95% CI, 1.11-1.19) and diabetes (1.08 ng/dl; 95% CI, 1.06-1.10). In central CH, when TSH was less than or equal to 0.02 mU/liter, mean FT(4) was 1.27 ng/dl (95% CI, 1.24-1.29). When FT(4) was within the reference range (0.78-1.79 ng/dl), 43% of the TSH measurements in thyroidal CH were more than 4.0 mU/liter, compared with 18% in autoimmune thyroid disease and 0% in type 1 diabetes mellitus; in central CH, 95% of TSH measurements were less than 0.4 mU/liter. CONCLUSIONS: In T(4)-supplemented patients with thyroidal CH, when TSH concentrations are established within the reference range, FT(4) concentrations tend to be elevated, and vice versa. Because this phenomenon could not be observed in acquired thyroidal hypothyroidism, we hypothesize that a pre- and/or perinatal hypothyroid state shifts the setpoint of the thyroid's regulatory system. In central CH, when FT(4) concentrations are established within the reference range, the pituitary secretes only minute amounts of TSH. For monitoring T(4) supplementation, reference ranges for FT(4) and TSH should be adapted to the etiology of hypothyroidism.

Adolescent↗

Human thyroid peroxidase (TPO) isoforms, TPO-1 and TPO-2: analysis of protein expression in Graves' thyroid tissue.

Thyroid peroxidase (TPO) is the key enzyme involved in the biosynthesis of thyroid hormones and is an important autoantigen in autoimmune thyroid disease. Different messenger RNA species coding for TPO are present in thyroid tissue, including the species coding for a 933-amino acid protein (termed TPO-1) and a second in which exon 10 is deleted and which is 57 residues shorter (termed TPO-2). However, it is not known whether the smaller, TPO-2 isoform is expressed as a protein in thyroid cells. In SDS-PAGE under reducing conditions, TPO appears in the thyroid microsome and purified protein preparations as a closely migrating double band of approximately 105 (larger form) and 100 kilodaltons (smaller form). We investigated the presence of the isoform TPO-2 polypeptide in Graves' thyroid tissue using rabbit antisera to three different synthetic peptides from exon 10 (specific for TPO-1) and a polyclonal rabbit and monoclonal anti-TPO antibody (both of which are specific for the two forms of TPO). The larger and smaller forms of TPO were purified by electroelution after gel electrophoresis of highly purified natural TPO from Graves' thyroid microsomes. Both of the purified forms of TPO react with all three anti-exon 10 peptide antibodies, the polyclonal anti-TPO and the monoclonal antibody anti-TPO. This shows that both forms of TPO contain exon 10-encoded polypeptide of TPO-1. Interestingly, the proportion of the larger and smaller forms of TPO varied in different Graves' thyroid microsome preparations. To investigate the presence of the smaller TPO-2 isoform in the purified natural TPO preparation, affinity depletion of TPO-1 using the anti-exon 10 peptide antibodies was carried out. The binding of anti-exon 10 peptide antibodies to the immunodepleted TPO-1 fraction was considerably diminished in comparison to binding of polyclonal anti-TPO, suggesting the presence of small amounts (< 10%) of TPO-2 expressed as a protein in thyroid cells. Our results extend previous observations by showing that the alternatively spliced form of TPO, in which exon 10 is excised, is expressed at low levels in Graves' thyroid tissue. Furthermore, we confirm that both the larger and smaller forms of TPO observed on gel electrophoresis contain TPO-1, suggesting that the difference is caused by posttranslational modifications. The presence of small amounts of TPO-2 in Graves' thyroid glands argues for its role in thyroid function, which remains to be clarified.

Amino Acid Sequence↗

Thyroid morphology in lethal non-thyroidal illness: a post-mortem study.

OBJECTIVE: Non-thyroidal illness (NTI) is associated with alterations in thyroid hormone metabolism. Whether morphological changes of the thyroid gland accompany NTI is unknown. The aim of the present study was to describe thyroid morphology in patients with lethal non-thyroidal disease. DESIGN: In an autopsy study 267 cases have been examined. METHODS: Clinical data were obtained from medical records. Subjects were patients with chronic disease (group A), intensive care patients (group B) or persons who had died suddenly without pre-existing illnesses (group C). Patients (n = 93) who did not fit into one of these categories and subjects with pre-existing thyroid disorders were excluded. Thyroid histology was assessed semi-quantitatively: grade I <25%, grade II 25--50% or grade III >75% occupation of the thyroid gland by follicles with a diameter <200 microm. RESULTS: Mean thyroid weight was 19.9 g in group A (n=75, age 19--96 (median 75) years, 48 males); 25.7 g in group B (n=64, age 24--93 (median 69) years, 43 males); and 26.0 g in group C (n=35, age 31--89 (median 69) years, 22 males) (P<0.0005, A vs B/C). Grade I thyroid histology was present in 6 out of 75 patients with chronic illness, in 3 out of 64 intensive care patients and in 33 out of 35 sudden-death subjects. Grade III thyroid histology occurred in 30 out of 75 chronically ill patients, in 17 out of 64 intensive care patients and in 0 out of 35 sudden-death subjects (P<0.0005, C vs A/B). CONCLUSIONS: NTI is associated with reduced thyroid follicular size that is accompanied by lower thyroid weight in chronically ill patients but not significantly in intensive care patients.

Acute Disease↗

[Chronic urticaria with alterations of the thyroid function and thyroid peroxidase antibodies].

Chronic urticaria is a frequent pathology, characterized by the presence of hives and/or angioedema lasting longer than 6 weeks. In an important number of patients it behaves as an autoimmune illness, frequently associated with alterations in thyroid function and thyroid antibodies. We herein describe a consecutive series of 70 patients with a diagnosis of chronic urticaria. Seven (10%) had a diagnosis of thyroid illness previous to their first consultation. Thyroid function and thyroid antibodies were studied in the remaining 63 patients by measuring the level of serum thyrotropin and the titer of peroxidase antibodies. Abnormal thyrotropin levels were detected in 11 (17%) patients, who in conjunction with the 7 patients with previous thyroid illness, add up to 18 (26%) with altered thyroid function. From 61 patients who were tested for thyroid peroxidase antibodies, 22 (36%) were positive. Of 57 patients without a diagnosis of previous thyroid disease, in whom both the levels of serum thyrotropin and the presence of thyroid peroxidase antibodies had been studied, 24 (42%) presented at least one altered study. Given the high percentage of thyroid alterations in our series of patients, it seems clinically relevant to study the thyroid function and the presence of thyroid peroxidase antibodies in patients with chronic urticaria.

Adolescent↗

Thyroid neoplasia, autoimmune thyroiditis, and hypothyroidism in persons exposed to iodine 131 from the hanford nuclear site.

CONTEXT: Approximately 740,000 Ci (2.73 x 10(16) Bq) of iodine 131 (131I) were released to the atmosphere from the Hanford Nuclear Site in Washington State from 1944 through 1957. The risk of thyroid disease resulting from prolonged environmental 131I exposure is poorly understood. OBJECTIVE: The Hanford Thyroid Disease Study (HTDS) was conducted to determine if thyroid disease is increased among persons exposed as children to atmospheric releases of 131I from Hanford. DESIGN: Retrospective cohort study. Exposure could have occurred from December 1944 through 1957. Follow-up occurred until the time of the HTDS examination (December 1992-September 1997). Participants' thyroid radiation doses from Hanford's 131I releases were estimated from interview data regarding residence and dietary histories. SETTING: The cohort included a sample of all births from 1940 through 1946 to mothers with usual residence in 1 of 7 counties in eastern Washington State. PARTICIPANTS: Of 5199 individuals identified, 4350 were located alive and 3440 were evaluable; ie, had sufficient data for dose estimation and received an HTDS evaluation for thyroid disease, including a thyroid ultrasound, physical examination, and fine needle biopsy if required to evaluate thyroid nodularity. MAIN OUTCOME MEASURES: Thyroid cancer, benign thyroid nodules, total neoplasia, any thyroid nodules, autoimmune thyroiditis, and hypothyroidism. RESULTS: There was no evidence of a relationship between Hanford radiation dose and the cumulative incidence of any of the outcomes. These results remained unchanged after taking into account several factors that might confound the relationship between radiation dose and the outcomes of interest. CONCLUSION: These results do not support the hypothesis that exposure during infancy and childhood to 131I at the dose levels (median, 97 mGy; mean, 174 mGy) and exposure circumstances experienced by our study participants increases the risk of the forms of thyroid disease evaluated in this study.

Cohort Studies↗

Thyroid hemiagenesis with subacute thyroiditis.

A 58-year-old woman with thyroid hemiagenesis associated with subacute thyroiditis is described. Physical examinations revealed a firm nodule with spontaneous pain and tenderness in the left thyroid lobe. A serum thyroid hormone levels were elevated and thyroid scintiscan with 99mTc pertechnetate showed an extremely low uptake, we made a diagnosis of subacute thyroiditis. A 201Tl thyroid scan demonstrated an enlarged left lobe and absence of the right lobe. Ultrasonography of the thyroid gland revealed an enlarged left lobe occupied mostly with a hypoechoic region. An incidental finding was absence of the right lobe. Two months later thyroid function returned to normal. A follow-up thyroid scintiscan revealed a normal left lobe but absent right lobe. The diagnosis of hemiagenesis was confirmed by CT scan. This appears to be the first case report of thyroid hemiagenesis associated with subacute thyroiditis.

Blood Cell Count↗

Thyroid function, autoimmune thyroiditis and coeliac disease in juvenile idiopathic arthritis.

OBJECTIVES: Autoimmune diseases have been associated with some organ non-specific rheumatological disorders such as rheumatoid arthritis and systemic lupus erythematosus; however, few studies have been performed in an extensive cohort of children with juvenile idiopathic arthritis (JIA). Our objective was to evaluate the thyroid function and the prevalence of antithyroid antibodies, autoimmune thyroiditis and coeliac disease in children with JIA. METHODS: One hundred and fifty-one children (120 female, 31 male, median age 8.3 yr, range 2.4-16.9 yr) with JIA were evaluated. All patients underwent thyroid function tests (u-TSH, free T(4) and free T(3)), antithyroglobulin (TgA) and antiperoxidase (TPOA) antibodies, antigliadin, anti-endomysium and antitransglutaminase antibodies. All patients with raised thyroid stimulating hormone levels, low thyroid hormone levels or positive TPOA and/or TgA values had a thyroid high-resolution sonography examination. Coeliac disease was confirmed by jejunal biopsy if the specific antibodies profile was positive. One hundred and fifty-eight age- and sex-matched Caucasian children from the same geographical area acted as controls. RESULTS: Fourteen (9.3%) patients showed subclinical hypothyroidism, 17 (11.9%) patients showed autoimmune thyroiditis with nine patients also showing a non-homogeneous thyroid parenchyma at ultrasound evaluation. Coeliac disease was demonstrated in 10 (6.6%) patients. Compared with controls, JIA patients had higher prevalence of subclinical hypothyroidism (P < 0.01), autoimmune thyroiditis (P < 0.0001) and coeliac disease (P < 0.005). CONCLUSIONS: JIA children have an increased prevalence of autoimmune thyroiditis, subclinical hypothyroidism and coeliac disease. These data seem to suggest careful monitoring of thyroid function, thyroid autoantibodies and coeliac disease in JIA children.

Adolescent↗

Persistent viral infection of the thyroid gland: alteration of thyroid function in the absence of tissue injury.

The possible role of viruses as the cause of some thyroid disorders was evaluated in three strains of mice neonatally infected with lymphocytic choriomeningitis virus. We report the first definitive evidence that viruses can persist in the thyroid gland, particularly thyroid epithelial cells in which thyroglobulin is synthesized. Concomitant with the infection of these cells was a significant reduction in the level of thyroglobulin mRNA and circulating thyroid hormones. Another virus that causes persistent infection but does not replicate in the thyroid gland failed to alter serum levels of thyroid hormones, indicating the thyroid dysfunction was not a generalized result of stress accompanying a persistent infection. This alteration in thyroid homeostasis during persistent infection with lymphocytic choriomeningitis virus is not caused by autoantibodies to the thyroid. Moreover, despite infection of the thyroid gland, neither necrosis nor inflammation occurs. Thyroid dysfunction was noted both when persistence was initiated at birth and in utero during congenital infection. These observations in an experimental model raise the issue that viruses may play a role in the pathogenesis of some thyroid disorders in man.

Animals↗

Reversible changes of the histological abnormalities of the thyroid in patients with painless thyroiditis.

The histological abnormalities on percutaneous needle biopsy of the thyroid were investigated in two patients (cases 1 and 2) with transient thyrotoxicosis and low radioactive iodine uptake by the thyroid and in a patient (case 3) with transient hypothyroidism which might be the consequence of transient thyrotoxicosis. The most characteristic findings of lymphocytic thyroiditis, such as extensive lymphocyte infiltration with collapsed follicles and degeneration of follicular cells of the thyroid, were found in case 1, in whom the thyroid biopsy was performed in the thyrotoxic phase. Ashkanazy cells were not present and fibrosis was not observed in this specimen. Histological examination of the thyroid biopsy specimen, which was obtained in the recovery phase in case 1, revealed well preserved thyroid follicles and slight lymphocytic infiltration. In addition, papillary infoldings of cuboidal epithelium were found in cases 2 and 3, in whom the thyroid biopsy was done in the hypothyroid phase. The follow-up biopsy of the thyroid was performed in the recovery phase in case 3. The biopsy specimen showed focal lymphocytic infiltration and the follicles lined by low cuboidal cells without papillary infoldings. In all biopsy specimens, there was no evidence of subacute thyroiditis, as characterized by granulomatous changes and breakdown of colloid follicles with foreign body giant cell reaction. The present findings revealed that the histological abnormalities, such as lymphocytic infiltration and follicular epithelial changes of the thyroid, observed in the patients with painless thyroiditis, can improve spontaneously during the course of several months.

Adult↗

Acute spontaneous hemorrhagic degeneration of the thyroid nodule with subacute thyroiditis-like symptoms and laboratory findings.

Seventeen consecutive patients (3 men and 14 women, aged 14-75 years) with a hemorrhagic degeneration of the thyroid nodule, which was confirmed by both ultrasonography and either reddish or brown fluid evacuated by fine-needle aspiration, were classified as either acute type with an episode of abrupt painful swelling of the thyroid (n = 4), or chronic type in which a painless thyroid nodule was incidentally found (n = 13). One of the four acute type patients demonstrated subacute thyroiditis-like symptoms and laboratory findings including transient painful thyrotoxicosis associated with high serum levels of thyroid hormones and thyroglobulin (Tg), a suppressed serum TSH level, a low thyroidal radioactive iodine uptake (RAIU), and accelerated erythrocyte sedimentation rate (ESR). In the other three acute type patients the serum level of Tg increased markedly, the serum thyroid hormones level increased in one, the thyroidal RAIU was low in two, and the ESR was accelerated in one. In the thirteen chronic type patients, the serum levels of the thyroid hormones and the thyroidal RAIU were within the normal range, and few inflammatory signs were observed. These findings suggest that acute hemorrhagic degeneration of the thyroid nodule may thus cause transient subacute thyroiditis-like symptoms and laboratory findings.

Acute Disease↗