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Absence of three regular thyroid arteries replaced by an unusual lowest thyroid artery (A. thyroidea ima): a case report.

During routine dissection of an 89-year-old female donor both inferior thyroid aa. as well as the left superior thyroid a. were found to be absent, whereas the right superior thyroid a. came from the right common carotid. A large lowest thyroid a. rose from the left internal thoracic a. at the level of the first intercostal space. Up to this point the internal thoracic a. was of immense diameter, almost reaching that of the lateral part of the subclavian. The lowest thyroid a. ascended in an oblique and sigmoid course to the thyroid gland. Slightly left of the median line it bifurcated into two branches. Both had a winding course in front of the trachea before entering the base of the thyroid gland. Other arterial variations of minor significance were also observed in this unique case. The clinical impact lies in the localisation, course and size of the lowest thyroid a. reported.

Aged↗

The foetal thyroid of the dromedary: its relation to body weight and dimensions and to the weight of the Dam's thyroid.

Growth and iodine content of the thyroid glands in relation to body weight, length [total (BCVRT), crown-rump (CR), and curved crown-rump (CVR)], chest circumference (CC), and age were investigated in 83 camel foetuses from 70 to 355 days of gestation (mean gestation length 390 days). Weight and iodine content of the dam's thyroid were also studied. Highly significant (P less than 0.01) correlations of 0.883, 0.797, 0.798, 0.792, and 0.813 were obtained between foetal thyroid weights on the one hand and body weight, BCVRT, CR, CVR, and CC on the other hand. A significant (P less than 0.05) correlation of 0.345 was obtained between weights of the foetal thyroid and dam's thyroid. The relative weight of the foetal thyroid to body weight was 0.045% at 70-99 days of gestation, but decreased to 0.028 (0.023 to 0.036%) in the subsequent stages. Iodine trapping by the foetal thyroid was first detected at 100-129 days of gestation. Total iodine then increased until 310 days, but decreased thereafter. The foetal thyroid has 4 to 25 times higher avidity to iodine accumulation than that of the dam.

Animals↗

Alteration in the transmission of TSH-message to thyroid target in a transplantable rat thyroid tumor.

Plasma membranes derived from a transplantable rat thyroid tumor (line 1-5G in Wollman's classification), which is unresponsive to thyrotropin (TSH) but is responsive to dibutyryl 3', 5' cAMP, have been evaluated to localize the defect. TSH binding in tumor plasma membrane is slightly lower than in normal rat thyroid membranes. No change in affinity, but simply a lower capacity was observed. The glycoprotein component of the TSH receptor exhibits similar binding and solubilization properties to the glycoprotein component derived from normal rat thyroid. Analogously to normal rat thyroid membranes, gangliosides more complex than N-acetylneuraminylgalactosylglucosyl-ceramide (GM3) are also present in tumor line 1-5G membranes. Phospholipid content of tumor line 1-5G is 50% lower than that of normal rat thyroid. At variance also with normal rat thyroid, 32P incorporation in tumor line 1-5G phospholipids such as phosphatidylserine and phosphatidylethanolamine is not modified after in vitro incubation with TSH. An even more pronounced effect by TSH on 32P incorporation into phosphatidylinositol is evident in tumor line 1-5G by comparison to normal. The 1-5G thyroid tumor membranes has a 12-fold higher basal adenylate cyclase activity than that of rat thyroid membranes. The high basal adenylate cyclase activity is associated with high ADP ribosylation activity. Both enzymes of tumor are only slightly responsive to TSH. These results suggest that the block in the transmission of TSH message to the cell machinery is localized to the regulatory domains between TSH receptor and adenylate cyclase catalytic subunit.

Adenosine Diphosphate Ribose↗

Uptake of amiodarone by thyroidal and non-thyroidal cell lines.

Amiodarone perturbs thyroid function, causing overt hypothyroidism or hyperthyroidism in 15% of patients. Changes in thyroid function are likely due, at least in part, to amiodarone and/or desethylamiodarone (DEA) concentration into the thyroid gland, but mechanisms whereby the drug uptake occurred are not known. Thyroidal (FRTL-5) or non-thyroidal [Chinese hamster ovary wild-type (CHOwt) or CHO stably transfected with NIS (CHO-NIS)] cells were exposed to 10 microM amiodarone or DEA. Cellular content of both drugs was measured by HPLC and normalized by protein concentration. Cellular concentration of the two drugs was higher in FRTL-5 (mean +/- SD 17.2 +/- 1.2 microg/mg protein of amiodarone and 18.9 +/- 0.7 microg/mg protein of DEA) than in CHO-NIS and CHOwt cells (10.8 +/- 0.8 microg/mg protein and 12.8 +/- 0.2 microg/mg protein, respectively, of amiodarone (p < 0.004); 11.9 +/- 0.1 microg/mg protein and 11 +/- 0.2 microg/mg protein, respectively, of DEA (p < 0.0002). DEA concentration was higher than that of amiodarone in all cell lines (p < 0.002). Differences between FRTL-5 and CHO cell lines were not dependent on TSH: in fact, cellular content of either drug did not change in the presence or absence of TSH in the culture medium. NIS did not intervene in amiodarone or DEA entry into thyroid cells, since amiodarone and DEA content was the same in CHOwt and CHO-NIS cells; in addition, KClO4 inhibited NIS function, but had no effect on drug uptake by the cells. At variance, 80 microM DEA reduced 125I uptake by CHO-NIS cells by 40% at 30 min without affecting cell viability. In conclusion, mechanisms whereby amiodarone is taken up by thyroid cells remain largely unknown, but the two main factors involved in thyroid-specific cellular transport, ie, NIS and TSH, seem to be excluded.

Amiodarone↗

Post-surgical ablation of thyroid residues with radioiodine in Ukrainian children and adolescents affected by post-Chernobyl differentiated thyroid cancer.

Post-surgical ablation of thyroid residues with 131-iodine (131-I) is usually recommended after near-total thyroidectomy in high-risk patients, including children, with differentiated thyroid cancer (DTC). We report here the results of post-surgical radioiodine thyroid ablation in 249 children and adolescents of Ukraine with post-Chernobyl DTC initially treated with near-total thyroidectomy at the Institute of Endocrinology and Metabolism in Kiev, during a 2-year period. The patients' age at the time of the Chernobyl accident (1986), ranged from <1 to 14 yr in 223 subjects (children) and from 15 to 18 yr in 26 subjects (adolescents). Six weeks after surgery a diagnostic 131-I whole body scan revealed the presence of residual thyroid tissue in all cases. All patients received one or more courses of radioiodine therapy, for a total of 468 courses. One hundred and twenty-nine out of 249 patients (51.8%) were successfully ablated. The total number of treatment courses needed in these patients was 219. Most patients required multiple doses of radioiodine, only 63 required a single dose. One hundred and twenty patients (48.2%) treated with radioiodine were not ablated and are still under treatment program. The clinical features and the amount of thyroid residue were not different in ablated or not-ablated patients. Our results indicate that in this particular population of post-Chernobyl thyroid carcinomas, thyroid ablation is a rather difficult task. Only 51.8% were successfully ablated. Possible explanation for this finding may be the young age of the patients, other particular features of post-Chernobyl thyroid carcinoma or technical aspects, such as less radical surgical procedures.

Adolescent↗

Detection of asymptomatic differentiated thyroid carcinoma by neck ultrasonographic screening for familial nonmedullary thyroid carcinoma.

Mass screening for the purpose of detecting thyroid cancer at its earliest stage may not be recommended at the present time, but screening focused on certain risk groups is advocated. Familial nonmedullary thyroid carcinoma (FNMTC) is a distinct clinical entity with a high incidence of multifocality and association with multiple benign nodules. FNMTC patients have shorter disease-free survival than do sporadic disease patients because of frequent locoregional recurrence. Screening by neck ultrasonography was performed for symptom-free family members of patients with FNMTC. A total of 149 subjects representing 53 FNMTC families were examined in this study. The average age of the patients was 41.0+/-19.0 years (range 3-76 years) with a female/male ratio of 104:45. At least one thyroid nodule was found in 77 (51.7%) of the 149 patients. Surgery was performed in 18 patients, and thyroid cancer was discovered in 15 of them (10.1%; 14 women, 1 man; 32-61 years of age). Papillary thyroid cancer (PTC) was found in 14 and follicular thyroid cancer combined with PTC in 1. The tumors averaged 9.1+/-5.4 mm (3-21 mm) in greatest diameter. Intraglandular metastases were found in 7 (47%) of the 15 patients with thyroid cancer. Lymph node metastases were found in 6 (43%). Ultrasonographic screening for FNMTC family members may enable the discovery of asymptomatic thyroid cancer. Because of the high incidence of intraglandular and lymph node metastases, we recommend screening with ultrasonography for early detection in family members of patients with FNMTC.

Adolescent↗

Thyroid cell responses to thyrotropin and 12-O-tetradecanoyl-phorbol-13-acetate: translocation of protein kinase C and phosphorylation of thyroid cell polypeptide substrates.

Not all of the effects of thyroid-stimulating hormone (TSH) on the thyroid are mediated by activation of the adenylate cyclase-cyclic AMP system, indicating that other control systems must also exist. Although a calcium-phospholipid-dependent protein kinase (protein kinase C) and specific substrates had been identified in thyroid tissue, their responsiveness to TSH and other stimulators has not been determined. In thyroid cells which had been preloaded with [32P]orthophosphate, TSH and 12-O-tetradecanoyl-phorbol-13-acetate (TPA) increased the phosphorylation of a 33K polypeptide substrate within 5 min in a dose-dependent fashion. The effect was observed with 1 mU/ml TSH and 3 nM TPA and was maximal with 100 mU/ml TSH and 100 nM TPA. The biologically inactive analog of TPA, 4 alpha-phorbol, had no effect. Isobutylmethylxanthine (IBMX) decreased the phosphorylation of the 33K polypeptide and inhibited the effect of TSH and TPA, indicating that the phosphorylation is not mediated by cyclic AMP. TSH and IBMX, but not TPA, augmented phosphorylation of a 38K polypeptide, suggesting involvement of cyclic AMP. In contrast TPA, but not TSH, increased the phosphorylation of 58K and 28K polypeptides. TSH, but not TPA or 4 alpha-phorbol, elevated the cyclic AMP level of thyroid slices. Incubation of thyroid slices with TSH or TPA significantly decreased protein kinase C activity in the 100,000g cytosol fraction and increased it in an extract of plasma membranes. The effect was present within 5 min and was maximal by 30 min. The effect was observed with 100 mU/ml TSH or 1 nM TPA. The stimulation by TSH or TPA of protein kinase C and its translocation from the cytosol to the plasma membranes of thyroid tissue may provide another mechanism for control of thyroid cell metabolism.

1-Methyl-3-isobutylxanthine↗

Thyroid disease and mental illness: a study of thyroid disease in psychiatric admissions.

The notes of 1007 consecutive admissions to a District General Hospital adult psychiatry unit were examined retrospectively to establish the role of the thyroid disease detected in routine management. Thyroid function tests were performed on 300 admissions, leaving 707 untested. Ten had abnormal results (3.3% of admissions tested), accounted for by nine patients with affective disorder. Two of the nine settled spontaneously, but seven cases (2.3%) had sustained abnormality. Five of the seven had a known history of thyroid disease, leaving two new findings of hypothyroidism who presented with no clinical signs other than their mental illness (0.7% of admissions tested). In five cases, which included the two new findings, the thyroid disease had been judged to precipitate the mental illness. All cases except one transitory abnormality occurred in females. When the results of this and other surveys are compared with the figures for thyroid disease in the general population, the value of screening psychiatric patients seems questionable. However, diagnosis is important in a few cases where thyroid disease apparently contributes to the mental illness. For psychiatric patients aged up to 65, elimination of unnecessary thyroid function tests without sacrificing detection may be possible by restricting use to female patients with affective disorder, patients with a past or family history of thyroid disease or with presenile dementia. Abnormal results obtained during the acute phase of the illness may be transitory and require confirmation.

Adult↗

Thyroid-specific T cells in the normal Wistar rat. I. Characterization of lymph node T cell reactivity to syngeneic thyroid cells and thyroglobulin.

Wistar rats are susceptible to the induction of experimental autoimmune thyroiditis (EAT) and recently a cloned Wistar thyroid epithelial cell line (WRT) has become available. In this study we have examined the in vitro proliferative response of Wistar rat lymphoid cells to the WRT cells as a model for better understanding thyroid cell-T cell interactions. Lymph node (LN) cells from normal Wistar rats showed an early and vigorous response to syngeneic thyroid cells (WRT). Further examination of the Wistar phenomenon revealed that unpurified lymphoid cells were also able to mount a proliferative response to rat thyroglobulin. The Wistar LN cell response to WRT cells consisted of T cell proliferation that was both MHC class I and class II restricted. There was a greater proliferation of CD8+ than CD4+ T cells, but WRT-stimulated lymphoblast cells were not cytotoxic to 51Cr-labeled WRT cell targets. These data suggest that normal Wistar rats have circulating thyroid-specific T cells that may be related to their known susceptibility to EAT. Furthermore, the interaction between such thyroid-specific T cells and cloned syngeneic thyroid cells offers a unique model for the further investigation of thyroid-immune interactions and the escape from tolerance induction.

Animals↗

Thyroidal ANF: a possible mediator of autocrine regulation in the porcine thyroid gland.

Atrial natriuretic factor immunoreactivity (ir-ANF) was examined in thyroid tissue sections and cultured thyroid cells using immunohistochemical staining with a monoclonal anti-ANF antibody. Localization of ir-ANF in perinuclear granules in cultured cells and in the basal region of follicular cells in sectioned tissue suggests that ir-ANF is a basally secreted product. Thyroidal ir-ANF was also characterized using reversed phase high performance liquid chromatography (RP-HPLC) of acidic thyroid extracts. An ir-ANF peak coeluting with synthetic rat ANF(99-126) suggests that thyroidal ir-ANF may be identical in form to circulating atrial ANF. However, the detection of ir-ANF in cultured thyroid cells confirms that the immunoreactivity is locally produced. Saturation analysis revealed high affinity ANF receptors (Kd = 0.1 nM; MBC = 17.2 fmol/mg protein) on these cultured cells, and a competition study demonstrated the ability of extracted thyroidal ir-ANF to inhibit 125I rat ANF binding to the membrane receptors. The evidence presented here suggests that ir-ANF in the thyroid may be secreted locally to exert an autocrine effect on neighboring follicular cells.

Animals↗

A novel tumor marker, Niban, is expressed in subsets of thyroid tumors and Hashimoto's thyroiditis.

Niban is a recently identified molecular marker of renal carcinogenesis in the Tsc2 gene-mutant Eker rat. Niban expression is most dramatically increased in the early stage of renal carcinogenesis and might decline during malignant progression. Niban is also expressed in various histologic types of human renal cell carcinoma. Therefore, Niban might be a good marker for renal carcinogenesis in both animal models and humans. In the present study, we examined Niban expression in various thyroid lesions by immunohistochemical staining using polyclonal rabbit antihuman Niban antibody. Normal thyroid tissue never stained for Niban. Niban was most frequently expressed in tumors with oxyphilic cytoplasm, including oxyphilic variants of papillary carcinoma (4/4 = 100%), oxyphilic variants of follicular adenoma (7/7 = 100%), and oxyphilic variants of follicular carcinoma (5/5 = 100%). Eighty-one percent (44/54) of papillary carcinoma cases, including microcarcinomas, and follicular variants were also positively stained for Niban at variable intensities. Follicular carcinomas were less frequently and less intensely stained. In nonneoplastic lesions, cells were rarely positively stained. In Hashimoto's thyroiditis, scattered cells with oxyphilic cell metaplasia were weakly Niban-positive. Reverse transcriptase-polymerase chain reaction and Western blot analysis of frozen tissue confirmed Niban expression at the molecular level in 4 cases of papillary carcinoma. Taken together, Niban expression is up-regulated in various types of thyroid tumors. We postulate that Niban expression may play an important role in the tumorigenic process of the thyroid in several scenarios. (1) Niban expression may be closely related to the carcinogenic process, especially from the early stage of papillary thyroid carcinoma. (2) Niban may be closely associated with altered mitochondrial functions in preneoplastic and neoplastic processes of the thyroid. (3) Niban may be a molecular marker of the oxyphilic phenotype under various conditions. Further functional studies of Niban will clarify the role of Niban in various thyroid lesions.

Biomarkers, Tumor↗

Human Thyroid Oxidases genes promoter activity in thyrocytes does not appear to be functionally dependent on Thyroid Transcription Factor-1 or Pax8.

Thyroid Oxidases (ThOX/DUOX) genes encode proteins that are thought to play a crucial role in the biosynthesis of thyroid hormone by providing the oxidizing agent required to allow the organification of iodine. The expression of these genes is not restricted to the thyroid, but the corresponding mRNAs are found in the thyrocyte more abundantly than in several other cell types. It raises the question whether the same transcription factors, namely Thyroid Transcription Factor-1 (TTF-1) and Pax8, that control the expression of other genes involved in the differentiated thyroid function, also regulate ThOX/DUOX gene transcription in the thyrocyte. We set up a functional co-transfection assay in which fusion proteins composed of the DNA-binding domain of either TTF-1 or Pax8 fused to the repressive domain of the drosophila engrailed protein were used to competitively counteract the activity of endogenous TTF-1 or Pax8 factor in the differentiated thyroid cell line PCCl3. Contrary to the Thyroglobulin or Thyroid Peroxidase promoter, the known regulatory elements of the human ThOX/DUOX genes displayed no reduction in transcriptional activity when either TTF-1 or Pax8 competitor was produced in the cell, indicating that the presently characterized control elements of human ThOX/DUOX genes are not responsive to these thyroid-specific transcription factors.

Animals↗

[Anti-thyroid peroxidase in non-neoplastic thyroid pathology].

Anti-thyroid peroxidase antibodies were prospectively assayed and compared with anti-microsome and anti-thyroglobulin antibodies in 203 patients (188 women, 15 men; mean age 42 +/- 14 years). These patients consulted for hyperthyroidism (n = 42, including 18 with Graves' disease), fumary hypothyroidism (n = 50, including 20 at the diagnosis stage), euthyroid diffuse or nodular goitre (n = 81) or benign euthyroid nodule (n = 14). Sixteen patients examined for fatigue, gynecomastia, menstrual disorders or overweight had normal thyroid function. Anti-thyroid peroxidase, anti-microsome and anti-thyroglobulin antibodies were assayed by radioimmunology or indirect immunofluorescence. Anti-thyroid peroxidase antibodies were most frequently present in patients with autoimmune thyroid diseases, such as Graves' disease (72%) or primary hypothyroidism (70%), and correlated with anti-microsome antibody levels (r = 0.87; p less than 0.001). Anti-thyroid peroxidase antibodies were absent in patients with benign euthyroid nodule; they were present in 22% of patients with euthyroid goitre and in 12% of control patients; their level decreased during replacement therapy for hypothyroidism. It is concluded that radioimmunological assays of anti-thyroid peroxidase antibodies should replace anti-microsome and anti-thyroglobulin antibodies in thyroid evaluation.

Adult↗

Intranodal benign thyroid tissue: significance of HBME-1 in differentiation from metastatic papillary thyroid carcinoma.

The aim of this study was to determine the significance of HBME-1 immunostaining in the differentiation between intranodal benign thyroid tissue and metastatic papillary thyroid carcinoma in the lymph node. Immunohistochemically we examined normal-appearing intranodal thyroid tissue in four patients who did not show evidence of papillary carcinoma histologically or clinically. We also examined follicular-pattern-predominant papillary carcinoma with metastatic foci in the lymph nodes. Normal-appearing intranodal thyroid tissue and normal thyroid showed no immunopositivity for HBME-1. In contrast, all papillary carcinomas in both the lymph nodes and thyroid demonstrated strong positivity for HBME-1. HBME-1 was predominantly positive for the luminal surface of the tumor cells. The immunopositivity of the cuboidal and low columnar carcinoma cells was more intensive than that of the flat-shaped cells in the lymph nodes and thyroid. The results probably indicate that HBME-1 immunostaining is helpful in distinguishing between intranodal benign thyroid tissue and metastatic papillary carcinoma in lymph nodes. We emphasize that the HBME-1 reactivity should be evaluated in connection with the histological findings, and that positive and negative controls stained in parallel are necessary.

Aged↗

Relation between serum interleukin-6 and thyroid hormone concentrations in 270 hospital in-patients with non-thyroidal illness.

OBJECTIVES: Non-thyroidal illness (NTI) is frequently accompanied by alterations in circulating thyroid hormone concentrations, despite patients remaining clinically euthyroid. The mechanisms accounting for these changes in circulating thyroid hormone concentrations remain unknown. Much attention has focussed on the role of inflammatory cytokines which are known to be important mediators of disease. The aim of this study was to investigate the role of the cytokine interleukin-6 (IL-6) in alterations of thyroid hormone metabolism seen in NTI. DESIGN: Longitudinal study of hospital in-patients, correlating serum IL-6 concentrations with circulating thyroid hormone concentrations. PATIENTS: Two hundred and seventy in-patients recruited consecutively, excluding those with known or suspected thyroid disorder. The patients were divided into 5 subgroups reflecting the nature of their NTI and comprised 41 patients with liver disease, 99 with renal disease, 19 intensive care (ITU) patients, 22 with cardiac disease and 89 patients with general medical, or surgical conditions. MEASUREMENTS: Serum IL-6 concentrations were determined using a commercially obtained immunoassay (IL-6 Quantikine assay, R&D Systems, Abingdon, UK). Serum total T4 and total T3 were measured using chemiluminescent immunometric assays (Kodak Clinical Diagnostics Ltd, Amersham, UK) and serum TSH was measured using a third-generation chemiluminescent immunometric assay (Amerlite TSH 30, Kodak Clinical Diagnostics Ltd, Amersham, UK). RESULTS: Ninety-three patients studied (35%) had a serum T3 below the normal range (<1.0 nmol/l), 89 patients (33%) had a serum T4 below the normal range (<65 nmol/l) and in 58 patients (21%) both serum T3 and T4 were below the normal range. There was a significant negative correlation between serum total T3 and IL-6 (r = -0.219; P < 0.001) and total T4 and IL-6 (r = -0.32; P = 0.32), but not between TSH and IL-6 (r = -0.075; P = 0.22). The ITU patient subgroup had the highest IL-6 concentrations (229.3 +/- 48.1 ng/l, mean +/- standard error), whilst also having the lowest T3 (0.93 +/- 0.08 nmol/l), TSH (0.79 +/- 0.25 mU/l) and T4 concentrations (66.6 +/- 7.3 nmol/l). The subgroup of patients under general medical or surgical care had least disturbance of their T3 (low in 19%) and T4 (low in 8%) concentrations, whilst also having the lowest mean IL-6 concentration (39.0 +/- 5.3 ng/l). The renal patient subgroup, whilst including a high proportion of patients with low T3 (39%) and T4 (45%) concentration, demonstrated only modest elevation of IL-6 concentrations (mean 41.4 +/- 8.5 ng/l). CONCLUSIONS: Our data revealed a statistical relation between elevated serum IL-6 concentrations and alterations in circulating thyroid hormone concentrations seen in NTI; however, the findings in patients with renal disease suggest that circulating IL-6 is not the only factor responsible for alteration in thyroid hormone metabolism in NTI.

Euthyroid Sick Syndromes↗

Thyrocyte integration, and thyroid folliculogenesis and tissue regeneration: perspective for thyroid tissue engineering.

The thyroid gland is composed of many ball-like structures called thyroid follicles, which are supported by the interfollicular extracellular matrix (ECM) and a capillary network. The component thyrocytes are highly integrated in their specific structural and functional polarization. In conventional monolayer and floating culture systems, thyrocytes cannot organize themselves into follicles with normal polarity. In contrast, in 3-D collagen gel culture, thyrocytes easily form stable follicles with physiological polarity. Integration of thyrocyte growth and differentiation results ultimately in thyroid folliculogenesis. This culture method and subacute thyroiditis are two promising models for addressing mechanisms of folliculogenesis, because thyroid-follicle formation actively occurs both in the culture system and at the regenerative phase of the disorder. The understanding of the mechanistic basis of folliculogenesis is prerequisite for generation of artificial thyroid tissue, which would enable a more physiological strategy to the treatment of hypothyroidism caused by various diseases and surgical processes than conventional hormone replacement therapy. We review here thyrocyte integration, and thyroid folliculogenesis and tissue regeneration. We also briefly discuss a perspective for thyroid tissue regeneration and engineering.

Animals↗

Avian thyroid development in chemically contaminated environments: is there evidence of alterations in thyroid function and development?

Poor reproductive success, developmental abnormalities, and behavioral alterations in fish-eating birds in some Great Lakes areas have led to more than 35 years of toxicological studies and residue monitoring of herring gull (Larus argentatus) populations. Polyhalogenated aromatic hydrocarbons (PHAHs), especially polychlorinated biphenyls (PCBs), are widespread contaminants in the Great Lakes ecosystem. The introduction of regulations and elimination of point sources since the 1970s have resulted in decreased PHAHs in fish-eating bird eggs and tissues. PCB exposure is associated with thyroid disruption (hypothyroidism) in mammals, but much less is known of PCB effects on avian thyroid function. Our 1998-2000 studies of herring gulls from the Great Lakes show that both pipping embryos and prefledglings from highly contaminated sites have marked depletion of thyroid gland hormone stores compared with similarly aged gulls at the reference sites. However, organismal hypothyroidism was not apparent in many embryo and chick collections where severe depletion of thyroid gland hormone was observed. Adults, sampled at two high PCB sites and a low PCB site in the Great Lakes and the maritime reference colony in 2001, showed no differences in organismal thyroid status across sites, but gulls from the high sites had enlarged thyroid glands and depressed thyroid gland hormone stores. Here we discuss the evidence that ecological exposure to PHAHs are responsible for thyroid deficiencies in gulls and that during development these deficiencies lead to developmental abnormalities in young gulls from highly contaminated Great Lakes sites.

Animals↗

Is familial non-medullary thyroid carcinoma more aggressive than sporadic thyroid cancer? A multicenter series.

BACKGROUND: The aggressiveness of familial non-medullary thyroid cancer (FNMTC) has been a subject of debate. The purpose of the study was to determine whether FNMTC is more aggressive than sporadic thyroid cancer. METHODS: A multicenter retrospective matched-case control study of FNMTC versus sporadic non-medullary thyroid cancer was conducted. Disease-free survival (time to recurrence) for both groups was compared. RESULTS: Forty-eight familial cases were compared with 144 age-, gender-, and stage-matched controls. Patients with FNMTC had a significantly shorter disease-free survival compared with sporadic non medullary thyroid cancer. Patients with FNMTC who presented with evidence of distant metastasis, or who were from families with more than 2 thyroid cancer-affected members, had the worst prognosis. The available staging systems were less likely to predict the outcome in patients with FNMTC than in patients with sporadic non-medullary thyroid cancer unless one accounted for the strength of family history in the staging system. CONCLUSIONS: FNMTC is more aggressive than sporadic non-medullary thyroid cancer. The best predictors of a poor outcome in patients with FNMTC are the number of family members affected by thyroid cancer and evidence of distant metastasis.

Adult↗