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PubMed2005

Exaggerated TSH responses to TRH in patients with goiter and 'normal' basal TSH levels.

BACKGROUND/AIM: The availability of sensitive thyrotropin (TSH) assays decreased the diagnostic value of thyrotropin-releasing hormone stimulation tests (TRH-ST) in subclinical hypothyroidism. In this study we aimed to evaluate the relation between basal and stimulated serum TSH levels on TRH-ST and to determine the prevalence of patients with normal basal serum TSH and exaggerated TSH responses. METHODS: 179 patients (117 girls, 123 pubertal) with a median age of 12 (2.7-21.4) years who presented with goiter were enrolled and evaluated for their pubertal stage, height, thyroid autoimmunity, ultrasonography, thyroid function, and TRH-ST. Serum TSH concentrations were determined by sensitive assays. At TRH-ST, a peak serum TSH level >25 mIU/l was considered as an exaggerated response. RESULTS: 30 (17%) patients had an exaggerated TSH response. In patients with serum TSH levels between 2 and 4.68 mIU/l (upper half the normal range), an exaggerated TSH response was observed in 19.5%. A positive correlation between basal and TRH-stimulated TSH levels was determined (r = 0.536, p < 0.01). In patients with an exaggerated TSH response, 23 had normal (discordant) and 7 had high basal TSH levels (concordant). The mean basal serum TSH level was lower in the discordant group compared to the concordant group (p < 0.01). CONCLUSION: Basal serum TSH levels might not be sufficient for diagnosing subclinical hypothyroidism. Stimulated TSH levels on TRH-ST are valuable, especially when serum TSH concentrations are in the upper half of the normal range.

Adolescent↗
PubMed1987

Increased thyroidal T4/T3 ratio in nodular and paranodular tissues of nontoxic goiter following suppressive treatment with thyroid hormones.

The effect of suppressive treatment with thyroid hormones on thyroidal iodothyronines and T4/T3 ratio in nodular and paranodular tissues was investigated in 12 patients with nontoxic goiter. Results were compared to those from 11 nontreated patients. Continuous thyroid hormone administration produced a significant increase in thyroidal T4 and T4/T3 ratio in nodular tissues while T3 remained unchanged. In paranodular tissues a significant rise of T4/T3 ratio, an insignificant increase in T4 and a decrease in T3 were observed following the administration of thyroid hormones. The results are very similar to those obtained in paranodular tissue of autonomously functioning thyroid nodule, and are probably the consequence of suppressed TSH secretion, as TSH predominantly stimulates the synthesis of T3 and/or thyroidal T4 monodeiodination.

Goiter, Nodular↗
PubMed1986

Retrosternal goiter and chylothorax: case report.

We describe a case of chylothorax associated with a retrosternal goiter. Such an association has not been previously reported. The chylothorax was probably caused by compression of the thoracic duct and brachiocephalic vessels.

Aged↗
PubMedDate not supplied

Multinucleated giant cells in fine needle aspirates. Can they help differentiate papillary thyroid cancer from benign nodular goiter?

OBJECTIVE: To determine whether multinucleated giant cells (MGCs) in fine needle aspirates can help differentiate papillary thyroid carcinoma (PTC) from benign nodular goiter (BNG). STUDY DESIGN: Specimens from 100 cases of PTC and 100 cases of BNG with surgical and pathologic proof were randomly retrieved. The morphologic characteristics and frequency distribution of the maximal size and number of MGC nuclei were analyzed. A retrospective review of medical records was also undertaken. RESULTS: MGCs were twice as frequent (40%) in PTC than in BNG (26%) (odds ratio = 1.90). Most MGCs in BNG tended to be smaller and ovoid, with foamy cytoplasm, and had fewer nuclei. No MGC in BNG was > 116 microns in diameter or had > 27 nuclei. In contrast, MGCs in PTC were more diverse in size, shape, cytoplasm and number of nuclei. No significant association was found between the presence or nature of MGCs and disease extent in PTC. CONCLUSION: The presence of large MGCs with dense cytoplasm in a thyroid nodule without clinical evidence of thyroiditis should prompt careful exclusion of associated PTC.

Biopsy, Needle↗
PubMed1992

Identification of a mutation in the coding sequence of the human thyroid peroxidase gene causing congenital goiter.

Thyroid peroxidase (TPO) is the key enzyme in the synthesis of thyroid hormones, and the TPO defects are believed to be the most prevalent causes of the inborn errors of thyroid metabolism. We investigated an adopted boy with iodide organification defect, who presented with florid hypothyroidism at the age of 4 mo, poorly complied with thyroxine treatment, and developed a compressive goiter necessitating partial resection at the age of 12 yr. Biochemical studies revealed the absence of TPO activity in the resected tissue. Genomic DNA studies identified a 4 base-pair insertion in the eighth exon of the TPO gene, and showed that the patient was homozygous for this frameshift mutation. The direct genetic diagnosis of this mutation can be made by digestion of polymerase chain reaction products with NaeI restriction enzyme. This will help assessing its prevalence among the heterogenous genetic group of TPO defects.

Amino Acid Sequence↗
PubMedDate not supplied

Frequency of thyroid carcinoma in a recent series of 539 consecutive thyroidectomies for multinodular goiter.

AIMS AND BACKGROUND: The aim of the study was to analyze the frequency of thyroid carcinoma in a consecutive series of 539 thyroidectomies for multinodular goiter (MNG) and to assess the influence of sex and age as cancer risk factors. METHODS: In a 2-year period, 539 patients underwent subtotal or total thyroidectomy for MNG at the institute of General Surgery, University of Padova, Padova, Italy: 455 were females and 84 males (F/M = 5.5/1); mean age was 46 years (min. 17, max 78). Only 17 patients (3.1%) (16 females and 1 male) were aged 21 years or less. RESULTS: A malignancy was found in 41 patients: 38 females and 3 males; 39 older and 2 younger than 21 years. The frequency of cancer in MNG was 7.6%: 8.3% in females and 3.6% in males; 7.5% in patients older than 21 and 11.7% under 21 years. CONCLUSIONS: The combination of MNG and carcinoma should always be carefully considered but not overemphasized, and the policy of surgically treating all patients with MNG is not justified. Sex and age cannot be considered as factors of a higher risk of cancer.

Adult↗
PubMed1977

Enhanced thyroxine metabolism and high uptake goiters in rats after a single dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Nine days after treatment of rats with a single dose (25 microgram/kg) of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), the 1 h biliary excretion of [125I]-thyroxine (T4) was increased 4-fold and the [125I]T4 bile:plasma ratio and the biliary clearance rate of plasma [125I]T4 were increased 10-fold. The proportion of biliary 125I present as T4-glucuronide was larger in TCDD-treated rats. Unexpectedly, TCDD did not influence the 30 min biliary excretion of [125I]triiodothyronine (T3), the [125I]T3 bile:plasma ratio, and the biliary clearance rate of plasma [125I]T3. TCDD also elevated serum thyrotropin concentrations, produced goiters and increased thyroid 131I uptake. Serum T4 concentrations were reduced to half of normal in TCDD-treated animals, but their serum T3 levels were elevated. Sephadex uptake of serum [125I]T3 was reduced in the TCDD group.

Animals↗
PubMed1978

Hereditary congenital goiter with thyroglobulin deficiency in a breed of goats.

Hereditary congenital goiter occurring in an inbred breed of goats is reported. The goitrous goats were severely hypothyroid. Thyroglobulin-related antigens could only be detected by radioimmunoassay in amounts of 0.03% of the total protein concentration in the 105,000 x g supernate of the goitrous gland, which corresponded with 8 microgram soluble thyroglobulin-related antigens/g tissue. After treatment with digitonin, 4 microgram thyroglobulin-related antigens/g tissue could be extracted from the sediment. This means that the gland contained about 12 microgram thyroglobulin-related antigens/g tissue (normal about 100 mg/g). However, no thyroglobulin (19S) could be detected by ultracentrifugation experiments, immunodiffusion, or immunoelectrophoresis. Iodinated proteins with sedimentation constants of 3-9S were found. Among these iodinated macromolecular compounds, iodinated "albumin" and some non-hydrolysable iodinated material was found. These last mentioned components were also found in the blood, indicating a leakage from the gland. As described for comparable cases, these results indicate a defect in thyroglobulin synthesis or its regulation.

Animals↗
PubMed1978

Euthyroidism via iodide supplementation in hereditary congenital goiter with thyroglobulin deficiency.

We have studied hereditary congenital goiter in an inbred strain of goats. On a normal diet, the goats were hypothyroid and iodide taken up by the gland was released rapidly in the form of iodinated macromolecular material. This resulted in a low thyroidal iodine pool. An extremely low amount of thyroglobulin-related antigens (12 microgram/g tissue; normal, 100 mg/g tissue) was detected in the goitrous gland by RIA. Addition of 1 mg I-/day to the diet made the goats euthyroid and the serum protein-bound iodine increased to high values. Even under these conditions, however, the amount of thyroglobulin-related antigens was not significantly elevated (19 microgram/g tissue). On sucrose gradient, these antigens sedimented in the 7S region. No thyroglobulin-related antigens sedimented at 12S or 19S. Besides iodoalbumin, a heterogeneous group of abnormal iodoproteins containing T3 and T4 was observed with this high iodide intake and may have accounted for the hormone production. The abnormal iodoproteins had a molecular weight of 300,000-500,000 and a sedimentation value of about 7S. From these findings, we conclude that these goats were unable to synthesize thyroglobulin but with excess iodide, there was sufficient formation of T3 and T4 in the abnormal iodoproteins to make the animals euthyroid.

Animals↗
PubMed1986

Increased follicular heterogeneity in experimental colloid goiter produced by refeeding iodine excess after thyroid hyperplasia.

Delayed morphological changes induced in mouse hyperplastic thyroid by refeeding iodine were analyzed by light and electron microscopy, stereology, and autoradiography. Thyroid hyperplasia was induced by a low iodine diet supplemented with 0.25% propylthiouracil for 10 days. Involution was obtained by discontinuing the propylthiouracil and returning either to a moderate iodine diet [(MID) 1 microgram I/day] or to an iodine-rich diet [(HID) 10 micrograms I/day] for 40 days. In other experiments, three cycles of hyperplasia (8 days) and subsequent involution (8 days) with MID or HID were brought about. Control animals were fed MID or HID. All animals were killed when 12-14 weeks old after injection of 10-50 microCi 125I. Double labeling, with repeated injections of [3H]thymidine from day 0 to day 7 of involution followed by 125I injection 4 h before killing, was also performed. When involutions were performed with MID, most morphological variables returned to control values. However, when involution was brought about with HID, the glandular weight, the number of follicles, and the relative volume of follicular lumina remained larger than in controls. Moreover, the 125I-labeling pattern of the follicles was altered. The proportions of unlabeled, and unevenly or partly labeled, follicles, which were fewer than 5% in control groups, represented 25-35% of all follicles after involution with HID, whereas they were unchanged with MID. In unlabeled follicles the epithelium was flattened, with a reduced number of microvilli. Partly labeled follicles were of two types. In some follicles a persistent ring reaction was observed, suggesting an abnormally slow mixing of thyroglobulin. In others, the 125I labeling was restricted to areas adjacent to the apex of a reduced number of cells, suggesting that some cells were iodinating thyroglobulin, whereas others were not. There was no relationship between the follicular 125I labeling and the frequency of [3H]thymidine-labeled cells. These results indicate that refeeding iodine excess after hyperplasia leads to the formation of a colloid goiter with new follicles, and to an increased heterogeneity of iodine metabolism among follicles and among cells.

Animals↗
PubMed1987

Inherited congenital goiter in mice.

Congenital goiter (cog), a new autosomal recessive mutation in mice, has been mapped to the central region of chromosome 15. Young adult mutant mice are characterized by a reduced rate of growth, mild anemia, hypothyroidism, as indicated by significantly lower total serum T4 and T3, and elevated serum TSH. Thyroids from mutant mice are hypertrophied, deficient in colloid, show a reduced accumulation of iodine that is partially susceptible to perchlorate ion discharge, have modestly elevated serum immunoreactive thyroglobulin (Tg) levels, but are markedly deficient in glandular immunoreactive Tg content. Thyroid hormone therapy corrects the growth deficiency and prevents the thyroid hypertrophy resulting from excessive stimulation by TSH. These findings suggest that the cog mutant gene results in primary hypothyroidism in response to either defective synthesis or processing of Tg.

Aging↗
PubMed1989

Abnormal properties of thyroglobulin in mice with inherited congenital goiter (cog/cog).

A recessive autosomal mutation (cog) in mice that results in congenital goiter was recently described. Since the mutation has been linked to the thyroglobulin (TG) gene, we have studied the immunological and physical properties of TG in cog/cog mice. +/Cog mice, which are phenotypically normal, were used as controls. In a mouse TG RIA the displacement curve produced by cog/cog thyroid extract was not parallel to normal murine TG, and at maximum displacement 15.4% of the tracer was still bound to the antibody. Extract from +/cog thyroid tissue produced parallel and complete displacement. Sucrose density gradient velocity centrifugation followed by RIA was used to determine the sedimentation properties of cog/cog TG. An abnormal pattern was obtained; a small peak in the 3-8S area and a broad, poorly defined peak at 12S and extending to above 27S were present. By comparison, +/cog thyroids had sharp peaks at 19S and 27S. These findings suggest that normal TG contains some immunological determinants that are absent, and some that are altered, in cog/cog TG. They also indicate that the association of 12S subunits to form 19S TG in cog/cog mice is weak and abnormal. Thyroid tissue was labeled with Na125I in vivo and with [35S] methionine in vitro. In cog/cog mice iodine was incorporated predominantly into albumin and other non-TG proteins. However, by polyacrylamide gradient gel electrophoresis, distinct 125I-labeled bands comigrating with normal TG were present. The bands migrating with TG were also precipitable with anti-TG antiserum. In +/cog mice TG was the predominant iodinated molecule. With [35S]methionine labeling, cog/cog and +/cog thyroids formed TG with the same electrophoretic mobilities. These data indicate the cog/cog thyroids synthesize TG of normal, or very nearly normal, size. The immunological and sedimentation properties of this TG are abnormal, supporting the possibility that the cog mutation is in the TG gene.

Animals↗
PubMed1992

Effect of in vivo administration of recombinant acidic fibroblast growth factor on thyroid function in the rat: induction of colloid goiter.

We have recently demonstrated that the iv administration of 0.6-60 micrograms/kg.day of acidic fibroblast growth factor (acidic FGF) increases thyroid weight in male and female rats. Interestingly, measurement of serum TSH and thyroid hormones in rats treated with 6 micrograms/kg.day acidic FGF for 30 days revealed only a slight increase in serum T4 and reverse T3 concentrations. Since thyroid function was only examined 24 h after the 30th daily treatment, we performed a series of experiments to evaluate the effects of acidic FGF on thyroid function following single and 6 multiple injections of acidic FGF. There was a small increase in the serum TSH concentrations at 2, 4, 8, and 24 h after a single high dose iv injection of acidic FGF (60 micrograms/kg). In contrast, serum T3 concentrations were slightly decreased at 2, 4, and 8 h after acidic FGF administration. There was no effect of a single injection of acidic FGF on serum T4, reverse T3, or thyroglobulin concentrations. After 6 days of treatment, there was a 34% increase in the thyroid weights of rats treated with acidic FGF. Analysis of serum hormones revealed a slight increase in serum TSH, T3, and T4 concentrations in acidic FGF-treated rats, but no change in serum reverse T3 or thyroglobulin concentrations. There was no effect of acidic FGF administration on thyroid radioiodine uptake, the intrathyroidal metabolism of radioiodine, or the relative amounts of thyroidal thyroglobulin or peroxidase messenger RNAs, or on liver 5'-deiodinase activity. In hypophysectomized rats, with no detectable levels of serum TSH, acidic FGF failed to increase thyroid weight. These data suggest that FGFs may participate with TSH in the regulation of thyroid weight and colloid accumulation, and that autocrine or paracrine growth factors may be involved in the pathogenesis of colloid goiter.

Animals↗
PubMed2004

Two distinct compound heterozygous constellations (R277X/IVS34-1G>C and R277X/R1511X) in the thyroglobulin (TG) gene in affected individuals of a Brazilian kindred with congenital goiter and defective TG synthesis.

In this study, we have extended our initial molecular studies of a nonconsanguineous family with two affected siblings and one of their nephews with congenital goiter, hypothyroidism, and marked impairment of thyroglobulin synthesis. Genomic DNA sequencing revealed that the index patient (affected nephew) was heterozygous for a single base change of a cytosine to a thymine at nucleotide 886 in exon 7 (886C>T, mother's mutation) in one allele and for a novel guanine to cytosine transversion at position -1 of the splice acceptor site in intron 34 (IVS34-1G>C, father's mutation) in the other allele. The two affected siblings inherited the 886C>T mutation from their mother and a previously reported cytosine to thymine transition at nucleotide 4588 in exon 22 from their father (4588C>T). The 886C>T and 4588C>T substitutions resulted in premature stop codons at amino acids 277 (R277X) and 1511 (R1511X), respectively. In vitro transcription analysis showed that the exon 35 is skipped entirely when the IVS34-1G>C mutation is present, whereas the wild-type allele is correctly spliced. SSCP (exon 7 and 35) and restriction analysis (exon 22) using Taq I indicated that the two affected siblings, the affected nephew, his mother, and his unaffected brother were all heterozygous for the R277X mutation. The two affected siblings, their father, and three unaffected siblings were all heterozygous for the R1511X mutation, whereas the affected nephew and his father were heterozygous for the IVS34-1G>C mutation. Moreover, in this kindred, we have characterized polymorphisms (insertion/deletion, microsatellite, and single nucleotide polymorphism) located within introns 18 and 29 and exon 44 that are associated with the described mutations. Haplotype analysis with these polymorphic markers in two unrelated Brazilian families (present family studied and previously reported family) harboring the R277X mutation suggests a founder effect for the R277X mutation. In conclusion, the affected individuals of this family are either compound heterozygous for R277X/IVS34-1G>C or R277X/R1511X. This observation further supports that thyroglobulin gene mutations display significant intraallelic heterogeneity.

Amino Acid Sequence↗
PubMed2006

Clinical case seminar: metastatic follicular thyroid carcinoma arising from congenital goiter as a result of a novel splice donor site mutation in the thyroglobulin gene.

CONTEXT: Defects in thyroglobulin (Tg) synthesis are one of the causes of thyroid dyshormonogenesis. Only a few mutations in the Tg gene have been described. OBJECTIVES: We describe a novel Tg gene mutation and discuss the mechanisms by which it causes dyshormonogenesis with subsequent malignant transformation. CASES: Two siblings aged 21 and 19 yr presented with recurrent goiters for which they had undergone multiple thyroid surgeries since early childhood. The older sibling was diagnosed with metastatic follicular thyroid carcinoma at age 15 yr. METHODS: The entire coding region and intron-exon boundaries of the Tg gene were amplified and sequenced from the patients. We also sequenced the boundaries of exon 5 and intron 5 from both parents. RT-PCR amplification of a cDNA fragment encompassing exons 4-6 was also performed. RESULTS: A homozygous G to A point mutation at position +1 of the splice donor site of intron 5 (g.IVS5+1G-->A) was detected in both patients, whereas a monoallelic mutation was found in their parents. RT-PCR amplification of a cDNA fragment covering exons 4-6 revealed a 191-bp fragment in the patients and 351- and 191-bp fragments in the parents. Sequence analysis of these two fragments confirmed deletion of exon 5 in the 191-bp fragment. CONCLUSIONS: Aberrant splicing occurred as a result of the g.IVS5+1G-->A mutation, which caused fusion of exons 4 and 6, resulting in the frame shift at codon position 141 and a premature stop codon at position 147 (FS141-->147X). The malignant transformation is likely a result of prolonged TSH stimulation.

Adenocarcinoma, Follicular↗
PubMed1977

Hypothyroidism in an area of endemic goiter and cretinism in Central Java, Indonesia.

In an area of severe endemic goiter in Central Java, Indonesia, clinical overt or mild hypothyroidism appeared to be present in 7 out of 20 cretins and also in 12 out of 94 non-cretinous subjects, all 5-20 years of age, living in the village of Sengi. Hypothyroidism was not found in a control group of 70 subjects of the same age living in Londjong just outside the edemia. In hypothyroid subjects the plasma PBI-concentration was 0.98+/-0.32 mug/100 ml (mean+/-SD) vs. 2.72+/-1.24 mug/100 ml in euthyroid subjects from Sengi and 4.86+/-0.80 mug/100 ml in controls from Londjong. Values for T3 were 56.3+/-3.17 ng/100 ml in hypothyroids, 140.5+/-38.5 ng/100 ml in euthyroids from Sengi and 121.6+/-27.4 ng/100 ml in controls. The TSH levels (geometric mean and range) in these 3 groups were, respectively, 210.1 (108.0-342), 15.6 (3.0-372) and 4.1 (0.8-7.0) muU/ml. The differences between the mean concentration of PBI, T3 and TSH in the hypothyroid and euthyroid groups were highly significant (P less than 0.001). These data strengthen the clinical diagnosis of hypothyroidism in cretins as well as in non-cretinous subjects. All hypothyroid subjects had a PBI less than 1.8 mug/100 ml and T3 less than 120 ng/100 ml and TSH greater than 100 muU/ml. In 8 hypothyroid subjects, restudied 18 months after iodized oil injection, hypothyroidism was either corrected or markedly improved. It therefore appears that iodine deficiency per se in postnatal life may lead to (juvenile) hypothyroidism, which can be corrected by iodine therapy. Our findings have implications for the definition and diagnosis of endemic cretinism. Not all hypothyroid subjects in an area of endemic iodine deficiency should be classified as cretins.

Adolescent↗
PubMed1978

3,3',5'-triiodothyronine, thyroxine, triiodothyronine, and thyrotropin levels in maternal and cord blood sera from endemic goiter regions of Brazil.

T4, T3, rT3, and TSH were measured in cord blood of infants born in mild to severe endemic goiter areas and nonendemic urban areas in South and North America. A significantly high rT3 concentration was found in newborns living in the urban area of South America as compared to a Canadian newborn population. There were no differences among the various thyroid parameters in the groups of newborns studied. Blood from goitrous mothers showed significantly higher concentrations of T3 and TSH than nongoitrous mothers. However, these changes did not affect the concentrations of thyroid hormones, rT3, or TSH in the fetal circulation.

Brazil↗
PubMed1986

Thyroid growth immunoglobulins in large multinodular endemic goiters: effect of iodized oil.

Iodized oil (IO) was administered to 10 goitrous patients recently emigrated to São Paulo (SP) from iodine deficiency areas and to 42 goitrous patients from 2 Brazilian chronic iodine deficiency regions, Loreto and Luziania (L). Thyroid growth-promoting immunoglobulin G (IgG) thyroid-stimulating antibody, serum thyroglobulin (Tg), TSH, and thyroid hormones were measured before and 1 yr after IO administration. In all patients there was a remarkable reduction of gland mass associated with a significant decrease (P less than 0.01) in both basal serum Tg and peak Tg levels after bovine TSH administration. The mean percent Tg increase after bovine TSH treatment was reduced to 82% above basal levels compared with 224% before IO. Mean serum TSH levels, elevated only in the L group [7.3 +/- 11 (+/- SD) microU/ml] decreased to the normal range after IO (2.5 +/- 2.1 microU/ml). Serum T3 and T4 concentrations did not change greatly. Tests for microsomal antibodies were negative before and after IO. IgG concentrates of serum obtained before and after IO were tested for their ability to stimulate incorporation of [3H]thymidine into DNA or to increase intracellular generation of cAMP in FRTL-5 cells. Thymidine incorporation activity was found in 8 of 10 patients from SP [316 +/- 37% (+/- SEM); range, 140-480%] and 25 of 42 patients in the L group (mean, 206 +/- 14; range, 120-500%) before IO. Stimulation of thymidine incorporation reflected true growth-promoting activity, as confirmed by experiments measuring cell number, was not accounted for by TSH in the preparation, and reflected IgG action because it was abolished by absorption with antihuman IgG. IgG from only 1 patient in group SP and 4 patients in group L stimulated intracellular production of cAMP in FRTL-5 cells. All patients except 1 in both groups had no IgG stimulation (less than 120%) of growth-promoting activity 1 yr after IO treatment. There was a significant positive correlation between thyroid growth-promoting activity and serum Tg concentrations (r = 0.58; P less than 0.001), but no significant correlation was found with other parameters (TSH, T4, and T3). We conclude that growth-promoting IgGs lacking ability to stimulate cAMP production may play a role in the large multinodular goiters due to chronic iodine deficiency.

Adenylyl Cyclases↗