Pendrin expression in nodular and non-nodular thyroid tissues

Introduction: Different mechanisms for the expression of pendrin which is an apical iodide transporter have been reported in nodular thyroid tissues compared to normal thyroid. The aim of the present study was to determine the alterations of pendrin expression in nodular and surrounding non-nodular thyroid tissues and clarify the role of pendrin in the functional behaviour of nodular lesions. Material and methods: Twenty-six nodular and paired non-nodular normal thyroid tissues were collected at the same centre. Patients were divided into two groups based on the function of the dominant thyroid nodule; hot nodules (n = 18) and cold nodules (n = 8). mRNA levels of pendrin were evaluated by quantitative RT-PCR. Pendrin protein expression was determined by immunohistochemical analysis. Results of dominant nodules were compared to non-nodular thyroid tissue of the same patient. Results: No statistically significant difference was found with respect to qualitative and quantitative measurements of pendrin expression between hot and cold nodules. However, percent immunohistochemical staining of pendrin was significantly higher in both hot and cold nodules compared to non-nodular thyroid tissue of the same patients. RT-PCR revealed comparable mRNA levels of pendrin gene between hot nodules and corresponding normal thyroid tissues. However, in cold nodules, significantly decreased mRNA levels of pendrin were observed compared to normal thyroid tissue. mRNA levels of pendrin showed significant positive correlation with TSH in corresponding non-nodular thyroid tissues. Conclusions: The present study demonstrates that expression of pendrin could not be influenced by TSH in thyroid nodules and expression level of pendrin seems not to have an effect on nodule function. (Endokrynol Pol 2013; 64 (3): 208–214)Wstęp: W guzkowej tkance tarczycowej opisano odmienny od pozaguzkowej tkanki tarczycowej mechanizm ekspresji pendryny — transportera jodu zlokalizowanego w części szczytowej komórki. Celem badania było ustalenie zmian w ekspresji pendryny w guzkowej tkance tarczycowej i otaczającej ją pozaguzkowej tkance tarczycowej, aby wyjaśnić rolę pendryny w zachowaniu czynnościowym zmian guzkowych. Materiał i metody: W tym samym ośrodku pobrano 26 wycinków guzkowej tkanki tarczycowej i sparowanych wycinków pozaguzkowej prawidłowej tkanki tarczycowej. Pacjentów podzielono na dwie grupy w zależności od statusu czynnościowego guzka dominującego: grupę z guzkami gorącymi (n = 18) i grupę z guzkami zimnymi (n = 8). Poziom mRNA i pendryny oznaczono ilościowo metodą RT-PCR. Ekspresję białka pendryny oznaczono metodą immunohistochemiczną. Wyniki dla guzków dominujących porównano z wynikami dla tkanki pozaguzkowej u tego samego pacjenta. Wyniki: Nie stwierdzono statystycznie znamiennych różnic pomiędzy guzkami gorącymi i zimnymi, jeżeli chodzi o wyniki oznaczenia ilościowego i jakościowego ekspresji pendryny. Procentowe barwienie immunohistochemiczne w kierunku pendryny było natomiast znamiennie większe zarówno w przypadku guzków gorących, jak i zimnych w porównaniu z tkanką pozaguzkową u tych samych pacjentów. RT-PCR wykazało porównywalne poziomy mRNA genu kodującego pendrynę w guzkach gorących i prawidłowej tkance tarczycowej u tych samych pacjentów. Z kolei w przypadku guzków zimnych stwierdzono znamiennie niższe poziomy pendryny w porównaniu z prawidłową tkanką tarczycową. Stwierdzono też korelację dodatnią poziomu mRNA pendryny i poziomu TSH w korespondujących tkankach pozaguzkowych. Wnioski: W przeprowadzonym badaniu wykazano, że na ekspresję pendryny nie może mieć wpływu TSH w guzkach tarczycy oraz że poziom ekspresji pendryny nie wydaje się wpływać na czynność guzków. (Endokrynol Pol 2013; 64 (3):208–214

Pendrin expression in nodular and non-nodular thyroid tissues

Introduction: Different mechanisms for the expression of pendrin which is an apical iodide transporter have been reported in nodular thyroid tissues compared to normal thyroid. The aim of the present study was to determine the alterations of pendrin expression in nodular and surrounding non-nodular thyroid tissues and clarify the role of pendrin in the functional behaviour of nodular lesions

The predictive value of CTLA-4 and Tg polymorphisms in the recurrence of Graves' disease after antithyroid withdrawal

Graves' disease (GD) is a multifactorial disease that develops as a result of complex interactions between genetic and environmental factors. The aim of our study is to determine the frequency of cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4) A/G and TG C/T exon 33 SNPs (Tg E33SNP) in GD and to evaluate the relation between recurrence and these polymorphisms. A total of 187 subjects, including 97 previously treated GD patients and 90 age and gender matched control subjects were studied. We examined the relationship between the A/G and C/T polymorphism and various clinical and laboratory variables among patients with GD. TT genotype frequency in the GD patients was significantly higher than the controls. Number of recurrent patients was significantly higher in AG and GG carriers in comparison to AA carriers (57% and 45% vs 14%,p = 0.0001). CTLA-4 AG genotype had an eightfold (OR: 8.050; 95 % CI: 2.87-22.5; p = 0.0001) and GG genotype had a sevenfold (OR: 7.025; 95% CI: 1.67-29.4; p = 0.007) increase in the risk of recurrence in the patients with GD. In conclusion, early interpretation for definitive treatment procedures (i.e., radioactive iodine or surgery) may be considered in the patients with G allielle and E33SNP of Tg gene is conformed the susceptibility to GD in a Turkish population and having TT genotype increases the susceptibility to GD

An unusual patient with hypercalciuria, recurrent nephrolithiasis, hypomagnesemia and G227R mutation of paracellin-1

A 19-year-old female patient with hypercalciuria and recurrent nephrolithiasis/urinary tract infection unresponsive to thiazide type diuretics is presented. The patient first experienced nephrolithiasis at the age of 4 years. Afterwards, recurrent passages of stones and urinary tract infection occurred. On diagnostic evaluation at the age of 19 years, she also had hypocitraturia and hypomagnesemia. Her serum calcium concentrations were near the lower limit of normal (8.5-8.8 mg/dl; normal range: 8.5-10.5), her serum magnesium concentrations were 1.15-1.24 mg/dl (normal range: 1.4-2.5) and urinary calcium excretion was 900 mg/24 h. PTH concentrations were increased (110-156 pg/ml; normal range: 10-65). We tried to treat the patient with hydrochlorothiazide at a dose of 50 mg/day. During treatment with thiazide diuretics, PTH concentration remained high and the patient had recurrent urinary tract infections and passages of stones. Serum magnesium concentration did not normalize even under the parenteral magnesium infusion. Her mother had a history of nephrolithiasis 20 years ago. Severe hypomagnesemia in association with hypercalciuria/urinary stones is reported as a rare autosomal recessive disorder caused by impaired reabsorption of magnesium and calcium in the thick assending limp of Henle's loop. Recent studies showed that mutations in the CLDN16 gene encoding paracellin-1 cause the disorder. In exon 4, a homozygous nucleotide exchange (G679C) was identified for the patient. This results in a point mutation at position Glycine227, which is replaced by an Arginine residue (G227R). The mother was heterozygous for this mutation. G227 is located in the fourth transmembrane domain and is highly conserved in the claudin gene family. This case indicates the pathogenetic role of paracellin-1 mutation in familial hypomagnesemia with hypercalciuria and nephrocalcinosis and further underlines the risk of stone formation in heterozygous mutation carriers. Copyright (c) 2006 S. Karger AG, Basel

RELATIONSHIP BETWEEN ADENOMAWEIGHT AND PREOPERATIVE BIOCHEMICAL PARAMETERS IN PRIMARY HYPERPARATHYROIDISM

Objective: The aim of this study was to determine the relationships between parathyroid adenoma weight and preoperative biochemical indices such as parathyroid hormone, calcium, phosphate, alkaline phosphatase, and urinary calcium excretion in patients with primary hyperparathyroidism