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M Centanni, R Cesareo, O Verallo, M Brinelli, G Canettieri, N Viceconti and M Andreoli


Objective: The aim of the study was to analyse the relationship between the ocular parameters, namely intraocular pressure (IOP), and the early forms of subclinical hypothyroidism.

Design: Fifty-three subjects (9 male and 44 female) aged from 18 to 45 years (mean 32±7 years) were selected for this study. Twenty-nine met the criteria of subclinical hypothyroidism and 24 euthyroid subjects, age- and sex-matched, were used as controls.

Methods: All individuals underwent a complete ocular examination, including visual field examination and serial measurement of IOP by means of a Goldmann tonometer. A tonographic examination was also performed.

Results: The hypothyroid patients showed a substantially higher pressure in both eyes compared with control subjects (right eye=17·52±4·74 vs 13·42±1·95 mmHg, p<0.0001; left eye=17·55±3·99 vs 13·71±1·55 mmHg, p<0.0001). Indeed, the tonometric pressure exceeded 18 mmHg in 11 out of the 29 (38%) patients in the right eye and in 8 out of 29 (27%) patients in the left eye. The outflow index was normal in all subjects except in two hypothyroid patients. After two months of L-thyroxine (L-T4) replacement therapy, only one patient continued to show tonometric values above 18 mmHg and the hypothyroid patients showed a significant reduction in mean IOP in both eyes compared with pretreatment values (right eye=14·96± 1·32 mmHg. p<0.0097; left eye=15·03± 1·38 mmHg, p<0.0018). Treatment did not lead to any change in the outflow indices; however, the C value (outflow coefficient at the sclerocorneal corner) returned to normal in the two patients with increased pre-treatment tonographic values.

Conclusions: These findings indicate that the intraocular pressure is increased even in subclinical hypothyroid patients and that, at this early stage, the impairment is fully reversible with L-T4 therapy.

European Journal of Endocrinology 136 595–598

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M Centanni, G Canettieri, N Viceconti, R Sibilla, A Bei and M Andreoli

OBJECTIVE: We have studied the effect of tryptophan on cellular [(125)I]tri-iodothyronine (T3) uptake by mouse thymocytes. MATERIALS AND METHODS: Mouse thymocytes (20 x 10(6 )cells/ml) were suspended in Krebs-Ringer solution buffered by Tris-HCl and incubation (23 degrees C at pH7.45+/-0.6), in the presence or absence of 1mM tryptophan, was started by adding 25 pM [(125)I]T3. At the end of incubation, samples were cooled in ice, centrifuged over a 30% sucrose cushion and the cell-associated radioactivity was measured in the pellet. RESULTS: Tryptophan reduced both the total and the saturable fraction of [(125)I]T3 uptake by 44% (P=0.0009) and 60% (P=0.0006) respectively, following 1 min of incubation. This effect was specific and dose-dependent, being maximal at 5mM concentration (-82%). In contrast, the pre-exposure of cells to tryptophan for up to 2h had no effect on the subsequent uptake of [(125)I]T3, in the absence of tryptophan. The effect of D-tryptophan on saturable T3 uptake was not different from that obtained using the L-stereoisomer. Tryptophan reduced the V(max) of the initial rate of saturable [(125)I]T3 uptake by two-thirds without affecting the apparent K(m) (2.2 nM) of the process, thus indicating the non-competitive nature of the inhibition. In sodium-free medium the saturable [(125)I]T3 uptake was reduced by 43%. The inhibitory effect of tryptophan on [(125)I]T3 uptake was exerted in both the presence and the absence of sodium. In fact, the inhibitory effect of tryptophan on T3 transport was greater and significantly different (P=0.0046) from that obtained by sodium depletion alone. CONCLUSIONS: Tryptophan interferes with both the sodium-dependent and -independent components of [(125)I]T3 uptake by a dose-dependent, non-competitive mechanism which operates in cis-modality at the plasma membrane level of mouse thymocytes.

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N Brusca, C Virili, M Cellini, S Capriello, L Gargano, R Salvatori, M Centanni and M G Santaguida


Autonomously functioning thyroid areas may be associated with subclinical or overt hyperthyroidism, but may exist even in the presence of normal TSH. This study was aimed at comparing the rate of autonomously functioning areas and their cardiac sequelae in patients with nodular goitre studied with the usual and a novel approach.

Design and methods

In total 490 adult outpatients with thyroid nodular goitre, living in a mild iodine-deficient area, were selected in our referral centre for thyroid diseases from 2009 to 2014 on the basis of a suspicion of thyroid functional autonomy. They were divided in three groups according to a non-conventional approach (excessive response to thyroxine treatment: group 1) or conventional approach (low/normal TSH with clinical suspicion or low TSH: groups 2 and 3). All patients of the study with the suspicion of thyroid functional autonomy underwent thyroid scan with radioactive iodine (I131) uptake (RAIU).


The percentage of confirmed thyroid functional autonomy was 319/490, being significantly higher in group 3 than in groups 1 and 2 (81.5 vs 64.7 vs 52.6%; chi-square P < 0.0001). However, the diagnosis with non-conventional approach was made at a significant earlier age (P < 0.0001). Cardiac arrhythmias as well as atrial fibrillation were similarly detected by conventional and non-conventional approaches (chi-square test: P = 0.2537; P = 0.8425).


The hyper-responsiveness to thyroxine treatment should induce the suspicion of thyroid functional autonomy at an early stage, allowing to detect autonomous functioning areas in apparently euthyroid patients.

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S C Del Duca, M G Santaguida, N Brusca, I Gatto, M Cellini, L Gargano, C Verga Falzacappa, F M Frattaroli, C Virili and M Centanni


Thyroxine (T4) requirement after total thyroidectomy for differentiated thyroid carcinoma (DTC) is a debated issue. As most of the studies in the area have been retrospective and/or performed with heterogeneous therapeutic approaches, we designed our study to determine T4 requirement in the same patients and treatment settings, before and after total thyroidectomy.

Design, patients and methods

This was a longitudinal study including 23 goitrous patients treated with T4 in an individually tailored fashion. All patients exhibited a stable TSH (median TSH=0.28 mU/l) at a stable T4 dose for at least 1 year before surgery (median T4 dose=1.50 μg/kg per day). The patients underwent total thyroidectomy based on cancer suspicion or compressive symptoms. Eventually diagnosed as having DTC (pT1b-pT2N0) and following surgical and radiometabolic treatment, they were treated with the same pre-surgical doses of T4.


Three months after surgery,using the same pre-surgical dose, median TSH increased up to 5.38 mU/l (P<0.0001) and so the T4 dose had to be increased (median T4 dose=1.95 μg/kg per day; +30%; P<0.0001). Once divided by patients' age, we observed that, after thyroidectomy and maintaining the same pre-surgical dose, serum TSH significantly increased both in younger and in older patients (median TSH=4.57 and 6.11 mU/l respectively). Serum TSH was restored to the pre-surgical level by increasing the dose up to 1.95 and 1.77 μg/kg per day (+25 and +21%) respectively.


Following the same treatment regimen, a thyroidectomized patient requires one-third higher therapeutic T4 dose than before surgery. Despite this increase, the dose of T4 needed in our patients remains significantly lower than that previously described in athyreotic patients.

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FS Celi, G Canettieri, D Mentuccia, L Proietti-Pannunzi, A Fumarola, R Sibilla, V Predazzi, M Ferraro, M Andreoli and M Centanni

OBJECTIVE: The selenoenzyme type 2 iodothyronine 5' deiodinase (DII) catalyzes the conversion of thyroxine into its active form tri-iodothyronine (T3), modulating thyroid hormone homeostasis in a local, tissue-specific manner. The amphibian, rodent and human cDNAs encoding this enzyme have been recently cloned and expressed. At present, little information regarding the genomic structure of mammalian DII is available. DESIGN AND METHODS: The complete structure, including intron-exon junctions, of the human DII (hDII) gene was obtained by long PCR and rapid amplification of cDNA ends (RACE). Chromosomal assignment of the hDII gene was performed by fluorescence in situ hybridization using a highly specific probe. RESULTS AND CONCLUSIONS: Our data demonstrated that hDII is a single copy gene located on chromosome 14, position 14q24.3. The gene spans over 15 kb, and the 7 kb transcript is encoded by three exons of 149 bp, 273 bp and 6.6 kb separated respectively by two 274 bp and 7.4 kb introns. A restriction map of the hDII gene is also reported. These data will help in further studies of the role of DII in the maintenance of peripheral thyroid hormone homeostasis.