Hypertrophy and hyperplasia during goitre growth and involution in rats separate bioeffects of TSH and iodine

Stübner, D.; Gärtner, Roland; Greil, W.; Gropper, K.; Brabant, Georg; Permanetter, W.; Horn, K.; Pickardt, C. R.

doi:10.1530/acta.0.1160537

Cited by 58 publications

(24 citation statements)

References 15 publications

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“…In vitro, stimulatory effects of TSH on thyroid cell growth (1), as well as no or even inhibitory effects of TSH on thyroid cell prolife¬ ration (2,3) have been reported. In epidemiological studies, elevated basal TSH levels in patients with endemic goitre could only be demonstrated in areas with severe iodine deficiency (4).…”

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confidence: 99%

Unaltered pulsatile and circadian TSH release in euthyroid patients with endemic goitre

Weber

Krause

Gaffga

et al. 1991

Acta Endocrinologica

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To evaluate the pathophysiological role of TSH in goitrogenesis we investigated pulsatile TSH secretion in 11 patients with a non-toxic goitre and in 11 healthy controls. Thyroid volume was 40 \m=+-\10 ml in the goitre group and 15 \m=+-\4 ml in the controls as measured by ultrasound. Blood was sampled continously via an indwelling venous catheter at 10-min intervals over 24 h. Neither the mean 24-h serum TSH levels (goitre 1.1 \ m=+-\0.5 vs controls 0.9 \m=+-\0.4 mU/l) nor the nocturnal surge of TSH were significantly different between the two groups. The average of the TSH pulse frequency (goitre 10.8 \ m=+-\ 3.7 vs controls 9.6 \m=+-\3.5 pulses/24-h) and of the TSH pulse amplitude (goitre 0.4 \ m=+-\0.2 vs controls 0.3 \ m=+-\0.1 mU TSH/l as analysed by DESADE programme (detection of secretory activity by discrete deconvolution) did not differ in the two groups. Furthermore, there was no correlation between the volume of the thyroid gland and the dynamics of the TSH secretion. We conclude that our data do not suggest a relevant pathophysiological role of TSH secretion in the development of non-toxic goitre in man.The pathophysiological role of TSH in the devel¬ opment of endemic goitre is still controversial, and no clear evidence exists for an altered secretion of the hormone. In vitro, stimulatory effects of TSH on thyroid cell growth (1), as well as no or even inhibitory effects of TSH on thyroid cell prolife¬ ration (2,3) have been reported. In epidemiological studies, elevated basal TSH levels in patients with endemic goitre could only be demonstrated in areas with severe iodine deficiency (4). In areas with mild or moderate iodine deficiency, as e.g. the FRG, basal TSH levels and TSH responses after TRH stimulation in patients with endemic goitre are not different from those observed in normal controls (5). In a recent clinical study, Gutekunst et al. (6) have even described lower basal TSH levels in German patients with endemic goitre as com¬ pared with the Swedish population with sufficient iodine supply and normal thyroid volume.It has been shown since 1986 that TSH, like other pituitary hormones, is secreted in a pulsatile manner (7,8). Nevertheless, in former studies ex¬ amining the pathophysiological significance of TSH for goitrogenesis in man, the dynamics of pi¬ tuitary TSH secretion were not taken into account.If the pituitary TSH secretion really plays an im¬ portant role in goitrogenesis one could expect an altered pulsatile TSH secretion in patients with en¬ demic goitre. Thus, the aim of the present study was to investigate pulsatile and circadian TSH se¬ cretion with a continous blood sampling technique in patients with non-toxic goitre and in controls. Subjects and MethodsEleven healthy subjects and 11 patients with a non-toxic goitre were studied. Each group consisted of 5 females and 6 males. The mean age was 25 ± 3 years in the controls and 25 ± 5 years in the goitre group. Subjects were selected on the basis of their thyroid volume as mea¬ sured by ultrasound. Ultrasound was performed...

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confidence: 99%

Unaltered pulsatile and circadian TSH release in euthyroid patients with endemic goitre

Weber

Krause

Gaffga

et al. 1991

Acta Endocrinologica

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“…Thyroid hypertrophy is mainly stimulated by TSH while thyroid hyperplasia is regulated by the intracellular iodine level [31]. Thus, it may be beneficial to give iodine in addition to treatment with L -T 4 .…”

Section: Discussionmentioning

confidence: 99%

The Comparison of Thyroxine versus Thyroxine plus Oral Iodine in the Treatment of Congenital Hypothyroidism due to Iodine Deficiency

Kurtoğlu

Köroğlu²,

Baştuğ³

et al. 2014

Horm Res Paediatr

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Aim: Iodine deficiency is one of the most important causes of congenital hypothyroidism. In addition to thyroid hormone replacement, iodine supplementation is also given to newborns with congenital hypothyroidism due to iodine deficiency. We aimed to determine whether it is beneficial to administer iodine supplementation in addition to the L-thyroxine (L-T₄) treatment of newborns with congenital hypothyroidism due to iodine deficiency. Materials and Methods: Of 51 newborns, 26 who were diagnosed with congenital hypothyroidism due to iodine deficiency were treated with L-T₄. The remaining 25 cases were given L-T₄ plus 100 μg/day of oral iodine. Free triiodothyronine (fT₃), free thyroxine (fT₄), thyroid-stimulating hormone (TSH), thyroglobulin (TG), thyroid volume, urine iodine and breast milk iodine levels were measured in the first and third months of treatment, and the data were compared between the two groups. Results: First- and third-month values of fT₃, fT₄, TSH, TG and thyroid volume for both groups were statistically similar. There was no significant difference between the two groups in respect to falling levels of fT₃ and TSH, the rate of increase of fT₄ levels or the shrinkage rate of thyroid volume. Conclusion: In this study, the addition of oral iodine to L-T₄ treatment provided no benefit compared to treatment with L-T₄ alone.

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“…[11]. Inwieweit dies übertragbar ist für funktionell inaktive Knoten muss weiteren Untersuchungen vorbehalten sein, ist aber eher unwahrscheinlich.…”

Section: Pathophysiologieunclassified

Pathophysiologie der Knotenstruma: Konsequenzen für die Therapie und Rezidivprophylaxe

Gärtner¹

2005

Viszeralchirurgie

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ZusammenfassungJodmangel ist die wesentlichste Ursache für die Entstehung von diffusen (hyperplastischen) und multinodösen Strumen (benignen Neoplasien). Die Schilddrüse gehört zu den Organen mit den häufigsten benignen Neoplasien, welche durch somatische Mutationen entstehen, wobei es offenbar auch eine familiäre genetische Prädisposition gibt, denn nicht alle Menschen in einem Jodmangelgebiet entwickeln Knotenstrumen. Diese treten familiär gehäuft auf. In Deutschland werden bei etwa 25-35 % aller Erwachsenen Knotenstrumen nachgewiesen. Angesichts der Häufigkeit von funktionell inaktiven, benignen Knotenstrumen gibt es nur sehr wenig kontrollierte Studien, die den klinisch wichtigen Effekt einer medikamentösen Therapie belegen, näm-lich nicht nur die Verhinderung bzw. Verzögerung des Wachstums, sondern vor allem eine Verhinderung der malignen Entartung und die Prävention der Entstehung weitere Knoten, bzw. Rezidivknoten nach Strumaoperation. Eine TSH-suppressive Therapie kann eine Rezidivstruma nicht sicher verhindern. Aus pathophysiologischer Sicht sollte die Jodidsubstitution bevorzugt eingesetzt werden, denn wir wissen, dass sie keine negativen Wirkungen hat, wenn eine Autonomie ausgeschlossen ist. Prospektive, kontrollierte und langjährige Studien sind dringend notwendig, um zu zeigen, welche der konservativen Therapiemöglichkeiten am effektivsten ist, die oben angeführten, wichtigsten Therapieziele zu erreichen. SchlüsselwörterKnotenstruma · Schilddrüsen-Neoplasie · Jodmangel · TSHsuppressive Therapie AbstractIodine deficiency is the main cause of the development of diffuse (hyperplastic) and multinodular goitre (benign neoplasia). The thyroid is one of the organs with the highest prevalence of benign neoplasias, probably because it has the potential for growth even in adulthood. Somatic mutations are responsible for the development of thyroid nodules, but there also seems to be a familiar genetic background, facilitating the development of benign thyroid neoplasia. In Germany 25-35 % of adult people are suffering from nodular goitre. There are limited controlled studies, which show the effect of a TSH suppressive therapy or iodine supplementation or both on the main goals of a conservative therapy, which are: prevention of malignant dedifferentiation, development of new nodules and growth inhibition or involution. But we know from meta-analyses that a TSH-suppressive therapy does not prevent recurrence of nodular goitre after surgery. From pathophysiological point of view, iodine supplementation, probably in combination with antioxidants should prevent the development of new nodules and probably malignant dedifferentiation. Prospective, controlled studies are still necessary to evaluate the best treatment of nodular goitre and prevention of recurrence after thyroid surgery.

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Hypertrophy and hyperplasia during goitre growth and involution in rats separate bioeffects of TSH and iodine

Abstract: Goitre growth was investigated in rats receiving a low iodine diet (< 0.1 \ g=m\ giodine/g) and either 1 g/l KClO4 or 1 g/l propylthiouracil (PTU), or a combination of KClO4 or PTU with 50.82 nmol/l T3 in tap water for 3 weeks. To investigate goitre involution, rats with iodine-deficient

Cited by 58 publications

References 15 publications

Unaltered pulsatile and circadian TSH release in euthyroid patients with endemic goitre

Unaltered pulsatile and circadian TSH release in euthyroid patients with endemic goitre

The Comparison of Thyroxine versus Thyroxine plus Oral Iodine in the Treatment of Congenital Hypothyroidism due to Iodine Deficiency

Pathophysiologie der Knotenstruma: Konsequenzen für die Therapie und Rezidivprophylaxe

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