Dynamics of thyroid diseases and thyroid‐axis gland masses

Kohanim, Yael Korem; Milo, Tomer; Raz, Moriya; Karin, Omer; Bär, A.; Mayo, Avi; Cohen, Netta Mendelson; Toledano, Yoel; Alon, Uri

doi:10.15252/msb.202210919

Cited by 16 publications

(25 citation statements)

References 69 publications

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“…This explains the delays in TSH normalization after correction of hypo- and hyperthyroidism (hysteresis). In these disease states, it normally takes weeks to months for the abnormal levels of thyroid hormones or TSH to alter the pituitary or thyroid cell mass ( 29 ); our study shows that even acute, significant elevations of TSH might stimulate thyroid cell growth.…”

Section: Discussionmentioning

confidence: 70%

Benign thyroid nodules respond to a single administration of 0.3mg recombinant human thyrotropin with highly variable volume increase

et al. 2023

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IntroductionThe nature of thyroid nodules is heterogenous. Most of them are benign and, in the absence of pressure symptoms of adjunct structures, no treatment is needed. Our objective was to investigate the acute effects of a low dose of recombinant human TSH (rhTSH) on the volume of benign thyroid nodules.Methodswe studied 27 nodules (14 isoechoic and 13 hypoechoic) in 15 (11 women and 4 men; mean age: 51.0 ± 15.9 years) consecutive patients with one to three well-separated asymptomatic benign thyroid nodules. All subjects were euthyroid, with negative thyroid antibodies, and none received levothyroxine. The total thyroid volume and thyroid nodule volume were sonographically determined by two independent examiners (P.B. and M.M.) before, 48 hours and 6 months post intramuscular (IM) administration of 0.3mg rhTSH, and the mean values of the two examiners’ measurements were used; thyroid function tests were obtained at the same time points.ResultsThe mean volume of isoechoic nodules increased by 57.3%, of hypoechoic nodules by 46.6% and of the surrounding thyroid parenchyma by 70.4% 48 hours post-rhTSH; mean volumes had returned to baseline levels 6 months later. A large variance in the volume change responses was observed. The relative change in nodule volume (defined as the percent change in nodule volume divided by the percent change in the surrounding parenchyma) from baseline to 48 hours was significantly higher in isoechoic versus hypoechoic nodules (p<0.05).ConclusionsA single dose of 0.3 mg rhTSH transiently increased the volume of benign thyroid nodules. The increase was more pronounced in isoechoic nodules and had a great variability. Our findings could be useful in the management of benign thyroid nodules, by helping in understanding which nodules would be more responsive to TSH suppression therapy.

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Section: Discussionmentioning

confidence: 70%

Benign thyroid nodules respond to a single administration of 0.3mg recombinant human thyrotropin with highly variable volume increase

et al. 2023

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“…As beta cell functional mass approaches C, its growth rate slows down, according to a linear term adapted from carrying capacity in ecology and in cellular replication (25,26,27). In this model, there is sufficient compensation when B is much smaller than the carrying capacity, where we can approximate and return to the Topp model.…”

Section: Resultsmentioning

confidence: 99%

Quantification of beta cell carrying capacity in prediabetes

Woller,

Tamir,

Bar

et al. 2024

Preprint

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Prediabetes, a subclinical state of high glucose, carries a risk of transition to diabetes. One cause of prediabetes is insulin resistance, which impairs the ability of insulin to control blood glucose. However, many individuals with high insulin resistance retain normal glucose due to compensation by enhanced insulin secretion by beta cells. Individuals seem to differ in their maximum compensation level, termed beta cell carrying capacity, such that low carrying capacity is associated with a higher risk of prediabetes and diabetes. Carrying capacity has not been quantified using a mathematical model and cannot be estimated directly from measured glucose and insulin levels in patients, unlike insulin resistance and beta cell function which can be estimated using HOMA-IR and HOMA-B formula.Here we present a mathematical model of beta cell compensation and carrying capacity, and develop a new formula called HOMA-C to estimate it from glucose and insulin measurements. HOMA-C estimates the maximal potential beta cell function of an individual, rather than the current beta cell function. We test this approach using longitudinal cohorts of prediabetic people, finding 10-fold variation in carrying capacity. Low carrying capacity is associated with higher risk of transitioning to diabetes. We estimate the timescales of beta cell compensation and insulin resistance using large datasets, showing that, unlike previous mathematical models, the new model can explain the slow rise in glucose over decades. Our mathematical understanding of beta cell carrying capacity may help to assess the risk of prediabetes in each individual.

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“…Other examples are the adjustable sizes of endocrine glands, such as those in the HPA axis, which provide dynamic compensation for physiological changes, but can result in dysregulation. 102 , 103 , 104 , 105 , 106 …”

Section: Discussionmentioning

confidence: 99%