Browsing by Author "Duntas, Leonidas (7003597705)"

Adiposopathy, defined as functionally disturbed adipose tissue mainly composed of large adipocytes and induced by chronic excess of food intake, has been associated with immune, metabolic and endocrine derangements promoting inflammation and, eventually, cardiovascular disease. Adiposopathy may positively influence thyrotropin-stimulating hormone, by raising leptin levels, and triggering autoimmunity. In this regard, it is hypothesized that the increased thyrotropin-stimulating hormone is independent of the negative regulation of the thyroid hormone, thereby constituting a secondary phenomenon and not a causal effect. Replacement therapy with thyroid hormones should therefore be applied following strict individualized consideration. Leptin is involved in the immune response and neuroendocrine appetite regulation, while leptin resistance may further promote autoimmune disease. The lipid derangement in adiposopathy may be aggravated in the presence of hypothyroidism and thus considerably augment cardiovascular risk. Lifestyle-modification counselling, including low-fat dietary intake and regular physical exercise, is today the cornerstone of adiposopathy treatment. Meanwhile, new drug formulations, such as leptin and leptin analogs, 5-HT2C-receptor agonist, and potent thyromimetics, currently comprise a promising armamentarium against adiposity and adiposopathy. © 2012 Expert Reviews Ltd.

Aging and its underlying pathophysiological background has always attracted the attention of the scientific society. Defined as the gradual, time-dependent, heterogeneous decline of physiological functions, aging is orchestrated by a plethora of molecular mechanisms, which vividly interact to alter body homeostasis. The ability of an organism to adjust to these alterations, in conjunction with the dynamic effect of various environmental stimuli across lifespan, promotes longevity, frailty or disease. Endocrine function undergoes major changes during aging, as well. Specifically, alterations in hormonal networks and concomitant hormonal deficits/excess, augmented by poor sensitivity of tissues to their action, take place. As hypothalamic-pituitary unit is the central regulator of crucial body functions, these alterations can be translated in significant clinical sequelae that can impair the quality of life and promote frailty and disease. Delineating the hormonal signaling alterations that occur across lifespan and exploring possible remedial interventions could possibly help us improve the quality of life of the elderly and promote longevity. © 2017 European Society of Endocrinology Printed in Great Britain.

Aging and its underlying pathophysiological background has always attracted the attention of the scientific society. Defined as the gradual, time-dependent, heterogeneous decline of physiological functions, aging is orchestrated by a plethora of molecular mechanisms, which vividly interact to alter body homeostasis. The ability of an organism to adjust to these alterations, in conjunction with the dynamic effect of various environmental stimuli across lifespan, promotes longevity, frailty or disease. Endocrine function undergoes major changes during aging, as well. Specifically, alterations in hormonal networks and concomitant hormonal deficits/excess, augmented by poor sensitivity of tissues to their action, take place. As hypothalamic-pituitary unit is the central regulator of crucial body functions, these alterations can be translated in significant clinical sequelae that can impair the quality of life and promote frailty and disease. Delineating the hormonal signaling alterations that occur across lifespan and exploring possible remedial interventions could possibly help us improve the quality of life of the elderly and promote longevity. © 2017 European Society of Endocrinology Printed in Great Britain.

Purpose: Levothyroxine (LT4) is commonly prescribed, but there is evidence strongly suggesting that a significant proportion of these patients are on treatment without solid evidence of hypothyroidism. Small trials on treatment discontinuation, did not detect any predictors of success. Therefore, we conducted this study in an attempt to identify predicting factors for successful LT4 withdrawal. Methods: In 802 consecutive patients (83% females, mean age 48 ± 16 years) on LT4 treatment for 8.8 ± 7.3 years without a solid diagnosis of hypothyroidism, therapy was abruptly discontinued. A total of 387 persons were followed up for up to 4 months (group A) and 415 individuals who were euthyroid at 4 months post LT4 discontinuation, were followed up for up to 60 months (group B). Recurrent hypothyroidism was defined if thyrotropin (TSH) level exceeded 4.5mIU/L. Results: Among the entire cohort, 182 patients (23%) became hypothyroid, 40% of group A and 7% of group B (p < 0.001). The Τhyroid treatment Discrimination Index (T4RxDI), the product of TSH levels multiplied by the daily LT4 dose divided by BMI, was calculated. In group A, successful LT4 withdrawal was strongly indicated by a T4RxDI value < 2.78 (72% sensitivity, 66% specificity), while in group B, the corresponding value was 3.75 (100% sensitivity, 48% specificity). Conclusions: Our findings reveal considerable overuse of LT4 and propose a T4RxDI product of < 3 as a valuable predictive factor of recurrent hypothyroidism, justifying a treatment discontinuation trial. If hypothyroidism does not resume within 4 months, the risk of developing long-term hypothyroidism is likely to be minimal. © The Author(s), under exclusive licence to Italian Society of Endocrinology (SIE) 2025.

Purpose: Levothyroxine (LT4) is commonly prescribed, but there is evidence strongly suggesting that a significant proportion of these patients are on treatment without solid evidence of hypothyroidism. Small trials on treatment discontinuation, did not detect any predictors of success. Therefore, we conducted this study in an attempt to identify predicting factors for successful LT4 withdrawal. Methods: In 802 consecutive patients (83% females, mean age 48 ± 16 years) on LT4 treatment for 8.8 ± 7.3 years without a solid diagnosis of hypothyroidism, therapy was abruptly discontinued. A total of 387 persons were followed up for up to 4 months (group A) and 415 individuals who were euthyroid at 4 months post LT4 discontinuation, were followed up for up to 60 months (group B). Recurrent hypothyroidism was defined if thyrotropin (TSH) level exceeded 4.5mIU/L. Results: Among the entire cohort, 182 patients (23%) became hypothyroid, 40% of group A and 7% of group B (p < 0.001). The Τhyroid treatment Discrimination Index (T4RxDI), the product of TSH levels multiplied by the daily LT4 dose divided by BMI, was calculated. In group A, successful LT4 withdrawal was strongly indicated by a T4RxDI value < 2.78 (72% sensitivity, 66% specificity), while in group B, the corresponding value was 3.75 (100% sensitivity, 48% specificity). Conclusions: Our findings reveal considerable overuse of LT4 and propose a T4RxDI product of < 3 as a valuable predictive factor of recurrent hypothyroidism, justifying a treatment discontinuation trial. If hypothyroidism does not resume within 4 months, the risk of developing long-term hypothyroidism is likely to be minimal. © The Author(s), under exclusive licence to Italian Society of Endocrinology (SIE) 2025.