Adult growth hormone deficiency (AGHD) is nowadays recognized as a distinct clinical entity and replacement therapy has become a standard practice. Reflecting on the accumulated evidence, questions nevertheless arise. Should all AGHD patients be treated? What dose of GH should be given and for how long? What are the real long-term benefits, in particular regarding life expectancy? if the diagnosis of severe GHD is firmly established and if there is no contra-indication (such as an active cancer or uncontrolled diabetes), it is worthwile initiating GH replacement therapy. Treatment can indeed correct the abnormal body composition, improve various adverse cardiovascular parameters and risk factors, increase muscle strength and bone mineral density and, although to a variable degree, improve the patient's quality of life and psychological well-being. Treatment should be started with very low doses to avoid side-effects related to fluid retention and should then be gradually titrated against IGF-I values, clinical response and individual tolerance.There is unfortunately no confirmed predictive factor for the overall therapeutic response in a given individual. Thus, the decision to whether or not pursue the therapy will depend on the ratio of perceived and expected benefits over cost and risks of treatment, as well as on the persistent motivation of the patient.
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http://dx.doi.org/10.1179/acb.2010.002 | DOI Listing |
Sci Rep
December 2024
Department of Psychiatry and Behavioral Sciences and Weill Center for Neurosciences, University of California, San Francisco, CA, 94107, USA.
Telomere attrition is a hallmark of biological aging, contributing to cellular replicative senescence. However, few studies have examined the determinants of telomere attrition in vivo in humans. Mitochondrial Health Index (MHI), a composite marker integrating mitochondrial energy-transformation capacity and content, may be one important mediator of telomere attrition, as it could impact telomerase activity, a direct regulator of telomere maintenance.
View Article and Find Full Text PDFNat Commun
December 2024
Institute of Pathology, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.
Pathogenic activating mutations in the fibroblast growth factor receptor 3 (FGFR3) drive disease maintenance and progression in urothelial cancer. 10-15% of muscle-invasive and metastatic urothelial cancer (MIBC/mUC) are FGFR3-mutant. Selective targeting of FGFR3 hotspot mutations with tyrosine kinase inhibitors (e.
View Article and Find Full Text PDFFront Physiol
December 2024
Department of Zoology, Acharya Narendra Dev College, University of Delhi, New Delhi, India.
Introduction: , the vector of multiple arboviral diseases, is a prime health concern worldwide. The surge in borne diseases emphasizes the urgent need for efficient vector control measures. Synthetic pesticides used traditionally, however, present environmental concerns and issues like resistance development, causing the use of higher chemical doses.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
December 2024
Department of Pediatric Diabetes and Endocrinology, Clinique Pédiatrique, Centre Hospitalier, Luxembourg, Luxembourg.
Aims: To compare impact of pump treatment and continuous glucose monitoring (CGM) with predictive low glucose suspend (SmartGuard) or user initiated CGM (iscCGM) on sleep and hypoglycemia fear in children with type 1 Diabetes and parents.
Methods: Secondary analysis of data from 5 weeks pump treatment with iscCGM (A) or SmartGuard (B) open label, single center, randomized cross-over study was performed. At baseline and end of treatment arms, sleep and fear of hypoglycemia were evaluated using ActiGraph and questionnaires.
Front Endocrinol (Lausanne)
December 2024
Department of Obstetrics and Gynecology, Hefei Maternal and Child Health Hospital, Hefei, China.
Objective: Gestational diabetes mellitus (GDM) is a common complication during pregnancy and increases the risk of metabolic diseases in offspring. We hypothesize that the poor intrauterine environment in pregnant women with GDM may lead to chromosomal DNA damage and telomere damage in umbilical cord blood cells, providing evidence of an association between intrauterine programming and increased long-term metabolic disease risk in offspring.
Methods: We measured telomere length (TL), serum telomerase (TE) activity, and oxidative stress markers in umbilical cord blood mononuclear cells (CBMCs) from pregnant women with GDM (N=200) and healthy controls (Ctrls) (N=200) and analysed the associations of TL with demographic characteristics, biochemical indicators, and blood glucose levels.
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