2015
DOI: 10.1530/endoabs.37.ep652
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IGF1 deficiency in newly diagnosed Graves' disease patients

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Cited by 3 publications
(4 citation statements)
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“…In a study of patients with new onset Graves' disease, 18.4% had IGF-1 deficiency as defined by serum levels less than 2 standard deviations below normal values for age. 161 No study has been performed linking IGF-1 levels and hearing loss in GD patients. It is unclear whether topical application of IGF-1 would help prevent hearing-related complications secondary to teprotumumab therapy.…”
Section: Infectionsmentioning
confidence: 99%
“…In a study of patients with new onset Graves' disease, 18.4% had IGF-1 deficiency as defined by serum levels less than 2 standard deviations below normal values for age. 161 No study has been performed linking IGF-1 levels and hearing loss in GD patients. It is unclear whether topical application of IGF-1 would help prevent hearing-related complications secondary to teprotumumab therapy.…”
Section: Infectionsmentioning
confidence: 99%
“…12,13 However, there is also evidence to suggest that IGF1 administration can stimulate regulatory T cells to dampen the immune response. 1420…”
Section: Introductionmentioning
confidence: 99%
“…12,13 However, there is also evidence to suggest that IGF1 administration can stimulate regulatory T cells to dampen the immune response. [14][15][16][17][18][19][20] Systemic lupus erythematosus (SLE) is the prototypic autoimmune disease, characterised by abnormalities in T-cell and B-cell functionality and a diverse clinical presentation that can lead to organ failure and premature mortality due to an excess of cardiovascular events. 19,21 GH therapy has been used by SLE patients to increase IGF1 levels in spite of the lack of evidence for a possible role of the GH/IGF1 pathway in the pathogenesis of SLE.…”
Section: Introductionmentioning
confidence: 99%
“…Furthermore, complexes containing thyrotropin, IGF-1R and INSR have been detected in orbital fibroblasts and thyroid epithelial cells, the IGF axis is required to maintain thyrotropin signaling, and anti-IGF-1R autoantibodies that activate IGF-1R are detectable in patients with GD [87,90,91]. Thus, although cross-talk between thyrotropin and IGF signaling has been recognized for over 30 years, it is only recently that IGF-1R activation has been implicated in driving the immunopathogenesis of GD [87,88,92,93].…”
Section: Thyroid Eye Diseasementioning
confidence: 99%