SUN-095 Persistent IGF-1 elevation in a patient with previously diagnosed acquired growth hormone deficiency

Abstract Disclosure: J.L. Azocar Villalobos: None. K. Gonzales: None. Background: Insulin-like growth factor-1 (IGF-1) is primarily synthesized in the liver and mediates growth hormone (GH) effects. IGF-1 elevations are typically associated with pituitary somatotroph tumors and rarely ectopic GH secretion. When both etiologies are ruled out, other contributing factors should be considered. Inflammatory cytokines are known to impair the GH-IFG-1 axis. Anti-inflammatory therapies, laboratory assay performance, biological variability, and effects of other medications on this axis should be considered in unexplained IGF-1 elevations. Clinical Case A 47-year-old female, G2P2, with reactive arthritis and osteoporosis was diagnosed with anterior panhypopituitarism secondary to peripartum hypotension. She had been treated with disease-modifying and anti-inflammatory agents prior to the diagnosis of panhypopituitarism, but had discontinued treatments prior to her endocrine evaluation. At the time of diagnosis of panhypopituitarism, she had an insulin tolerance test that resulted in a glucose of 26 mg/dL, peak serum cortisol of 5.9 μg/dL (n > 15 μg/dL), and a peak GH of 0.25 ng/mL (<5.1 ng/mL). FreeT4 (FT4) was 0.8 ng/dL (n 0.7-1.6 ng/dL). Hydrocortisone, levothyroxine, and recombinant GH (rGH) were started.The patient began treatment with adalimubab and presented to endocrinology clinic several years later. She had discontinued rGH therapy two years prior. Biochemistries at that time revealed a mildly elevated IGF-1 of 223 ng/mL (n 82-219 ng/mL), AM cortisol of 1.7 μg/dL, and FT4 1.6 ng/dL. Physical examination showed no signs of acromegaly.Three months later, IGF-1 was 260 ng/mL with a normal GH of 1.98 ng/mL. An oral glucose tolerance test (OGTT) showed GH suppression to 0.15 ng/mL at 120 min (n < 0.3 ng/mL). IGFBP-3 was 4.8 ng/mL (n 2.67-6.19 ng/mL), and growth hormone releasing hormone (GHRH) was 4 pg/mL (n 5-18 pg/mL). IGF-1 via mass spectrometry was 232 ng/mL (n 44-227 ng/mL). Brain MRI showed no pituitary mass.The exact cause of the mild but persistent IGF-1 elevations in this case remain unclear, but treatment with an anti-TNF alpha inhibitor may have contributed. Several studies have identified unique impacts of inflammatory cytokines on mediation of the GH-IGF-1 axis, and some have demonstrated amelioration with rises in IGF-1 levels in response to glucocorticoids and anti-TNF alpha inhibitors. Assay performance seemed less likely given the consistent elevations on different platforms, although the elevations may have reflected normal individual biological variation for the assays. Conclusion: Persistent elevations in IGF-1 concentrations among patients without clinical or confirmatory biochemical evidence of acromegaly can create diagnostic uncertainty. Laboratory findings should be interpreted in the context of patient-specific factors, and consideration of other potential etiologies may negate the need for more extensive evaluations. Presentation: Sunday, July 13, 2025