UT Medical School - Houston Houston, United States
Disclosure(s):
Catherine dos Reis Schevz, medical doctor: No financial relationships to disclose
Background
Elevated IGF-1 is typically associated with growth hormone excess from pituitary adenoma. Testosterone therapy may increase IGF-1, occasionally mimicking acromegaly without GH excess.
Case Presentation
A 71-year-old male with hypogonadism on testosterone replacement therapy presented with intermittent elevation of IGF-1 and acromegaloid features, including coarse facial changes, prognathism, large feet, also joint pain, obstructive sleep apnea, prediabetes, hypertension and erythrocytosis. Longitudinal laboratory evaluation demonstrated a temporal correlation between supraphysiologic testosterone levels (peak 1124 ng/dL) and elevated IGF-1 (302 ng/mL), while lower testosterone levels were associated with lower IGF-1 values. Oral glucose tolerance testing showed appropriate growth hormone suppression, excluding biochemical acromegaly. Pituitary MRI revealed no adenoma, and other pituitary hormones were within normal limits.
Discussion
In this context, patients may present with elevated IGF-1 despite preserved GH suppression and the causes could be metabolic, pharmacological, and physiological influences, including testosterone therapy, dopamine agonist use, chronic kidney disease, pregnancy and hyperthyroidism. Testosterone therapy is an important modulator of the GH–IGF-1 axis and may increase circulating IGF-1 through androgen receptor–mediated transcription, stimulation of GH secretion, and direct hepatic effects independent of pathological GH excess, causing positive hormonal feedback. Nevertheless, sustained IGF-1 elevation itself may be associated with the development of acromegaloid features and, consequently, a higher risk of acromegaly-related comorbidities, such as obstructive sleep apnea, erythrocytosis, hypertension and benign colon polyps. These observations highlight that peripheral hormonal modulation can influence both biochemical markers and clinical phenotype independently of pituitary tumor activity.
Conclusion
Testosterone replacement therapy can elevate IGF-1 through GH-dependent and independent mechanisms and produce acromegaloid features. Awareness of this association, combined with confirmatory GH suppression testing, allows accurate diagnosis, prevents misclassification as acromegaly, and guides appropriate surveillance.
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