# The Journey of Acromegaly Towards Treatment: A Single-Center Study

**Authors:** Varvara Chalmantzi, Sophia Vlachou, Maria Eleni Chondrogianni, Maria Panagaki, Ariadni Spyroglou, Marina Tsoli, Eva Kassi, Gregory Kaltsas, Krystallenia I. Alexandraki

PMC · DOI: 10.3390/jpm16020085 · 2026-02-02

## TL;DR

This study tracks how patients with acromegaly are treated over time, focusing on factors like age, surgery, and biochemical outcomes.

## Contribution

The study provides insights into treatment patterns and outcomes in acromegaly, particularly in elderly patients.

## Key findings

- Biochemical control was achieved in 85% of patients.
- Higher IGF-1/ULN ratios at diagnosis tend to predict non-remission.
- Older patients were less likely to undergo surgery and had longer diagnostic delays.

## Abstract

Background: In the era of personalized medicine, the overall therapeutic approach has progressed throughout the years in acromegaly, but biochemical control of the disease is not achieved in a significant proportion of patients. This study aims to systematically record the journey of patients with acromegaly in the context of adenomas characteristics, therapeutic approaches and comorbidities in acromegaly with an emphasis in elderly. Method: In this retrospective study 79 patients were diagnosed with acromegaly between 1971 and 2023. Results: The dataset consisted of 43 (54%) female and 36 male (46%) with an overall mean age ± SD at diagnosis at 45 ± 13 years. 57 (73%) underwent one surgical procedure. Medical treatment with one agent was reported in 36 patients (67%), almost all by somatostatin analogs (89%). Radiotherapy was offered in 14 patients (18%). Disease remission was documented in 67 (85%) patients. IGF1/ULN at diagnosis displayed a tendency to predict non-remission. A diagnostic delay of less than five years was reported in 28 cases (65%) and patients reporting longer delays were older at diagnosis (58 ± 6 years). Patients diagnosed at or above the age of 60 were less likely to undergo a surgical procedure compared to patients diagnosed before the age of 60. Conclusions: Biochemical control was the most frequent disease outcome. A higher IGF-1/ULN ratio tends to predict non-remission. Longer diagnostic delay was reported with advancing age and older patients were less likely to follow surgical procedures.

## Linked entities

- **Diseases:** acromegaly (MONDO:0019933)

## Full-text entities

- **Genes:** GH1 (growth hormone 1) [NCBI Gene 2688] {aka GH, GH-N, GHB5, GHN, IGHD1A, IGHD1B}, CDH1 (cadherin 1) [NCBI Gene 999] {aka Arc-1, BCDS1, CD324, CDHE, ECAD, LCAM}, AIP (AHR interacting HSP90 co-chaperone) [NCBI Gene 9049] {aka ARA9, FKBP16, FKBP37, PITA1, SMTPHN, XAP-2}, MTOR (mechanistic target of rapamycin kinase) [NCBI Gene 2475] {aka FRAP, FRAP1, FRAP2, RAFT1, RAPT1, SKS}, SSTR5 (somatostatin receptor 5) [NCBI Gene 6755] {aka SS-5-R, SST5}, GGH (gamma-glutamyl hydrolase) [NCBI Gene 8836] {aka GATD10, GH}, VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422] {aka L-VEGF, MVCD1, VEGF, VPF}, SSTR2 (somatostatin receptor 2) [NCBI Gene 6752] {aka SST2}, IGF1 (insulin like growth factor 1) [NCBI Gene 3479] {aka IGF, IGF-I, IGFI, MGF}
- **Diseases:** ectopic (MESH:C566852), colon adenomas (MESH:D003108), breast cancer (MESH:D001943), type 2 diabetes (MESH:D003924), multiple endocrine neoplasia syndrome (MESH:D009377), Vertebral fractures (MESH:C535781), Excess GH (MESH:C531600), Ischemic disease (MESH:D017202), hypertrophy (MESH:D006984), cardiovascular disease (MESH:D002318), myocardial infarction (MESH:D009203), Osteoporosis (MESH:D010024), bone (MESH:D001847), pituitary diseases (MESH:D010900), Acromegalic (MESH:D000172), colorectal and thyroid (MESH:D015179), death (MESH:D003643), thyroid cancer (MESH:D013964), Hypertension (MESH:D006973), left ventricular hypertrophy (MESH:D017379), adrenal lesions (MESH:D000307), metabolic disorders (MESH:D008659), type 3 tumors (MESH:C565335), Micro- and macroadenomas (MESH:C536681), Osteopenia (MESH:D001851), diastolic dysfunction (MESH:D018487), hepatic steatosis (MESH:D005234), adenoma (MESH:D000236), Neoplasia (MESH:D009369), Valvular lesions (MESH:D006349), diabetes (MESH:D003920), Pituitary tumors (MESH:D010911), hyperglycemia (MESH:D006943), Hyperlipidemia (MESH:D006949), injury to (MESH:D014947), dyslipidemia (MESH:D050171), fractures (MESH:D050723), thyroid nodules (MESH:D016606)
- **Chemicals:** dopamine (MESH:D004298), glucose (MESH:D005947), lipid (MESH:D008055), Pegvisomant (MESH:C406545), SSA (-), cabergoline (MESH:D000077465), octreotide (MESH:D015282), Bromocriptine (MESH:D001971), triglycerides (MESH:D014280)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12941836/full.md

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Source: https://tomesphere.com/paper/PMC12941836