Elevated Levels of Activin-A, TNF-Alpha and IL-6 in Acromegaly


Dogan K., Yildiz S. N., SARIAKÇALI B., DUMAN G., BOLAT S.

NEUROCHEMICAL JOURNAL, cilt.15, sa.3, ss.325-330, 2021 (SCI-Expanded) identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 15 Sayı: 3
  • Basım Tarihi: 2021
  • Doi Numarası: 10.1134/s181971242103003x
  • Dergi Adı: NEUROCHEMICAL JOURNAL
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED)
  • Sayfa Sayıları: ss.325-330
  • Anahtar Kelimeler: acromegaly, tumor necrosis factor-alpha, interleukin-6, activin A, residual pituitary tumor, serum, inflammation, comorbidity, GROWTH-HORMONE-SECRETION, INHIBITION, ANTAGONIST
  • Sivas Cumhuriyet Üniversitesi Adresli: Evet

Özet

Although systemic inflammation has been linked to acromegaly, little is known about the abnormalities in cytokine networks during the disease. The aim of this study was to evaluate the serum concentrations of tumor necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6), and activin-A in acromegaly, and to investigate the relationship between TNF-alpha, IL-6, activin-A and comorbidities of acromegaly. A total of 56 subjects were recruited to the study. Serum samples were collected from 31 acromegaly patients and 25 healthy control subjects. Serum activin-A, IL-6 and TNF-alpha were determined using the enzyme-linked immunosorbent assay. Circulating levels of activin-A, TNF-alpha, and IL-6 were higher in patients than in the control group. Receiver operating characteristic analysis for activin-A for the differentiation of acromegaly patients from healthy control subjects showed an area under the curve of 0.90. Higher activin-A levels were determined in patients with residual pituitary tumor. These findings provide evidence for the role of activin-A, TNF-alpha and IL-6 in acromegaly. Serum activin-A levels could be used as a novel biomarker to diagnose acromegaly. These findings confirm previous studies that inflammation might be involved in the pathogenesis of acromegaly. Finally, treatment strategies targeting the regulation of inflammation cannot be sufficient alone in reducing comorbidities.