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A review by Iriana Maharani, MD, highlights the role of TGF-β1 as a potential biomarker in chronic rhinosinusitis with and without nasal polyps.

Transforming growth factor beta 1 (TGF-β1) has been identified as a key molecular factor in the pathophysiology of chronic rhinosinusitis with nasal polyps (CRSwNP). However, the exact role and pathological significance of TGF-β1 in CRSwNP remain poorly understood because of inconsistencies in study methodologies and findings.

In a recent systematic review, Iriana Maharani, MD, and colleagues sought to clarify the role of TGF-β1 in the pathogenesis of CRSwNP and to determine whether TGF-β1 can be a reliable biomarker for this inflammatory condition. They reported their findings in Acta Oto-Laryngologica.

The researchers conducted a systematic literature review across three databases to investigate TGF-β1 levels in CRSwNP, chronic rhinosinusitis without nasal polyps (CRSsNP), and healthy controls. Data were extracted on TGF-β1 levels, methodological approaches, and clinical correlations.

They identified 12 articles for review. The analysis included data from a total of 77 patients in the control group, 102 patients with CRSsNP, and 354 patients with CRSwNP. The average age for the three groups was 28.28 years for the control group, 34.75 years for CRSsNP, and 34.17 years for CRSwNP.

Data revealed a distinct elevation of TGF-β1 in CRSsNP compared with the CRSwNP and control groups. The CRSsNP exhibited significantly elevated TGF-β1 with values reaching 23,998.70 pg/mL, suggesting a pronounced inflammatory response in CRSsNP, which may play an important role in its pathophysiology. Furthermore, the consistently high TGF-β1 levels across various measurements support the theory that TGF-β1 is an important factor in CRSsNP, according to the authors.

Compared with CRSsNP, the CRSwNP displayed a broader range of TGF-β1 levels, ranging from 30.767 pg/mL to 15,017.75 pg/mL. Although some individual’s measurements in the CRSwNP approached those of CRSsNP, the overall levels were generally lower, placing the controls between CRSwNP and CRSsNP.

“These results highlight a marked elevation of TGF-β1 in CRSsNP compared to both control and CRSwNP groups, suggesting a significant role of TGF-β1 in the pathophysiology of CRSsNP,” the authors said, “In contrast, CRSwNP displays a broad spectrum of TGF-β1 levels, which may indicate diverse disease activity or individual patient variability.”