Turkish journal of medical sciences · 2025
Can mac-2 binding protein glycosylation isomer serve as a biomarker for predicting pulmonary arterial pressure and pulmonary hypertension in systemic sclerosis?
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Mercan Rıdvan, Gökten Dilara Bulut, Kara Sonat Pınar, Üzüm Neslihan Melik, Güzel Savaş
Аннотация
BACKGROUND/AIM: This study aimed to explore the role of Mac-2 binding protein glycosylation isomer (M2BPGi) serum levels as a biomarker that could contribute to understanding organ involvement and the overall disease process in systemic sclerosis (SSc).
MATERIALS AND METHODS: The cross-sectional study examined 108 patients with SSc. Seventy-two people were included in the control group. Demographic and clinical characteristics of the patients, laboratory and radiological findings, pulmonary function tests and echocardiography results, and presence of pulmonary hypertension (PHT) based on echocardiographic evaluation were recorded. Venous blood samples of 5 mL were collected from individuals. Human M2BPGi levels in the samples were measured using a specific kit.
RESULTS: There was no significant difference between the M2BPGi levels in the patient (median = 4749.69 pg/mL, mean = 5351.75 ± 2483.97) and the control group (median = 4638.07, mean = 4611.86 ± 1333.15) (p = 0.071). Considering pulmonary arterial pressure (PAP) status, the average M2BPGi level in the normal PAP group was 5898.15 ± 2555.61 pg/mL, while it was 4258.96 ± 1973.08 pg/mL in the increased PAP group. The difference between these groups was statistically significant (p: 0.021). Examining PHT status, the average M2BPGi level was 5942.01 ± 2579.14 pg/mL in the group without PHT, decreasing to 4264.44 ± 1917.63 pg/mL in the group with PHT. There is a significant relationship regarding PHT (p: 0.016).
CONCLUSION: This study explores the relationship between M2BPGi and systemic involvements in SSc. It demonstrates a significant relationship between M2BPGi and PAP and PHT, suggesting that M2BPGi might serve as a noninvasive biomarker for predicting both PAP and PHT.
MATERIALS AND METHODS: The cross-sectional study examined 108 patients with SSc. Seventy-two people were included in the control group. Demographic and clinical characteristics of the patients, laboratory and radiological findings, pulmonary function tests and echocardiography results, and presence of pulmonary hypertension (PHT) based on echocardiographic evaluation were recorded. Venous blood samples of 5 mL were collected from individuals. Human M2BPGi levels in the samples were measured using a specific kit.
RESULTS: There was no significant difference between the M2BPGi levels in the patient (median = 4749.69 pg/mL, mean = 5351.75 ± 2483.97) and the control group (median = 4638.07, mean = 4611.86 ± 1333.15) (p = 0.071). Considering pulmonary arterial pressure (PAP) status, the average M2BPGi level in the normal PAP group was 5898.15 ± 2555.61 pg/mL, while it was 4258.96 ± 1973.08 pg/mL in the increased PAP group. The difference between these groups was statistically significant (p: 0.021). Examining PHT status, the average M2BPGi level was 5942.01 ± 2579.14 pg/mL in the group without PHT, decreasing to 4264.44 ± 1917.63 pg/mL in the group with PHT. There is a significant relationship regarding PHT (p: 0.016).
CONCLUSION: This study explores the relationship between M2BPGi and systemic involvements in SSc. It demonstrates a significant relationship between M2BPGi and PAP and PHT, suggesting that M2BPGi might serve as a noninvasive biomarker for predicting both PAP and PHT.