Plasma α-Glutathione S-Transferase in Patients with Chronic Mesenteric Ischemia and Median Arcuate Ligament Syndrome.
biomarker
chronic mesenteric ischemia
intestinal ischemia
median arcuate ligament syndrome
α-GST
Journal
Vascular health and risk management
ISSN: 1178-2048
Titre abrégé: Vasc Health Risk Manag
Pays: New Zealand
ID NLM: 101273479
Informations de publication
Date de publication:
2022
2022
Historique:
received:
09
03
2022
accepted:
14
07
2022
entrez:
29
7
2022
pubmed:
30
7
2022
medline:
2
8
2022
Statut:
epublish
Résumé
Chronic mesenteric ischemia (CMI) due to either atherosclerosis of the mesenteric arteries or median arcuate ligament syndrome (MALS) is an underdiagnosed entity. The etiology of MALS and its existence have been debated and questioned. We aimed to identify plasma biomarkers indicating mesenteric ischemia in patients with CMI and MALS. Plasma α-glutathione S-transferase (α-GST), intestinal fatty acid-binding protein (I-FABP), citrulline, and ischemia modified albumin (IMA) were analyzed in fifty-eight patients with CMI (Group A, n=44) and MALS (Group B, n=14) before and after revascularization. The plasma levels of these potential biomarkers were compared with those of healthy individuals (Group C, n=16). Group comparison was performed with the Mann-Whitney Plasma levels of α-GST were significantly raised in the patients with CMI (7.8 ng/mL, p<0.001) and MALS (8.4 ng/mL, p<0.001), as compared with the control Group C (3.3 ng/mL). The threshold for normal median plasma α-GST levels of 4 ng/mL yielded a sensitivity of 93% and 86%, specificity of 86% and 88%, respectively, for the diagnosis of CMI due to atherosclerosis and MALS. AUC of ROC curves was 0.96 (p<0.0001) for CMI and 0.85 (p<0.002) for MALS. The patient groups did not differ from the healthy controls in any other biomarkers. Plasma α-GST levels are elevated in CMI and MALS patients. Elevated plasma levels of α-GST suggest ischemia as the etiology of MALS.
Sections du résumé
Background
UNASSIGNED
Chronic mesenteric ischemia (CMI) due to either atherosclerosis of the mesenteric arteries or median arcuate ligament syndrome (MALS) is an underdiagnosed entity. The etiology of MALS and its existence have been debated and questioned. We aimed to identify plasma biomarkers indicating mesenteric ischemia in patients with CMI and MALS.
Methods
UNASSIGNED
Plasma α-glutathione S-transferase (α-GST), intestinal fatty acid-binding protein (I-FABP), citrulline, and ischemia modified albumin (IMA) were analyzed in fifty-eight patients with CMI (Group A, n=44) and MALS (Group B, n=14) before and after revascularization. The plasma levels of these potential biomarkers were compared with those of healthy individuals (Group C, n=16). Group comparison was performed with the Mann-Whitney
Results
UNASSIGNED
Plasma levels of α-GST were significantly raised in the patients with CMI (7.8 ng/mL, p<0.001) and MALS (8.4 ng/mL, p<0.001), as compared with the control Group C (3.3 ng/mL). The threshold for normal median plasma α-GST levels of 4 ng/mL yielded a sensitivity of 93% and 86%, specificity of 86% and 88%, respectively, for the diagnosis of CMI due to atherosclerosis and MALS. AUC of ROC curves was 0.96 (p<0.0001) for CMI and 0.85 (p<0.002) for MALS. The patient groups did not differ from the healthy controls in any other biomarkers.
Conclusion
UNASSIGNED
Plasma α-GST levels are elevated in CMI and MALS patients. Elevated plasma levels of α-GST suggest ischemia as the etiology of MALS.
Identifiants
pubmed: 35903288
doi: 10.2147/VHRM.S365625
pii: 365625
pmc: PMC9315055
doi:
Substances chimiques
Biomarkers
0
Serum Albumin
0
Glutathione Transferase
EC 2.5.1.18
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
567-574Informations de copyright
© 2022 Kazmi et al.
Déclaration de conflit d'intérêts
Dr Asle Wilhelm Medhus reports grants from Takeda, outside the submitted work. The authors report no other conflicts of interest in this work.
Références
Eur J Vasc Endovasc Surg. 2017 Apr;53(4):460-510
pubmed: 28359440
Vasc Health Risk Manag. 2022 Apr 08;18:233-243
pubmed: 35431549
Clin Transl Gastroenterol. 2020 Aug;11(8):e00200
pubmed: 32955192
Vasc Health Risk Manag. 2020 Aug 10;16:331-341
pubmed: 32982262
N Engl J Med. 1985 Jan 17;312(3):159-63
pubmed: 2981404
Br J Surg. 1999 Oct;86(10):1349-53
pubmed: 10540149
Ann Transl Med. 2018 Sep;6(17):341
pubmed: 30306080
United European Gastroenterol J. 2020 May;8(4):371-395
pubmed: 32297566
Radiology. 1982 Apr;143(1):29-36
pubmed: 7063747
J Vasc Surg. 1991 Oct;14(4):511-8; discussion 518-20
pubmed: 1920649
Ann Transl Med. 2019 Aug;7(16):394
pubmed: 31555708
Perspect Vasc Surg Endovasc Ther. 2007 Sep;19(3):259-63
pubmed: 17911551
Am J Emerg Med. 2008 Feb;26(2):202-5
pubmed: 18272103
World J Surg. 2012 Apr;36(4):793-9
pubmed: 22354487
Intern Emerg Med. 2017 Sep;12(6):821-836
pubmed: 28478489
Langenbecks Arch Surg. 1999 Jun;384(3):233-8
pubmed: 10437610
Br J Surg. 2006 Nov;93(11):1377-82
pubmed: 17022013
Paediatr Anaesth. 2000;10(4):395-8
pubmed: 10886696
World J Surg. 2009 Jul;33(7):1374-83
pubmed: 19424744
J Vasc Bras. 2020 Dec 11;19:e20200186
pubmed: 34211533
Semin Nucl Med. 1978 Oct;8(4):283-98
pubmed: 112681
N Engl J Med. 2016 Mar 10;374(10):959-68
pubmed: 26962730
JAMA Surg. 2016 May 1;151(5):471-7
pubmed: 26934394
Clin Exp Gastroenterol. 2017 Apr 28;10:75-81
pubmed: 28496350
Scand J Clin Lab Invest. 2019 Nov;79(7):541-549
pubmed: 31560225
World J Gastroenterol. 2013 Mar 7;19(9):1338-41
pubmed: 23538325
Eur J Gastroenterol Hepatol. 2009 Mar;21(3):278-82
pubmed: 19279473
J Vasc Surg. 2018 May;67(5):1598-1605
pubmed: 29571626
Gut. 1995 May;36(5):788-91
pubmed: 7797132
Am J Pathol. 2010 May;176(5):2283-91
pubmed: 20348235
J Thromb Thrombolysis. 2012 May;33(4):355-61
pubmed: 22081293
Support Care Cancer. 2017 Sep;25(9):2933-2941
pubmed: 28536886
J Vasc Surg. 2006 Aug;44(2):277-81
pubmed: 16890853
Can J Gastroenterol Hepatol. 2019 Oct 20;2019:5850787
pubmed: 31772928
Minerva Gastroenterol Dietol. 1999 Sep;45(3):181-5
pubmed: 16498328
Ann Vasc Surg. 2016 Jan;30:22-7
pubmed: 26365109