Portal hypertensive gastropathy is associated with iron deficiency anemia

Benedikt Simbrunner, Andrea Beer, Katharina Wöran, Fabian Schmitz, Christian Primas, Marlene Wewalka, Matthias Pinter, Werner Dolak, Bernhard Scheiner, Andreas Puespoek, Michael Trauner, Georg Oberhuber, Mattias Mandorfer, Thomas Reiberger, Benedikt Simbrunner, Andrea Beer, Katharina Wöran, Fabian Schmitz, Christian Primas, Marlene Wewalka, Matthias Pinter, Werner Dolak, Bernhard Scheiner, Andreas Puespoek, Michael Trauner, Georg Oberhuber, Mattias Mandorfer, Thomas Reiberger

Abstract

Background and aims: Portal hypertensive gastropathy (PHG) is common in patients with cirrhosis and may cause bleeding. This study systematically explored the independent impact of patient characteristics, portal hypertension and hepatic dysfunction on PHG severity and associated anemia.

Methods: Patients with cirrhosis undergoing endoscopy were included in this retrospective analysis and PHG was endoscopically graded as absent, mild or severe. Clinical and laboratory parameters and hepatic venous pressure gradient (HVPG) were assessed with respect to an association with severity of PHG.

Results: A total of 110 patients (mean age: 57 years, 69% male) with mostly alcoholic liver disease (49%) or viral hepatitis (30%) were included: 15 (13.6%) patients had no PHG, 59 (53.6%) had mild PHG, and 36 (32.7%) had severe PHG. Severe PHG was significantly associated with male sex (83.3% vs. 62.2% in no or mild PHG; p = 0.024) and higher Child-Turcotte-Pugh (CTP) stage (CTP-C: 38.9% vs. 27.0% in no or mild PHG; p = 0.030), while MELD was similar (p = 0.253). Patients with severe PHG had significantly lower hemoglobin values (11.2 ± 0.4 g/dL vs. 12.4 ± 0.2 g/dL; p = 0.008) and a higher prevalence of iron-deficiency anemia (IDA: 48.5% vs. 26.9%; p = 0.032). Interestingly, HVPG was not significantly higher in severe PHG (median 20 mm Hg) vs. mild PHG (19 mm Hg) and no PHG (18 mm Hg; p = 0.252). On multivariate analysis, CTP score (odds ratio, OR: 1.25, 95% confidence interval, CI 1.02-1.53; p = 0.033) was independently associated with severe PHG, while only a trend towards an independent association with IDA was observed (OR: 2.28, 95% CI 0.91-5.72; p = 0.078).

Conclusion: The CTP score but not HVPG or MELD were risk factors for severe PHG. Importantly, anemia and especially IDA are significantly more common in patients with severe PHG.

Keywords: Anemia; Cirrhosis; Endoscopy; Iron deficiency; Portal hypertension.

Conflict of interest statement

B. Simbrunner received travel support from AbbVie and Gilead. M. Pinter is an investigator for Bayer, BMS, and Lilly, he received speaker fees from Bayer, BMS, Eisai, and MSD, he is a consultant for Bayer, BMS, Ipsen, Eisai, and Lilly, and he received travel support from Bayer and BMS. B. Scheiner received travel support from Abbvie and Gilead. M. Trauner received speaker fees from BMS, Falk Foundation, Gilead and MSD; advisory board fees from Albireo, Falk Pharma GmbH, Genfit, Gilead, Intercept, MSD, Novartis, Phenex and Regulus. He further received travel grants from Abbvie, Falk, Gilead and Intercept and unrestricted research grants from Albireo, Cymabay, Falk, Gilead, Intercept, MSD and Takeda. M. Mandorfer has served as a speaker and/or consultant and/or advisory board member for AbbVie, Bristol-Myers Squibb, Gilead, W. L. Gore & Associates and Janssen. T. Reiberger received grant support from Abbvie, Boehringer-Ingelheim, Gilead, MSD, Philips Healthcare, Gore; speakers fees from Abbvie, Gilead, Gore, Intercept, Roche, MSD; consulting/advisory board fee from Abbvie, Bayer, Boehringer-Ingelheim, Gilead, MSD, Siemens and travel support from Boehringer-Ingelheim, Gilead and Roche. A. Beer, K. Wöran, F. Schmitz, C. Primas, M. Wewalka, W. Dolak, A. Puespoek and G. Oberhuber declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
Patient flow chart. aData on HVPG missing in n = 47 (42.7%), available in n = 10, n = 34, n = 19 of patients without PHG, mild and severe PHG, respectively. bData on IDA missing in n = 10 patients (9.1%), available in n = 11, n = 56, n = 33 of patients without PHG, mild and severe PHG, respectively. GI gastrointestinal, PHG portal hypertensive gastropathy, MELD model for end-stage liver disease, HVPG hepatic venous pressure gradient, IDA iron-deficiency anemia
Fig. 2
Fig. 2
Prevalence and severity of portal hypertensive gastropathy according to a gender, b Child-Turcotte-Pugh stage and c severity of portal hypertension. PHG portal hypertensive gastropathy, HVPG hepatic venous pressure gradient
Fig. 3
Fig. 3
a Hemoglobin levels, b prevalence of anemia and c iron deficiency anemia according to severity of PHG. PHG Portal hypertensive gastropathy, G1–G3 grades 1–3, IDA Iron-deficiency anemia

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Source: PubMed

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