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Review
. 2023 Dec 21;16(1):35.
doi: 10.3390/nu16010035.

Portal Hypertension in Malnutrition and Sarcopenia in Decompensated Cirrhosis-Pathogenesis, Implications and Therapeutic Opportunities

Ryma Terbah  1   2 , Adam Testro  1   2 , Paul Gow  1   2 , Avik Majumdar  1   2 , Marie Sinclair  1   2
Affiliations
Review

Portal Hypertension in Malnutrition and Sarcopenia in Decompensated Cirrhosis-Pathogenesis, Implications and Therapeutic Opportunities

Ryma Terbah et al. Nutrients. .

Abstract

Malnutrition and sarcopenia are highly prevalent in patients with decompensated cirrhosis and are associated with poorer clinical outcomes. Their pathophysiology is complex and multifactorial, with protein-calorie malnutrition, systemic inflammation, reduced glycogen stores and hormonal imbalances all well reported. The direct contribution of portal hypertension to these driving factors is however not widely documented in the literature. This review details the specific mechanisms by which portal hypertension directly contributes to the development of malnutrition and sarcopenia in cirrhosis. We summarise the existing literature describing treatment strategies that specifically aim to reduce portal pressures and their impact on nutritional and muscle outcomes, which is particularly relevant to those with end-stage disease awaiting liver transplantation.

Keywords: cirrhosis; malnutrition; portal hypertension; sarcopenia.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 2
Figure 2
Complications of portal hypertension and their role in sarcopenia. Flowchart outlining how the complications of portal hypertension contribute to the development of sarcopenia. ↑ = increased; ↓ = decreased; BCAA = branched chain amino acid; TCA = tricarboxylic acid; mTOR = mammalian target of rapamycin.
Figure 1
Figure 1
Pathophysiology of portal hypertension. Flowchart describing the development of portal hypertension in cirrhosis. ↑ = increased; ↓ = decreased; NO = nitric oxide; VEGF = vascular endothelial growth factor; RAAS = renin–aldosterone–angiotensin system.
Figure 3
Figure 3
The urea cycle and the tricarboxylic acid cycle. (a) Flowchart describing the steps of the urea cycle; (b) flowchart describing the steps of the tricarboxylic acid cycle.
Figure 4
Figure 4
The effect of inflammation on muscle. Flowchart outlining the effect of inflammation on muscle. ↑ = increased; ↓ = decreased; mTOR = mammalian target of rapamycin; UPP = ubiquitin proteasome pathway.
See this image and copyright information in PMC

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