RPR Predicts Short-Term Acute Decompensation in Alcohol-Related Cirrhosis: Digestive and Liver Disease | 2026

Introduction:

Patients with alcohol-related cirrhosis and non-acute decompensation (NAD) may appear sufficiently stable for outpatient management but remain at substantial risk of rapidly progressing to hospitalisation-requiring acute decompensation (AD). This prospective multicentre study evaluated whether a simple routinely available marker—the red cell distribution width-to-platelet ratio (RPR)—could identify patients at high short-term risk.

Why is this important?

NAD should not be considered a stable clinical state.

In this cohort, 38.5% progressed to acute decompensation within only 3 months.

Portal hypertension and systemic inflammation are major drivers of deterioration.

RPR potentially captures both:

RDW → inflammation, oxidative stress and altered erythropoiesis

Platelet count → portal hypertension/hypersplenism

Both measurements are already available from a routine CBC.

Key Results:

Derivation cohort: 260 patients

Acute decompensation within 3 months: 100/260 (38.5%)

RPR had the best discrimination among evaluated non-invasive tests:

AUC: 0.888

Optimal RPR threshold: 0.159

Sensitivity: 90.0%

Specificity: 78.1%

Negative predictive value: 92.6%

Increasing RPR remained independently associated with AD:

adjusted HR 1.040 per 0.01 increase

95% CI 1.021–1.060; P<0.001

External Validation:

Performance remained strong in an independent cohort of 75 patients:

AUC: 0.836

Negative predictive value: 95.3%

The particularly high NPV suggests that RPR may potentially be useful as a rule-out/risk-triage tool for identifying NAD patients less likely to deteriorate over the following 3 months.

Clinical Implication:

The concept is attractive because RPR requires no additional laboratory testing, imaging or invasive portal-pressure assessment.

A potential clinical pathway could be:

Alcohol-related cirrhosis + NAD → calculate RPR → identify high-risk phenotype → closer surveillance and earlier intervention

Conversely, a low-risk RPR may help identify patients with a relatively low probability of short-term hospitalization-requiring deterioration.

What Makes RPR Biologically Interesting?

Rather than representing a single disease pathway, RPR may integrate two important components of cirrhosis progression:

Systemic inflammation / altered erythropoiesis (↑RDW) + portal hypertension (↓platelets) → ↑RPR → increased decompensation risk

This may explain why the composite ratio performed better than several conventional non-invasive measures.

Caution:

This should not yet be treated as a stand-alone clinical decision threshold. The study included a relatively specific population—patients with alcohol-related decompensated advanced chronic liver disease and ongoing NAD—and the external validation cohort was modest (n=75).

RDW and platelet count can also be influenced by alcohol exposure, nutritional deficiency, anemia, infection, bone-marrow abnormalities and hypersplenism. Whether the 0.159 threshold generalizes to other etiologies of cirrhosis remains uncertain.

Bottom Line:

In alcohol-related cirrhosis with non-acute decompensation, RPR was a simple and powerful predictor of hospitalization-requiring acute decompensation within 3 months (AUC 0.888; externally validated AUC 0.836). Its greatest practical attraction is simplicity: two routine CBC parameters may help identify apparently stable outpatients who are actually at high short-term risk of deterioration.