RESUMO
Background and aims: Malnutrition is a common comorbidity in cirrhotic patients and confers a poorer prognosis. Vitamin C (VC) is a micronutrient essential for human health. Vitamin C deficiency (VCD) can lead to scurvy and may impair immune and liver functions. Although previously thought to be rare in developed countries, VCD is now well described in patients with pneumonia, COVID19 and upper gastrointestinal bleeding (UGIB). The prevalence and clinical significance of VCD in cirrhosis remains poorly studied. Method: Patients with cirrhosis admitted to 3 metropolitan tertiary centres in Australia were prospectively included over a 10-month period in 2021. Fasting VC levels were collected on admission and we recorded demographic data and clinical outcomes. The primary outcomes were the prevalence of VCD (defined as VC level <23 mcmol/L) and severe VCD (SVCD), defined as <11 mcmol/L. Secondary outcomes included mortality, intensive care admission, length of stay (LOS) and rate of infection. Results: 117 patients were included. Mean age was 57.1 ± 13.9 years, 59.0% were male and 23.9% belonged to the lowest socioeconomic decile. The most common aetiologies of cirrhosis were alcohol (62.4%), viral hepatitis (24.0%) and non-alcoholic fatty liver disease (18.8%). Median MELD scorewas 29 (IQR 22–36) and Child Pugh (CP) grades were 12.8% A, 46.2% B and 41.0% C. Most patients (74.4%) were hospitalised with complications of decompensated cirrhosis, including ascites (59.0%), encephalopathy (31.6%) and variceal bleeding (11.1%). Median VC level was 34mcmol/L (IQR 16–55) and did not differ with age, gender, or aetiology of cirrhosis. Increasing CP grade correlated with significantly lower median VC levels (CP-A 46.0 mcmol/L vs. CPB 36.5 mcmol/L and CP-C 20.5 mcmol/L, p = 0.026). The prevalence of VCD and SVCD were 39.3% and 17.1% respectively. SVCD was more prevalent in patients with a body mass index <25 (28.3% vs 13.0%, p = 0.036). In-hospital mortality was 12.8% and did not differ by VCD status, however in the subgroup of patients presenting with UGIB, SVCD correlated with significantly higher mortality (50% vs 4.1%, p = 0.045). Bacteraemia was more frequent in patients with VCD (13.3% vs. 1.4%, p = 0.014) and SVCD (26.3% vs 2.1%, p < 0.001), which remained significant at multivariate analysis (OR for every 1mcmol/L increase in VC, 0.91 (95% CI: 0.83–0.99), p = 0.037). Overall infection rateswere higher in patients with SVCD (40.0% vs. 27.8%) although thiswas nonsignificant (p = 0.279). Median hospital LOS was 10 (IQR 6–18) days and did not differ by VCD status. (Figure Presented) Conclusion: VCD is common in hospitalised cirrhotic patients and prevalence increases with severity of liver disease. VCD increases the risk of infective complications and higher mortality was observed in patients with UGIB and SVCD. Further studies are required to assess the significance of VCD in cirrhosis and the impacts of VC replacement.
RESUMO
Background and Aim: Liver cirrhosis is a serious medical condition associated with high morbidity and mortality, and it represents the fifth leading cause of death in adult patients. Malnutrition is a commonly recognized comorbidity in the population with cirrhosis and is associated with a poor prognosis. Ascorbic acid is a water-soluble vitamin present in most plant foods. Dietary deficiency leads to scurvy and may impair liver functions, such as the conversion of cholesterol to bile acids. Vitamin C deficiency (VCD) has traditionally been considered very uncommon in developed countries. However, recent studies indicate a significant prevalence in multiple subgroups, including patients presenting with pneumonia, coronavirus disease 2019 (COVID-19), and upper gastrointestinal bleeding. The prevalence of VCD in the population with cirrhosis remains poorly studied. The aim of this study was to investigate the prevalence of VCD in hospitalized patients with liver cirrhosis and the association between VCD and clinical outcomes. Methods: Patients with liver cirrhosis admitted to three Victorian metropolitan hospitals were prospectively recruited over a 4-month period (January to April 2021). Fasting vitamin C levels were obtained on admission. Baseline demographic data and clinical outcomes were recorded. The primary outcome was the prevalence of VCD, defined as a vitamin C level < 23 mcmol/L, with severe deficiency defined as <12 mcmol/L. Secondary outcomes included mortality, intensive care unit (ICU) admission, and hospital length of stay (LOS). Patients were risk stratified using the Model for End-Stage Liver Disease (MELD) score. Results: A total of 48 patients were included. The median patient age was 59 years (IQR, 50-69), 60% were male, and the median MELD score was 19 (IQR, 14-25). The most common etiologies of cirrhosis were alcohol related (60%), non-alcoholic fatty liver disease (NAFLD) (25%), and hepatitis B (19%). Most patients (83.3%) were admitted with complications of decompensated liver disease, most often ascites (47.9%), hepatic encephalopathy (33.3%), and upper gastrointestinal bleeding (27.1%). Mean vitamin C level on admission was 38 ± 12 mcmol/L. VCD was present in 18 patients (37.5%), with severe deficiency noted in eight (16.7%). VCD was most common in patients with NAFLD (42%), followed by those with hepatitis B (34%) and alcohol-related cirrhosis (31%), although no statistically significant difference in prevalence was found between etiologies of cirrhosis. No significant associations were found between VCD and MELD score, albumin levels, or the nature of the decompensating event. In terms of patient outcomes, inpatient mortality was 6.3%, 16.7% of patients required ICU admission, and the median LOS was 10 days (IQR, 6-16). No significant differences in mortality, ICU admission, or LOS stay were noted between patients with and without VCD, although this may be a result of type II error. Conclusion: VCD is prevalent in hospitalized patients with cirrhosis, with 37.5% noted to have VCD and 16.7% having severe deficiency. Further studies are required to assess the clinical significance of VCD deficiency in cirrhotic patients and the impacts of vitamin C replacement.