Procalcitonin as a Predictive Marker of Incident Liver Disease
ABSTRACT Background and Aims Previous studies have shown that procalcitonin (PCT) concentration is elevated in patients with liver disease without evidence of bacterial infection. We aimed to investigate the association between elevated PCT and the future risk of liver disease. Method PCT was measur...
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| Veröffentlicht in: | Liver international Jg. 45; H. 6; S. e70132 - n/a |
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01.06.2025
John Wiley and Sons Inc |
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| Abstract | ABSTRACT
Background and Aims
Previous studies have shown that procalcitonin (PCT) concentration is elevated in patients with liver disease without evidence of bacterial infection. We aimed to investigate the association between elevated PCT and the future risk of liver disease.
Method
PCT was measured in 3897 individuals without known liver disease in the Malmö Diet and Cancer Cardiovascular Cohort (MDC‐CC) and in 3854 individuals in the Malmö Preventive Project cohort (MPP). Cox proportional hazards regression models were used to analyse the risk of register‐verified incident liver disease by PCT levels. We performed our analyses in a pooled sample of both the MPP and MDC‐CC cohorts, as well as separate analyses for each cohort.
Results
70 subjects in MDC‐CC and 49 subjects in MPP were diagnosed with non‐viral liver disease during a median follow‐up of 27.1 and 14.8 years, respectively. In multivariate adjusted models in the pooled sample, individuals with high PCT (> 0.05 ng/mL) had a significantly increased risk of developing liver disease compared to subjects with PCT concentrations below the cutoff (hazard ratio (HR) 3.4, 95% confidence interval (CI) 2.07–5.63, p < 0.001). The HR per standard deviation increase of log‐transformed PCT was 1.56 (95% CI 1.32–1.85, p < 0.001) in multivariate adjusted models. Separate cohort‐specific sensitivity analyses, including additional adjustment for C‐reactive protein, showed similar effect estimates as the pooled analyses.
Conclusions
Elevated concentration of PCT independently predicts non‐viral liver disease. These findings could have implications for risk assessment but also highlight the possibility of PCT as a direct cause of hepatocyte damage. |
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| AbstractList | Previous studies have shown that procalcitonin (PCT) concentration is elevated in patients with liver disease without evidence of bacterial infection. We aimed to investigate the association between elevated PCT and the future risk of liver disease.BACKGROUND AND AIMSPrevious studies have shown that procalcitonin (PCT) concentration is elevated in patients with liver disease without evidence of bacterial infection. We aimed to investigate the association between elevated PCT and the future risk of liver disease.PCT was measured in 3897 individuals without known liver disease in the Malmö Diet and Cancer Cardiovascular Cohort (MDC-CC) and in 3854 individuals in the Malmö Preventive Project cohort (MPP). Cox proportional hazards regression models were used to analyse the risk of register-verified incident liver disease by PCT levels. We performed our analyses in a pooled sample of both the MPP and MDC-CC cohorts, as well as separate analyses for each cohort.METHODPCT was measured in 3897 individuals without known liver disease in the Malmö Diet and Cancer Cardiovascular Cohort (MDC-CC) and in 3854 individuals in the Malmö Preventive Project cohort (MPP). Cox proportional hazards regression models were used to analyse the risk of register-verified incident liver disease by PCT levels. We performed our analyses in a pooled sample of both the MPP and MDC-CC cohorts, as well as separate analyses for each cohort.70 subjects in MDC-CC and 49 subjects in MPP were diagnosed with non-viral liver disease during a median follow-up of 27.1 and 14.8 years, respectively. In multivariate adjusted models in the pooled sample, individuals with high PCT (> 0.05 ng/mL) had a significantly increased risk of developing liver disease compared to subjects with PCT concentrations below the cutoff (hazard ratio (HR) 3.4, 95% confidence interval (CI) 2.07-5.63, p < 0.001). The HR per standard deviation increase of log-transformed PCT was 1.56 (95% CI 1.32-1.85, p < 0.001) in multivariate adjusted models. Separate cohort-specific sensitivity analyses, including additional adjustment for C-reactive protein, showed similar effect estimates as the pooled analyses.RESULTS70 subjects in MDC-CC and 49 subjects in MPP were diagnosed with non-viral liver disease during a median follow-up of 27.1 and 14.8 years, respectively. In multivariate adjusted models in the pooled sample, individuals with high PCT (> 0.05 ng/mL) had a significantly increased risk of developing liver disease compared to subjects with PCT concentrations below the cutoff (hazard ratio (HR) 3.4, 95% confidence interval (CI) 2.07-5.63, p < 0.001). The HR per standard deviation increase of log-transformed PCT was 1.56 (95% CI 1.32-1.85, p < 0.001) in multivariate adjusted models. Separate cohort-specific sensitivity analyses, including additional adjustment for C-reactive protein, showed similar effect estimates as the pooled analyses.Elevated concentration of PCT independently predicts non-viral liver disease. These findings could have implications for risk assessment but also highlight the possibility of PCT as a direct cause of hepatocyte damage.CONCLUSIONSElevated concentration of PCT independently predicts non-viral liver disease. These findings could have implications for risk assessment but also highlight the possibility of PCT as a direct cause of hepatocyte damage. ABSTRACT Background and Aims Previous studies have shown that procalcitonin (PCT) concentration is elevated in patients with liver disease without evidence of bacterial infection. We aimed to investigate the association between elevated PCT and the future risk of liver disease. Method PCT was measured in 3897 individuals without known liver disease in the Malmö Diet and Cancer Cardiovascular Cohort (MDC‐CC) and in 3854 individuals in the Malmö Preventive Project cohort (MPP). Cox proportional hazards regression models were used to analyse the risk of register‐verified incident liver disease by PCT levels. We performed our analyses in a pooled sample of both the MPP and MDC‐CC cohorts, as well as separate analyses for each cohort. Results 70 subjects in MDC‐CC and 49 subjects in MPP were diagnosed with non‐viral liver disease during a median follow‐up of 27.1 and 14.8 years, respectively. In multivariate adjusted models in the pooled sample, individuals with high PCT (> 0.05 ng/mL) had a significantly increased risk of developing liver disease compared to subjects with PCT concentrations below the cutoff (hazard ratio (HR) 3.4, 95% confidence interval (CI) 2.07–5.63, p < 0.001). The HR per standard deviation increase of log‐transformed PCT was 1.56 (95% CI 1.32–1.85, p < 0.001) in multivariate adjusted models. Separate cohort‐specific sensitivity analyses, including additional adjustment for C‐reactive protein, showed similar effect estimates as the pooled analyses. Conclusions Elevated concentration of PCT independently predicts non‐viral liver disease. These findings could have implications for risk assessment but also highlight the possibility of PCT as a direct cause of hepatocyte damage. Previous studies have shown that procalcitonin (PCT) concentration is elevated in patients with liver disease without evidence of bacterial infection. We aimed to investigate the association between elevated PCT and the future risk of liver disease. PCT was measured in 3897 individuals without known liver disease in the Malmö Diet and Cancer Cardiovascular Cohort (MDC-CC) and in 3854 individuals in the Malmö Preventive Project cohort (MPP). Cox proportional hazards regression models were used to analyse the risk of register-verified incident liver disease by PCT levels. We performed our analyses in a pooled sample of both the MPP and MDC-CC cohorts, as well as separate analyses for each cohort. 70 subjects in MDC-CC and 49 subjects in MPP were diagnosed with non-viral liver disease during a median follow-up of 27.1 and 14.8 years, respectively. In multivariate adjusted models in the pooled sample, individuals with high PCT (> 0.05 ng/mL) had a significantly increased risk of developing liver disease compared to subjects with PCT concentrations below the cutoff (hazard ratio (HR) 3.4, 95% confidence interval (CI) 2.07-5.63, p < 0.001). The HR per standard deviation increase of log-transformed PCT was 1.56 (95% CI 1.32-1.85, p < 0.001) in multivariate adjusted models. Separate cohort-specific sensitivity analyses, including additional adjustment for C-reactive protein, showed similar effect estimates as the pooled analyses. Elevated concentration of PCT independently predicts non-viral liver disease. These findings could have implications for risk assessment but also highlight the possibility of PCT as a direct cause of hepatocyte damage. Background and Aims Previous studies have shown that procalcitonin (PCT) concentration is elevated in patients with liver disease without evidence of bacterial infection. We aimed to investigate the association between elevated PCT and the future risk of liver disease. Method PCT was measured in 3897 individuals without known liver disease in the Malmö Diet and Cancer Cardiovascular Cohort (MDC‐CC) and in 3854 individuals in the Malmö Preventive Project cohort (MPP). Cox proportional hazards regression models were used to analyse the risk of register‐verified incident liver disease by PCT levels. We performed our analyses in a pooled sample of both the MPP and MDC‐CC cohorts, as well as separate analyses for each cohort. Results 70 subjects in MDC‐CC and 49 subjects in MPP were diagnosed with non‐viral liver disease during a median follow‐up of 27.1 and 14.8 years, respectively. In multivariate adjusted models in the pooled sample, individuals with high PCT (> 0.05 ng/mL) had a significantly increased risk of developing liver disease compared to subjects with PCT concentrations below the cutoff (hazard ratio (HR) 3.4, 95% confidence interval (CI) 2.07–5.63, p < 0.001). The HR per standard deviation increase of log‐transformed PCT was 1.56 (95% CI 1.32–1.85, p < 0.001) in multivariate adjusted models. Separate cohort‐specific sensitivity analyses, including additional adjustment for C‐reactive protein, showed similar effect estimates as the pooled analyses. Conclusions Elevated concentration of PCT independently predicts non‐viral liver disease. These findings could have implications for risk assessment but also highlight the possibility of PCT as a direct cause of hepatocyte damage. Background and Aims: Previous studies have shown that procalcitonin (PCT) concentration is elevated in patients with liver disease without evidence of bacterial infection. We aimed to investigate the association between elevated PCT and the future risk of liver disease. Method: PCT was measured in 3897 individuals without known liver disease in the Malmö Diet and Cancer Cardiovascular Cohort (MDC-CC) and in 3854 individuals in the Malmö Preventive Project cohort (MPP). Cox proportional hazards regression models were used to analyse the risk of register-verified incident liver disease by PCT levels. We performed our analyses in a pooled sample of both the MPP and MDC-CC cohorts, as well as separate analyses for each cohort. Results: 70 subjects in MDC-CC and 49 subjects in MPP were diagnosed with non-viral liver disease during a median follow-up of 27.1 and 14.8 years, respectively. In multivariate adjusted models in the pooled sample, individuals with high PCT (> 0.05 ng/mL) had a significantly increased riskof developing liver disease compared to subjects with PCT concentrations below the cutoff (hazard ratio (HR) 3.4, 95% confidence interval (CI) 2.07–5.63, p < 0.001). The HR per standard deviation increase of log-transformed PCT was 1.56 (95% CI 1.32–1.85, p < 0.001) in multivariate adjusted models. Separate cohort-specific sensitivity analyses, including additional adjustment for C-reactive protein, showed similar effect estimates as the pooled analyses. Conclusions: Elevated concentration of PCT independently predicts non-viral liver disease. These findings could have implications for risk assessment but also highlight the possibility of PCT as a direct cause of hepatocyte damage. |
| Author | Enhörning, Sofia Pihlsgård, Mats Finnberg‐Kim, Amanda Önnerhag, Kristina Melander, Olle |
| AuthorAffiliation | 4 Department of Internal Medicine Skåne University Hospital Malmö Sweden 1 Department of Clinical Sciences in Malmö Lund University Malmö Sweden 2 Department of Gastroenterology and Hepatology Skåne University Hospital Malmö Sweden 3 Perinatal and Cardiovascular Epidemiology, Lund University Diabetes Centre Department of Clinical Sciences in Malmö, Lund University Malmö Sweden |
| AuthorAffiliation_xml | – name: 3 Perinatal and Cardiovascular Epidemiology, Lund University Diabetes Centre Department of Clinical Sciences in Malmö, Lund University Malmö Sweden – name: 4 Department of Internal Medicine Skåne University Hospital Malmö Sweden – name: 2 Department of Gastroenterology and Hepatology Skåne University Hospital Malmö Sweden – name: 1 Department of Clinical Sciences in Malmö Lund University Malmö Sweden |
| Author_xml | – sequence: 1 givenname: Amanda orcidid: 0009-0006-0023-719X surname: Finnberg‐Kim fullname: Finnberg‐Kim, Amanda email: amanda.finnberg‐kim@med.lu.se organization: Skåne University Hospital – sequence: 2 givenname: Mats surname: Pihlsgård fullname: Pihlsgård, Mats organization: Department of Clinical Sciences in Malmö, Lund University – sequence: 3 givenname: Kristina surname: Önnerhag fullname: Önnerhag, Kristina organization: Skåne University Hospital – sequence: 4 givenname: Olle surname: Melander fullname: Melander, Olle organization: Skåne University Hospital – sequence: 5 givenname: Sofia surname: Enhörning fullname: Enhörning, Sofia organization: Skåne University Hospital |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/40353301$$D View this record in MEDLINE/PubMed |
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| Keywords | risk assessment procalcitonin liver disease C‐reactive protein liver cirrhosis |
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| Notes | Handling Editor Funding Dr. Luca Valenti Dr. Enhörning was supported by grants from the Swedish Research Council (2022–01771), the Swedish Society for Medical Research (SG‐22‐0076), the Åke Wiberg Foundation (M21‐0041), the Maggie Stephen Foundation (20222029), the Albert Påhlsson Foundation (211214SE), the Crafoord Foundation (20210603), the Swedish Society of Medicine (SLS‐959724), the Swedish Heart and Lung Foundation (20200126), Skåne University Hospital and Region Skåne (2020–0358). ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Handling Editor: Dr. Luca Valenti Funding: Dr. Enhörning was supported by grants from the Swedish Research Council (2022–01771), the Swedish Society for Medical Research (SG‐22‐0076), the Åke Wiberg Foundation (M21‐0041), the Maggie Stephen Foundation (20222029), the Albert Påhlsson Foundation (211214SE), the Crafoord Foundation (20210603), the Swedish Society of Medicine (SLS‐959724), the Swedish Heart and Lung Foundation (20200126), Skåne University Hospital and Region Skåne (2020–0358). |
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| Snippet | ABSTRACT
Background and Aims
Previous studies have shown that procalcitonin (PCT) concentration is elevated in patients with liver disease without evidence of... Previous studies have shown that procalcitonin (PCT) concentration is elevated in patients with liver disease without evidence of bacterial infection. We aimed... Background and Aims Previous studies have shown that procalcitonin (PCT) concentration is elevated in patients with liver disease without evidence of bacterial... Background and Aims: Previous studies have shown that procalcitonin (PCT) concentration is elevated in patients with liver disease without evidence of... |
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| SubjectTerms | Aged Bacterial diseases Biomarkers - blood C-reactive protein Clinical Medicine Confidence intervals Female Gastroenterologi och hepatologi Gastroenterology and Hepatology Humans Incidence Klinisk medicin Liver liver cirrhosis liver disease Liver diseases Liver Diseases - blood Liver Diseases - diagnosis Liver Diseases - epidemiology Male Medical and Health Sciences Medicin och hälsovetenskap Middle Aged Multivariate Analysis Original Predictive Value of Tests Procalcitonin Procalcitonin - blood Proportional Hazards Models Regression analysis Regression models Risk assessment Risk Factors Sensitivity analysis Statistical analysis Sweden - epidemiology |
| Title | Procalcitonin as a Predictive Marker of Incident Liver Disease |
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