Liver stiffness predicts variceal bleeding in HIV/HCV-coinfected patients with compensated cirrhosis

Nicolás Merchante1, Antonio Rivero-Juárez, Francisco Téllez

  • 1aUnidad Clínica de Enfermedades Infecciosas y Microbiología, Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario de Valme, Sevilla bUnidad de Enfermedades Infecciosas, Instituto Maimónides de Investigación Biomédica de Córdoba (IMIBIC), Hospital Universitario Reina Sofía, Universidad de Córdoba (UCO), Córdoba cUnidad de Gestión Clínica de Enfermedades Infecciosas y Microbiología, Hospital de La Línea de la Concepción, AGS Campo de Gibraltar, Cádiz dUnidad de Gestión Clínica de Enfermedades Infecciosas, Complejo Hospitalario de Huelva, Huelva eUnidad de Enfermedades Infecciosas, Hospital Universitario Virgen Macarena, Sevilla fUnidad de Gestión Clínica de Enfermedades Infecciosas, Hospital Virgen de la Victoria, Complejo Hospitalario de Málaga, Málaga gUnidad de Enfermedades Infecciosas, Complejo Hospitalario de Jaén, Jaén, Spain.

AIDS (London, England)
|December 7, 2016
PubMed

Insights

Liver stiffness measurement effectively predicts portal hypertensive gastrointestinal bleeding (PHGB) risk in HIV/HCV-coinfected patients. A liver stiffness below 21 kPa safely excludes PHGB, allowing avoidance of upper gastrointestinal endoscopy (UGE).

Area of Science:

  • Hepatology
  • Infectious Diseases
  • Gastroenterology

Background:

  • Hepatitis C virus (HCV) and human immunodeficiency virus (HIV) coinfection often leads to liver cirrhosis.
  • Esophageal varices are a common complication, posing a bleeding risk.
  • Upper gastrointestinal endoscopy (UGE) is used for screening, but its routine use is debated.

Purpose of the Study:

  • To evaluate liver stiffness as a predictor of portal hypertensive gastrointestinal bleeding (PHGB).
  • To assess the safety of avoiding UGE in HIV/HCV-coinfected patients with compensated cirrhosis based on liver stiffness measurements.

Main Methods:

  • A prospective study of 446 HIV/HCV-coinfected patients with newly diagnosed compensated cirrhosis.
  • Liver stiffness was measured using transient elastography.
  • Patients were followed for the development of PHGB, with UGE use changing based on liver stiffness thresholds.

Main Results:

  • No patient with baseline liver stiffness below 21 kPa developed PHGB during a median follow-up of 49 months.
  • The negative predictive value of liver stiffness < 21 kPa for PHGB was 100%.
  • All 15 patients who experienced PHGB had baseline liver stiffness of at least 21 kPa.

Conclusions:

  • Liver stiffness measurement is a reliable, non-invasive tool to identify patients at very low risk of PHGB.
  • A liver stiffness threshold of 21 kPa can safely guide the decision to forgo UGE screening for esophageal varices in this population.
  • This strategy can reduce healthcare costs and patient burden without compromising safety.
Abstract

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