Journal of clinical and experimental hepatology · 2026
Clinicopathological Profile and Outcomes of Severe Hepatitis A Outbreak in India: A Multicenter Cross-sectional Study.
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Valsan Arun Koottumakkal, Nair Gowri Priya, Verma Nipun, Panackel Charles, Shenoy Kotacherry Trivikrama, Ahamed Hasim, Sebastian Benoy, Nandakumar Raghavan, Devadas Krishnadas, Sivakumar Priyanka, Nair Priya, Koshy Anoop Koshy, Mohan Nimitha Kattikoloth, Gutjahr Georg, Sudhindran Surendran, Mohamed Zubair, Raja Rajat, Eapen George, Krishnamoorthy Smitha, Taparia Yashowardhan, Venu Arathi, Sivaprasadan Saraswathy, Narayanankutty Anila, Duseja Ajay, Ajee Kurunjipadath Lakshmanan
Аннотация
BACKGROUND: A resurgence of hepatitis A virus (HAV) outbreak unfolded in the state of Kerala despite high sanitation and socioeconomic standards. Clinicians observed a possible new emerging phenotype marked by atypical features like persistent fever after the appearance of clinical jaundice, early renal and pulmonary involvement, and hemophagocytic lymphohistiocytosis (HLH).
METHODS: We conducted a multicenter, hospital-based study across six tertiary care centers, prospectively enrolling patients with serologically confirmed HAV (anti-HAV IgM positive) presenting with acute liver injury. Patients with ≥2 atypical manifestations (persistent fever, acute kidney injury [AKI], HLH, or pulmonary involvement) comprised the a-HAV arm, while outpatients with usual symptoms (u-HAV) served as the comparator.
RESULTS: A total of 324 patients (a-HAV: 179, u-HAV: 145) were included (mean age: 32 ± 12.8, 68.2% males). The a-HAV arm had a significantly higher incidence of hepatomegaly (64% vs 44%), splenomegaly (30% vs 17%), ascites (30% vs 9%), encephalopathy (21%), prolonged cholestasis (19%), higher mean levels of total leukocyte count (TLC), bilirubin, aspartate aminotransferase, international normalized ratio (INR), triglycerides, ferritin, and lactate dehydrogenase. Atypical features included continuing fever (93%), pulmonary complications (16.8%), AKI (13.4%), and HLH (12.8%). a-HAV required aggressive therapeutic interventions with higher steroid use (30% vs 4.1%), plasma exchange (21%; mean: 2.68 ± 1.26 cycles, 2240 ± 634.45 mL exchanged), continuous renal replacement therapy (7.8%), and mechanical ventilation (10%). Also, progression to acute-on-chronic liver failure (7.3%), autoantibodies (18%), metabolic acidosis (6.7%), readmissions (9%), and mortality (11.7%) were higher in the a-HAV arm. On multivariable analysis, the model incorporating baseline ammonia (odds ratio [OR]: 1.11), TLC (OR: 2.21), and INR (OR: 7.20) demonstrated the highest discriminative performance for 90-day mortality (area under the receiver operating characteristic curve: 0.994). Genotyping revealed the strain to be of genotype IIIA.
CONCLUSION: The study provides a strong indication regarding the changing clinical presentation and virulence of HAV. Unlike previous outbreaks, a significant number of patients had severe presentations marked by immune dysregulation and multiorgan involvement. Early recognition and tailored management are the keys to improving patient outcomes.
METHODS: We conducted a multicenter, hospital-based study across six tertiary care centers, prospectively enrolling patients with serologically confirmed HAV (anti-HAV IgM positive) presenting with acute liver injury. Patients with ≥2 atypical manifestations (persistent fever, acute kidney injury [AKI], HLH, or pulmonary involvement) comprised the a-HAV arm, while outpatients with usual symptoms (u-HAV) served as the comparator.
RESULTS: A total of 324 patients (a-HAV: 179, u-HAV: 145) were included (mean age: 32 ± 12.8, 68.2% males). The a-HAV arm had a significantly higher incidence of hepatomegaly (64% vs 44%), splenomegaly (30% vs 17%), ascites (30% vs 9%), encephalopathy (21%), prolonged cholestasis (19%), higher mean levels of total leukocyte count (TLC), bilirubin, aspartate aminotransferase, international normalized ratio (INR), triglycerides, ferritin, and lactate dehydrogenase. Atypical features included continuing fever (93%), pulmonary complications (16.8%), AKI (13.4%), and HLH (12.8%). a-HAV required aggressive therapeutic interventions with higher steroid use (30% vs 4.1%), plasma exchange (21%; mean: 2.68 ± 1.26 cycles, 2240 ± 634.45 mL exchanged), continuous renal replacement therapy (7.8%), and mechanical ventilation (10%). Also, progression to acute-on-chronic liver failure (7.3%), autoantibodies (18%), metabolic acidosis (6.7%), readmissions (9%), and mortality (11.7%) were higher in the a-HAV arm. On multivariable analysis, the model incorporating baseline ammonia (odds ratio [OR]: 1.11), TLC (OR: 2.21), and INR (OR: 7.20) demonstrated the highest discriminative performance for 90-day mortality (area under the receiver operating characteristic curve: 0.994). Genotyping revealed the strain to be of genotype IIIA.
CONCLUSION: The study provides a strong indication regarding the changing clinical presentation and virulence of HAV. Unlike previous outbreaks, a significant number of patients had severe presentations marked by immune dysregulation and multiorgan involvement. Early recognition and tailored management are the keys to improving patient outcomes.