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Case Reports
. 2016 Jan 6;5(1):e1.
doi: 10.1038/emi.2016.1.

Prevalence and characteristics of hypoxic hepatitis in the largest single-centre cohort of avian influenza A(H7N9) virus-infected patients with severe liver impairment in the intensive care unit

Affiliations
Case Reports

Prevalence and characteristics of hypoxic hepatitis in the largest single-centre cohort of avian influenza A(H7N9) virus-infected patients with severe liver impairment in the intensive care unit

YiMin Zhang et al. Emerg Microbes Infect. .

Erratum in

Abstract

Avian influenza A(H7N9) virus (A(H7N9)) emerged in February 2013. Liver impairment of unknown cause is present in 29% of patients with A(H7N9) infection, some of whom experience severe liver injury. Hypoxic hepatitis (HH) is a type of acute severe liver injury characterized by an abrupt, massive increase in serum aminotransferases resulting from anoxic centrilobular necrosis of liver cells. In the intensive care unit (ICU), the prevalence of HH is ∼1%-2%. Here, we report a 1.8% (2/112) incidence of HH in the largest single-centre cohort of ICU patients with A(H7N9) infection. Both HH patients presented with multiple organ failure (MOF) involving respiratory, cardiac, circulatory and renal failure and had a history of chronic heart disease. On admission, severe liver impairment was found. Peak alanine aminotransferase (ALT) and aspartate aminotransferase (AST) values were 937 and 1281 U/L, and 3117 and 3029 U/L, respectively, in the two patients. Unfortunately, both patients died due to deterioration of MOF. A post-mortem biopsy in case 1 confirmed the presence of centrilobular necrosis of the liver, and real-time reverse transcription polymerase chain reaction of A(H7N9)-specific genes was negative, which excluded A(H7N9)-related hepatitis. The incidence of HH in A(H7N9) patients is similar to that in ICU patients with other aetiologies. It seems that patients with A(H7N9) infection and a history of chronic heart disease with a low left ventricular ejection fraction on admission are susceptible to HH, which presents as a marked elevation in ALT at the time of admission.

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Figures

Figure 1
Figure 1
Radiographic and ultrasound findings in case 1. (A) Chest radiograph at the time of admission showed bilateral pulmonary infiltration with consolidation. (B) Ultrasound image showed a dilated hepatic vein (left branch, 1.22 cm; middle branch, 0.61 cm and right branch, 1.36 cm). (C) Ultrasound image showed slowed hepatic vein flow (middle branch, 9.14 mm/s). (D) Echocardiogram showed a dilated left ventricle (LVIDd 56.46 mm) and cardiac failure (LVEF 42%) with weakened left-ventricular wall motion. LVEF, left ventricular ejection fraction; LVIDd, left ventricular internal diameter at end-diastole.
Figure 2
Figure 2
Dynamic changes in biochemical test results in case 1. (A) Changes in ALT, AST and LDH values during the hospital stay. (B) Changes in TB and INR values during the hospital stay. ALT, alanine aminotransferase; AST, aspartate aminotransferase; INR, international normalized ratio; LDH, lactate dehydrogenase; TB, total bilirubin.
Figure 3
Figure 3
Histological findings in case 1. (A) Centrilobular necrosis in the liver without inflammation (haematoxylin and eosin, 10×). (B) Dilated sinusoids with coagulative necrosis (haematoxylin and eosin, 40×). (C) Reactive type II pneumocytes and hyaline membrane in the lung (haematoxylin and eosin, 20×). (D) Renal tubular degeneration and necrosis (haematoxylin and eosin, 20×).
Figure 4
Figure 4
Radiographic and ultrasound findings in case 2. (A) Chest radiograph at the time of admission showed bilateral pulmonary infiltration. (B) Chest radiograph on day 2 compared with that at admission showed progression of the bilateral pulmonary infiltration and consolidation. (C) Chest radiograph on day 4 showed progression of bilateral pulmonary infiltration and consolidation compared with day 2. (D) Echocardiogram at the time of admission showed cardiac failure (LVEF 37.5%). LVEF, left ventricular ejection fraction.
Figure 5
Figure 5
Dynamic changes in biochemical test results in case 2. (A) Changes in ALT, AST and LDH values during the hospital stay. (B) Changes in TB and INR values during the hospital stay. ALT, alanine aminotransferase; AST, aspartate aminotransferase; INR, international normalized ratio; LDH, lactate dehydrogenase; TB, total bilirubin.

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References

    1. 1Gao R, Cao B, Hu Y et al. Human infection with a novel avian-origin influenza A (H7N9) virus. N Engl J Med 2013; 368: 1888–1897. - PubMed
    1. 2World Health Organization. WHO risk assessment of human infection with avian influenza A(H7N9) virus as of 23 February 2015. Geneva: WHO, 2015. Available at http://www.who.int/influenza/human_animal_interface/influenza_h7n9/RiskA... 2015. (accessed 8 August 2015).
    1. 3Li Q, Zhou L, Zhou M et al. Epidemiology of human infections with avian influenza A(H7N9) virus in China. N Engl J Med 2014; 370: 520–532. - PMC - PubMed
    1. 4Wiwanitkit V. H7N9 influenza-the laboratory presentations: a letter to editor. Asian Pac J Trop Biomed 2013; 3: 584–585. - PMC - PubMed
    1. 5Zhang J, Zhao Y, Chen Y. Laboratory findings in patients with avian-origin influenza A (H7N9) virus infections. J Med Virol 2014; 86: 895–898. - PubMed

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