Liver international : official journal of the International Association for the Study of the Liver · 2015
Hepatosplenic schistosomiasis is characterised by high blood markers of translocation, inflammation and fibrosis.
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Sinkala Edford, Kapulu Melissa C, Besa Ellen, Zyambo Kanekwa, Chisoso Ng'andu J, Foster Graham R, Kelly Paul
Аннотация
BACKGROUND & AIMS: Cirrhosis is the main cause of portal hypertension worldwide but schistosomiasis dominates in much of the tropics. The seroprevalence of Schistosoma mansoni is up to 77% in endemic parts of Zambia. Morbidity is attributed to portal hypertension causing variceal bleeding which can be fatal. Bacterial translocation is associated with portal hypertension in cirrhosis but this is almost unexplored in hepatosplenic schistosomiasis. Liver biopsy is usually used to assess fibrosis although it is invasive and prone to sampling error. We aimed to investigate translocation, fibrosis and inflammatory makers in a case-control study of schistosomiasis at the University Teaching Hospital, Lusaka, Zambia.
METHODS: Patients had oesophageal varices, but were negative for human immunodeficiency virus, hepatitis B and C viruses. Plasma lipopolysaccharide binding protein was used as a marker of translocation while hyaluronan and laminin measured liver fibrosis. Inflammatory markers were measured in blood. Controls were patients with non-specific abdominal pain who had normal endoscopy.
RESULTS: Median (interquartile range) lipopolysaccharide binding protein was elevated in patients [44.3 ng/ml (35.7, 57.1)] compared to controls [30.7 ng/ml (30.4, 35.5), P < 0.0001]. Hyaluronan was higher in patients [111.6 ng/ml (39.1, 240.3)] compared to controls [21.0 ng/ml (12.4, 37.6), P < 0.0001] and so was laminin [2.2 μg/ml (1.0, 3.7)] compared to controls [0.9 μg/ml (0.7, 1.2), P = 0.0015]. Inflammatory markers, except C-reactive protein, were elevated in patients.
CONCLUSIONS: These data suggest that the bacterial translocation contributes to systemic inflammation in hepatosplenic schistosomiasis. Elevated fibrotic markers suggest they may be useful in diagnosing and monitoring periportal fibrosis.
METHODS: Patients had oesophageal varices, but were negative for human immunodeficiency virus, hepatitis B and C viruses. Plasma lipopolysaccharide binding protein was used as a marker of translocation while hyaluronan and laminin measured liver fibrosis. Inflammatory markers were measured in blood. Controls were patients with non-specific abdominal pain who had normal endoscopy.
RESULTS: Median (interquartile range) lipopolysaccharide binding protein was elevated in patients [44.3 ng/ml (35.7, 57.1)] compared to controls [30.7 ng/ml (30.4, 35.5), P < 0.0001]. Hyaluronan was higher in patients [111.6 ng/ml (39.1, 240.3)] compared to controls [21.0 ng/ml (12.4, 37.6), P < 0.0001] and so was laminin [2.2 μg/ml (1.0, 3.7)] compared to controls [0.9 μg/ml (0.7, 1.2), P = 0.0015]. Inflammatory markers, except C-reactive protein, were elevated in patients.
CONCLUSIONS: These data suggest that the bacterial translocation contributes to systemic inflammation in hepatosplenic schistosomiasis. Elevated fibrotic markers suggest they may be useful in diagnosing and monitoring periportal fibrosis.