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. 2020 Feb 4;20(1):30.
doi: 10.1186/s12876-020-1180-0.

Clinical characteristics, CT signs, and pathological findings of Pyrrolizidine alkaloids-induced sinusoidal obstructive syndrome: a retrospective study

Fang Liu  1 , Xinxin Rong  2 , Hui Guo  3 , Dong Xu  4 , Chang Liu  2 , Lingling Meng  2 , Xiaoqian Yang  2 , Tingting Guo  5 , Xuefeng Kan  5 , Yuhu Song  6
Affiliations

Clinical characteristics, CT signs, and pathological findings of Pyrrolizidine alkaloids-induced sinusoidal obstructive syndrome: a retrospective study

Fang Liu et al. BMC Gastroenterol. .

Abstract

Background: One major etiology of hepatic sinusoidal obstruction syndrome (HSOS) in China is the intake of pyrrolizidine alkaloids (PAs). Since PAs-induced HSOS is a rare disease that has not been clearly characterized until now, the aim of this study was to investigate clinical characteristics, CT features, and pathological findings of PA-induced HSOS.

Methods: This retrospective cohort study included 116 patients with PAs-induced HSOS and 68 patients with Budd-Chiari syndrome from Jan 2006 to Sep 2016. We collected medical records of the patients, and reviewed image features of CT, and analyzed pathological findings.

Results: Common clinical manifestations of PAs-induced HSOS were abdominal distention (98.26%), ascites (100%), jaundice (52.94%), abdominal pain (36.36%). Abnormal liver function was observed in most of PAs-induced HSOS. On CT scan, common findings included: ascites, hepatomegaly, the thickening of gallbladder wall, pleural effusion, patchy liver enhancement, and heterogeneous hypoattenuation. Most of the patients had a low ascitic total protein (< 25 g/L) and a high SAAG (≥ 11.0 g/L). In acute stage, pathologic features were massive sinusoidal dilatation, sinusoidal congestion, the extravasation of erythrocytes, hepatocellular necrosis, the accumulation of macrophages, the deposition of hemosiderin. In subacute stage, complete loss of pericentral hepatocytes, sinusoidal dilatation, the deposition of pigment granules were observed.

Conclusions: The PAs-induced HSOS patients displayed distinct clinical characteristics, imaging features, and pathological findings, which provided some evidences for the diagnosis of PAs-induced HSOS.

Trial registration: ChiCTR-DRD-17010709.

Keywords: Ascites; Clinical manifestations; Hepatic sinusoidal obstruction syndrome; Histology; Pyrrolizidine alkaloid.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
Flowchart of the patients’ enrollment
Fig. 2
Fig. 2
Elderly male patients diagnosed with gynura segetum-induced HSOS received contrast-enhanced CT and MRI scan. a-d images of plain and contrast-enhanced CT scan; a plain CT scan; b arterial phase; c porta-venous phase; patchy liver enhancement (arrow) and heterogeneous hypoattenuation (arrowhead) were shown; d equilibrium phases. e-f: images of pre-contrast and portal-venous phase on dynamic contrast-enhanced MRI scan;e pre-contrast MRI scan; f portal-venous phase of MRI scan. Heterogeneous hypointensity (arrowhead) and patchy enhancement (arrow) were shown
Fig. 3
Fig. 3
Histology of the patients and rat model of PAs-induced HSOS. a: early pathological changes of the PAs-induced HSOS patients; b: sub-acute pathological changes of the PAs-induced HSOS patients; c: the livers from normal mice were stained by H&E; d: 24 h after senecionine administration, the livers from the senecionine-treated mice were stained by H&E; e:48 h after monocrotaline administration, the livers from the rats with PAs-induced HSOS were stained by H&E; F: 2 weeks after monocrotaline administration, pathological changes of the rats with PAs-induced HSOS
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