Evidence map›Paper›PMID 42866000›Full record

ArticleJournal of clinical and translational hepatology2026

Clinicopathological Evolution of Pyrrolizidine Alkaloid-induced Liver Injury: Transition From SOS to PSVD?

Si Zhao, Feng Zhang, Yao Liu, Shuyan Zeng, Han Zhang, Jingjing Tu, Hui Xu, Qin Yin, Wei Zhang, Bing Xu and 5 more

Abstract read
In one paragraph

Article in Journal of clinical and translational hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors.

Si ZhaoDepartment of Gastroenterology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, China.
Feng ZhangDepartment of Gastroenterology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, China.
Yao LiuDepartment of Pathology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, China.
Shuyan ZengDepartment of Gastroenterology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, China.
Han ZhangDepartment of Gastroenterology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, China.
Jingjing TuDepartment of Gastroenterology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, China.
Hui XuDepartment of Gastroenterology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, China.
Qin YinDepartment of Gastroenterology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, China.
Wei ZhangDepartment of Gastroenterology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, China.
Bing XuDepartment of Gastroenterology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, China.
Jiangqiang XiaoDepartment of Gastroenterology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, China.
Lei WangDepartment of Gastroenterology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, China.
Juan Carlos García-PagánHepatic Hemodynamic Unit, Hospital Clínic, Clínic Barcelona, ERN-RareLiver (Health Care Provider of the European Reference Network on Rare Liver Disorders), CSUR Centro de referencia del Sistema Nacional de Salud en Enfermedad Hepática Vascular Compleja en adultos. Barcelona, Spain. Liver disease and the vascular system group (LiVas), FRCB-IDIBAPS (Fundació de Recerca Clínic Barcelona-Institut d'Investigacions Biomèdiques August Pi i Sunyer), Barcelona, Spain. CIBEREHD (Centro de Investigación Biomédica en Red Enfermedades Hepáticas y Digestivas), Madrid, Spain.
Jun ChenDepartment of Pathology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, China.ORCID https://orcid.org/0000-0003-3905-4615
Yuzheng ZhugeDepartment of Gastroenterology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, China.ORCID https://orcid.org/0000-0002-3829-5831

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background and Aims: Hepatic sinusoidal obstruction syndrome (SOS) is characterized by hepatic sinusoidal endothelial cell injury and detachment, hepatic sinusoidal congestion, and hepatic cell necrosis. Currently, limited data exist concerning changes during the recovery period, especially histopathological changes. The purpose of this study was to investigate the evolution of pathology in patients with pyrrolizidine alkaloid (PA)-induced SOS and in a monocrotaline-induced SOS rat model. Methods: Patients diagnosed with PA-induced SOS who underwent liver biopsy after achieving clinical remission were consecutively enrolled in this retrospective study. To compare the clinical and pathological differences between patients with acute and convalescent SOS, a 2:1 matched analysis was performed based on age, sex, treatment regimen, and baseline Drum Tower Severity Scoring (DTSS) during the acute phase. Additionally, an animal model of PA-induced SOS was established through the administration of monocrotaline. Results: Fourteen consecutive patients with SOS who had adequate liver biopsy specimens obtained during recovery were identified. During convalescence, most laboratory and imaging findings, such as the map-like enhancement observed on computed tomography, also disappeared. However, histopathological analysis revealed a distinct shift from hepatic sinusoidal endothelial cell injury in the acute phase to portal tract abnormalities, primarily characterized by portal vein stricture, in the recovery phase. These pathological changes were corroborated in our animal model. Conclusions: Our study suggests that both patients with PA-induced SOS and rats in the convalescent stage may exhibit porto-sinusoidal vascular disease-like changes. Regular follow-up and dynamic pathological assessment are therefore recommended to facilitate the early detection of potential signs of portal hypertension.

Indexed as

Obliterative portal venopathyPathologyPorto-sinusoidal vascular diseasePyrrolizidine alkaloids-induced liver injurySinusoidal obstruction syndrome

Identifiers

PMID42866000
PMCPMC13655728

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.