Evidence map›Paper›PMID 42112040›Full record

ReviewMiddle East journal of digestive diseases2025

Insights into Non-Alcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis: The Role of Fibrinogen and Pepsinogen.

Zahra Eslami, Alireza Norouzi

Abstract readReview
In one paragraph

Review in Middle East journal of digestive diseases, 2025. 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

2 authors.

Zahra EslamiDepartment of Clinical Biochemistry, Golestan University of Medical Sciences, Golestan, Iran.ORCID https://orcid.org/0000-0002-3187-3977
Alireza NorouziGolestan Research Center of Gastroenterology and Hepatology, Golestan University of Medical Sciences, Gorgan, Iran.ORCID https://orcid.org/0000-0003-4227-7350

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Fibrinogen is a multifunctional protein that contributes to inflammatory processes. Elevated levels of fibrinogen have been associated with increased liver fibrosis and disease severity of non-alcoholic steatohepatitis (NASH). Fibrinogen appears to interact with other factors implicated in NASH pathophysiology, such as activation of immune cells to induce pro-inflammatory cytokines and cellular signaling pathways. Additionally, fibrinogen-mediated pathways may disrupt normal tissue repair processes. Pepsinogen, the inactive precursor of pepsin and a specific functional enzyme in the gastric mucosa, is a serological marker with subtypes closely related to different gastrointestinal diseases. Changes in pepsinogen levels in liver disease are not entirely understood and likely relate to many factors, including inflammation, altered gastrin levels, and Methods: Databases searched included PubMed, Google Scholar, and Scopus from 2005 to 2024, and the following keywords were used: fibrinogen, pepsinogen, non-alcoholic steatohepatitis, NASH, non-alcoholic fatty liver disease, NAFLD, and fibrosis. Results: As a potential biomarker for NASH, measuring fibrinogen levels could offer valuable insights into disease diagnosis and progression monitoring. On the other hand, pepsinogen is involved in gut health and liver function, contributing to liver inflammation and fibrosis through mechanisms like the gut-liver axis and signaling pathways. Conclusion: Overall, both fibrinogen and pepsinogen appear to have a more significant negative impact on liver health and the progression of NAFLD than beneficial effects. Integrating assessments of fibrinogen and pepsinogen into clinical practice could facilitate earlier intervention strategies aimed at slowing disease progression.

Indexed as

FibrinogenInflammationLiver fibrosisNon-alcoholic fatty liver diseaseNon-alcoholic steatohepatitisPepsinogen

Identifiers

PMID42112040
PMCPMC13150696

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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.