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The pan-PPAR agonist lanifibranor reduces portal pressure independent of fibrosis reduction through the splanchnic vasculature.

Biomed Pharmacother

January 2025

Department of Internal Medicine and Pediatrics, Hepatology Research Unit, Ghent University, Ghent, Belgium; Liver Research Center Ghent, Ghent University, Ghent University Hospital, Ghent, Belgium. Electronic address:

Portal hypertension (PH) can cause severe complications in patients with advanced chronic liver disease (aCLD). The pan-peroxisome proliferator-activated receptor (pan-PPAR) agonist lanifibranor reduces portal pressure in preclinical models of aCLD. Since the effect on PH might be secondary to fibrosis improvement, we investigated the effect of lanifibranor on PH, hepatic and splanchnic angiogenesis in mouse models of fibrotic and prehepatic non-fibrotic PH.

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A 36-year-old woman diagnosed with complicated cholecystolithiasis underwent elective laparoscopic cholecystectomy (LC), then converted to open cholecystectomy because of a massive intraoperative bleeding. Hemostasis was performed with clipping and suturing the source of bleeding. In post-operative period, the patient suffered from persistent anemia associated with hemoperitoneum diagnosed through abdominal CT scanning, in absence of any sign of active bleeding.

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Background: Hepatic artery infusion pump (HAIP) chemotherapy is a locoregional treatment for intrahepatic malignancies. HAIPs are surgically implanted, and the catheter tip is typically inserted into a ligated gastroduodenal artery stump. Potential complications at the catheter insertion site include dehiscence, pseudoaneurysm or extravasation, and adjacent hepatic arterial stenosis and thrombosis.

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Pemigatinib suppresses liver fibrosis and subsequent osteodystrophy in mice.

Hepatol Commun

January 2025

Department of Veterinary Medical Science, Veterinary Pharmacology, Graduate School of Agriculture and Life Sciences, The University of Tokyo, Tokyo, Japan.

Background: Liver fibrosis could lead to serious secondary diseases, including osteodystrophy. The interaction between liver and bone has not been fully elucidated, thus existing therapies for osteodystrophy secondary to liver fibrosis are often ineffective. FGF23 was initially found as an endocrine regulator of phosphate homeostasis, but recently, its involvement in fibrosis has been suggested.

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Background: Liver fibrosis is caused by chronic toxic or cholestatic liver injury. Fibrosis results from the recruitment of myeloid cells into the injured liver, the release of inflammatory and fibrogenic cytokines, and the activation of myofibroblasts, which secrete extracellular matrix, mostly collagen type I. Hepatic myofibroblasts originate from liver-resident mesenchymal cells, including HSCs and bone marrow-derived CD45+ collagen type I+ expressing fibrocytes.

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