Background: Oxaliplatin is one of the key drugs for the treatment of colorectal cancer, although it is known to cause hepatic sinusoidal injury.
Method: Thirty-one patients underwent modified FOLFOX6 therapy from April 2006 and December 2009 at our hospital. Four patients were excluded from this study because they had too many intervals in their therapeutic courses. The size of the spleen and the blood platelet count were analyzed before and after 6 months of FOLFOX therapy. The spleen was measured using CT scan, and the splenic index(SI=length×width×height)was evaluated.
Results: After 6 months of treatment, the mean SI was increased from 229 cm3 to 323 cm3(p<0. 01). At the same time, the mean platelet count was decreased from 26. 9 ×10 / / 4 mm3 to 17. 1×104 mm3(p<0. 01). A negative correlation was found between the ratio of SI and the platelet count after 6 months of treatment to baseline(r=-0. 42, p=0. 030). SI increased by>50% in 12 patients (44. 4%). The platelet count decreased more severely in patients whose SI increased by>50%(p=0. 028).
Conclusions: Splenomegaly and thrombocytopenia were observed in patients who underwent FOLFOX therapy. These are candidate parameters for evaluating hepatic sinusoidal injury.
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J Med Case Rep
January 2025
Department of Hepatic Biliary Pancreatic Medicine, First Hospital of Jilin University, 1 Xinmin Avenue, Changchun, 130021, China.
Background: Dyskeratosis congenita is a rare genetic disease due to telomere biology disorder and characterized by heterogeneous clinical manifestations and severe complications. "Porto-sinusoidal vascular disease" has been recently proposed, according to new diagnostic criteria, to replace the term "idiopathic non-cirrhotic portal hypertension." TERT plays an important role in telomeric DNA repair and replication.
View Article and Find Full Text PDFJ Toxicol Pathol
January 2025
The Institute of Environmental Toxicology, 4321 Uchimoriya-machi, Joso-shi, Ibaraki 303-0043, Japan.
Cystic degeneration (CD) in the liver is a cyst-like lesion composed of one or more pseudocysts lacking lining cells, occurring spontaneously in rats older than 12 months, with a male predilection. In this study, 32 CDs were identified in 23 out of 104 non-treated, control male Sprague-Dawley rats from two combined chronic toxicity and carcinogenicity studies with agrochemicals. They were examined histologically, histochemically, and immunohistochemically to assess the pathogenesis and pathological significance of CD, focusing on pseudocapillarization in aged rat liver.
View Article and Find Full Text PDFJ Control Release
January 2025
Department of Pharmaceutical Engineering, China Pharmaceutical University, Nanjing 211198, China. Electronic address:
Liver fibrosis is a prevalent liver disease associated with significant morbidity, and the activation of hepatic stellate cells (HSCs) serves as the primary causative factor driving the progression of liver fibrosis. However, capillarization of liver sinusoidal endothelial cells (LSECs) induced by hepatic fibrosis can reduce nitric oxide (NO) production and bioavailability, which consequently loses the ability to retain HSCs dormant, leading to amplified HSCs activation. Herein, an elaborate micelle (VN-M@BN) loaded with benazepril (BN) was constructed by self-assembly of polymeric NO donor, aiming for the controlled release of NO in liver fibrosis lesions thereby impeding the progression of liver fibrosis.
View Article and Find Full Text PDFMetab Brain Dis
January 2025
Institute of Liver and Biliary Sciences, New Delhi, India.
Hepatic encephalopathy (HE) is traditionally associated with hepatic parenchymal diseases, such as acute liver failure and cirrhosis. Its prevalence in non-cirrhotic portal hypertension (NCPH) patients, extrahepatic portal vein obstruction (EHPVO), and non-cirrhotic portal fibrosis (NCPF) is less well described. HE in NCPH allows one to study the effect of portosystemic shunting and ammonia without significant hepatic parenchymal injury.
View Article and Find Full Text PDFJ Oncol Pharm Pract
January 2025
Department of Pharmacy Practice, Massachusetts College of Pharmacy and Health Sciences School of Pharmacy, Boston, MA, USA.
Purpose: Sinusoidal obstructive syndrome (SOS)/veno-occlusive disease (VOD) is a serious complication in hematopoietic stem-cell transplant (HSCT) patients. Gemtuzumab-ozogamicin (GO) and InO are known to cause SOS/VOD in leukemic and transplant populations. Due to limited data on ursodiol prophylaxis in non-HSCT patients, we aimed to assess hepatotoxicity, SOS/VOD incidences, time to hepatotoxicity, and confirmed SOS/VOD in adults receiving GO or InO ± ursodiol.
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