Severe sinusoidal lesions: a serious and overlooked complication of oxaliplatin-containing chemotherapy?

Arotçarena, Ramuntxo; Cales, Valérie; Berthélemy, Philippe; Parent, Yves; Malet, Maxime; Etcharry, F; Ferrari, S.; Pariente, Alexandre

doi:10.1016/s0399-8320(06)73542-4

Cited by 51 publications

(43 citation statements)

References 8 publications

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“…[50][51][52] It has been demonstrated that 5-fluorouracil and irinotecan are responsible for hepatic steatosis and nonalcoholic steatohepatitis, which may increase postoperative morbidity. 48,50,51 One concern is that higher intrahepatic concentrations of oxaliplatin, 5-FU, and irinotecan achieved by HAI would increase this histologic toxicity.…”

Section: Discussionmentioning

confidence: 99%

Rescue chemotherapy using multidrug chronomodulated hepatic arterial infusion for patients with heavily pretreated metastatic colorectal cancer

Bouchahda

Adam

Giacchetti

et al. 2009

Cancer

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Original carbohydrate‐based acrylamides bearing one azide group in C‐2 or C‐6 position namely, 2‐[(2‐deoxy‐2‐azido‐α‐D‐mannopyranosyloxy)ethanamido]‐ethyl acrylamide (II) and 2‐[(6‐deoxy‐6‐azido‐α‐D‐glucopyranosyloxy)ethanamido]‐ethyl acrylamide (III), and their azide‐free analogue, 2‐[(α‐D‐glucopyranosyloxy)ethanamido]‐ethyl acrylamide (I), have been designed. Whereas the reversible addition fragmentation chain transfer (RAFT) process ensured the preparation of well‐defined glycopolymers from I, the polymerization of monomers II and III proved to be challenging at temperatures compatible with a thermally initiated radical process, due to the presumed concomitant 1,3‐cycloaddition reactions between the azide and the acrylamide moieties. In contrast to III, for which no polymer could be obtained under any conditions, performing the RAFT polymerization of II at 30 °C clearly favored the radical polymerization and conferred a controlled character to the process, affording well‐defined azide‐functionalized glycopolymers and block copolymers. The presence of numerous azide moieties was finally exploited to introduce carbohydrates onto the glycopolymer backbone through copper catalyzed azide‐alkyne cycloaddition. © 2011 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem, 2011

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Section: Discussionmentioning

confidence: 99%

Rescue chemotherapy using multidrug chronomodulated hepatic arterial infusion for patients with heavily pretreated metastatic colorectal cancer

Bouchahda

Adam

Giacchetti

et al. 2009

Cancer

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“…In fact, since our initial report (1), several groups have confirmed the existence of oxaliplatin-related SOS in 25% to 36% of treated patients. This has led to concerns that oxaliplatin-associated hepatotoxicity may decrease the chances of curative liver surgery by increasing morbidity through preoperative hemorrhage, postoperative liver failure, delayed regeneration, and portal hypertension (4)(5)(6)(7)(8)(9)(10)(11)(12)(13). Rare fatal cases have been reported, inducing a group of experts to publish a cautionary note on the use of chemotherapy before surgical liver resection (14).…”

Section: Introductionmentioning

confidence: 99%

Gene Expression Profiling Provides Insights into Pathways of Oxaliplatin-Related Sinusoidal Obstruction Syndrome in Humans

Rubbia‐Brandt

Tauzin

Brézault

et al. 2011

Molecular Cancer Therapeutics

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Sinusoidal obstruction syndrome (SOS; formerly veno-occlusive disease) is a well-established complication of hematopoietic stem cell transplantation, pyrrolizidine alkaloid intoxication, and widely used chemotherapeutic agents such as oxaliplatin. It is associated with substantial morbidity and mortality. Pathogenesis of SOS in humans is poorly understood. To explore its molecular mechanisms, we used Affymetrix U133 Plus 2.0 microarrays to investigate the gene expression profile of 11 human livers with oxaliplatin-related SOS and compared it to 12 matched controls. Hierarchical clustering analysis showed that profiles from SOS and controls formed distinct clusters. To identify functional networks and gene ontologies, data were analyzed by the Ingenuity Pathway Analysis Tool. A total of 913 genes were differentially expressed in SOS: 613 being upregulated and 300 downregulated. Reverse transcriptase-PCR results showed excellent concordance with microarray data. Pathway analysis showed major gene upregulation in six pathways in SOS compared with controls: acute phase response (notably interleukin 6), coagulation system (Serpine1, THBD, and VWF), hepatic fibrosis/hepatic stellate cell activation (COL3a1, COL3a2, PDGF-A, TIMP1, and MMP2), and oxidative stress. Angiogenic factors (VEGF-C) and hypoxic factors (HIF1A) were upregulated. The most significant increase was seen in CCL20 mRNA. In conclusion, oxaliplatin-related SOS can be readily distinguished according to morphologic characteristics but also by a molecular signature. Global gene analysis provides new insights into mechanisms underlying chemotherapy-related hepatotoxicity in humans and potential targets relating to its diagnosis, prevention, and treatment. Activation of VEGF and coagulation (vWF) pathways could partially explain at a molecular level the clinical observations that bevacizumab and aspirin have a preventive effect in SOS.

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“…Moreover, a case of NRH that developed after the administration of neoadjuvant oxaliplatin-containing chemotherapy for colon cancer was reported in 2006 (10). Recently, the incidence of NRH following treatment with oxaliplatin-based chemotherapy has increased (11).…”

Section: (A) (B) (C)mentioning

confidence: 99%

“…Oxaliplatin potentially causes injury to endothelial cells as it stimulates the overproduction of reactive oxygen species and depletion of glutathione in endothelial cells followed by the unregulated expression of matrix metalloproteinase (MMP)-2 and MMP-9 (14) and the rupture of the sinusoidal barrier, with the possible extravasation of erythrocytes in the space of Disse and formation of perisinusoidal fibrosis. Moreover, NRH is attributed to the development of chronic ischemia in centrilobular zones (10); this process is thought to be due to the effects of ischemic atrophy associated with secondary nodular hyperplasia in regions with a favorable blood flow. In the present case, treatment with oxaliplatin may have induced a circulatory disturbance, thus leading to the development of NRH.…”

Section: (A) (B) (C)mentioning

confidence: 99%

Development of Nodular Regenerative Hyperplasia (NRH) with Portal Hypertension Following the Administration of Oxaliplatin for the Recurrence of Colon Cancer

et al. 2015

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Nodular regenerative hyperplasia (NRH) is associated with autoimmune and hematologic diseases and may lead to portal hypertension. We herein report a case of NRH diagnosed based on a liver biopsy. A 63-yearold woman developed esophageal varices and splenomegaly. She had undergone surgery for transverse colon cancer 24 years earlier and received systemic chemotherapy (FOLFOX4 including oxaliplatin) to treat lymph node metastasis 21 years after the operation. The present liver biopsy confirmed NRH, and, after two years, she received endoscopic injection sclerotherapy. Oxaliplatin was suspected to be the causative agent of NRH in this case. Therefore, physicians must consider the possibility of NRH in patients who receive chemotherapy.

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Severe sinusoidal lesions: a serious and overlooked complication of oxaliplatin-containing chemotherapy?

Cited by 51 publications

References 8 publications

Rescue chemotherapy using multidrug chronomodulated hepatic arterial infusion for patients with heavily pretreated metastatic colorectal cancer

Rescue chemotherapy using multidrug chronomodulated hepatic arterial infusion for patients with heavily pretreated metastatic colorectal cancer

Gene Expression Profiling Provides Insights into Pathways of Oxaliplatin-Related Sinusoidal Obstruction Syndrome in Humans

Development of Nodular Regenerative Hyperplasia (NRH) with Portal Hypertension Following the Administration of Oxaliplatin for the Recurrence of Colon Cancer

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