Reversible Nodular Regenerative Hyperplasia/Sinusoidal Obstruction Syndrome Due to Oxaliplatin Toxicity

2016 ◽  
Vol 111 ◽  
pp. S887-S888
Author(s):  
Maheedhar Gedela ◽  
Khalil Aloreidi ◽  
David Bean ◽  
Lokesh Jha
Keyword(s):  
Sinusoidal Obstruction Syndrome ◽  
Nodular Regenerative Hyperplasia

scholarly journals Hepatotoxicity during 6-thioguanine treatment in inflammatory bowel disease and childhood acute lymphoblastic leukaemia: a systematic review

2019 ◽  
Author(s):  
Linea Natalie Toksvang ◽  
Magnus Strøh Schmidt ◽  
Sofie Arup ◽  
Rikke Hebo Larsen ◽  
Thomas Leth Frandsen ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukaemia ◽  
Lymphoblastic Leukaemia ◽  
Case Reports ◽  
Sinusoidal Obstruction Syndrome ◽  
Nodular Regenerative Hyperplasia ◽  
Childhood Acute Lymphoblastic Leukaemia ◽  
Inflammatory Bowel Disorder ◽  
Registration Number ◽  
Inflammatory Bowel ◽  
Randomised Controlled

ABSTRACTBackgroundThe recently established association between higher levels of DNA-incorporated thioguanine nucleotides and lower relapse risk in childhood acute lymphoblastic leukaemia (ALL) calls for reassessment of prolonged 6-thioguanine (6TG) treatment, while avoiding the risk of hepatotoxicity.ObjectivesTo assess the incidence of hepatotoxicity in patients treated with 6TG, and to explore if a safe dose of continuous 6TG can be established.Data sourcesDatabases, conference proceedings, and reference lists of included studies were systematically searched for 6TG and synonyms from 1998–2018.MethodsWe included studies of patients with ALL or inflammatory bowel disorder (IBD) treated with 6TG, excluding studies with 6TG as part of an intensive chemotherapy regimen. We uploaded a protocol to PROSPERO (registration number CRD42018089424). Database and manual searches yielded 1823 unique records. Of these, 395 full-texts were screened for eligibility. Finally, 134 reports representing 42 studies were included.Results and conclusionsWe included data from 42 studies of ALL and IBD patients; four randomised controlled trials (RCTs) including 3,993 patients, 20 observational studies including 796 patients, and 18 case reports including 60 patients. Hepatotoxicity in the form of sinusoidal obstruction syndrome (SOS) occurred in 9–25% of the ALL patients in two of the four included RCTs using 6TG doses of 40–60 mg/m2/day, and long-term hepatotoxicity in the form of nodular regenerative hyperplasia (NRH) was reported in 2.5%. In IBD patients treated with 6TG doses of approximately 23 mg/m2/day, NRH occurred in 14% of patients; SOS has not been reported. At a 6TG dose of approximately 12 mg/m2/day, NRH was reported in 6% of IBD patients, which is similar to the background incidence. According to this review, doses at or below 12 mg/m2/day are rarely associated with notable hepatotoxicity and can probably be considered safe.

scholarly journals Porto-Sinusoidal Vascular Disease Associated to Oxaliplatin: An Entity to Think about It

Cells ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 1506 ◽  
Author(s):  
Angela Puente ◽  
Jose Ignacio Fortea ◽  
Carmen Del Pozo ◽  
Patricia Huelin ◽  
Maria Luisa Cagigal ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Vascular Disease ◽  
Chronic Hypoxia ◽  
Glutathione Transferase ◽  
Portal Pressure ◽  
Unknown Etiology ◽  
Sinusoidal Obstruction Syndrome ◽  
Nodular Regenerative Hyperplasia ◽  
Blood Capillaries ◽  
Sinusoidal Cells

Portal sinusoidal vascular disease is a presinusoidal cause of portal hypertension (PHT) of unknown etiology, characterized by typical manifestations of PHT (esophageal varices, ascites, portosystemic collaterals), plaquetopenia and splenomegaly with a gradient of portal pressure slightly increased, according to the presinusoidal nature of the PHT. A few cases in the literature have shown a relationship between oxaliplatin and the development of presinusoidal portal hypertension, years after the chemotherapy for colorectal cancer (therefore, different to sinusoidal obstruction syndrome). There are three mechanisms through which oxaliplatin can cause sinusoidal damage: (1) damage at the level of endothelial cells and stimulates the release of free radicals and depletion of glutathione transferase, with altering the integrity of the sinusoidal cells. The damage in the endothelial sinusoidal cells allows to erythrocytes to across into the Dissé space and formation of perisinusoidal fibrosis, (2) the appearance of nodular regenerative hyperplasia is favored by the chronic hypoxia of the centrilobular areas and, finally, (3) oxaliplatin can generate an obliteration of the blood capillaries and zones of parenchymal extinction. These three facts can develop, in a minority of cases, the appearance of a presinusoidal increase of portal pressure, which typically appears years after the completion of chemotherapy and sometimes is underdiagnosed until variceal bleeding, ascites or encephalopathy appear. The knowledge of this pathology is essential to be able to perform an early diagnostic and consult to the hepatologist.

Nodular Regenerative Hyperplasia of the Liver in an Infant: Case Report

2002 ◽  
Vol 47 (6) ◽  
pp. 689 ◽  
Author(s):  
Ho Kyun Kim ◽  
Young Hwan Lee ◽  
Duck Soo Chung ◽  
Ok Dong Kim ◽  
Jin Bok Whang ◽  
...  
Keyword(s):  
Case Report ◽  
Nodular Regenerative Hyperplasia ◽  
Infant Case

scholarly journals Endothelial cell dysfunction: a key determinant for the outcome of allogeneic stem cell transplantation

2021 ◽  
Author(s):  
Thomas Luft ◽  
Peter Dreger ◽  
Aleksandar Radujkovic
Keyword(s):  
Stem Cell ◽  
Stem Cell Transplantation ◽  
Cell Transplantation ◽  
Current Status ◽  
Sinusoidal Obstruction Syndrome ◽  
Hematopoietic Stem ◽  
Cell Dysfunction ◽  
Management Of Complications ◽  
Life Threatening

AbstractAllogeneic hematopoietic stem cell transplantation (alloSCT) carries the promise of cure for many malignant and non-malignant diseases of the lympho-hematopoietic system. Although outcome has improved considerably since the pioneering Seattle achievements more than 5 decades ago, non-relapse mortality (NRM) remains a major burden of alloSCT. There is increasing evidence that endothelial dysfunction is involved in many of the life-threatening complications of alloSCT, such as sinusoidal obstruction syndrome/venoocclusive disease, transplant-associated thrombotic microangiopathy, and refractory acute graft-versus host disease. This review delineates the role of the endothelium in severe complications after alloSCT and describes the current status of search for biomarkers predicting endothelial complications, including markers of endothelial vulnerability and markers of endothelial injury. Finally, implications of our current understanding of transplant-associated endothelial pathology for prevention and management of complications after alloSCT are discussed.

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