Pathology of Gastrointestinal and Liver Complications of Hematopoietic Stem Cell Transplantation

Mourad, Nathalie; Michel, René P.; Marcus, Victoria

doi:10.5858/arpa.2018-0282-ra

Cited by 13 publications

(7 citation statements)

References 92 publications

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“…In addition, imaging techniques or liver biopsy may be needed to verify the diagnosis. Pathological changes in liver tissue are similar to those seen in patients with oxaliplatin-induced SOS: sinusoidal dilation with digestion by erythrocytes, hepatocellular necrosis, and fibrosis in late stages [ 55 ].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Vascular Endothelial Growth Factor Protects against the Development of Oxaliplatin-Induced Sinusoidal Obstruction Syndrome in Wild-Type but Not in CD39-Null Mice

Knitter

Duwe

Beierle

et al. 2022

Cancers

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(1) Background: Sinusoidal obstruction syndrome (SOS) after oxaliplatin-based chemotherapy is associated with unfavorable outcomes after partial hepatectomy for colorectal liver metastases (CLM). Bevacizumab, a monoclonal antibody against vascular endothelial growth factor (VEGF), may prevent SOS development. We investigated the impact of VEGF-inhibition on the development of SOS in a murine model. (2) Methods: Male wild-type and CD39-null mice received oxaliplatin, additional anti-VEGF (OxAV), or controls, and were sacrificed or subjected to major partial hepatectomy (MH). Specimen were used for histological analysis of SOS. Liver damage was assessed by plasma transaminases. The VEGF pathway was elucidated by quantitative PCR of liver tissue and protein analysis of plasma. (3) Results: Mice treated with oxaliplatin developed SOS. Concomitant anti-VEGF facilitated a reduced incidence of SOS, but not in CD39-null mice. SOS was associated with increased plasma VEGF-A and decreased hepatocyte growth factor (HGF). After OxAV treatment, VEGF-R2 was upregulated in wild-type but downregulated in CD39-null mice. Oxaliplatin alone was associated with higher liver damage after MH than in mice with concomitant VEGF-inhibition. (4) Conclusions: We established a murine model of oxaliplatin-induced SOS and provided novel evidence on the protective effect of VEGF-inhibition against the development of SOS that may be associated with changes in the pathway of VEGF and its receptor VEGF-R2.

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Section: Discussionmentioning

confidence: 99%

Inhibition of Vascular Endothelial Growth Factor Protects against the Development of Oxaliplatin-Induced Sinusoidal Obstruction Syndrome in Wild-Type but Not in CD39-Null Mice

Knitter

Duwe

Beierle

et al. 2022

Cancers

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“…Then, antibiotic therapy, especially with anaerobic coverage, should be provided and treatment should be continued until the clinical symptoms are alleviated (8). Despite intensive medical treatment, surgical intervention should be considered in patients with persistent bleeding, perforation, and clinical worsen-ing (9). Continuation of chemotherapy without complete healing increases the risk of developing new NE (10).…”

Section: Discussionmentioning

confidence: 99%

Neoadjuvant Doxorubicin and Docetaxel in Breast Cancer Patients Applied Neutropenic Enterocolitis

Aslan¹

2020

Erciyes Med J

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Neutropenic enterocolitis is an acute complication of neutropenia induced by chemotherapy, characterized by inflammatory processes involving the colon and cecum that can lead to necrosis, hemorrhage, perforation, and septicemia. Usually, this condition develops after use of cytotoxic drugs, and fever and abdominal pain are the main symptoms. We present a case of a 38 year old female patient with breast cancer who received doxorubicin and docetaxel and presented typhlitis.

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“…Histologic examination is the gold standard for the diagnosis of NE[19]. However, colonoscopy is relatively contraindicated in NE patients, as air insufflation may result in bowel perforation[5,20].…”

Section: Pathology Findingsmentioning

confidence: 99%

Neutropenic enterocolitis: A clinico-pathological review

Xia

Zhang

2019

WJGP

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Neutropenic enterocolitis (NE) is a predominantly cecum-based disease with high mortality seen in patients post chemotherapy. The pathogenesis of NE is poorly understood and probably multifactorial involving mucosal injury, neutropenia, and impaired host defense to intestinal organisms. The clinical presentation is characterized as ileocolonic inflammation and bowel wall thickening in patients with neutropenia, fever, and abdominal pain. The pathological features of NE include patchy necrosis, hemorrhage, ulcer, edema, perforation, infiltrating organisms, and characteristically, depletion of inflammatory cells (neutrophils). NE should always be considered as a possible diagnosis in immunosuppressed patients, especially those receiving chemotherapy. High clinical and histological diagnostic discordance rate exists. High index of clinical suspicion and prompt appropriate personalized management are essential to achieve a lower mortality rate.

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Pathology of Gastrointestinal and Liver Complications of Hematopoietic Stem Cell Transplantation

Cited by 13 publications

References 92 publications

Inhibition of Vascular Endothelial Growth Factor Protects against the Development of Oxaliplatin-Induced Sinusoidal Obstruction Syndrome in Wild-Type but Not in CD39-Null Mice

Inhibition of Vascular Endothelial Growth Factor Protects against the Development of Oxaliplatin-Induced Sinusoidal Obstruction Syndrome in Wild-Type but Not in CD39-Null Mice

Neoadjuvant Doxorubicin and Docetaxel in Breast Cancer Patients Applied Neutropenic Enterocolitis

Neutropenic enterocolitis: A clinico-pathological review

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