Vitamin B12 Deficiency Anemia and Polyneuropathy Due to Chronic Radiation Enteritis

Fukuda, Hiroyuki; Takekuma, Munetaka; Hirashima, Yasuyuki

doi:10.2169/internalmedicine.3695-19

Cited by 6 publications

(6 citation statements)

References 13 publications

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“…At the same time, this study also found that there was no correlation between HEP and EPO levels, which was consistent with our previous research results [10][11][12]. This is because HEP is an important factor leading to anemia in tumors or other chronic inflammatory diseases.…”

Section: Discusssupporting

confidence: 92%

“…At the same time, the nutritional indicators ALB and PA were both significantly lower after radiotherapy than before, indicating that radiotherapy can also deteriorate the nutritional status of patients. In addition, ALB and PA were both positively correlated with HB, suggesting that the deterioration of nutritional status could cause or aggravate anemia, which was also consistent with literature [6,7].…”

Section: Discusssupporting

confidence: 90%

“…Anemia can be caused by tumor patients' own factors such as hemorrhage and malnutrition as well as intervention measures such as surgery, radiotherapy and chemotherapy, so the incidence of anemia is high, even up to 90% [1][2][3]8]. In this study, the number of anemia cases after radiotherapy was significantly higher than that before radiotherapy, and the actual HB level after radiotherapy was also significantly lower than that before radiotherapy and the control group, which was consistent with the results of literature both native and foreign [9][10][11], indicating that radiotherapy does have inhibitory or damage effects on the hematopoietic system.…”

Section: Discusssupporting

confidence: 89%

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Effect of Radiotherapy on HB Level and Nutritional Status of Tumor Patients and Its Relationship with Hepcidin and EPO

Tiantian¹,

Zhang²,

Zuo³

et al. 2021

AJCEM

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We studied the expression features of Hepcidin (HEP), Erythropoietin (EPO), Albumin (ALB) and Prealbumin (PA), and the pathogenesis of anemia in tumor patients caused by radiotherapy. We tested the hemoglobin (HB) concentration in 446 cancer patients who received radiotherapy, and measured the serum HEP, EPO, ALB and PA n 92 cases to explore the pathogenesis of anemia caused by radiotherapy. The results were: (1) The HB level before and after radiotherapy in 446 patients were 119.85±19.87g/L and 116.32±24.25g/L (t=2.5211, P<0.05). The cases of anemia before and after radiotherapy were 146 cases and 175 cases (χ 2 =4.09, P<0.05). (2) The HB level before and after radiotherapy in 92 patients and in 20 cases of control group were respectively 127.33±17.12, 119.41±17.05 and 132.80±11.80g/L, the difference was statistically significant (F=11.70, P<0.01). The anemia cases were 14 and 27, respectively, which were also statistically significant (χ 2 =8.68, P<0.01). (3) The HEP level before and after radiotherapy in 92 patients and in 20 cases of control group were 3.38±2.48, 2.37±1.37 and 3.22±1.10mg/mL respectively, the difference was statistically significant (F=3.88, P<0.05). (4) EPO level before and after radiotherapy in 92 patients and in 20 controls were 5.05±3.50, 5.75±1.99 and 3.81±1.15mg/mL respectively, the difference was statistically significant (F=9.18, P<0.01). (5) The levels of ALB and PA before radiotherapy in 92 patients were higher than those after radiotherapy. ( 6) HEP was negatively correlated with HB before radiotherapy (r=-0.2938, t=2.9089, P<0.01), but HEP was not correlated with HB after radiotherapy (r=-0.0111, P>0.05). (7) There were positive correlation between ALB and HB before and after radiotherapy (all P<0.01). (8) There were positive correlation between PA and HB before and after radiotherapy (all P<0.01). Therefore, Radiotherapy could cause anemia and deteriorate nutritional status in cancer patients. Anemia negatively feedback inhibited the expression of HEP, while EPO was highly compensatory.

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Section: Discusssupporting

confidence: 92%

Section: Discusssupporting

confidence: 90%

Section: Discusssupporting

confidence: 89%

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Effect of Radiotherapy on HB Level and Nutritional Status of Tumor Patients and Its Relationship with Hepcidin and EPO

Tiantian¹,

Zhang²,

Zuo³

et al. 2021

AJCEM

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“…Patients with diabetes mellitus and hyperglycemia are at an increased risk of developing CRC and are associated with a poor prognosis; a positive correlation between altered glycolytic metabolism and tumor recurrence was observed in patients after preoperative chemotherapy [16][17][18][19]. One of the common chemotherapeutic side effects was enteric malabsorption, which led to colonic retention of dietary sugars and accounts for high glucose (HG) delivery through the apical route to CRC cells [20,21]. Despite the indisputable roles of increased glucose uptake and altered glucose metabolism in tumor progression, the underlying mechanisms of glucose-mediated chemoresistance remain incompletely understood.…”

Section: Introductionmentioning

confidence: 99%

Glucose Conferred Irinotecan Chemoresistance through Divergent Actions of Pyruvate and ATP in Cell Death and Proliferation of Colorectal Cancer

Huang

Pai

2022

Oncology

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Altered glucose metabolism is associated with chemoresistance in colorectal cancer (CRC). This study aimed to illustrate the molecular mechanisms of glucose-mediated chemoresistance against irinotecan, a topoisomerase I inhibitor, focusing on the distinct roles of metabolites such as pyruvate and ATP in modulating cell death and proliferation. Four human CRC cell lines, tumorspheres, and mouse xenograft models were treated with various doses of irinotecan in the presence of high concentrations of glucose, pyruvate, or ATP-encapsulated liposomes. In this study, human CRC cell lines treated with irinotecan in high glucose displayed increased cell viability and larger xenograft tumor sizes in mouse models compared to those treated in normal glucose concentrations. Irinotecan induced apoptosis and necroptosis, both mitigated by high glucose. Liposomal ATP prevented irinotecan-induced apoptosis, while it did not affect necroptosis. In contrast, pyruvate attenuated the receptor-interacting protein kinase (RIP) 1/3-dependent necroptosis via free radical scavenging without modulating apoptotic levels. Regarding the cell cycle, liposomal ATP aggravated irinotecan-induced G0/G1 shift, whereas pyruvate diminished the G0/G1 shift, showing opposite effects on proliferation. Last, tumorsphere structural damage, an index of solid tumor responsiveness to chemotherapy, was determined. Liposomal ATP increased tumorsphere size while pyruvate prevented the deformation of spheroid mass. In conclusion, glucose metabolites confer tumor chemoresistance via multiple modes of action. Glycolytic pyruvate attenuated irinotecan-induced necroptosis and potentiated drug insensitivity by shifting cells from a proliferative to quiescent state. On the other hand, ATP decreased irinotecan-induced apoptosis and promoted active cell proliferation, contributing to tumor recurrence. Our findings challenged the traditional view of ATP as the main factor for irinotecan chemoresistance and provided novel insights of pyruvate acting as an antioxidant responsible for drug insensitivity, which may shed light to the development of new therapies against recalcitrant cancers.

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“…Patients with diabetes mellitus and hyperglycemia are at increased risk of developing CRC, and a positive correlation was observed between altered glycolytic metabolism and tumor recurrence in patients after preoperative chemotherapy [16][17][18]. In addition, enteric malabsorption, as a chemotherapeutic side effect, leads to colonic retention of dietary sugars, which accounts for an alternative route for high glucose delivery to CRC cells [19,20]. Despite the irrefutable roles of high glucose uptake and altered glucose metabolism contributing to tumor growth, the underlying mechanisms of glucose-mediated tumor chemoresistance remain incompletely understood.…”

Section: Introductionmentioning

confidence: 99%

Divergent Actions of Pyruvate and ATP in Glucose-mediated Irinotecan Chemoresistance in Colorectal Cancer

Huang

Pai

2021

Preprint

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Background: Altered glucose metabolism is associated with chemoresistance in colorectal cancer (CRC). The aim of this study was to illustrate the molecular mechanisms of glucose-mediated chemoresistance against irinotecan, a topoisomerase I inhibitor, focusing on the distinct roles of metabolites such as pyruvate and ATP in modulating cell death and proliferation. Methods: Four human CRC cell lines, tumorspheres, and mouse xenograft models were treated with various doses of irinotecan in the presence of high concentrations of glucose, pyruvate or ATP-encapsulated liposomes. Cell apoptosis was measured by DNA fragmentation and caspase activities, and necroptosis was evaluated by immunoprecipitation of receptor-interacting protein kinase (RIP) 1/3 complex. Cell cycles were assessed by flow cytometric analysis.Results: Human CRC cell lines treated with irinotecan in the presence of high glucose displayed increased cell viability and larger xenograft tumor sizes in mouse models compared to those treated in the presence of normal glucose. Irinotecan induced apoptosis and necroptosis, both of which were mitigated by high glucose. Liposomal ATP prevented irinotecan-induced apoptosis, while it had no effect on necroptosis. In contrast, pyruvate attenuated the RIP1/3-dependent necroptosis via free radical scavenging, without modulating apoptotic levels. Regarding the cell cycle, liposomal ATP aggravated irinotecan-induced G0/G1 shift whereas pyruvate diminished the G0/G1 shift, showing opposite effects on proliferation. Last, tumorsphere structural damage, an index of solid tumor responsiveness to chemotherapy, was determined. Liposomal ATP increased tumorsphere sizes while pyruvate prevented the deformation of spheroid mass. Conclusions: Glucose metabolites confer tumor chemoresistance via multiple modes of action. Glycolytic pyruvate attenuated irinotecan-induced necroptosis and potentiated drug insensitivity by shifting cells from a proliferative to quiescent state. On the other hand, ATP decreased irinotecan-induced apoptosis and promoted active cell proliferation, which might contribute to tumor recurrence.

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Vitamin B12 Deficiency Anemia and Polyneuropathy Due to Chronic Radiation Enteritis

Cited by 6 publications

References 13 publications

Effect of Radiotherapy on HB Level and Nutritional Status of Tumor Patients and Its Relationship with Hepcidin and EPO

Effect of Radiotherapy on HB Level and Nutritional Status of Tumor Patients and Its Relationship with Hepcidin and EPO

Glucose Conferred Irinotecan Chemoresistance through Divergent Actions of Pyruvate and ATP in Cell Death and Proliferation of Colorectal Cancer

Divergent Actions of Pyruvate and ATP in Glucose-mediated Irinotecan Chemoresistance in Colorectal Cancer

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