Secondary diabetes associated with 5‐fluorouracil‐based chemotherapy regimens in non‐diabetic patients with colorectal cancer: results from a single‐centre cohort study

Feng, Jiexiong; Yuan, Xianglin; Li, M.; Fang, Jun; Xie, Tian; Zhou, Yanli; Zhu, Yaowu; Luo, Min; Lin, Mao Shin; Ye, D.-W.

doi:10.1111/j.1463-1318.2012.03097.x

Cited by 66 publications

(56 citation statements)

References 20 publications

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“…In 5-FU treated colorectal cancer patients (adjuvant and palliative setting) 23% developed hyperglycaemia (11% impaired fasting glucose, 12% diabetes). 75% of patients who developed diabetes did so during chemotherapy treatment, the other 25% approximately a year after 5-FU treatment [46]. There was no difference in baseline BMI between patients who developed diabetes and those that did not, however, there was no correction for weight-changes during or after therapy.…”

Section: Chemotherapycontrasting

confidence: 43%

Cancer-drug induced insulin resistance: Innocent bystander or unusual suspect

Ariaans

Jong

Gietema

et al. 2015

Cancer Treatment Reviews

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Section: Chemotherapycontrasting

confidence: 43%

Cancer-drug induced insulin resistance: Innocent bystander or unusual suspect

Ariaans

Jong

Gietema

et al. 2015

Cancer Treatment Reviews

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“…Two of these risk factors (male gender and the combination of Hispanic ethnicity with unrelated donor) are novel, while the other risk factors for hyperglycemia are well established, including: greater BMI, which promotes insulin resistance [25]; tacrolimus [29], which impairs insulin secretion [30]; glucocorticoids (administered on Day 1), which cause impaired glucose uptake, enhanced gluconeogenesis, and increased glycogenolysis [31]; myeloablative conditioning with total body irradiation, which like chemotherapy, may damage islet beta cells directly [32,33]; and TPN, which is associated with profound hyperglycemia even when used per clinical guidelines in HSCT recipients [34]. From Table 3, it is clear that a patient would have needed nearly all of these risk factors to develop severe hyperglycemia, which corresponds to nearly double (190%) the MSG level estimated for a patient with none of the factors.…”

Section: Discussionmentioning

confidence: 99%

Severe Hyperglycemia Immediately After Allogeneic Hematopoietic Stem-Cell Transplantation is Predictive of Acute Graft-Versus-Host Disease

et al. 2012

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Background Stress hyperglycemia and acute graft versus host disease (GVHD), the major early complication of hematopoietic stem-cell transplantation (HSCT), are both associated with excessive release of inflammatory cytokines. We investigated whether new-onset hyperglycemia immediately after HSCT predicts acute GVHD. Methods We studied nondiabetic adult recipients of human leukocyte antigen(HLA)-matched HSCT (peripheral blood stem-cells) for acute leukemia. Using mean morning serum glucose on Day 1–10, we classified hyperglycemia as: mild (6.11–8.33 mmol/L), moderate (8.34–9.98), severe (minimum 9.99). Subjects GVHD-free on Day 10 were followed Day 11–100 for grade II-IV acute GVHD or competing event (relapse or death). Evaluation utilized cumulative incidence-based proportional hazards regression. Results Subjects (n=328) were age 18–74, median 49 years. Per body mass index (BMI), 25.0% were obese (BMI 30–48), 33.8% overweight (25–<30), 30.8% normal weight (21–;<25), and 10.4% lean (18–;<21). Mild, moderate, or severe hyperglycemia occurred Day 1–10 in 50.0%, 21.3%, and 16.8% of subjects, respectively. Cumulative incidence on Day 100 was 44.8(±2.8)% acute GVHD and 7.9(±1.5)% competing event. Among normal-to-overweight subjects (n=212), severe hyperglycemia developed in 14.2% (n=30) and more than doubled the risk of acute GVHD (hazards ratio, HR, 2.71, 95% CI 1.58–4.65, adjusted for donor/recipient characteristics, prophylactic regimen, and mucositis). In contrast, among obese subjects (n=82), severe hyperglycemia developed in 30.5% (n=25) but did not significantly affect risk of GVHD. (No lean subjects (n=34) developed severe hyperglycemia.) Hyperglycemia that was less than severe had an effect indistinguishable from normoglycemia. Conclusions In nondiabetic patients, severe hyperglycemia immediately after allogeneic HSCT indicates increased likelihood of acute GVHD. This association is absent in obese patients, who may be primed by obesity-induced inflammation to develop severe hyperglycemia even without experiencing the cytokine storm that is essential to GVHD pathogenesis.

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“…Diet control alone was applied to 13 patients (31%), and hyperglycemia was spontaneously remitted in seven patients (17%). Intravenous glucocorticoids were administered in 14 of the 42 diabetes patients (33.3%), with a median accumulated dose of 47.5 mg (12.5 mg per cycle) [11]. …”

Section: Hyperglycemia In Cancer Patientsmentioning

confidence: 99%

“…Chemotherapy treatment may cause diabetes to develop earlier in susceptible women. Weight gain, estrogen suppression, and glucocorticoids are risk factors [11161718]. …”

Section: Hyperglycemia In Cancer Patientsmentioning

confidence: 99%

Acute Hyperglycemia Associated with Anti-Cancer Medication

Hwangbo

Lee

2017

Endocrinol Metab

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Hyperglycemia during chemotherapy occurs in approximately 10% to 30% of patients. Glucocorticoids and L-asparaginase are well known to cause acute hyperglycemia during chemotherapy. Long-term hyperglycemia is also frequently observed, especially in patients with hematologic malignancies treated with L-asparaginase-based regimens and total body irradiation. Glucocorticoid-induced hyperglycemia often develops because of increased insulin resistance, diminished insulin secretion, and exaggerated hepatic glucose output. Screening strategies for this condition include random glucose testing, hemoglobin A1c testing, oral glucose loading, and fasting plasma glucose screens. The management of hyperglycemia starts with insulin or sulfonylurea, depending on the type, dose, and delivery of the glucocorticoid formulation. Mammalian target of rapamycin (mTOR) inhibitors are associated with a high incidence of hyperglycemia, ranging from 13% to 50%. Immunotherapy, such as anti-programmed death 1 (PD-1) antibody treatment, induces hyperglycemia with a prevalence of 0.1%. The proposed mechanism of immunotherapy-induced hyperglycemia is an autoimmune process (insulitis). Withdrawal of the PD-1 inhibitor is the primary treatment for severe hyperglycemia. The efficacy of glucocorticoid therapy is not fully established and the decision to resume PD-1 inhibitor therapy depends on the severity of the hyperglycemia. Diabetic patients should achieve optimized glycemic control before initiating treatment, and glucose levels should be monitored periodically in patients initiating mTOR inhibitor or PD-1 inhibitor therapy. With regard to hyperglycemia caused by anti-cancer therapy, frequent monitoring and proper management are important for promoting the efficacy of anti-cancer therapy and improving patients' quality of life.

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Secondary diabetes associated with 5‐fluorouracil‐based chemotherapy regimens in non‐diabetic patients with colorectal cancer: results from a single‐centre cohort study

Abstract: Secondary diabetes associated with 5-FU-based chemotherapy occurs in around 10% of CRC patients, with a significant negative impact on treatment and clinical outcome. 5-FU-related diabetes should be regarded as a common side effect of 5-FU treatment.

Cited by 66 publications

References 20 publications

Cancer-drug induced insulin resistance: Innocent bystander or unusual suspect

Cancer-drug induced insulin resistance: Innocent bystander or unusual suspect

Severe Hyperglycemia Immediately After Allogeneic Hematopoietic Stem-Cell Transplantation is Predictive of Acute Graft-Versus-Host Disease

Acute Hyperglycemia Associated with Anti-Cancer Medication

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