Investigating the nutritional status characteristics of terminal cancer patients by the type of cancer

Health expenditures and financial burden among patients with major gastrointestinal cancers relative to other common cancers in the United States

Malnutrition is common in patients undergoing surgery for cancers and is a risk factor for postoperative outcomes. Body composition provides information for precise nutrition intervention in perioperative period for improving patients' postoperative outcomes. The aim was to determine changes in parameters of body composition and nutritional status of cancer patients during perioperative period. A total of 92 patients diagnosed with cancer were divided into gastrointestinal and non-gastrointestinal cancer group according to different cancer types. The patients body composition assessed by bioelectrical impedance vector analysis (BIVA) on the day before surgery, postoperative day 1 and 1 day before discharge. The changes between two groups were compared and the correlation between body composition and preoperative serum nutritional indexes was analyzed. The nutritional status of all patients become worse after surgery, and phase angle (PA) continued to decrease in the perioperative period. Fat-free mass (FFM), fat-free mass index (FFMI), skeletal muscle mass (SMM), extracellular water (ECW), total body water (TBW), hydration, and body cell mass (BCM) rise slightly and then fall in the postoperative period in patients with gastrointestinal cancer, and had a sustained increase in non-gastrointestinal patients, respectively (P<0.05). Postoperative body composition changes in patients with gastrointestinal cancer are related to preoperative albumin, pre-albumin, hemoglobin, and C-reactive protein (P<0.05), whereas postoperative body composition changes in patients with non-gastrointestinal cancer are related to age (P<0.05). Significant changes in body composition both in patients with gastrointestinal cancer and non-gastrointestinal cancer during perioperative period are observed. Changes in body composition for the cancer patients who undergoing surgery are related to age and preoperative serum nutrition index.

830 Background: Aspirin has been shown to reduce the risk of various gastrointestinal (GI) and non-GI cancers 1,2 . However, little was known about at what age aspirin should be started for maximal chemoprotective better on GI cancer. Furthermore, the randomised controlled trial on aspirin for primary prevention use in healthy elderly (ASPREE) showed no association between aspirin and cancer incidence despite the limitation of short follow-up duration 3 . The current study aims to investigate the 20-year risk of cancer using aspirin in a territory-wide Hong Kong population cohort. Methods: The study included all aspirin users from 2000 to 2019, and non-aspirin users matched by age and sex at a ratio of 1:2. Enrolled subjects with a history of cancer at enrolment, cancer incidence or death within 6 months were excluded. The incidence of individual GI and non-GI cancer was presented as the primary outcome. Baseline characteristics between aspirin and non-aspirin users were adjusted in the survival analysis by inverse probability of treatment weighting (IPTW). The fine-grey model has been used to address bias from competing risk of death. The sub-distribution hazard ratio was presented for the association of aspirin use and risk of GI and non-GI cancers. Results: The current study included 538,147 aspirin users and 968,378 non-users with a mean age of 64.8 years. A total number of 36,683 cases of GI cancer (2.4%) and 47,196 cases of non-GI cancers (3.1%) were observed. Aspirin was associated with a lower risk of several common individual GI cancers, including colorectal cancer (SHR 0.78, 95% CI 0.76-0.81), liver cancer (SHR 0.67, 95% CI 0.64-0.70), stomach cancer (SHR 0.79, 95% CI 0.75-0.84) and pancreatic cancer (SHR 0.85, 95% CI 0.79-0.91), but not oesophageal cancer. On the other hand, aspirin was associated with a lower risk of prostate cancer (SHR 0.95, 95% CI 0.91-1.00) and breast cancer (SHR 0.76, 95% CI 0.73-0.79), but not lung cancer and kidney cancer. In overall, aspirin was associated with a 24% lower risk of GI cancers (SHR 0.76, 95% CI 0.74-0.78) and a 3% lower risk of non-GI cancers (SHR 0.97, 95% CI 0.95-0.99). Conclusions: Aspirin was associated with a lower risk of most GI cancers, including colorectal cancer, liver cancer, stomach cancer and pancreatic cancer, but not most non-GI cancers. In general, results on the effect of aspirin on GI cancer prevention were consistent with the previously presented 10-year cohort. 1. Bosetti C, Santucci C, Gallus S, Martinetti M, La Vecchia C. Aspirin and the Risk of Colorectal and Other Digestive Tract Cancers: An Updated Meta-analysis through 2019. Ann Oncol. 2020;31(5):558-568. 2. Santucci C, Gallus S, Martinetti M, La Vecchia C, Bosetti C. Aspirin and the risk of nondigestive tract cancers: An updated meta-analysis to 2019. Int J Cancer. 2021;148(6):1372-1382. 3. McNeil JJ, Gibbs P, Orchard SG, et al. Effect of Aspirin on Cancer Incidence and Mortality in Older Adults. J Natl Cancer Inst. 2021;113(3):258-265.

e21523 Background: Older adults undergoing chemotherapy for GI cancers are at increased risk of HOS due to treatment related toxicity; however, there are limited data regarding which individuals are at greatest risk. We therefore sought to identify risk factors for HOS among older adults with GI cancers receiving chemotherapy. Methods: We performed a secondary analysis of patients age ≥ 65 years with GI cancer who participated in either of 2 prospective studies used to develop (n = 500) and validate (n = 250) a geriatric assessment (GA) based chemotherapy toxicity score for older adults with cancer. The incidence of HOS within 30 days post treatment was determined. The following patient characteristics were captured pre-chemotherapy: demographics, cancer type, stage, laboratory values, chemotherapy type, and GA measures (functional status, comorbidity, psychological state, cognitive function, nutritional status, and social support). Univariate and multivariate logistic regressions were used to estimate the odds ratio (OR) to identify risk factors. Results: A total of 199 adults age 65+ (median 73; range 65-94) with GI cancers (colorectal 43%, gastric/esophageal 25%, pancreas/biliary 32%; Stage I-III 42%, stage IV 58%) receiving chemotherapy (67% poly-chemotherapy) were included. 5-FU chemotherapy was administered alone or in combination in 126 (63%) patients. Sixty five (33%) patients had ≥1 HOS (1 HOS: 55, 2 HOS: 9, 3 HOS: 1). In univariate analysis, hospitalized patients were more likely to be female (p = 0.02), have stage IV disease (p = 0.03), have a diagnosis of non-colorectal GI cancer (p = 0.04), have poly-pharmacy (≥ 5 medications, p &lt; 0.01), decreased hearing (p = 0.05), cardiac comorbidity (p &lt; 0.01), and low serum albumin (p = 0.05). On multivariate analyses, patients who were female (OR = 2.06, 95% CI: 1.05-4.06), with cardiac comorbidity (OR = 3.73, 95% CI: 1.78-7.83), or a diagnosis of stage IV non-colorectal GI cancer (OR = 3.75, 95% CI: 1.50-9.39) were more likely to be hospitalized. Conclusions: HOS during chemotherapy treatment are common among older adults with GI cancers. Female sex, cardiac comorbidity, and a diagnosis of stage IV non-colorectal GI cancer are risk factors for HOS.

Background: Patients with cancer showed a high incidence of venous thromboembolism (VTE) with a poor prognosis. The risk factors for VTE in different types of cancers may differ.Methods: The clinical features and laboratory test results of cancer patients with VTE in Henan Provincial People's Hospital from 2014 to 2020 were evaluated and compared.Results: Among the eligible patients, gastrointestinal cancer (GI cancer), lung cancer and gynecological cancer accounted for the top three. This study included 49 patients with GI cancer, 31 with lung cancer and 31 with gynecological cancer. The proportion of patients who underwent surgery in GI cancer or gynecological cancer group was significantly higher than that for lung cancer (69.4% and 80.6% vs 12.9%, both P<0.001). Red blood cell (RBC) and hemoglobin (HGB) levels were lower in the gynecological cancer group than that in the lung cancer group (P = 0.014 and 0.029, respectively), while red cell distribution width (RDW) was higher in the GI cancer group than that in the lung cancer group and gynecological cancer group (P = 0.047 and 0.010, respectively). Prothrom bin time (PT) was shorter in the gynecological cancer group than that in the GI and lung cancer group (P = 0.003 and P = 0.002, respectively). The activated partial thromboplastin time (APTT) in the lung cancer group was longer than that in the GI and gynecological cancer group (P = 0.029 and 0.003, respectively). There was no difference in LOS and successful treatment rate among the groups. However, the VTE cure rate in the gynecological cancer group is higher than that in the GI cancer group (90.3% vs 61.2%, P = 0.005). The probability of continuing to take anticoagulants after discharge in the gynecological cancer group is lower than that in the GI and lung cancer groups (6.5% vs 30.6% and 32.3%, P = 0.011 and 0.022 respectively).Conclusion: VTE risk factors of different types of cancers and laboratory test results were not exactly the same. Thrombosis prevention and treatment should be implemented according to the characteristics of the different types of cancer.

To assess the effects of poor nutritional and psychological status on tolerance of cancer treatment and the recovery of physical performance status in patients with gastrointestinal cancer. An epidemiological survey with respect to nutritional and psychological status in patients with gastrointestinal cancer was conducted among 182 operated patients in four provincial-level hospitals from December 2005 to June 2006. The food frequency survey method, state-trait anxiety inventory (STAI) and depression status inventory (DSI) were used to obtain information about the diet and psychological status in the patients. Nutritional status in the participants was reflected by serum albumin (Alb), hemoglobin (HB) and body mass index (BMI). Alb, protein intake and anxiety were associated with the severity of side effects of treatment. The adjusted relative risk (RR) for Alb, protein intake and anxiety was 3.30 (95% CI: 1.08, 10.10, P = 0.03), 3.25 (95% CI: 1.06, 9.90, P = 0.04) and 1.48 (95% CI: 1.29, 1.70, P < 0.0001), respectively. Moreover, calorie intake, HB and depression were associated with the recovery of physical performance status in the patients. Adjusted relative risk was 2.12 (95% CI: 1.09, 4.03, P = 0.028), 2.05 (95% CI: 1.08, 3.88, P = 0.026) and 1.07 (95% CI: 1.02, 1.12, P = 0.007), respectively. Both poor nutrition status and psychological status are independent risk factors for severe side effects of cancer treatment, and have impact on the recovery of physical performance status in patients after treatment.

Gastrointestinal tract cancers account for approximately one-third of cancer-related deaths. Early diagnosis and effective treatment are the most important ways to prevent cancer-related morbidity and mortality. ROMO1 has been shown to play an important role in many types of cancer. However, the biological function of ROMO1 is still poorly understood in gastrointestinal system cancers. The aim of this study is to reveal the expression change and oncogenic role of ROMO in gastrointestinal system cancers. Gene Expression Profiling Interactive Analysis (GEPIA), UALCAN, TIMER, GeneMANIA, TISIDB, and STRING were applied to assess the biological function of ROMO1 in gastrointestinal cancers (colon adenocarcinoma (COAD), esophageal carcinoma (ESCA), liver hepatocellular carcinoma (LIHC), pancreatic adenocarcinoma (PAAD), and stomach adenocarcinoma (STAD)). ROMO1 is significantly increased in COAD, ESCA, LUHC, and PAAD, and the overexpression of ROMO1 is associated with clinicopathological features. In addition, ROMO1 has been found to be closely associated with tumor-infiltrating immune cells in gastrointestinal cancers. ROMO1 is closely related to the inner mitochondrial membrane proteins (TIMM) family. The study revealed that ROMO1 is of significant clinical importance for gastrointestinal cancers and may have potential clinical utility in treatment and prognosis. Functional tests on cell lines derived from these particular gastrointestinal cancers can also be performed in vitro to evaluate the impact of the ROMO1 gene and other factors, like potential drugs, on the expression of these genes and the development and progression of the cancer.

BackgroundIn aging populations, the number of people with high cholesterol levels is increasing. Appropriate management of high cholesterol levels with drugs such as statins may prevent secondary diseases. Despite many studies on the effects of statins on various types of cancer, the effectiveness of lipid-lowering therapy in preventing cancer remains controversial. This study aimed to evaluate its long-term effect on developing gastrointestinal (GI) cancer in patients with dyslipidemia.MethodsThis study used the National Health Insurance Sampling (NHIS) cohort data (2002–2015), which included patients with dyslipidemia without diabetes, and measured patients’ adherence to lipid-lowering therapy using the medication possession ratio. We used the Cox proportional hazard ratio (HR) to identify the association between the continuity of lipid-lowering therapy and the risk of GI cancer. We also evaluated the association between a combination of lipid-lowering drugs and a reduced risk of GI cancer.ResultsA total of 49,351 patients were diagnosed with dyslipidemia, of which 579 were diagnosed with GI cancer. Patients with higher adherence to lipid-lowering therapy had a significantly reduced risk of GI cancer compared to patients without drugs, and high adherence was associated with a reduced incidence of all types of GI cancer. Specifically, the combination of statins and ezetimibe or fibrates appears to reduce GI cancer risk effectively. Overall, the continuity of lipid-lowering therapy had a protective effect on GI cancer in middle-aged and elderly patients with dyslipidemia compared to non-users.ConclusionsOur findings suggest that the continuity of lipid-lowering therapy is vital in patients with dyslipidemia. In addition, for individuals vulnerable to GI cancer, combination therapy may be associated with more effective protection against GI cancer. Healthcare providers need patient education and monitoring to improve drug adherence in patients with dyslipidemia.

The miR-200 Family: Central Player for Gain and Loss of the Epithelial Phenotype

283 Background: Cancers of the esophagus, stomach, pancreas, gallbladder, liver, bile duct, colon and rectum will account for 17% of incident cancer diagnoses and 26% of cancer-related deaths in the US in 2019. We developed a methylation-based cfDNA early multi-cancer detection test that also can predict the tissue of origin (TOO) of these and other cancers types; performance of this test for gastrointestinal (GI) tract cancers is reported here. Methods: The Circulating Cell-free Genome Atlas (CCGA; NCT02889978) study is a prospective, multi-center, observational, case-control study with longitudinal follow-up, enrolling individuals with cancer ( &gt; 20 cancers, all stages, newly diagnosed) and without cancer. Plasma cfDNA was subjected to a cross-validated targeted methylation (TM) sequencing assay. Methylation fragments were combined across targeted genomic regions and assigned a probability of cancer and a predicted TOO. GI cancer classes were upper GI (esophagus/stomach, n = 67), pancreas/gallbladder/extrahepatic bile duct (n = 95), liver/intrahepatic bile duct (n = 29), and colon/rectum (n = 121). Results: Detection across all GI cancers was 82% (95% CI 77-86) at a &gt; 99% pre-set specificity. Overall predicted TOO accuracy was 92% (88-95) among the samples for which TOO was predicted (6/255 had indeterminate predicted TOO). The table shows performance by GI cancer type. Conclusions: Simultaneous detection at high specificity ( &gt; 99%) of multiple cancer types, including GI cancers across stages at high sensitivity (82%), was shown using TM analysis of cfDNA. Accurate (92%) localization of cancers to specific regions of the GI tract was also achieved. Detection of multiple GI cancers from a single noninvasive blood test could be a practical method for detecting GI and other cancers, and may facilitate diagnostic work-ups. Clinical trial information: NCT02889978. [Table: see text]

Effect of daily aspirin on long-term risk of death due to cancer: analysis of individual patient data from randomised trials

Special Series: Advances in GI Cancer.

e16382 Background: The relation between cancer and thrombotic events has been well established over the past decade. Cancer is a prothrombotic state and thrombosis is the second most common cause of death in cancer. While portal vein thrombosis (PVT) has been extensively studied in individuals with Hepatocellular Carcinoma (HCC), its significance in other Gastrointestinal (GI) cancers is often overlooked. This study aims to investigate the prevalence and prognostic impact of PVT across various GI cancers. Methods: A retrospective analysis was performed on the National Inpatient Sample database (2018-2020) and the ICD-10 codes to identify the patients &gt; 18 years old with primary diagnosis of GI cancers (pancreatic, HCC, gastric, small intestinal[SI], colorectal). Prevalence of PVT in individual GI cancers and effect of PVT on mortality, length of stay and Hospital cost utilization was studied. Multivariable regression analyses were performed adjusting for demographics, hospital-level characteristics, and relevant comorbidities. These included Age, Sex, Race, obesity, Smoking, Hypertension, Diabetes, CKD, liver disease, CHF, CAD, Hypothyroidism. Results: Our study analyzed data from 2,313,888 individuals with GI cancers, Including HCC, Gastric cancer, SI cancer, colorectal and pancreatic cancer, The incidence of PVT varied across cancer types, with 12.9% in pancreatic cancer, 0.74% in HCC, 0.99% in gastric cancer, 0.47% in colorectal cancer, and 3.6% in pancreatic cancer. Multivariate regression analysis, adjusting for confounders, revealed a significant association between PVT and increased mortality in various GI cancers. Specifically, the odds ratio (OR) for mortality in pancreatic cancer was 1.31 (p &lt; 0.001), in HCC was 1.39 (p &lt; 0.001), in gastric cancer was 1.88 (p &lt; 0.001), and in colorectal cancer was 2.10 (p &lt; 0.001). However, the incidence of mortality in SI cancer did not yield a significant result OR 1.42 [p- value 0.369] [Table 1]. Additionally, Our findings revealed an increase in length of stay and total healthcare resource utilization across all GI cancers for individuals with PVT compared to without PVT. Conclusions: There is a statistically significant effect of symptomatic and asymptomatic PVT on mortality in various other GI cancers in addition to HCC, which has been established and studied widely. Further prospective studies are needed to study the effect of diagnosing PVT earlier in the disease to predict mortality and other major complications in GI cancers.[Table: see text]

ImportanceEarly-onset gastrointestinal (GI) cancer is typically defined as GI cancer diagnosed in individuals younger than 50 years. The incidence of early-onset GI cancer is rising globally, and early-onset GI cancers represent the most rapidly increasing early-onset cancer in the US.ObservationsWorldwide, among early-onset GI cancers reported in 2022, colorectal cancer (CRC) was the most common (54.3%; 184 709 cases), followed by gastric cancer (23.8%; 80 885 cases), esophageal cancer (13.2%; 45 056 cases), and pancreatic cancer (8.6%; 29 402 cases). In the US, among early-onset GI cancers reported in 2022, 20 805 individuals were diagnosed with early-onset CRC, 2689 with early-onset gastric, 2657 with early-onset pancreatic, and 875 with early-onset esophageal cancer. Most early-onset GI cancers are associated with modifiable risk factors including obesity, poor-quality diet (eg, sugar-sweetened beverages, ultraprocessed foods), sedentary lifestyle, cigarette smoking, and alcohol consumption. Nonmodifiable risk factors include family history, hereditary syndromes (eg, Lynch syndrome), and inflammatory bowel disease for patients with early-onset CRC. Approximately 15% to 30% of early-onset GI cancers have pathogenic germline variants in genes such as DNA mismatch repair genes and BRCA1/2. All patients with early-onset GI cancers should undergo germline and somatic genetic testing to guide treatment, screen for other cancers (eg, endometrial cancer in Lynch syndrome), and assess familial risk. Treatment for early-onset GI cancers is similar to later-onset GI cancers and may include chemotherapy, surgery, radiation, and therapies such as poly–adenosine diphosphate ribose polymerase inhibitors for BRCA-associated pancreatic cancer. Compared with GI cancers diagnosed after age 50 years, patients with early-onset GI cancers typically receive more treatments but often have similar or shorter survival. Specialized centers and multidisciplinary teams can support patients with challenges around fertility preservation, parenting with cancer, financial difficulty, and psychosocial distress. Currently, screening is not recommended for most early-onset GI cancers, although in the US, screening for CRC is recommended for average-risk individuals starting at age 45 years. High-risk individuals (eg, those with Lynch syndrome, a first-degree relative with CRC, or advanced colorectal adenoma) should begin CRC screening earlier, at an age determined by the specific risk factor.Conclusions and RelevanceEarly-onset GI cancers, typically defined as cancer diagnosed in individuals younger than 50 years, are among the largest subset of early-onset cancers globally. Treatment is similar to later-onset GI cancers and typically involves a combination of chemotherapy, surgery, and radiation, depending on the cancer type and stage. The prognosis for patients with early-onset GI cancers is similar to or worse than that for patients with later-onset GI cancers, highlighting the need for improved methods of prevention and early detection.

Background Many studies have shown the link between the pretreatment serum transthyretin and prognosis in gastrointestinal (GI) cancers. However, based on the conclusion, the initial findings were inconsistent. Hence, this meta-analysis was performed to identify the prognostic values of the pretreatment serum transthyretin in GI cancers. Methods Previous studies published before November 2018 were collected from a comprehensive literature search of several databases. The pooled hazard ratios (HRs) and 95% confidence intervals (CIs) were applied in the assessment of the intensity of associations. Also, the publication bias and the robustness of merged data were assessed. All statistical analyses were undertaken using STATA/SE 14.1. Results The combined data indicated that the pretreatment serum transthyretin level was related to the prognosis in GI cancers. The group with reduced pretreatment transthyretin had a significantly worse overall survival (OS) (HR = 1.71, 95% CI: 1.37-2.05). The subgroup analysis for OS further showed the predictive value of transthyretin. In addition, the low serum transthyretin level could be an unfavorable factor for recurrence-free survival (RFS) or progression-free survival (PFS) (HR = 1.66, 95% CI: 1.14-2.18) in GI cancers. Conclusion The low pretreatment serum transthyretin level implies an unfavorable prognosis for patients with GI cancers. The monitoring of pretreatment transthyretin level could contribute to the risk stratification and individualized therapy in GI cancers.