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Muscle loss, inflammation, and frailty are prevalent among older cancer patients. We aimed to evaluate whether inflammatory markers could identify muscle loss, and if muscle measures differed between frail and non-frail patients.

A total of 115 patients ≥70 years old with solid tumors were included. Inflammation was measured using the Glasgow Prognostic Score (GPS), which is based on C-reactive protein (CRP) and albumin levels, and CRP alone. Frailty was evaluated using a modified geriatric assessment (mGA) of eight domains affecting older patients' health status. Computed tomography-derived muscle measures were collected at the level of the third lumbar vertebra.

Patients with GPS=2 and CRP>27 mg/l exhibited poorer muscle measures compared to patients with lower levels. No associations between mGA-based frailty and muscle mass were found.

Inflammation has detrimental effects on muscle mass. However, GPS or CRP alone cannot be used to identify muscle loss, and muscle measures were not associated with frailty in this series.

Inflammation has detrimental effects on muscle mass. However, GPS or CRP alone cannot be used to identify muscle loss, and muscle measures were not associated with frailty in this series.

It remains unclear whether rectal cancers down-staged by preoperative chemoradiotherapy (CRT) have similar prognoses to those of the same stage without preoperative CRT. https://www.selleckchem.com/products/GDC-0449.html We compared prognoses of pT1 rectal cancer patients stratified by preoperative CRT.

We retrieved data of patients with pathological T1 rectal cancer between 2003 and 2020. Patients were divided into the "ypT1 group" who received preoperative CRT following surgery and the "pT1 group" who underwent surgery alone. Factors associated with relapse-free survival (RFS) were investigated.

Among 86 patients, ypT1 and pT1 groups comprised 18 and 68 patients, respectively. There was no significant difference in RFS between the groups (p=0.19). Tumor location within 5 cm from the anal verge was associated with recurrence (hazard ratio 0.13, p=0.034).

The prognosis of patients with ypT1 rectal cancer was similar to that of patients with pT1. Low tumor location was a poor prognostic factor.

The prognosis of patients with ypT1 rectal cancer was similar to that of patients with pT1. Low tumor location was a poor prognostic factor.

We evaluated the relationship between low bone mineral density (BMD), also called osteopenia, and prognosis in patients who underwent resection for pancreatic cancer (PC).

We enrolled 91 consecutive patients who underwent curative resections for PC between May 2009 and January 2019. Their BMDs were measured at the Th11 vertebra using computed tomography. Patients were then divided by age-adjusted standard BMD values into the osteopenia group (n=34) and the non-osteopenia group (n=57). Their overall survival (OS) and recurrence-free survival (RFS) were compared (log-rank test).

The two groups did not differ in age, BMI, tumor marker, operation time, blood loss, postoperative complications or stage. The osteopenia group had significantly worse 3-year rates for OS (46% vs. 30%, p=0.04) and RFS (41% vs. 26%, p=0.01). In multivariate analysis, osteopenia was an independent prognostic factor for RFS (HR=2.16, p=0.01).

Osteopenia is an adverse prognostic factor for patients with resected PC.

Osteopenia is an adverse prognostic factor for patients with resected PC.

Survival after allogeneic hematopoietic stem cell transplantation (allo-HSCT) has increased but so have long-term sequelae. New-onset post-transplant diabetes mellitus (PTDM) occurs frequently following allo-HSCT.

Study endpoints were incidence and risk factors of PDTM. We studied 599 adult patients suffering from either acute myeloid leukemia n=220), acute lymphoblastic leukemia (n=79), chronic myeloid leukemia (n=22), myelodysplastic syndrome/myeloproliferative neoplasm (n=105), chronic lymphocytic leukemia (n=37), lymphoma/myeloma (n=116, or non-malignant disorders (e.g. bone marrow failure, hemoglobinopathies) (n=20) who underwent myeloablative (466; 77.8%) or non-myeloablative (131; 21.9%) allo-HSCT between 2006 and 2016.

Altogether, 39 patients (6.5%) developed PTDM. In a competing-risk analysis, time to PTDM was associated with acute grade 2-4 graft-versus-host-disease (p=0.017). Further cardiovascular risk factors were hypertension (n=145; 24.2%), coronary artery disease (n=36, 6%), dyslipidemia (n=139; 23.3%), and stroke (n=12; 2%).

After allo-HSCT, a significant number of patients developed PTDM and patients with acute graft-versus-host-disease were found to have a higher risk for PTDM. Long-term and continuous follow-up for diabetes and cardiovascular risk factors after HSCT is important in order to be able to provide timely and appropriate treatment.

After allo-HSCT, a significant number of patients developed PTDM and patients with acute graft-versus-host-disease were found to have a higher risk for PTDM. Long-term and continuous follow-up for diabetes and cardiovascular risk factors after HSCT is important in order to be able to provide timely and appropriate treatment.

Capecitabine is a prodrug that is metabolized to its active form, 5-fluorouracil (5-FU), in three enzymatic steps. This prospective pharmacokinetic study evaluated cytidine deaminase (CDA) activity, the second drug-metabolizing enzyme that generates 5'-deoxy-5-fluorouridine (5'-DFUR) from 5'-deoxy-5-fluorocytidine (5'-DFCR), as well as creatinine clearance (CLcr).

Patients with colorectal cancer who received capecitabine plus oxaliplatin were selected. Pharmacokinetics of capecitabine and its metabolites, and CDA activity in plasma were analyzed.

Eighteen patients were examined. The area under the plasma concentration-time curve (AUC) of 5'-DFUR showed a significant inverse correlation with CLcr (p=0.003). The metabolic ratio, i.e. the ratios of the AUC of 5'-DFUR plus that of 5-FU to the AUC of 5'-DFCR, significantly increased when CLcr decreased (p=0.001) but did not depend on plasma CDA activity.

Metabolism of 5'-DFCR to form 5'-DFUR increased as CLcr decreased but the mechanism remains unknown.

Metabolism of 5'-DFCR to form 5'-DFUR increased as CLcr decreased but the mechanism remains unknown.