Rehabilitation nutrition support for a hemodialysis patient with protein-energy wasting and sarcopenic dysphagia: a case report

Abstract Background Patients with end-stage renal failure may exhibit sarcopenia and protein-energy wasting (PEW). We report a case of improvement in physical function, muscle mass, and muscle strength by management of rehabilitation nutrition in a maintenance hemodialysis patient with PEW and sarcopenia. Case presentation A 60-year-old man with an 8-year history of dialysis was admitted for pneumococcal meningitis. When he was transferred for rehabilitation 36 days following the onset, he was transferred to our hospital for rehabilitation and hemodialysis. On admission, energy intake was 1200 kcal/day, via a nasogastric tube, due to sarcopenic dysphagia. He was diagnosed with PEW, based on results from a biochemical examination, physical examination, and his low dietary intake. His height, dry weight, body mass index, Mini Nutritional Assessment-Short Form, albumin, C-reactive protein, and Geriatric Nutritional Risk Index were 166 cm, 46.5 kg, 16.9 kg/m2, 1 point, 2.1 g/dL, 0.22 mg/dL, and 63, respectively, indicating malnutrition. He was also diagnosed with sarcopenia because of low muscle mass, muscle strength, and physical function. Functional Independence Measure (FIM) was 58 points (motor 27, cognition 31). He was improved by a combination of rehabilitation including activities of daily living training, swallowing training, and nutrition management. Nutritional requirement was 1752 kcal/day of energy and 55.5 g/day (1.2 g/kg/day) of protein. Energy intake was added energy accumulation (300 kcal/day) to improve muscle mass and strength. On day 108, he was discharged to go home, he could walk outdoors, and his sarcopenic dysphagia improved. Conclusion Aggressive management of rehabilitation nutrition to increase dry weight may improve PEW and sarcopenic dysphagia in patients undergoing maintenance hemodialysis

MDR1, MRP1 and MRP2 Genotypes and In Vitro Chemosensitivity in Japanese Patients with Colorectal Adenocarcinomas

In our previous paper, the chemosensitivity of human colorectal adenocarcinoma was evaluated against 12 anticancer drugs including 5-fluorouracil (5-FU), 7-ethyl-10-hydroxycamptothecin (SN-38), mitomycin C (MMC) and cisplatin (CDDP), and it was found that the anticancer drugs were effective against those with a relatively high growth rate. MMC was effective for those with a relatively high mRNA expression of the multidrug resistance-associated protein 2 (MRP2), whereas no correlation was found for the multidrug resistant transporter MDR1 and MRP1. In this study, 3 genotypes of MDR1, 4 genotypes of MRP1, and 6 genotypes of MRP2 were additionally evaluated, and it was suggested that MDR1 C3435T and MRP2 G1249A were related with the susceptibility to colorectal adenocarcinoma. The chemosensitivity against 5-FU, SN-38, MMC and CDDP was independent of MDR1 C3435T, MRP1 G2168A, and MRP2 C-24T (C3972T), possibly due to no association with the growth rate of and mRNA expression levels of MDR1, MRP1 and MRP2 in the adenocarcinoma, however, MDR1 C3435T tended to be accompanied with a higher expression of MDR1 mRNA

Association of CD4-positive cell infiltration with response to vedolizumab in patients with ulcerative colitis

Abstract Not all patients with ulcerative colitis (UC) respond initially to treatment with biologic agents, and predicting their efficacy prior to treatment is difficult. Vedolizumab, a humanized monoclonal antibody against alpha 4 beta 7 (α4β7) integrin, suppresses immune cell migration by blocking the interaction between α4β7 integrin and mucosal addressin cell adhesion molecule 1. Reports about histological features that predict vedolizumab efficacy are scarce. So, we examined the association between histological features and vedolizumab efficacy. This was a multicenter, retrospective study of patients with UC treated with vedolizumab. Biopsy specimens taken from the colonic mucosa prior to vedolizumab induction were used, and the areas positively stained for CD4, CD68, and CD45 were calculated. Clinical and histological features were compared between those with and without remission at week 22, and the factors associated with clinical outcomes were identified. We enrolled 42 patients. Patients with a high CD4+ infiltration showed a better response to vedolizumab [odds ratio (OR) = 1.44, P = 0.014]. The concomitant use of corticosteroids and high Mayo scores had a negative association with the vedolizumab response (OR = 0.11, P = 0.008 and OR = 0.50, P = 0.009, respectively). Histological evaluation for CD4+ cell infiltration may be helpful in selecting patients who can benefit from vedolizumab

Dietary l-serine confers a competitive fitness advantage to Enterobacteriaceae in the inflamed gut

International audienceMetabolic reprogramming is associated with the adaptation of host cells to the disease environment, such as inflammation and cancer. However, little is known about microbial metabolic reprogramming or the role it plays in regulating the fitness of commensal and pathogenic bacteria in the gut. Here, we report that intestinal inflammation reprograms the metabolic pathways of Enterobacteriaceae, such as Escherichia coli LF82, in the gut to adapt to the inflammatory environment. We found that E. coli LF82 shifts its metabolism to catabolize L-serine in the inflamed gut in order to maximize its growth potential. However, L-serine catabolism has a minimal effect on its fitness in the healthy gut. In fact, the absence of genes involved in L-serine utilization reduces the competitive fitness of E. coli LF82 and Citrobacter rodentium only during inflammation. The concentration of luminal L-serine is largely dependent on dietary intake. Accordingly, withholding amino acids from the diet markedly reduces their availability in the gut lumen. Hence, inflammation-induced blooms of E. coli LF82 are significantly blunted when amino acids-particularly L-serine-are removed from the diet. Thus, the ability to catabolize L-serine increases bacterial fitness and provides Enterobacteriaceae with a growth advantage against competitors in the inflamed gut