Clostridium butyricum affects nutrition and immunology by modulating gut microbiota.

The gut microbiota has nutritional and protective functions. In patients with end-stage renal disease, changes in the gut microbiota disrupt their protective functions. Probiotics help maintain normal bowel function. However, their role in patients with end-stage renal disease is controversial. We investigated whether Clostridium butyricum affects the nutrition and immune function of patients with end-stage renal disease undergoing maintenance dialysis between 2014 and 2015; thirty-seven patients were included. The patients were divided into two groups: one in which C. butyricum was administered and one in which it was not. One tablet of the probiotics, which contained 20 mg of C. butyricum, was administered orally three times daily for 2 years in the C. butyricum group. The 16S rRNA genes were sequenced from stool samples of 14 (37.8%) patients in the C. butyricum group and 23 (62.2%) patients in the control group. The differences in the gut microbiota of the two groups were analyzed. The α-diversity index indicated that the C. butyricum group had significantly more operational taxonomic units and higher albumin and transferrin levels than the control group. The effector to target cell ratio was significantly higher in the C. butyricum group. In addition, interleukin-6 levels were significantly lower in the C. butyricum group, and inflammation was less severe in this group. The patients undergoing maintenance dialysis with C. butyricum had abundant gut microbiota. They also had a good nutritional status, low systemic inflammation, and a good immunological status.

Effect of increased blood flow rate on renal anemia and hepcidin concentration in hemodialysis patients.

BACKGROUND: Increasing the blood flow rate (BFR) is a useful method for increasing Kt/V and the clearance for low molecular solutes. Hemodialysis patients are often anemic due to hypoerythropoiesis and their chronic inflammatory state. Hepcidin, a hormone that regulates iron homeostasis, is considered as an indicator of iron deficiency in patients with end-stage renal disease. This study aimed to investigate the effects of an increased BFR during hemodialysis on serum hepcidin levels and anemia. METHODS: Between April 2014 and March 2016, 22 chronic dialysis patients (11 men [50.0 %]; mean [± standard deviation] age, 72 ± 12 years) undergoing maintenance hemodialysis treatment, thrice weekly, were enrolled and followed prospectively for 24 months. In April 2014, the BFR was 200 mL/min; in April 2015 this was increased to 400 mL/min, which was within acceptable limits. The dialysate flow rate remained stable at; 500mlL/min. Blood samples were collected in March 2015 and 2016. The primary endpoint was the comparison of the amounts of erythropoiesis-stimulating agent (ESA) required. RESULTS: The increased BFR increased the Kt/V and contributed to significantly decreased urea nitrogen (UN) (p = 0.015) and creatinine (Cr) (p = 0.005) levels. The dialysis efficiency was improved by increasing the BFR. Ferritin (p = 0.038), hepcidin (p = 0.041) and high-sensitivity interleukin-6 (p = 0.038) levels were also significantly reduced. The ESA administered was significantly reduced (p = 0.004) and the Erythropoietin Resistant Index (ERI) significantly improved (p = 0.031). The reduction rates in UN (p < 0.001), Cr (p < 0.001), and beta-2 microglobulin (p = 0.017) levels were significantly greater post the BFR increase compared to those prior to the BFR increase. However, hepcidin was not affected by the BFR change. CONCLUSIONS: Increasing BFR was associated with hemodialysis efficiency, and led to reduce inflammatory cytokine interleukin-6, but did not contribute to reduce C-reactive protein. This reduced hepcidin levels, ESA dosage and ERI. Hepcidin levels were significantly correlated with ferritin levels, and it remains to be seen whether reducing hepcidin leads to improve ESA and iron availability during anemia management.

Hemorrhoidectomy for elderly patients aged 75 years or more, before and after studies.

BACKGROUND: The incidence of hemorrhoids requiring hemorrhoidectomy among the elderly has been increasing. Old age is sometimes considered a contraindication for surgery. The relationship between age and complications of hemorrhoidectomy for elderly patients is not well established. This study aimed to compare the clinicopathological features and postoperative outcomes of hemorrhoidectomy in the elderly (≥75 years old) and non-elderly patients (<75 years old). METHODS: A total of 100 patients who underwent hemorrhoidectomy for hemorrhoids of Goligher classification grades 3 and 4 at our institution between 2014 and 2018 were enrolled. The clinical characteristics were compared between the elderly and non-elderly patients. Pain scores were measured at 6, 12, 24, and 48 h after surgery. The risk factors for postoperative complications were identified. RESULTS: A total of 34 patients were classified as elderly patients. In the elderly group, aspartate aminotransferase levels were higher while the albumin levels and cholinesterase levels were lower and the platelet counts were significantly lower. The blood urea nitrogen levels were higher and estimated glomerular filtration rates and hemoglobin levels were significantly lower in the elderly group. The pain scores significantly decreased at 48 h postoperatively compared to those recorded at 6 h postoperatively in both groups. Multivariate analysis identified Goligher classification grade 4 and high neutrophil to lymphocyte ratio at the indicators of complications. CONCLUSIONS: Hemorrhoids due to impairment of liver function and kidney function were dominant in elderly patients. Aging itself was not a risk factor for postoperative complications.

Plasma cell leukemia producing monoclonal immunoglobulin E.

A 78-year-old male with lumbar pain and dim consciousness presented the clinical pictures of plasma cell leukemia (PCL) producing a large amount of monoclonal immunoglobulin E (IgE)/kappa protein. Laboratory investigation demonstrated an elevated serum calcium level and renal dysfunction. Systemic bone X-ray survey disclosed only a solitary osteolytic lesion. Circulating plasma cells demonstrated CD19(-)/CD56(-) and MPC-1(-)/CD49e(-)/CD45(+/-), the latter indicating the immature phenotype of the tumor cells. Bone marrow was occupied with immature, atypical plasma cells, of which cytoplasms were positive for IgE by direct immunofluorescence analysis. Chromosomes revealed a translocation of (11;14)(q13;q32), which is concordant with cyclinD1-protein overexpression by immunohistochemistry. He was treated with dexamethasone and vincristine, which somewhat improved the laboratory findings. He died of tumor progression after 4-month admission. The clinical and biological characteristics of IgE-producing PCL, a very rare type of plasma cell dyscrasia, are discussed, reviewing the past literature.

Apoptosis-inducing protein derived from hepatocyte selectively induces apoptosis in lymphocytes.

The liver is where lymphocytes undergo activation-induced cell death (AICD) at the resolution phase of an immune response, which is crucial for homeostasis of the immune system and prevention of autoimmunity. Exploring the machinery of AICD in the liver, we found that a primary culture supernatant of murine hepatocytes had an antiproliferative effect on antigen-stimulated T clone and T lymphoma cells. Biological study showed that the antiproliferation was due to induction of apoptosis in a caspase-dependent manner. The apoptosis-inducing potential was sensitive to trypsin, heat (> 70 degrees ) and acid (< pH 5) treatment but could not be neutralized by anti-tumour necrosis factor-alpha, anti-Fas ligand, or anti-transforming growth factor-beta antibodies. Biochemical study of the isolated and purified apoptosis-inducing component from the supernatant showed that it was a protein with a molecular mass of about 68,000-70,000. It induced apoptotic change in murine T and B cells, and to a lesser degree, in human lymphoid cells, but not in macrophages. Biochemical and biological characteristics distinguish this protein from others that have been reported to induce apoptosis of lymphocytes. The identification of an apoptosis-inducing protein derived from murine hepatocytes, which selectively induces apoptosis in lymphocytes, suggests one possible mechanism for immune suppression in the liver.