Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report here the case of a patient suffering from hemophagocytic syndrome (HPS) associated with bile ductopenia. A 24-year old man was admitted after suffering fever, sore throat and general malaise for 7 days and jaundice for 2 days. Clinical studies showed hepatic dysfunction with hyperbilirubinemia. Epstein-Barr viral DNA from two bone marrow samples was detected. Bone marrow aspiration disclosed findings of HPS. Liver biopsy showed centrilobular cholestasis with lack of interlobular bile duct. Repeated therapeutic plasma exchange was effective for decreasing serum bilirubin and interleukin-6 levels. The patient received liver transplantation, however, he finally died of alveolar hemorrhage resulting from disseminated intravascular coagulation and acute rejection.
Ther Apher Dial 2006 Feb
PMID:Effect of plasma exchange on the circulating IL-6 levels in a patient with fatal hemophagocytic syndrome associated with bile ductopenia. 1655 42

Using changes in cell counts and levels of cancer antigen 125 (CA125), fibrinogen degradation product (FDP), and interleukin-6 (IL-6) in effluent before and after the use of icodextrin-based peritoneal dialysis solution (icodextrin), we evaluated the effects of icodextrin on peritoneal membrane. The subjects were 8 anuric patients (4 men, 4 women) who had been using a 2.5% glucose-based dialysis solution (glucose solution) for the overnight dwell. The mean age of the patients was 57.9 +/- 6.1 years, and their mean duration of continuous ambulatory peritoneal dialysis was 61.6 +/- 44.3 months. In all patients, chronic glomerulonephritis was the cause of end-stage renal disease. We changed the 2.5% glucose solution used for the 8-hour dwell to an icodextrin, and we compared cell counts in effluent and levels of IL-6, FDP, and CA125 in the overnight effluent before, and 12 and 36 weeks after, the switch to the icodextrin. When 2.5% glucose solution was used for the overnight 8-hour dwell, the mean cell count in the effluent was 5.5 +/- 3 cells/mm3. However, 12 and 36 weeks after the start of icodextrin, mean cell counts in effluent were significantly increased to 15.3 +/- 7.7 cells/mm3 (p < 0.01) and 16.5 +/- 11.2 cells/mm3 (p < 0.01) respectively. Values of effluent CA125, FDP, and IL-6 obtained during the use of a glucose solution were compared to values obtained 12 and 36 weeks after the start of icodextrin. Effluent levels of CA125 and IL-6 did not vary before and after the use of the icodextrin, but levels of FDP in the icodextrin effluent were higher than the levels found in the effluent of a 2.5% glucose solution (7278.8 +/- 2915 ng/mL before the start of icodextrin; 29,875 +/- 13,227 ng/mL 12 weeks after icodextrin introduction, p < 0.01; and 12,062.9 +/- 5684.6 ng/mL 36 weeks after icodextrin introduction). Icodextrin induced a subclinical inflammatory response in the peritoneum. Therefore, biocompatibility of an icodextrin solution is not always superior to that of a glucose solution, and further research is needed to clarify the influence of long-term icodextrin use on the peritoneum.
Adv Perit Dial 2005
PMID:Effect of icodextrin-based peritoneal dialysis solution on peritoneal membrane. 1668 79

The usefulness of icodextrin-containing peritoneal dialysis (PD) solution for the management of body fluid and blood pressure has been reported. However, icodextrin PD solution is a foreign solution in the body, and the possible induction of intraperitoneal inflammation has been reported. In this study, we investigated at 6-month intervals the influence of icodextrin solution on peritoneal permeability and inflammatory reactions in patients in whom glucose solution had been changed to icodextrin solution for the overnight dwell. We enrolled 9 anuric PD patients (5 men, 4 women) of mean age 58 +/- 5.9 years (range: 45.6-64.8 years) into the study. The patients' mean duration of PD was 61.9 +/- 42 months (range: 6.7-142.5 months). The cause of end-stage renal disease was chronic glomerulonephritis in all patients. For evaluation ofperitoneal permeability, we performed peritoneal equilibration tests (PETs) immediately after an overnight dwell and determined the dialysate-to-plasma ratios of creatinine (D/P Cr), beta2-microglobulin (D/P beta2m), albumin (D/P Alb), immunoglobulin G (D/P IgG), and alpha2-macroglobulin (D/P alpha2m). We also measured interleukin-6 (IL-6) and fibrinogen degradation products (FDPs) in overnight effluent as indices of inflammation and of the fibrinolysis-coagulation system. The evaluation was performed every 6 months for 24 months. The FDPs in effluent increased significantly at 6 months after the change to icodextrin solution, and IL-6 tended to increase. The D/P beta2m, D/P Alb, D/P IgG, and D/P alpha2m all significantly increased in the course of follow-up. In the PETs, the D/P Cr increased slightly, but the change was nonsignificant. At 30 months after the change to icodextrin solution, 1 patient was diagnosed as having a risk of encapsulating peritoneal sclerosis (pre-EPS). In this patient, rapid increases in IL-6, D/P Cr and macromolecular and small molecular D/P by PET were noted after the change to icodextrin solution. Steroids were administered after the diagnosis of pre-EPS, with the result that the IL-6 level rapidly decreased and the D/P Cr and D/P of small molecules and macromolecules slightly decreased. Icodextrin dialysis solution increased peritoneal permeability. Although the cause was unclear, icodextrin may have changed peritoneal reactivity. Long-term use of icodextrin PD solution requires further investigation.
Adv Perit Dial 2006
PMID:Impact on peritoneal membrane of use of icodextrin-based dialysis solution in peritoneal dialysis patients. 1698 33

Cachexia is common in end-stage renal disease (ESRD) patients, and it is an important risk factor for poor quality of life and increased mortality and morbidity. Chronic inflammation is an important cause of cachexia in ESRD patients. In the present review, we examine recent evidence suggesting that adipokines or adipocytokines such as leptin, adiponectin, resistin, tumor necrosis factor alpha, interleukin-6, and interleukin-1beta may play important roles in uremic cachexia. We also review the physiology and the potential roles of gut hormones, including ghrelin, peptide YY, and cholecystokinin in ESRD. Understanding the molecular pathophysiology of these novel hormones in ESRD may lead to novel therapeutic strategies.
Perit Dial Int 2007 Jun
PMID:Adipokines and gut hormones in end-stage renal disease. 1755 23

The removal of low molecular weight proteins such as beta(2)-microglobulin (beta(2)MG) is accelerated by using a 7.5% icodextrin-based peritoneal dialysis solution (ICO) dwell. To examine the possibility of peritoneal injury in ICO, we investigated the relationship between beta(2)MG and the injury markers in effluent. Sixteen ICO-treated patients (11 male and five female, mean age 50.1 +/- 10.9 years) with continuous ambulatory peritoneal dialysis (CAPD; mean duration 54.6 +/- 30.8 months) were studied. The patients were treated with ICO 2 L and 2.27% glucose-based solution 2 L for an 8-h dwell and the effluent was collected. We investigated the correlations between beta(2)MG and the injury markers (e.g. hyaluronic acid [HA], interleukin-6 [IL-6], matrix metalloproteinase-2 [MMP-2]) in each effluent sample. The beta(2)MG level in the ICO effluent was 8978 +/- 2431 microg/L, significantly higher than in the 2.27% glucose-based solution effluent (6454 +/- 2956 microg/L; P = 0.0032). The levels of HA and MMP-2 in ICO effluent were significantly higher than those in the 2.27% glucose-based solution effluent (P = 0.00214, P = 0.0113, respectively). There was a trend toward higher IL-6-values in ICO effluent, although no significant differences were seen. There were positive correlations between levels of various injury markers and beta(2)MG. We propose that the subclinical injury of the peritoneum by ICO treatment may accelerate peritoneal permeability to increase beta(2)MG in effluent. ICO's biocompatibility might not be superior to that of glucose-based solution.
Ther Apher Dial 2007 Aug
PMID:Relationship between effluent levels of beta(2)-microglobulin and peritoneal injury markers in 7.5% icodextrin-based peritoneal dialysis solution. 1766 36

Leptin is mainly produced by adipocytes and metabolized in the kidney. Leptin is taken up into the central nervous system by a saturable transport system, and controls appetite in rodents and in healthy subjects. Leptin acts on peripheral tissue and increases the inflammatory response by stimulating the production of tumor necrosis factor alpha, interleukin-6 and interleukin-12. In healthy humans, serum leptin concentration is related to the size of adipose tissue mass in the body. The majority of obese subjects have inappropriately high levels of circulating plasma leptin concentrations, indicating leptin resistance. In healthy subjects increased leptin concentration constitutes a biomarker for increased cardiovascular risk. On the other hand, a recent prospective long-term study in patients with chronic kidney disease stage 5 on hemodialysis therapy showed that reduced serum leptin concentration is an independent risk factor for mortality in these patients.
Semin Dial
PMID:Role of leptin in reverse epidemiology in chronic kidney disease. 1799 Dec

We examined peritoneal growth factors, mesothelial mass, and epithelial-to-mesenchymal transition (EMT) in response to peritoneal exposure to peritoneal dialysate with standard and low concentrations of glucose degradation products (GDPs). We randomized 56 incident continuous ambulatory peritoneal dialysis (CAPD) patients to receive either low-GDP (30 patients) or high-GDP (standard) peritoneal dialysis (PD) solution (26 patients). The effects of the PD solutions on EMT and peritoneal growth factors in overnight dialysate effluent were compared at 1, 6, and 12 months. Assessment of EMT was performed after human peritoneal mesothelial cells (HPMCs) were cultured from overnight effluent. The low-GDP solution group showed significantly higher dialysate levels of cancer antigen 125 (CA125), fibronectin, transforming growth factor beta(TGFbeta)-induced gene product (betaig-h3), and interleukin-6 (IL-6), but the rate of EMT was significantly lower in the low-GDP solution group during the initial 12 months of CAPD treatment. After adjusting peritoneal growth factors for dialysate CA125 concentration, the low-GDP solution group showed significantly lower ratios of fibronectin/CA125, betaig-h3/CA125, IL-6/CA125, TGFbeta/CA125, and vascular endothelial growth factor (VEGF)/CA125 than did patients in the high-GDP (standard) solution group. Factors associated with higher EMT were the type of solution (high in GDPs), the mass of HPMCs (low CA125), and higher VEGF/CA125. Adjustment of dialysate VEGF for effluent CA125 revealed a significant association with EMT. It suggests that fibroblastoid transition from HPMCs could be affected by the intraperitoneal VEGF per unit mass of HPMCs.
Perit Dial Int 2008 Jun
PMID:The association between the vascular endothelial growth factor-to-cancer antigen 125 ratio in peritoneal dialysis effluent and the epithelial-to-mesenchymal transition in continuous ambulatory peritoneal dialysis. 1855 37

Ultrafiltration failure (UFF) continues to be a major complication of peritoneal dialysis (PD), particularly long-term PD. Continuous exposure to bioincompatible PD solutions causes inflammation of the peritoneal membrane, which progressively undergoes fibrosis and angiogenesis and, ultimately, UFF. There is emerging evidence that epithelial-mesenchymal transition (EMT) of peritoneal mesothelial cells (MCs) may play an important role in the failure of peritoneal membrane function. Submesothelial myofibroblasts originating from MCs through EMT and from activated resident fibroblasts participate in inflammatory responses, extracellular matrix accumulation, and angiogenesis. High glucose and glucose degradation products from PD solutions are responsible for production of transforming growth factor beta (TGFbeta) and vascular endothelial growth factor (VEGF) by MCs, which induce EMT. Leptin and receptor for advanced glycation end-products (AGEs) augment myofibroblastic conversion through the TGFbeta signaling system. A reduction in osmotic conductance in addition to increased solute transport causes UFF. This situation may be caused by loss of aquaporin (AQP) function and formation of the submesothelial fibrotic layer. During PD, AQP1 plays an essential role in water permeability and ultrafiltration (UF), modulating processes such as endothelial permeability and angiogenesis. During a hypertonic dwell, AQP1 mediates 50% of UF. Insufficient AQP1 function may be causative for inadequate UFF. A significant amount of evidence from animal studies now exists to show that mast cells communicate with fibroblasts and are implicated in fibrogenesis, angiogenesis, and UFF. However, it is not confirmed in human studies that mast cells contribute to the fibrosis seen in the peritoneum of PD patients. The patterns of UFF in PD patients depend on duration of treatment. Inherently high small-solute transport status is associated with hypoalbuminemia and a greater comorbidity index. However, most of the variability in peritoneal transport remains unexplained, pointing to the potential role of genetic factors. Gene polymorphisms associated with peritoneal membrane transport have been identified. Recent studies have shown that VEGF, interleukin-6, endothelial NO synthase, AGE receptor, and RAS gene polymorphisms are associated with transport properties in PD patients. Current insights into the mechanisms of UFF will provide rationales for new therapeutic strategies.
Perit Dial Int 2009 Feb
PMID:Update on mechanisms of ultrafiltration failure. 1927 Feb

Encapsulating peritoneal sclerosis (EPS) is an intestinal obstruction syndrome in which peritoneal deterioration and intraperitoneal inflammation result in intestinal adhesions, which are covered with a fibrin capsule and which cause bowel obstruction. Here, we report the case of a patient with EPS suspected to result from the use of icodextrin peritoneal solution. In this patient, peritoneal permeability to high molecular weight solutes and effluent interleukin-6 (IL-6) levels increased after initiation on-to icodextrin solution. The patient developed symptoms of intestinal obstruction accompanied by intestinal edema 30 months after the start of icodextrin and after a peritoneal dialysis (PD) duration of 78 months. He was then diagnosed as being in a pre-EPS state. The use of icodextrin solution was discontinued, and the symptoms of intestinal obstruction improved after corticosteroid administration. Subsequently, he was managed on a combination of PD using glucose solution low in glucose degradation products and of twice-weekly hemodialysis, but he showed enhanced peritoneal permeability and increases in effluent IL-6. After a PD period of 98 months, severe symptoms of intestinal obstruction developed, and enterolysis was performed. The degeneration of the intestinal wall itself was slight, and the adhesions between the capsule and intestinal surface could be readily removed. In this patient, the degree of peritoneal deterioration and capsule formation differed from that of typical EPS. These findings suggest the promotion of capsule formation by icodextrin solution and the involvement of certain inflammatory reactions.
Adv Perit Dial 2009
PMID:A case of encapsulating peritoneal sclerosis suspected to result from the use of icodextrin peritoneal solution. 1988 16

Levels of fibroblast growth factor (FGF) 23, a phosphatonin, are frequently elevated in patients with end-stage renal disease (ESRD) who are on maintenance hemodialysis (MHD). However, the role of FGF23 remains unclear because renal FGF receptor function might be impaired. The present cross-sectional study examines a cohort of patients (n = 196) on MHD who were not undergoing therapy with lipid-lowering drugs including sevelamer. Non-fasting venous blood samples were withdrawn before the hemodialysis (HD) session on the third day after the previous HD session to measure serum levels of albumin, calcium (Ca), phosphate (P), alkaline phosphatase, intact parathyroid hormone (PTH), total cholesterol (C), high-density lipoprotein (HDL)-C, low-density lipoprotein(LDL)-C, oxidative LDL-C, high-sensitivity C-reactive protein (HsCRP), interleukin-6 (IL-6), and FGF23. Nutritional status was assessed using the geriatric nutritional risk index (GNRI). Carotid intima-medial thickness (CIMT) was assessed using a B-mode ultrasound scanner. FGF23 was positively correlated with P, Ca(alb)xP product, and intact PTH, and inversely correlated with C and non-HDL-C. In the higher FGF23 tertile, levels of both non-HDL-C and C were significantly decreased and CIMT was less elevated compared to the lower FGF23 tertile. Multivariate analysis showed that the higher FGF23 tertile was independently associated with decreases in C (adjusted r(2) = 0.14) and non-HDL-C (adjusted r(2) = 0.20) levels and with a less-pronounced increase in CIMT (adjusted r(2) = 0.14). High FGF23 appears to be an independent biomarker of a decrease in C and non-HDL-C that is negatively associated with atherosclerosis in patients on MHD.
Ther Apher Dial 2010 Jun
PMID:Impact of fibroblast growth factor 23 on lipids and atherosclerosis in hemodialysis patients. 2060 85


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