IgG myeloma with closed tetrameric Bence Jones proteinemia.
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Biomedical subjects
Publications and source records attributed to C Dominguez.
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OBJECTIVE: Our goal was to compare sensitivity, specificity, and predictive values of glucose and cytokines [interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor (TNF)] in amniotic fluid (AF) to detect an AF-positive culture. METHODS: Amniocentesis was performed on 113 patients with preterm labour (PTL) and intact membranes. Fluid was cultured for aerobic and anaerobic bacteria, and for mycoplasmas. AF analysis included cytokines and glucose determinations. RESULTS: The prevalence of positive AF cultures was 11.5% (13/113). Anaerobic bacteria were isolated in 9 patients (69.2%). The glucose <16 mg/dl and cytokines values; IL-1 >640 pg/ml, IL-6 >55,000 pg/ml, IL-8 >1,000 pg/ml, TNF >672 pg/ml, were significantly correlated (P < 0.01) with AF culture result. Glucose had a sensitivity of 69.2% and a specificity of 96% for the prediction of positive AF culture. The sensitivity and specificity of the cytokines ranged from 61.5-53.4% and 79.8-8.99%, respectively. CONCLUSIONS: In the diagnosis of the AF-positive culture, glucose <16 mg/dl is more sensitive than cytokines.
Chlorhexidine (CLX) is the most widely used antiseptic for wound and skin disinfection. Despite its potent bactericidal action, skin irritation is observed when it is used topically. This study aimed to evaluate the mechanisms underlying CLX-induced toxicity on human dermal fibroblasts with special emphasis on factors that may mediate or counteract its undesirable effects. Cells were exposed to CLX concentrations of 0.00005-0.025% for 3, 6, 8 or 24 h in the absence or presence of different concentrations of foetal calf serum (FCS) (2, 5 and 10%). Depletion of cell ATP occurred, in a time- and concentration-dependent manner, in all experimental conditions at [CLX] >0.001%. At 24 h of CLX exposure time, the decrease in intracellular ATP was produced from a 10-times lower CLX concentration (0.0001%). Concentrations > or =0.02% produced total loss of ATP. However, cell survival was maintained after CLX treatment for 3 and 8 h and CLX concentrations > or =0.005% were required to produce total cell death. CLX exerted an inhibitory concentration-dependent effect on DNA synthesis from concentrations as low as 0.0001%. Only FCS at 10% appeared to have a cytoprotective action against CLX-induced cytotoxicity.
OBJECTIVE: To evaluate protein and caloric intake in peritoneal dialysis (PD) patients on an incremental dialysis schedule, in an attempt to discriminate the influence of residual renal function (RRF) on these nutritional parameters. DESIGN: Prospective observational study. PATIENTS: Nine patients who had significant RRF at the beginning of PD therapy, which permitted a schedule of incremental PD (i.e., the number of peritoneal exchanges was increased as the RRF fell) in order to maintain the sum of renal and peritoneal clearance (weekly Kt/V urea) at approximately 2. METHODS: The mean adequacy parameters (urine and peritoneal Kt/V urea and creatinine clearance) along with the mean dietary energy (DEI) and protein intake (DPI) estimated by 3-day diet histories, were determined 6 and 9 months after the beginning of PD, when patients had RRF (period 1), and 6 and 9 months after the loss of RRF (period 2). The mean data obtained in both periods were compared. The best determinants for the changes in DEI and DPI after the loss of RRF were also investigated. RESULTS: Mean total Kt/V urea was very similar in both periods (2.16+/-0.32 vs 2.15+/-0.18), although creatinine clearance decreased significantly after the loss of RRF (74.41+/-12.28 L/week/1.73 m2 vs 56.78+/-11.77 L/week/1.73 m2, p = 0.0001). Absolute and normalized DPI values for actual body weight decreased after the loss of RRF (68.21+/-11.87 g/kg vs 59.27+/-13.66 g/kg, p = 0.02; and 1.17+/-0.32 g/kg/day vs 0.97+/-0.32 g/kg/day, p = 0.01). Although the energy delivered by peritoneal glucose uptake increased significantly after the loss of RRF, the mean total energy intake (DEI plus peritoneal glucose uptake) was very similar in both periods (2141+/-339 kcal/day vs 2010+/-303 kcal/day, p = 0.13). However, the mean total energy intake normalized for actual body weight decreased significantly after the loss of RRF (37.5+/-10.1 kcal/kg/day vs 32.8+/-8.9 kcal/kg/day, p = 0.02). The changes in DEI and DPI between periods 1 and 2 correlated negatively with the difference of the energy delivered by peritoneal glucose uptake (r = 0.65, p = 0.05, and r = 0.88, p = 0.001, respectively). The magnitude of DPI changes between both periods correlated significantly with the magnitude of urinary Kt/V urea changes (r = 0.77, p = 0.01). However, there was no correlation between the changes in DPI and the changes in total Kt/V urea, total or renal creatinine clearance, or the length of time on PD. CONCLUSIONS: The loss of RRF led to a reduction in dietary caloric and protein intake. The magnitude of the reduction in the DPI was strongly correlated with the increase in the energy delivered by peritoneal glucose uptake and with the decrease in the urinary Kt/V urea, but not with the total Kt/V urea.
BACKGROUND: Hypoalbuminemia is common in peritoneal dialysis (PD) patients; but the reduction in serum albumin levels (SAlb) that should be expected in stable PD patients is less clear. OBJECTIVES: To determine prospectively, in a group of stable PD patients without comorbid conditions, the changes in SAlb concentration and in the concentrations of the other serum protein fractions. To investigate the best determinants of a significant decrease in SAlb levels. DESIGN: Prospective observational study. METHODS: Seventeen PD patients in stable clinical condition, with no signs of systemic inflammatory response, were included in the study. SAlb and the electrophoretic pattern of serum proteins were determined immediately before PD start, and after 6, 9, 12, 15, 18, 21, and 24 months on PD. In each study period, clinical characteristics, adequacy parameters, protein catabolic rate (PNPNA: protein equivalent of non protein nitrogen appearance), and protein losses were determined. Patients were divided into two subgroups according to whether SAlb decreased less than 10%, or 10% or more, from baseline values after 24 months on PD. The main differences between the subgroups were investigated. RESULTS: Mean SAlb did not decrease significantly after 24 months on PD (from baseline 3.99 +/- 0.46 g/dL to 3.80 +/- 0.54 g/dL), though percentage SAlb values did (58.36% +/- 5.58% vs 55.15% +/- 5.42%, p < 0.01). A weak increase in alpha2-globulin was observed after 18 months on PD (from 10.62% +/- 2.53% to 12.96% +/- 2.51%, p = 0.001). Alpha-globulin showed a sustained increase from a mean baseline value of 3.51% +/- 1.09% to 6.83% +/- 2.13% after 24 months (p < 0.0001). Seven patients had a reduction in SAlb greater than 10% after 24 months on PD. Kt/V urea and residual renal function tended to be lower in patients whose SAlb decreased. Mean PNPNA was significantly lower in patients who had a reduction in SAlb (0.76 +/- 0.12 g/kg/day vs 0.96 +/- 0.12 g/kg/day, p < 0.0001). However, total protein loss was even greater in patients who had no SAlb reduction. CONCLUSIONS: After 24 months on PD, a mean reduction in SAlb of 10%-15% from baseline values should be expected only in those stable patients whose PNPNA is low.
OBJECTIVE: To investigate the risk factors associated with the development of peritonitis caused by enteral bacteria in peritoneal dialysis patients, including the prescription of gastric acid inhibitors as a potential risk factor. DESIGN: Retrospective single-center study. SETTING: Tertiary university hospital. PATIENTS AND MAIN OUTCOME MEASURES: Fifty-five patients who entered into our continuous ambulatory peritoneal dialysis (CAPD) program during the last 6 years were included. Multiple logistic regression analysis was used to establish the best determinants over the development of at least one episode of enteric peritonitis. The predictive variables included in the model were: age, gender, diabetic versus nondiabetic, polycystic versus nonpolycystic kidney diseases, history of constipation, presence or absence of moderate/severe malnutrition, peritoneal transport characteristics, peritoneal protein losses, rate of exit-site infections, rate of total peritonitis, intestinal abnormalities, and treatment with inhibitors of gastric acid secretion. RESULTS: The total number of peritonitis episodes during the studied period was 88, which clustered in 34 of 55 patients. Fourteen (16%) were caused by enteric micro-organisms in 10 patients: Escherichia coli (6), Klebsiella sp (2), Enterobacter sp (1), and Enterococcus sp (5). Nine of 10 patients who developed enteric peritonitis were on gastric acid inhibitors (3 patients on omeprazole and 6 patients on H2-antagonists), while 15 of 45 patients who did not develop enteric peritonitis were on gastric acid inhibitors (all of them on H2-blockers). There were temporal relationships between the start of gastric acid inhibitors and the development of enteric peritonitis in 6 of 9 patients who were on this medication. Four of 10 patients who developed enteric peritonitis had diverticulosis. Ten of 45 patients who did not develop enteric peritonitis had been diagnosed with diverticulosis of the colon or sigmoid prior to entry to CAPD. The unique patient who was not on gastric acid inhibitors and developed enteric peritonitis, had been diagnosed with chronic atrophic gastritis with achlorhydria. By multiple logistic regression analysis, the treatment with gastric acid inhibitors was the only independent variable that entered into the best predictive equation over the development of enteric peritonitis (log likelihood ratio = -26.077, odds ratio = 18; 95% CI odds ratio: 2 - 155). CONCLUSION: Gastric acid inhibitors may increase the risk for developing enteric peritonitis in peritoneal dialysis patients.