Biomedical subjects
Publications and source records attributed to R Wens.
Pseudomonas paucimobilis has rarely been reported as an opportunistic human pathogen. We report the isolation of this organism in two patients who developed peritonitis during the course of intermittent or continuous ambulatory peritoneal dialysis. The origin of the infection was related to contamination of the dialysate in the first patient but could not be determined in the second case.
We report one case of acute renal failure with oliguria, microscopic haematuria and normocytic anemia in a 86-year old Swedish woman. A full investigation led to the diagnosis of Goodpasture disease, an isolated form of Goodpasture syndrome. Goodpasture disease is and autoimmune disorder characterized by the development of autoantibodies to the NC1 domain of the alpha3 chain of type IV collagen, found mainly in glomerular basement membranes (GBM). When the disease affects both the lung and the kidney, it is called Goodpasture syndrome but the pulmonary or renal involvement can be isolated or separated in years. Its pathogenesis is not well known. It occurs essentially in Caucasian subjects, preferentially from Nordic and Anglo-Saxon countries (higher prevalence of HLA DR B1-15 and B1-4 group). Are also mentioned, the exposure to hydrocarbons, rustproof, insecticides and greasy solvents. The annual incidence of Goodpasture syndrome is rare and has been estimated in Europe to be about 0.5 to 1 case per million inhabitants. The isolated renal form represents about 1/3 of the cases. The clinical presentation is characterized by rapidly progressive renal failure with oliguria or anuria and in case of lung involvement, pulmonary hemorrhage responsible of hemoptysis, sometimes massive. Renal biopsy and immunofluorescence analysis play a key role in the diagnosis. The presence of both linear deposits of IgG along the glomerular basement membrane (GBM) and circulating anti-GBM antibodies is of paramount importance. The treatment, which depends on the degree of renal involvement, is based on the association of corticosteroids, cyclophosphamide and plasma exchanges.
Lymphocyte subpopulations were studied by immunofluorescence staining with monoclonal antibodies and laser flow cytometry in the blood of 23 hemodialysis patients before and after 3 months of treatment with recombinant human erythropoietin (rhEPO). Correction of anemia was accompanied by an increase in natural killer cells and a decrease in B lymphocytes. In the 11 patients (Group 1) with a baseline helper/suppressor (T4/T8) ratio greater than or equal to 2, the latter significantly decreased from 3.0 +/- 0.3 to 2.1 +/- 0.3 through both an increase in T8 cells and a decrease in T4 cells (p less than 0.005). Among the 12 patients with a pre-EPO T4/T8 ratio less than 2 (Group 2), no difference in T cell subsets was observed. The decrease in ferritin levels observed over the study period was not significant. In addition, the mean increase in hemoglobin levels during the first month of rhEPO therapy was greater in Group 2 than in Group 1 (1.1 +/- 0.3 vs. 0.6 +/- 0.3 g/dl, p less than 0.025). No change in any parameter was observed in eight control patients not receiving rhEPO. These results suggest that rhEPO can induce changes in lymphocyte subpopulations of hemodialysis patients through mechanism(s) yet to be clarified; conversely, the T4/T8 ratio might be a predictive factor for the erythropoietic response to rhEPO.
OBJECTIVE: Serious discrepancies between glycemia measurements obtained with an Accutrend Sensor (Boehringer Mannheim GmbH, Mannheim, Germany) type analyzer (based on a glucose dehydrogenase enzymatic reaction) and measurements obtained in the laboratory by a reference method (hexokinase) have been found in an insulin-requiring, diabetic, continuous ambulatory peritoneal dialysis (CAPD) patient treated with icodextrin 7.5% (Extraneal; Baxter Healthcare SA, Castlebar, Ireland), a new osmotic agent for peritoneal dialysis. We therefore investigated the respective role of the Analyzer and of the glucose polymer in this hitherto undescribed problem. DESIGN: Glycemia was measured simultaneously on venous blood using a reference laboratory technique, and on capillary blood using the Accutrend Sensor glucose analyzer in three groups of CAPD patients: 6 patients on Extraneal for at least 1 week, 6 patients receiving their first Extraneal exchange, and 8 patients never exposed to Extraneal. In the first group of patients, glycemia was also measured with another analyzer (Glucocard; Menarini Diagnostics, Firenze, Italy) using a different enzymatic reaction (glucose oxidase). In a separate study, whole blood of a normal subject was spiked with concentrated solutions of glucose and icodextrin and some of its metabolites (maltose, maltotriose, maltopentaose). Once again, comparative measurements of glycemia were performed with the Accutrend Sensor, with two other kits using a glucose dehydrogenase enzyme reaction, and with the hexokinase reference method. RESULTS: In 6 CAPD patients treated with once-daily exchanges with Extraneal for a minimum of 7 consecutive days, we confirmed overestimation of glycemia by the Accutrend Sensor of 65 +/- 26 mg/dL compared to reference values (p < 0.01), and of 69 +/- 25 mg/dL (p < 0.001) compared to measurements obtained with the Glucocard monitor. In 6 other CAPD patients studied at the end of one single icodextrin exchange, overestimation of 61 +/- 11 mg/dL was already present (p < 0.001). On the other hand, in 8 CAPD patients never treated with icodextrin, there was no discrepancy between the Accutrend Sensor readings and reference values. The measurements in spiked blood confirmed that only the Accutrend Sensor overestimates glycemia in the presence of maltose and glucose polymers. The overestimation decreased as the molecular size of the saccharides added to blood increased. There was no overestimation when other kits using a dehydrogenase enzyme were tested. CONCLUSION: The overestimation observed is probably related to the presence of oligosaccharides (mainly maltose), derivatives of glucose polymers present in Extraneal and absorbed via the peritoneal route, in the blood of patients treated with icodextrin. The glucose dehydrogenase characterizing the Accutrend Sensor, an enzyme of the pyrroloquinolinequinone class, very likely reacts with the free reducing group of the glucose molecule located at the end of each saccharide chain. This would not be the case for the Glucocard monitor using glucose oxidase, for other kits using glucose dehydrogenase, and for the reference method based on hexokinase. The Accutrend Sensor type of analyzers are therefore not suitable for regular monitoring of glycemia in diabetic PD patients treated with icodextrin.