[Treatment of severe acute iron poisoning].
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Biomedical subjects
Publications and source records attributed to M Friedberg.
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In a consecutive series of 38 patients with acute glomerulonephritis (GN), 17 showed serological or immunological signs of current or previous yersiniosis. None of these 17 patients had raised antistreptolysin-o titres. Only half of these patients had had clinical symptoms of Yersinia infection. Light microscopic examination revealed that 12 of the 17 patients had proliferative and 4 epimembranous GN. In 8 out of 14 biopsy specimens, Yersinia antigen could be demonstrated by immunoglobulins and complement. Immunofluorescence microscopy examination of all biopsy specimens containing sufficient tissue for a valid analysis showed deposits of complement and immunoglobulin G, most specimens also immunoglobulins A and M. It is considered highly likely that Y. ent. O:3 may be, and frequently is, an etiological factor for development of acute GN. It would be advisable not only to investigate all patients with acute GN for streptococcal infections, but also to carry out serological and bacteriological tests for Y. eng. O:3 infection and to institute an active therapeutic approach to acute infections caused by this bacterium.
Signs of damage to the glomerular basement membrane appearing as haematuria and proteinuria have been observed in 16 cases of proven acute yersiniosis. The infecting agent was Yersinia enterocolitica serotype O:3 in all. In a few cases a transient deterioration of the renal function was observed. The renal symptoms were not related to the acute febrile state, but seemed to appear about 14 days after the onset of yersiniosis and to be reversible in the observation period. Infection with other microorganisms known as nephritogenic was not found in spite of attempts to do so. Kidney biopsy was performed in one case and immunofluorescence microscopy showed deposits of immunoreactants. Based on these observations we suggest that acute glomerulonephritis can be included in the spectrum of complications of infection with Yersinia enterocolitica serotype O:3. The frequency of complicating glomerulonephritis in yersiniosis could not be estimated from this study.
The serum levels of 25-hydroxycholecalciferol (25-OHD3) and 1,25-dihydroxycholecalciferol[1,25-(OH)2D3] were measured simultaneously in nephrectomized patients on maintenance haemodialysis, in haemodialyzed patients with preserved kidneys who were receiving different vitamin D supplement, and in patients who had undergone renal transplantation. The results indicate that the production of 1,25-(OH)2D3 can be stimulated in patients with minimal residual renal excretory function by increasing the serum levels of 25-OHD3. Successful renal transplantation was followed by a rise in serum 1,25-(OH)2D3 concentrations.
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The frequency of wound infection was studied in 92 patients who had received cadaver kidneys. Wound drainage was performed in 26 patients and not performed in 66 patients. Wound infection was found in 31% of the wounds with drainage and in 14% of wounds without primary drainage. The results were compared with the frequency of 34% infected wounds in a previous report where wound drainage was performed routinely. It is advised that, when possible, wound drainage should be avoided.
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The relation between previous bloodtransfusions and renal allograft survival was studied retrospectively in 88 patients, who had been transplanted for the first time. The allograft survival rate was higher in the group who had received bloodtransfusion than in the group who had not. This difference was significantly greater when considering patients who had not previously been pregnant, e.g. patients without previous stimulation of the immuno system. The material shows no difference in allograft survival between previously transfused and non transfused patients, when considering age, sex or disease of kidney. In this retrospective study it is concluded that previous transfusions improved the prognosis of the transplantation. A prospective study has yet to be done, in order to enlighten the influence of various other factors on the allograft survival rate such as length of period or uraemia and of dialysis.
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In humans, oxoreducing 11beta-HSD-1 activity appears to be related to body fat distribution in male-type central obesity, but not in female-type peripheral obesity. We postulated that inhibition of 11beta-HSD-1 might have clinical therapeutic significance in oxoreducing mostly visceral fat and its metabolic activity. Our current study investigated the consequence at the cellular level of such inhibition. As an inhibitor of 11beta-HSD-1 activity, we used the licorice derivative carbenoxolone. Carbenoxolone has an inhibitory effect on the activity of both oxidizing 11beta-HSD-2, which converts cortisol to cortisone, and oxoreducing 11beta-HSD-1; yet, preadipocytes and adipocytes only express the latter. Preadipocytes were retrieved from omental and subcutaneous fat from healthy non-obese individuals and differentiated in vitro to mature adipocytes. Activity of 11beta-HSD-1 was assayed by measuring conversion of added 500 nM cortisone to cortisol. Expression of 11beta-HSD-1 mRNA was determined by real-time PCR, while lipolytic effects were determined by measuring glycerol and triglyceride concentration in the culture medium. Carbenoxolone decreased 11beta-HSD-1 activity in a dose-dependent manner with an IC-50 of 5X10 -6 M, but did not affect the expression of 11beta-HSD-1 mRNA. Cortisone stimulated subcutaneous, but not omental preadipocytes proliferation, an effect that was not abolished by carbenoxolone. Dexamethasone had a stimulatory effect on the maturation of both omental and subcutaneous preadipocytes. Carbenoxolone per se, either with or without cortisone, had a negative effect on preadipocyte maturation. Inhibiting 11beta-HSD-1 activity by carbenoxolone had no impact on leptin secretion. Thus, carbenoxolone has no effect on preadipocyte proliferation, but a dramatic inhibitory effect on preadipocyte differentiation into mature adipocytes. The mechanism is only partly related to its inhibitory effect on 11beta-HSD-1 activity. The present observations lend support to the presence of an intracrine loop of a hormone that is both produced from a precursor and active within the preadipocyte and adipocyte.
OBJECTIVE: The goals for maintenance dialysis treatment are to improve patient survival, reduce patient morbidity, and improve patient quality of life. This is the first randomized prospective study comparing automated peritoneal dialysis (APD) and continuous ambulatory peritoneal dialysis (CAPD) treatment with respect to quality of life and clinical outcomes in relation to therapy costs. DESIGN: A prospective, randomized multicenter study. SETTING: Three Danish CAPD units. PATIENTS: Thirty-four adequately dialyzed patients with high or high-average peritoneal transport characteristics were included in the study.Twenty-five patients completed the study. INTERVENTIONS: After randomization, 17 patients were allocated to APD treatment and 17 patients to CAPD treatment for a period of 6 months. Medical and biochemical parameters were evaluated at monthly controls in the CAPD units. Quality-of-life parameters were assessed at baseline and after 6 months by the self-administered short-form SF-36 generic health survey questionnaire supplemented with disease- and treatment-specific questions. Therapy costs were compared by evaluating dialysis-related expenses. MAIN OUTCOME MEASURES: Quality-of-life parameters, dialysis-related complications, dialysis-related expenses. RESULTS: The quality-of-life studies showed that significantly more time for work, family, and social activities was available to patients on APD compared to those on CAPD (p < 0.001). Although the difference was not significant, there was a tendency for less physical and emotional discomfort caused by dialysis fluid in the APD group. Sleep problems, on the other hand, tended to be more marked in the APD group. Any positive effect of APD compared to CAPD on dialysis-related hospital days or complication rates could not be confirmed. With larger patient samples, it is possible, however, that a significant difference might have been achieved. The running costs for APD treatment were US $75 per day and for CAPD treatment US $61 per day. CONCLUSION: If APD treatment can help to keep selected patients vocationally or socially active, paying the extra cost seems reasonable.