[Destructive spondylodiskopathy in beta 2 microglobulin-induced amyloidosis].
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Biomedical subjects
Publications and source records attributed to J Passlick.
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After six years of home haemodialysis and two years of continuous ambulatory peritoneal dialysis a 59-year-old woman developed an aluminium-induced osteopathy, myopathy and normochromic anaemia. She was at first treated with intravenous, then peritoneal, deferoxamine, 1 g every other day. Before treatment, 15.8 micrograms aluminium (Al) had been eliminated daily, with a peritoneal clearance of 0.3 ml/min; after intravenous deferoxamine a mean of 774.3 +/- 102.3 micrograms Al was eliminated per day, after peritoneal deferoxamine 646.7 +/- 89.6 micrograms of Al per day, with a peritoneal clearance of 2.2 +/- 0.9 (intravenous) and 1.9 +/- 0.7 ml/min (intraperitoneal). After four months of deferoxamine administration, mostly intraperitoneally as an out-patient, the osteomalacia clearly improved, as did the myopathy and anaemia.
Aluminum concentrations in the dialysate and serum of 14 patients on CAPD were measured every six months. Additionally, in ten of the patients Al elimination was measured after a bolus ingestion of 1800 mg aluminium-chloride-hydroxide-complex. There was no significant difference between serum Al concentrations initially (47.3 +/- 8.2 micrograms/l), at six months (55.4 +/- 9.5 micrograms/l), and after 12 months (44.3 +/- 10.1 micrograms/l) although the Al concentration in the dialysate had been decreased from 16.6 +/- 2.3 micrograms/l to 1.5 +/- 0.2 in the last six months. The Al concentrations in the effluent dialysate were 14.5 +/- 1.3 micrograms/l initially, 15.6 +/- 1.2 micrograms/l after six months and 11.9 +/- 2.6 micrograms/l after 12 months. During kinetic studies a constant rise of serum Al concentration was found until the fifth hour, from 29.9 +/- 2.5 to 42.5 +/- 4.0, and a decline after 24 hours to 32.4 +/- 3.0 micrograms/l. The quantity of Al eliminated was 41.1 +/- 8.7 micrograms/24 h, equivalent to 1.2% of the ingested dose. In patients with residual renal function, renal Al clearance was almost double the peritoneal one. These results indicate that Al elimination by CAPD is not efficient and ingestion of Al-containing phosphate binders can result in Al accumulation.
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1. Aluminium concentrations were measured in hair, plasma and bone samples from different groups of chronic renal insufficient patients and from a control group (75 healthy volunteers plus 21 deceased subjects). A cross-sectional study with 40 haemodialysis patients and two longitudinal studies were undertaken, the first comprising of 12 home haemodialysis patients and the second 16 patients undergoing continuous ambulatory peritoneal dialysis (CAPD). 2. Before introduction of water treatment by reverse osmosis, the hair aluminium levels of home haemodialysis patients were elevated compared to controls. Aluminium in the hair of all other groups were within the normal range. Hair aluminium levels were not related to the daily aluminium intake, nor to the cumulative aluminium intake, nor to bone and plasma aluminium concentrations. 3. Plasma aluminium concentrations in all patients were higher than in the controls. Dialysis without reverse osmosis water treatment increased aluminium plasma levels. After installation of reverse osmosis units there was a decrease in the aluminium concentrations in plasma. In CAPD patients insignificant increases in the aluminium levels in plasma were observed. When low contaminated dialysis fluid was available the plasma aluminium concentrations returned to the initial level. 4. Aluminium concentrations in bone were increased in renal insufficient patients compared with controls. Aluminium bone content increased with increasing cumulative aluminium intake by phosphate binding therapy. 5. Hair analysis is of very limited value for the diagnosis of aluminium exposure. Bone analysis is suitable for the assessment of the individual body burden.
To evaluate the pharmacokinetics of ofloxacin, a novel quinolone antibiotic, in patients with end-stage renal disease (ESRD) on continuous ambulatory peritoneal dialysis (CAPD), we investigated 6 patients in a single-dose study and 9 patients in a multiple-dose study, all without peritonitis. In the single-dose study, patients received 200 mg ofloxacin orally. Serum concentrations (Cmax) peaked at 3.1 +/- 0.3 mg/L (mean +/- SEM), 1.6 +/- 0.5 h after p.o. administration of the drug. Elimination half-life (t1/2) was 26.8 +/- 2.5 h. Peritoneal clearance accounted for 10% of the total body clearance. After 5-h dwell time, ofloxacin concentrations in the dialysate were 1.5 +/- 0.2 mg/L, which is above the MIC90 for most bacteria responsible for peritonitis in patients on CAPD. In the multiple dose study, 200 mg ofloxacin were administered twice, with a time interval of 12 h, followed by 200 mg for 9 days every morning. Mean trough serum levels were 2.6 +/- 1.0 mg/L, mean peak concentrations were 4.1 +/- 1.7 mg/L. Mean ofloxacin concentrations in the peritoneal effluent were 1.9 +/- 0.9 mg/L. It is concluded that an oral loading dose of 400 mg on the first day and a maintenance dose of 200 mg ofloxacin/day does not lead to significant accumulation, even though the elimination by the peritoneal route is only small. The proposed dosing regimen could be an adequate therapy of peritonitis and exit-site infections in patients on CAPD since levels reached in the dialysate effluent are bactericidal. The clinical usefulness in the treatment of peritonitis has to be proven in further studies.
Since dialysis solutions in CAPD are now nearly aluminum free, the only source for elevated aluminum levels are aluminum-containing phosphate binders. Elimination with CAPD is insufficient to prevent aluminum accumulation. Therefore, we investigated a phosphate binder consisting of calcium alginate, a natural polyuronic acid, containing 100 mg calcium/g substance in 14 patients on CAPD over a period of one year. The patients had previously been treated with aluminum-containing phosphate binders for a period of 24.3 +/- 21.3 months. During a period of 3 weeks before changing to the new phosphate binder the mean (+/- SD) serum phosphorus concentration was 1.8 +/- 0.4 mmol/l, while at the end of one year of treatment with calcium alginate the concentration was 1.6 +/- 0.4 mmol/l. In order to lower serum phosphorus to this level, it was necessary to increase the mean (+/- SD) amount of calcium alginate from 6.9 +/- 1.3 g per day at the beginning of the study to 8.3 +/- 2.1 g per day at the end. The mean (+/- SD) serum calcium concentration did not change throughout the study period. Serum levels of alkaline phosphatase, 1.25 (OH)2 vitamin D3, and intact parathyroid hormone did not change as well. The mean (+/- SD) serum aluminum level declined from 36.0 +/- 20 to 14.0 +/- 11.3 micrograms/l after 6 months (p less than 0.001). In conclusion, calcium alginate is a good alternative to aluminum-containing phosphate binders and to phosphate binders on a calcium base as it does not lead to hypercalcemia. It prevents aluminum intoxication and has no serious side effects.
Intestinal absorption of aluminum (Al) from the phosphate binder aluminum-hydroxide-chloride (PhosphonormR) and successive renal and peritoneal Al elimination were studied in 11 patients undergoing continuous ambulatory peritoneal dialysis (CAPD). Al was measured by atomic absorption spectrometry in serum, urine, and dialysis fluid. Al levels in serum of all patients increased in average from 28.6 micrograms/l immediately before to a peak level of 41.6 microgramsWl 4 h after intake of 342 mg Al. After 24 h serum Al (34.0 micrograms/l) was still increased. Elimination across the peritoneum increased from 5.6 micrograms Al during the first 4 h to peak levels of 12.9 micrograms between hour 8 and 12 and decreased to 8.1 micrograms during the last 12 h. The Al clearance of the peritoneum was 0.43 ml/min. In the 6 patients with residual diuresis the renal Al excretion was higher than the peritoneal removal (48.1 micrograms/24 h vs. 24.8 micrograms/24 h). The renal Al clearance amounted to 1.6 ml/min. Assuming a gastrointestinal absorption quotient of 0.1% it is concluded that Al removal by CAPD in patients receiving 342 mg Al/day is not sufficient to prevent Al accumulation. In patients with remaining diuresis, the renal Al elimination exceeds the Al removal by the peritoneum.
Treatment of diabetics with end-stage renal failure is still a hazard. We report on 33 insulin-dependent diabetic patients who were treated with CAPD over a period of up to 70 months. Seven of them have been transplanted. The evaluation of the clinical and biological parameters serum protein, phosphate, calcium, revealed acceptable values. Hemoglobin rose during the treatment period. Hypertension improved and medication was reduced. HbAlc levels were near normal with subcutaneous application of insulin. Peritonitis rate was 1/18 patient-months. Survival rate was comparable with other centers with 83% in the first and 62% in the second year. In 7 patients that have been transplanted no CAPD-related problems arose after transplantation. 6 of them are still doing well; one returned to CAPD because of graft failure. In conclusion, because of good control of hypertension, blood glucose and anemia and the avoidance of fluctuating volumes, we think CAPD to be the best method for diabetics awaiting transplantation and for those that cannot be transplanted.
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After suicidal ingestion of 9 g Propafenone, a 31-year-old woman showed unconsciousness, cerebral convulsions, respiratory depression, sinus arrest, ventricular tachycardia and recurrent atrioventricular block. The maximum Propafenone plasma level was 4,702 ng/ml. Only 67.2 mg of Propafenone were eliminated within 4 h of hemoperfusion. Successful therapy could be achieved by symptomatic intensive care treatment. Additionally, 2 X 25 ml of 20%-saline solution were infused. In this case no efficacy of hemoperfusion in the treatment of Propafenone intoxication could be documented.