Real time ultrasound for venous catheter placement.
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Biomedical subjects
Publications and source records attributed to D Brancaccio.
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BACKGROUND: Phosphate-induced hyperparathyroidism still represents an intriguing problem in dialysis patients. Postprandial hyperphosphataemia is considered to be the main stimulus to parathyroid hyperfunction, and therefore many efforts have focused on the use of phosphate binders to prevent phosphate absorption. METHODS: We investigated whether the pH-mediated gastric ionization of calcium phosphate dietary salts is necessary for its intestinal absorption. In eight normal subjects we measured 24-h urinary calcium phosphate excretion and the postprandial blood calcium phosphate profile after a meal containing 1 g of calcium and 2 g of phosphate salts in a crossover placebo-omeprazole study. On two occasions the subjects received either placebo or omeprazole 60 mg/day 2 days before and during the day test. RESULTS: Serum gastrin levels were measured as an indicator of achlorhydria and were 13.7 +/- 1 pg/ml after placebo and 30.4 +/- 4.7 after omeprazole (P < 0.003). Postprandial plasma phosphate profiles were not significantly different between the two studies (+36 +/- 8% after placebo and +24 +/- 8% after omeprazole, NS), while plasma calcium increased by +6.1 +/- 1% after placebo and decreased by -4.2 +/- 0.7% after omeprazole (P < 0.01). The 24-h urinary phosphate excretion was 1068 +/- 85 mg after placebo and 773 +/- 55 after omeprazole (P < 0.002), while the 24-h urinary calcium excretion was 360 +/- 21 after placebo and 238 +/- 15 after omeprazole (P < 0.0001). A negative relationship was observed between absolute changes in plasma gastrin and those in urinary calcium (P < 0.009) and phosphate (P < 0.05). CONCLUSIONS: The inhibition of gastric acid secretion by omeprazole significantly reduces both urinary phosphate and calcium excretion after an oral load. The behaviour of the postprandial calcium-phosphate plasma profile suggests that gastric acid inhibition is more effective in reducing calcium rather than phosphate dietary salts absorption in normal subjects.
Ten years after the pioneering data by Slatopolsky, there is growing evidence that calcitriol given intravenously is able to improve secondary hyperparathyroidism better than the traditional daily oral administration. However, the scenario is changing again after the observation that oral bolus therapy, in equivalent doses to the intravenous route, is also able to effectively control parathyroid hormone secretion. This review reports and comments on the most recent controlled and uncontrolled observations dealing with calcitriol therapy of hyperparathyroidism in patients with uremia. There are currently no convincing data about the superiority of one route of administration over the other, although intravenous boluses appear to be more attractive both from a theoretical (higher plasma levels and reduced action on intestinal receptors) and practical (compliance) point of view. The higher cost of the injectable drug is the crucial factor limiting its wider clinical use. Large and carefully designed controlled clinical trials are still awaited to elucidate the most important aspects of calcitriol treatment of secondary hyperparathyroidism, such as dose, interval, and route of administration.
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We studied with US both the knees of 32 long-term dialysis patients (mean dialysis age: 69.7 months), 7 of whom exhibited palpable joint swelling. In 29/32 patients, US scans were combined with knee X-ray films, patellar views included. In one case, opaque arthrography was performed too. US demonstrated the presence of fluid collections within both joint space and synovial cavities in 19/32 patients (59%). Their content was transonic or mildly hypoechoic. X-ray films were positive for amyloid bone involvement in 19/29 cases (66%), with evidence of intra-osseous cysts and cortical erosions. There was a good general agreement between the results obtained with the two techniques: therefore, in some cases only one examination was positive. Needle aspiration of synovial fluid was performed in 18/32 patients (56%). The 2 cases of diffusely hypoechoic collections yielded very dense jelly material, that was highly positive for beta-2-microglobulin. US is proposed, combined with conventional X-ray films, as a simple and reliable method for the diagnosis of articular amyloidosis in dialysis patients and for the follow-up of this disease.
Intravenous calcitriol is known to directly suppress PTH secretion and release. We evaluated the effect of four months of treatment with low-dose intravenous calcitriol on PTH levels in 83 hemodialysis patients. The criteria for including patients in the study were a serum PTH levels at least four times the normal limit, a serum total calcium less than 10 mg/dl and good control of the serum phosphorus level. All patients underwent standard bicarbonate or acetate dialysis; dialysate calcium level was maintained at the usual 3.5 mEq/liter concentration. Initial calcitriol dose was 0.87 +/- 0.02 (SEM) micrograms (0.015 micrograms/kg body wt) thrice weekly at the end of dialysis, and it was reduced in case of hypercalcemia or elevated calcium-phosphate product. Seven out of 83 patients dropped out during treatment. Among the 76 patients who completed the study, 58 (76%) showed a highly significant decrease of intact PTH levels (average reduction 48%) and of alkaline phosphatase levels after four months of therapy. Total serum calcium increased slightly but significantly in the responder group but remained unchanged in the non-responders. No significant changes in ionized calcium levels could be detected, even in responders. Treatment was well tolerated by patients, but 60% of them had transient episodes of hyperphosphatemia. Mean serum phosphate was 4.95 mg/dl at the beginning of the study. It increased significantly after four months of treatment in patients who showed a decrease of PTH levels, although it remained within acceptable limits, below 5.5 mg/dl. Twenty-eight of 76 patients (37%) reduced the dose of calcitriol because their calcium-phosphate products exceeded 60.(ABSTRACT TRUNCATED AT 250 WORDS)
Forty-four elements (Al, Sb, As, Ba, Be, B, Br, Cd, Ce, Co, Cr, Cs, Cu, Eu, Ga, Au, Hf, In, Ir, Fe, La, Lu, Mn, Hg, Mo, Nd, Ni, Pb, Rb, Sm, Sc, Se, Ag, Sr, Ta, Tb, Tl, Th, Sn, W, U, V, Zn, Zr) have been determined in the dialysate for hemodialysis (HD) and fluids for hemofiltration (HF) and continuous ambulatory peritoneal dialysis (CAPD). Multiple determinations have been performed for each dialysis fluid. Several trace elements (TE) showed remarkably elevated average levels; moreover, different bathes of the same commercial product may present a wide variability in TE concentration. The data point out the pivotal role of dialysis fluids in contributing to TE imbalance in dialysis patients and allow the assessment of the potential element exposure of patients on regular dialytic treatment. Patients on HD treatment would be exposed on a weekly basis to milligrams of Al, B, Ba, Br, Cu, Fe, Ni, Pb, Rb, Sr and Zn; on HF, the highest exposures are due to Al, B, Br, Fe, Pb and Zn; on CAPD to B, Br, Fe and Zn. The weekly exposure for several TE appears to be 50- to 12,000-fold higher than the corresponding values on the amount absorbed via the diet (HD: Au, Ba, Be, Ce, Ga, La, Sc, Ta, Th, V, Zr; HF: Be, Ce, Ta, Th, V, Zr; CAPD: Au, Be, Ce, Ga, V, Zr).(ABSTRACT TRUNCATED AT 250 WORDS)
An 85 KDa protein was purified by a multistep procedure (ultracentrifugation, HPLC, SDS-PAGE) from sera and amyloid deposits of patients on chronic hemodialysis and was characterized as a novel protein on the basis of its NH2 terminus (KVQLVE-V). This protein was formed by two subunits with Mr of 55 and 30 KDa and had affinity for Thyoflavin T, a fluorescent dye which was employed for labelling the protein prior HPLC. The 85 KDa was the only fluorescent component of ultracentrifugates from the serum of hemodialyzed patients while in amyloid fibrils it coexisted in roughly equimolar amounts with beta 2-microglobulin. This new high molecular weight protein which accumulates in uremia, could be co-responsible with beta 2-microglobulin for hemodialysis-related osteoarticular amyloidosis.
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Neurological derangement has been reported in haemodialysed patients receiving intravenous desferrioxamine (DFO) for aluminium-related disorders. The possible direct effects of desferrioxamine on EEG recordings were investigated in ten haemodialysed patients who underwent a DFO test 2 h after the end of dialysis. According to a commonly accepted protocol, 40 mg/kg body-weight of desferrioxamine was infused in 60 min. EEG recording was continuously performed, starting 30 min before and stopping 30 min after the desferrioxamine infusion. Besides visual inspection, EEG records were digitised, tapered, and spectrally analysed with Digital PDP 11/73 microcomputer. Basal EEG recording was normal in all patients. In three patients a progressive EEG slowing was detected by visual inspection during desferrioxamine infusion; in these cases automatic analysis revealed a 50% increase in power of slower frequencies 30 min after starting the infusion, when no changes in plasma aluminium concentrations are detected; a complete recovery was observed 30 min after desferrioxamine withdrawal. In one patient bilateral paroxysms of slow waves appeared, so we stopped desferrioxamine infusion. Two of the three patients who developed EEG abnormalities also had an increased aluminium body burden (positive DFO test). Results indicated that desferrioxamine per se can modify EEG in haemodialysis patients and that its effect is not mediated by acute increases of plasma aluminium concentrations. The finding of a positive DFO test in two of three patients with EEG changes may suggest that an aluminium-induced blood-brain barrier derangement could have played a role. However, prompt recovery after ceasing desferrioxamine infusion strongly suggests a direct role of desferrioxamine in the induction of EEG changes.(ABSTRACT TRUNCATED AT 250 WORDS)
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Amyloid arthropathy is an important complication of long-term hemodialysis. This condition may lead to destructive bone lesions and to severe functional impairment. We studied with sonography of both knees 32 long-term dialysis patients (mean dialytic age: 69.7 months), whose 7 were carrying palpable joint swellings. In 29/32 patients, ultrasound scans were associated with knee X-rays films, patellar views included. In one case, opaque arthrography was performed too. Sonography demonstrated the presence of fluid collections within the articular space and the synovial cavities in 19/32 patients (59%). Their content was transonic or mildly hypoechoic. X-ray films were positive for amyloid bone involvement in 19/29 cases (66%), with intra-osseous cysts and cortical erosions. There was a good general agreement between the results obtained with the two techniques: therefore, in some cases only one examination was positive. Sonography is proposed, in association with standard X-ray films, as a simple and reliable method for the diagnosis of articular amyloidosis in dialysis patients and for the follow-up of this disease.
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Thirty-nine trace metals were determined by neutron activation analysis (NAA) in nine salts (glucose, NaCl, KCl, CaCl2, MgCl2, Na-lactate, Na-acetate, NaHCO3 and NaOH), from different European producers, used in the preparation of dialysis fluids. Metal concentrations vary widely from less than 1 ng g-1 to several micrograms per gram. The data are used to assess the potential metal contribution of the salts to a hypothetical dialysis fluid. A comparison of these calculations with NAA of commercial haemodialysis solutions, and water used for their preparation, suggests that salts are the main source of metal contamination of the dialysate. Despite this, the chemical purity of the salts analyzed is considered to be good and it would be unrealistic to expect a clearly better chemical quality on a commercial scale. In order to protect the health of dialysis patients against abnormal metal exposure, toxicological research directed towards the estimation of the effective daily metal exposure and the determination of possible metal overloads in dialysis patients is necessary. A standardization of the dialysis systems actually used is also an important aspect if uncontrolled metal contamination of the dialysis fluid is to be avoided.
Substitution of calcium carbonate for aluminum hydroxide in patients on dialysis: effects on acidosis, parathyroid function, and calcemia. We studied the effects of substituting CaCO3 for aluminum-containing gels on metabolic acidosis and on the response of the parathyroid glands in 11 patients treated with chronic hemodialysis. The 8 men and 3 women were clinically stable, were known to be compliant, and had no clinical evidence of aluminum overload; they were not receiving vitamin D supplements; and they had been on dialysis for an average of 65.6 months (range: 13-188 months). After 3 weeks of CaCO3 administration plasma phosphate concentration remained well controlled, and plasma calcium concentration increased from 9.2 +/- 0.2 (2.3 +/- 0.1 mmol/l) to 10.1 +/- 0.2 mg/dl (2.5 +/- 0.1 mmol/l). Predialysis plasma bicarbonate concentration increased from 19.7 +/- 0.6 to 21.9 +/- 0.6 mmol/l. Plasma aluminum concentration decreased from 78.7 +/- 12.5 to 48.5 +/- 3.9 micrograms/l. Plasma PTH level increased from 2.0 +/- 0.7 to 3.3 +/- 0.8 ng/ml despite the concurrent increase in plasma calcium levels. All values returned to control levels following discontinuation of CaCO3 and resumption of aluminum gels. We conclude: (1) In addition to controlling hyperphosphatemia and increasing plasma calcium concentration, CaCO3 ameliorates metabolic acidosis. (2) Avoidance of oral aluminum intake is followed by prompt lowering of plasma aluminum levels. (3) PTH levels paradoxically increase despite the increment in plasma calcium concentration. The hypercalcemia seen with CaCO3 administration may be due, in part, to transient parathyroid hypersecretion that develops when aluminum administration is discontinued.