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Biomedical subjects

M Taccone-Gallucci

Publications and source records attributed to M Taccone-Gallucci.

49 records · Page 3Linked to original sources
PubMed1982

Evaluation of acid-base balance and pO2 with acetate dialysis in non-uremic patients.

The aim of our work was to evaluate the immediate effects of acetate-dialysis in patients with normal renal and respiratory function. For this purpose pH, pO2, pCO2 and HCO3- were monitored in arterial blood before dialysis, after 60, 120, 180 mns and at the end of each treatment in two groups of patients on chronic hemodialysis, a first group of schizophrenic patients and a second group of uremic patients. In the first group of patients the predialytic values were in the normal range. After hemodialysis HCO3- and pCO2 significantly decreased, both these changes were associated with a stable pH. The pO2 significantly decreased after 60 mns of dialysis. At the end of dialysis the pO2 increased without significant variation compared to predialytic values. In conclusion in non-uremic hemodialysis patients metabolic acidosis due to the loss of bicarbonate through the membrane is compensated by respiratory alkalosis. This respiratory alkalosis is not due to hypoventilation secondary to respiratory centre inhibition, but is mainly due to the pCO2 loss through the dialysis membranes.

Acetates↗
PubMed1981

[Bone histomorphometry: methodological criteria in the study of metabolic skeletal diseases].

The present study deals with the appropriate statistical approach to the histomorphometric technique carried out on bone tissue with the Merz and Schenk integrating eyepiece. Statistical analysis of the results obtained from ten bone biopsies of renal osteodystrophic patients enabled to calculate the values of standard errors for each histomorphometric parameter as a function of measured histological fields. The examination of 42 fields chosen at random on histological sections from different sites of the bone biopsy guarantees sufficiently low standard error values. This technique is of invaluable help in the study of metabolic bone diseases, and extremely useful in the evaluation of treatment trials in renal osteodystrophy.

Biopsy↗
PubMed1979

25-hydroxycholecalciferol in the treatment of renal osteodystrophy in haemodialysed patients.

The effects of 25-OHD3 on renal osteodystrophy have been studied in 6 patients on maintenance haemodialysis. Administration of 25-OHD3, 50 microgram/day, did not improve biochemical data and intestinal absorption of calcium. With a dose of 100 microgram/day in all patients an increase in blood calcium levels eventually reaching hypercalcemic values was observed. In two cases a fall in alkaline phosphatase toward normal values was noted. In the same cases the treatment-induced hyperphosphatemia, uncontrolled by AI(OH)3 supplementation and similarly high iPTH levels were observed. In two cases repeated bone biopsy following 8 months treatment and not show substantial improvement of bone lesions. In one case addition of 1,25-(OH)2D3 to the treatment with 25-OHD3 led to a more rapid improvement in biochemical parameters and iPTH serum levels. Doses of 25-OHD3 capable to correct blood calcium levels and intestinal absorption of calcium, may have minimal benefit on the osteitis fibrosa component of the bone lesion.

Adolescent↗
PubMedDate not supplied

Dialysis leukopenia and hypoxemia in a patient without measurable complement activity.

We have studied complement activity, total leukocyte counts, PO2 and acid-base balance during a single hemodialysis with cuprophan membranes in a patient with hereditary angioedema and C3NeF-positive chronic membranoproliferative glomerulonephritis. Before, during and after the dialytic procedure plasma complement activity (total hemolytic complement, classical and alternative pathway activities) was not detectable and no C3-conversion occurred, while profound leukopenia (from 8,500 to 1,800 leukocytes/microliter) and hypoxemia (from 101.8 to 86 mmHg PO2) were found within 20 min from the initiation of hemodialysis. Similar results were obtained by studying the same parameters during two additional hemodialytic procedures. In vitro experiments showed that the patient's C3 could not be converted, either by cuprophan or zymosan, a specific and potent complement activator, even under optimal experimental conditions. Our data demonstrate that complement activation is not the only possible mechanism responsible for early leukopenia (as well as hypoxemia) during dialysis with cuprophan membranes.

Acid-Base Equilibrium↗
PubMedDate not supplied

Disappearance of oxidative damage to red blood cell membranes in uremic patients following renal transplant.

Hemodialysis patients display increased oxidative damage to red blood cell (RBC) membranes, characterized by elevated levels of malonyldialdehyde (MDA), a short chain aldehyde produced by the oxidation of the polyunsaturated fatty acids (PUFA) in the RBC membranes. This is the result of a metabolic blockage of the pentose-phosphate shunt in uremic patients, which causes reduced detoxification of highly oxidative free radicals. The oxidative damage induces increased RBC rigidity and decreased RBC deformability, therefore favoring hemolysis. The aim of this work was to determine if a functioning renal graft would restore normal erythrocyte metabolism, reducing the oxidative damage. To this end, we have determined RBC MDA concentrations in 20 hemodialysis (HD) patients (RBC MDA 18.22 +/- 4.36 micrograms/ml packed RBC), 20 renal transplant (T) patients with well functioning grafts (serum creatinine less than 2 mg%) (RBC MDA 1.2 +/- 0.4 micrograms/ml packed RBC) (T vs. HD P less than 0.005) and 20 healthy controls (HC) (RBC MDA 1.44 +/- 0.6 micrograms/ml packed RBC) (HC vs. HD P less than 0.005; HC vs. T NS). Our findings show that a well-functioning renal graft restores normal RBC metabolism and eliminates the oxidative damage induced by uremia.

Adolescent↗
PubMedDate not supplied

Administration of GSH has no influence on the RBC membrane: oxidative damage to patients on hemodialysis.

In patients on hemodialysis, a metabolic block of the pentose phosphate shunt has been described that impairs the reduction of oxidized glutathione. The block results in lack of detoxication of the free hydroxyl radicals produced inside the red blood cell (RBC) and causes oxidative damage to the polyunsaturated fatty acids of the RBC membrane that results in formation of aldehydes. Malonyldialdehyde has been used as an index of the oxidative damage. In a study group of 13 patients on hemodialysis, the authors have tested whether administering reduced glutathione (GSH) at 1200 mg/day for 1 month could minimize oxidative damage to the RBC membranes and improve the hematologic parameters. Treatment with GSH was followed by significant improvement of hematocrit (P = 0.008), hemoglobin (P = 0.03), and RBC count (P = 0.0037); however, oxidative damage to the membranes was increased (P = 0.0004), which suggests that improvement of the hematologic parameters is not related to reduction of the oxidative damage. This is because oxidized glutathione, formed in the oxidative process, cannot be reduced back to GSH because of alteration of the pentose phosphate shunt.

Adult↗
PubMedDate not supplied

Vitamin E supplementation and oxidative status of peripheral blood mononuclear cells and lymphocyte subsets in hemodialysis patients.

Increased oxidative damage to cell membrane constituents causes profound changes in the membrane cytoarchitecture and modifications of the membrane physiological properties, e.g., the ability to respond to hormonal stimuli. In uremic patients receiving intermittent hemodialysis, a metabolic block of the phosphate pentose shunt has been described. This leads to insufficient detoxication of the hydroxyl radicals formed within the cells and therefore to increased oxidative damage to the polyunsaturated fatty acid constituents of the cell membranes. Vitamin E is known to reduce this oxidative damage and its harmful effects. We studied vitamin E (alpha-tocopherol acetate) administration in 10 chronically uremic patients receiving intermittent hemodialysis for positive effects on cell membrane-receptor response. The patients were studied before and after treatment for the extent of oxidative damage in peripheral mononuclear cells and for response to monoclonal antibodies to specific markers of T-lymphocyte subsets. After vitamin E treatment, oxidative damage decreased, and the membranes of peripheral mononuclear cells contained greater amounts of some unsaturated fatty acids. This is in agreement with a modification of the membrane phenotype markers of T-lymphocyte subsets and seems to confirm in vivo that changes in membrane structure first induced by increased oxidative damage due to the blockage of the phosphate pentose shunt can be reduced by the antioxidant action of vitamin E, which significantly influences the expression of membrane determinants.

Adult↗
PubMedDate not supplied

[Evaluation of cognitive functions in patients with chronic renal insufficiency].

Fifteen undialyzed and thirteen dialyzed patients affected by chronic renal failure were studied by means of an extensive neuropsychological battery with the aim of assessing the incidence of a deterioration of cognitive functions. Mean performances scores obtained by the two groups of patients were compared with analogous scores obtained by a group of control subjects similar as for literacy and age. The comparisons among the three groups did not reveal any difference as for performance scores obtained to various tasks nor for the global assessment derived for the entire battery. Furthermore our data do not point out any significative correlation between global performances on neuropsychological battery and blood levels of creatinine and urea nitrogen or duration of dialytic treatment of renal subjects. In conclusion, the results of our study do not show evidence of cognitive impairment in subjects affected by chronic renal failure and do not confirm the hypothesis of a detrimental effect of prolonged periods of dialytic treatment on cognitive functions.

Blood Urea Nitrogen↗
PubMedDate not supplied

Haematological changes induced by direct contact over a coated activated charcoal: in vivo and in vitro study.

In evaluating biocompatibility, haematological changes induced by ACCM in vivo and in vitro were studied. Twenty minutes after the start of haemoperfusion a significant fall in white blood cell number was found. After 60 minutes the leucopenia still occurred. In a previous work we suggested that complement activation is at least one of the possible mechanisms responsible for these phenomena. Moreover, our data showed a significant decrease in platelet number after 60 minutes of haemoperfusion. During the in vitro study, we found, using citrated blood, a significant correlation between aggregation response to ADP and collagen, either at different ACCM doses or at various periods of incubation. Our results suggest that the fall in platelets is due to platelet aggregation. The haemocoagulation study may have clinical importance in high-risk patients when haemoperfusion is required.

Adenosine Diphosphate↗