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P Todeschini

Publications and source records attributed to P Todeschini.

11 recordsLinked to original sources
PubMed1996

ELISA anti-HLA antibody screening identifies non-complement-fixing antibodies responsible for acute graft rejection. A case report.

We report on a kidney transplant recipient experiencing an unexpected early acute vascular graft rejection. Retrospective analysis of patient serum samples, utilizing a new ELISA HLA screening technique, revealed that the rejection crisis and the subsequent graft loss were due to a pretransplant donor-specific pre-sensitization caused by a non-complement-fixing antibody of IgG2 class. The case illustrates the clinical significance of non-complement-fixing anti-HLA antibodies. In addition it is shown that ELISA methods are suitable for detecting potentially harmful donor pre-sensitization in waiting-list patients not detectable by standard lymphocytotoxicity techniques. Hence ELISA could be an alternative to flow cytometry for this purpose. It is concluded that screening and cross-matching techniques which detect non-complement-fixing anti-HLA antibodies could improve graft outcome, and should form part of the immunological monitoring of kidney transplant waiting-list patients.

Adult↗
PubMed1993

Strategies in renal failure and the impact of lipids.

The main points to note in terms of strategies in renal failure and the impact of lipids are: 1) Timing and typing of dyslipidemia; 2) Occurrence of dyslipidemia in the course of strategies (conservative, dialysis and transplantation); 3) How the strategies can handle the impact of lipids. Analysis of point 1 confirms what a complex profile uremic dyslipidemia presents, involving the type, class, composition and enzyme systems involved in lipid metabolism. In conservative and dialysis, type IV (triglycerides) predominates; in transplantation, type II (cholesterol). Examination of point 2 shows the non obligatory relationship between dyslipidemia and the various strategies of treatment. Lipid abnormalities, type IV or II, occur in 50-60% of patients. Uremic factors for dyslipidemia include: 1) enhanced hepatic stimulation or altered removal in conservative strategies; 2) the same causes plus "specific" promotors in dialysis (dialysis fluid, plasticizer leaching; bioincompatibility, etc.); 3) steroid therapy and other "accessories" in transplantation. A genetic predisposition is very likely present in all patients. Point 3, finally, analyzes the various "supplements" that each strategy requires to cope with the lipid impact. Generic rules (ranging from doing nothing, to diet, drugs, etc.) are of value in all strategies when dyslipidemia occurs. More specific rules include: a) Conservative strategies: appropriate dietetic optimization and modulation (protein-lipid-carbohydrate ratio in terms of calories); b) Dialysis: timing treatment and improving biocompatibility; c) Transplantation: reducing steroids as much as possible.

Humans↗
PubMed1990

Hormonal changes in hemodialysis.

When chronic renal failure becomes advanced, the serum or tissue levels and/or the functions of most hormones are altered because of several interplaying mechanisms involving synthesis, transport, accumulation of inhibitors, abnormality of target organ responsiveness, and impaired renal clearance. As regular dialysis treatment is performed, most of these uremic hormone abnormalities are not reversed, and some of them may even get worse. The main endocrine derangements can be grouped as sexual hormone dysfunction, thyroid abnormalities, growth retardation, hormone-related disorders of metabolism, derangements of pressor substances, gastrointestinal peptide abnormalities, renal osteodystrophy, and anemia. The endocrine abnormalities play a major role as for the clinical and metabolic rehabilitation of dialysis patients.

Endocrine System Diseases↗
PubMed1985

[In-hospital and long-term prognosis in acute myocardial infarction. Comparative longitudinal study of 2 patient groups].

The in-hospital mortality, the causes of death, the actuarial survival curves were compared in two subsequent groups of patients admitted to our CCU for acute myocardial infarction: the first (group A) includes 791 pts, admitted from september '67 to december '72, the second (group B) includes 542 pts admitted from january '78 to june '80. The in-hospital mortality was significantly reduced in group B (A: 186/791, 23.5%; B: 72/542, 13,3%, p less than 0.01). This could be due to a reduction of the number of deaths for cardiogenic shock (A: 71/791, 9%; B: 30/542, 5.6%; p less than 0.01) and to reduction in the mortality rate for pulmonary oedema (from 6% to 1.5%, p less than 0.01), although the frequency of pulmonary oedema was the same during the two periods (A: 205 pts, 26%; B/156 pts 29%). We did not observe any significant difference in the long-term prognosis (54 months: A 79.3%, B 71.5%). The actuarial survival curves overlapped after the 1st semester after discharge. The most frequent cause of death during follow-up was a new myocardial infarction. None in the group A and only 3% in the group B were referred to the surgeon for coronary artery bypass grafting. We conclude that, in spite of a significant reduction of the in-hospital mortality, possibly related to the evolution in diagnosis and management of the disease, the long-term survival was not improved in a non-surgically treated population with myocardial infarction.

Adult↗
PubMed1981

Effect of nitroglycerin on ST potentials in the post-acute phase of myocardial infarction.

Thoracic electromaps were recorded before and after sublingual nitroglycerin (NG) in 26 subjects 15 and 30 days after acute myocardial infarction (MI), in order to evaluate the effect of the drug on injury potentials. Ten patients with documented left ventricular aneurysm were also studied 5 to 46 months after acute MI. Fifteen min after NG there was a significant decrease, compared with basal values, of ST segment elevations, blood pressure and rate-pressure product on both the 15th and 30th days. The degree of ST potentials reduction was not strictly related to the decrease of myocardial oxygen consumption, as indicated by the rate-pressure product. The response to NG on the 15th day did not predict accurately the evolution of injury potentials. In fact there was no significant correlation between percentages reduction of ST after NG on the 15th day and amplitudes of ST segment elevations present on the 30th day. In the patients with ventricular aneurysm, ST potential decrease and hemodynamic changes after NG were similar to those observed in the other groups studied. Our data suggest that it is not possible to differentiate between ST segment elevations associated with a dyssynergic area and those merely due to ischemic injury on the basis of NG sensitivity, and that ST segment elevations in the acute and subacute phase and long after MI have, at least in part, a similar electrophysiological significance.

Adult↗