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Biomedical subjects

S Casati

Publications and source records attributed to S Casati.

At least 19 recordsLinked to original sources
PubMed1990

Aluminium interference in the treatment of haemodialysis patients with recombinant human erythropoietin.

In nine chronic haemodialysis patients a desferrioxamine (DFO) load test (40 mg/kg body-weight) was performed 1 year after the beginning of treatment with recombinant human erythropoietin (rHuEpo). The patients were then divided into two groups. Group A comprised five patients with a greater mean aluminium (204 +/- 28 micrograms/l) than the four patients in group B. Group A was given a mean dose of 25.8 g (range 14-39 g) of DFO over 6 months. Group B (aluminium values 112 +/- 36 micrograms/l) was never treated with DFO. During the period of observation, plasma iron, serum ferritin and transferrin, as well as iron supplementation, did not differ between the groups. After DFO treatment a second DFO load test was performed. The mean predialysis aluminium value was significantly reduced in group A (204 +/- 28 vs 111 +/- 72 micrograms/l; P less than 0.05), while remaining unchanged in group B (112 +/- 36 vs 140 +/- 39 micrograms/l; P = ns). In both groups, the doses of rHuEpo necessary to maintain the same haemoglobin values decreased with time, but reduced significantly only in group A (298 +/- 105 vs 110 +/- 61 mu/kg per week; delta -63%; P less than 0.01). Thus, aluminium interferes with the response to rHuEpo in haemodialysis patients, and the correction of aluminium overload with DFO can allow a considerable sparing of rHuEpo.

Adult↗
PubMed1990

Response of renal transplanted patients to oral calcium load.

In a previous study we demonstrated that cyclosporin-treated renal transplanted patients have a reduced 1,25(OH)2D3 synthesis in comparison with azathioprine-treated transplanted patients. To assess the impact of this defect on intestinal calcium transport we compared the plasma calcium variation and the urinary calcium excretion in 14 cyclosporin-treated and in 12 azathioprine-treated patients, in fasting conditions and 4 hours after an oral calcium load (1 g). In ten cyclosporin patients we also correlated cyclosporin plasma values with plasma 1,25(OH)2D3 values before and after a 25(OH)D3 oral load. After the oral calcium load, plasma and urinary calcium increased significantly in the azathioprine group, while remaining unchanged in the cyclosporin group. A negative correlation between plasma concentrations of cyclosporin and the increment in 1,25(OH)2D3 after 25(OH)D3 oral load was also observed. Thus, our data suggest that cyclosporin impairs 1-alpha hydroxylase activity and alters the response to an oral calcium load.

Adult↗
PubMed1989

Haemodialysis efficiency after long-term treatment with recombinant human erythropoietin.

In 11 chronic haemodialysis patients we investigated whether the increase in haematocrit during recombinant human erythropoietin (rHuEPO) treatment might alter the long-term efficiency of haemodialysis. After correction of anaemia with rHuEPO (mean Ht 35 +/- 2% vs 19 +/- 2% at baseline) (p 0.001), mean predialysis creatinine and urea did not change, while predialysis phosphate (1.77 +/- 0.38 vs 1.51 +/- 0.29 mmol/l) were significantly increased (p 0.01). In six of the 11 rHuEPO treated patients a post- versus pre-dialysis haemoconcentration (haematocrit 44% vs 35%) not attributable to different ultrafiltration regimes, was observed. In these 6 patients mean predialysis phosphate, creatinine and urea tended to be higher, but not significantly, in comparison to he remaining 5 patients who did not haemoconcentrate. Dialyser clearances and total extractions for urea, creatinine, phosphate and inulin were compared to those of 11 matched haemodialysis patients with anaemia. No differences were observed either for small and middle molecule clearances or their extractions between rHuEPO and anaemic patients. In conclusion, dialysis efficiency is not affected if haematocrit values are kept about 35%.

Adult↗
PubMed1988

Death from cardiovascular disease in Italy, 1972-1981: decline in mortality rates and possible causes.

Mortality rates for cardiovascular disease vary widely between countries, and epidemiological patterns (trends in incidence rates, prevalence of risk factors, availability of medical care) are heterogeneous even among industrialized nations. We studied mortality from cardiovascular disease in Italy from 1972 to 1981 and compared mortality to trends in risk factors during the same period. Age-adjusted mortality rates for acute ischaemic heart disease (IHD) have increased in Italy from 1972 to reach a peak in 1978 (180.53/100,000 in males, 51.55/100,000 in females), then declined between 1978 and 1981, by 7% in males and 5% in females. The decline was more evident in males and in the younger age groups. Deaths from chronic IHD reached a peak in 1973 in females and in 1975 in males, then decreased, respectively by 24.8% and 35.7% until 1981. Mortality for cerebrovascular disease declined from 1972 to 1981 by 16.2% in males and 21.5% in females. Data from national statistics and sample surveys in different areas of Italy show an increase in total calorie intake, in animal proteins, fats and dairy products and raised average serum cholesterol levels plus an increase in smoking prevalence but a possible decline in blood pressure levels. The roles of hypertension treatment and of access to specialized medical care are discussed as possible contributors to the new declining trend of IHD, and the need is stressed for preventive strategies in health promotion.

Adult↗
PubMed1987

Improvement in the haemostatic defect of uraemia after treatment with recombinant human erythropoietin.

Patients with uraemia have a defect of primary haemostasis expressed as long skin bleeding times and reduced platelet adhesion to the arterial subendothelium. Transfusion of red cells shortens the bleeding time and stops bleeding symptoms in uraemia. This study investigated whether the efficacy of recombinant human erythropoietin in correcting anaemia and the improvement in haemostasis are correlated. Recombinant human erythropoietin was given to seven consecutive patients with chronic uraemia, a history of bleeding, severe anaemia (haematocrit below 23%), and long bleeding times (above 19 min). The progressive rise in haematocrit induced by increasing doses of recombinant human erythropoietin was paralleled by a pronounced shortening of the bleeding time. Platelet adhesion to the subendothelium of human umbilical arteries, very low before the study, increased greatly in all patients and became normal in six. None of the patients bled during the study period.

Adult↗
PubMed1987

Benefits and risks of protracted treatment with human recombinant erythropoietin in patients having haemodialysis.

Fourteen patients with uraemic anaemia and having regular haemodialysis were given human recombinant erythropoietin in increasing doses, beginning with 24 U/kg thrice weekly. One patient was dropped from the study because of recurrent thrombosis of vascular access sites. In the other 13 patients, followed up for a mean of 9.1 months (range 8-11), haemoglobin concentrations increased from 62 (SD 8) to 105 (9) g/l. No antierythropoietin antibodies were detected during the study. The correction of anaemia was associated with a tendency to hyperkalaemia and a mild increase of unconjugated bilirubinaemia. In eight previously hypertensive patients antihypertensive treatment had to be reinforced, but in normotensive patients blood pressure did not change. Thrombosis of arteriovenous fistulas occurred in two patients and a cerebral ischaemic lesion in one. Protracted treatment with human recombinant erythropoietin evidently can maintain normal haemoglobin concentrations in uraemic patients over time. Full correction of anaemia, however, may trigger some vascular problems, particularly in hypertensive patients and those with a tendency to thromboembolism.

Adult↗
PubMed1987

Extrarenal synthesis of 1,25-dihydroxyvitamin D: sensitivity to glucocorticoid treatment.

The response of circulating 1,25-dihydroxyvitamin D [1,25-(OH)2D] to challenge with vitamin D treatment both before and after 7-10 days of prednisone therapy (25 mg/day) was investigated in five anephric subjects, six patients with chronic renal failure (CRF), two patients with vitamin D intoxication and four patients with hypoparathyroidism. In anephric subjects serum 25-hydroxyvitamin D [25-(OH)D] rose from 58 +/- 48 (SD) to 377 +/- 221 (SD) nmol/l after administration of 150 micrograms of 25-(OH)D3 for 1 month. Serum 1,25-(OH)2D, which was barely detectable in only two out of five patients under basal conditions, rose to 30 +/- 21 pmol/l after 2 weeks of therapy with 25-(OH)D3, but fell to 10 +/- 5 pmol/l during prednisone treatment. In CRF patients circulating 1,25-(OH)2D rose from 37 +/- 24 to 58 +/- 24 pmol/l during 25-(OH)D3 therapy, but fell to 41 +/- 31 pmol/l during prednisone treatment. In two patients with rheumatoid arthritis, hypercalcaemia due to vitamin D intoxication was associated with raised levels of 1,25-(OH)2D (288 and 317 pmol/l). Administration of prednisone resulted in suppression of 1,25-(OH)2D levels (132 and 96 pmol/l respectively) and reduction of serum calcium to within the normal range. In the hypoparathyroid patients prednisone therapy did not affect circulating 25-(OH)D levels but serum 1,25-(OH)2D fell from 192 +/- 42 to 117 +/- 23 pmol/l and serum calcium from 2.41 +/- 0.21 to 2.20 +/- 0.05 mmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcifediol↗
PubMed1986

High plasma levels of protein C activity and antigen in the nephrotic syndrome.

Low plasma levels of antithrombin III due to excessive urinary loss are thought to be the cause of thrombotic complications in patients with the nephrotic syndrome. To see whether protein C (PC), another antithrombotic protein, is also reduced in plasma by the same mechanism, plasma and urinary protein C were determined in 24 patients with nephrotic syndrome and no thrombotic complication, and compared to plasma and urinary antithrombin III. Twenty patients (83%) had high plasma levels of protein C activity (mean +/- SD 157 +/- 41 U/dl) and antigen (158 +/- 41). Even though measurable amounts of PC antigen were found in the urines of all but two patients the urinary loss of protein C relative to its plasma concentration was about 40 times lower than that of antithrombin III. High protein C might help to counteract hypercoagulability in nephrotic syndrome.

Adolescent↗
PubMed1985

Treatment of arterial hypertension with nifedipine in patients with chronic renal insufficiency.

The acute and chronic antihypertensive effects of nifedipine were investigated in patients with chronic renal insufficiency (CRI). The acute effects were assessed after the administration either of a fast-release nifedipine capsule or a slow-release nifedipine tablet in 10 and 15 patients respectively. Both the preparations induced prompt and marked reduction of systolic and of diastolic blood pressure, but the capsules showed a shorter antihypertensive effect (2 hours) than tablets (more than 6 hours). The chronic effects of nifedipine tablets given in addition to the previous therapy was assessed in 25 patients with CRI and resistant hypertension. Both systolic and diastolic blood pressure values promptly fell and maintained within the normal range over the whole period of the study (12 months).

Blood Pressure↗