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E Cecchin

Publications and source records attributed to E Cecchin.

At least 19 recordsLinked to original sources

Relief of pruritus and decreases in plasma histamine concentrations during erythropoietin therapy in patients with uremia.

BACKGROUND: The pathophysiologic aspects of pruritus in patients with chronic renal insufficiency are poorly understood, and there is no universally effective treatment. The improvement of pruritus in several patients receiving erythropoietin therapy raised the possibility that erythropoietin affects uremic pruritus directly. METHODS: We undertook a 10-week placebo-controlled, double-blind, crossover study in a group of patients receiving hemodialysis who had severe pruritus, to investigate the effects of recombinant human erythropoietin on their pruritus and plasma histamine levels. Twenty patients with uremia, of whom 10 had severe pruritus and 10 did not, received erythropoietin (36 units per kilogram of body weight three times weekly) and placebo in random order, each for five weeks. The severity of pruritus was scored weekly, and plasma histamine levels were measured at the beginning and end of each five-week period. RESULTS: Eight of the 10 patients with pruritus had marked reductions in their pruritus scores during erythropoietin therapy. The mean (+/- SE) pruritus score decreased from 25 +/- 3 to 6 +/- 1 in these patients. The pruritus returned within one week after the discontinuation of therapy. The improvement was not related to the change in hemoglobin level. These eight patients were successfully treated again with low doses of erythropoietin (18 units per kilogram three times weekly), and the effect has persisted for six months. The patients with pruritus had elevated plasma histamine concentrations (20.7 +/- 2.7 nmol per liter), as compared with the patients without pruritus (4.2 +/- 0.6 nmol per liter; P less than 0.001) and normal subjects (2.1 +/- 0.2 nmol per liter; P less than 0.001). Therapy with erythropoietin induced a decrease in plasma histamine concentrations in both groups of patients with uremia, and recurrences of pruritus after the discontinuation of erythropoietin were accompanied by increases in plasma histamine concentrations. CONCLUSIONS: Erythropoietin therapy lowers plasma histamine concentrations in patients with uremia and can result in marked improvement of pruritus.

Double-Blind Method

Bardet-Biedl syndrome and cystinuria.

An unusual association of Bardet-Biedl syndrome with cystinuria was described in one patient. A 21-year-old male was admitted to hospital because of renal failure, severe deterioration of visual acuity, polydactyly, brachydactyly, and mental retardation. Laboratory investigations revealed a serum creatinine of 292 mumol/L (3.3 mg/dL) and a GFR of 25 mL/min per 1.73 m2. Quantitative ion exchange chromatography demonstrated an increased urinary excretion rate of cystine, lysine, arginine, and ornithine. The ophthalmologic examination showed a severe atypical retinal dystrophy. Visual acuity was severely deteriorated and the patient could only count the examining physician's fingers. The patient had been previously evaluated at the age of 7 years for polyuria, polydipsia, and growth failure. His workup at that time demonstrated nephrogenic diabetes insipidus, normal GFR, and a urinary amino acid pattern consistent with the cystinuric phenotype. There was mental retardation notwithstanding the normal ophthalmologic examination. Intravenous pyelography showed calyceal clubbing, calyceal cysts, and lobulated renal outlines of the fetal type. The patient was evaluated again at the age of 13 years for deterioration of visual acuity and the ophthalmologic examination showed an atypical retinal dystrophy, with sparse pigmentation, central and peripheral atrophy, attenuated vessels, and marked optic disk pallor. To our knowledge the association of Bardet-Biedl syndrome with cystinuria has never been reported. It is unlikely that cystinuria may have contributed to the kidney damage. The possibility that mental retardation has been induced or aggravated by cystinuria cannot be excluded.

Adult

Hepatic computed tomography for monitoring the iron status of haemodialysis patients with haemosiderosis treated with recombinant human erythropoietin.

1. A randomized, partial-crossover study was conducted in uraemic patients with dialysis-associated anaemia and transfusional iron overload to evaluate the effects of desferrioxamine chelation therapy and of recombinant human erythropoietin treatment on hepatic iron storage determined by computed tomography, as well as by serum ferritin concentration and transferrin saturation. 2. Twenty-one haemodialysis patients with moderate iron overload, confirmed by values of serum ferritin concentration, transferrin saturation and hepatic computed tomography density exceeding 1000 micrograms/l, 45% and 68 Hounsfield units respectively, were randomly allocated to three groups and were followed for 12 months. 3. During the first 6 months group 1 (n = 7) received desferrioxamine chelation therapy (30 mg/kg intravenously three times a week) and group 2 (n = 7) underwent recombinant human erythropoietin treatment (36 units/kg intravenously three times a week). Thereafter, in the second 6 months of observation patients in group 1 were switched to receive recombinant human erythropoietin. Because of a poor response in the desferrioxamine-treated group in the initial 6 months, patients in group 2 continued on the maintenance dose of recombinant human erythropoietin (18 units/kg three times a week) until the end of the trial. Patients in group 3 (n = 7) were maintained on placebo throughout the study. 4. In comparison with placebo, recombinant human erythropoietin treatment, but not desferrioxamine chelation therapy, reduced serum ferritin concentration, transferrin saturation and hepatic computed tomography density, and was associated with a rise in haemoglobin and packed cell volume. Hepatic computed tomography density, serum ferritin concentration and transferrin saturation decreased in 13 out of 14 patients (93%) during treatment with recombinant human erythropoietin.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Asymptomatic autoimmune thyroiditis and thyroid dysfunction in Alport's syndrome. A report of three families.

The purpose of this study was to investigate the significance of serum antithyroid antibodies in Alport's syndrome. Thyroid microsomal and thyroglobulin antibodies were assessed in three families with Alport's syndrome for a total of 11 patients and 17 healthy relatives, as well as in 40 haemodialysis patients and in 40 healthy subjects. Thyroid function tests, including the measurement of serum total thyroxine (TT4), total triiodothyronine (TT3), free thyroxine (fT4) and free triiodothyronine (fT3) concentrations, and thyrotropin-releasing hormone (TRH) stimulation tests were performed in all patients and subjects. Among patients with Alport's syndrome, five (45%) had elevated titres of thyroid microsomal antibodies and eight (73%) had positive titres of thyroglobulin antibodies, whereas only one healthy relative (6%) had circulating antithyroid antibodies. Fine-needle aspiration biopsy of the thyroid demonstrated a lymphocytic infiltration that indicated the existence of asymptomatic autoimmune thyroiditis in all five patients with elevated thyroid microsomal antibody titres. The prevalence of antithyroid antibodies in healthy subjects and in haemodialysis patients was 7.5% and 12.5% respectively. Functional tests demonstrated a thyroid dysfunction in four of five patients with asymptomatic autoimmune thyroiditis. Two patients had evidence of subclinical hypothyroidism. Two other patients, both with end-stage renal failure, showed a blunted TSH response to TRH, increased fT4 and elevated borderline fT3. The present study indicates that elevated titres of serum antithyroid antibodies may be detected in patients with Alport's syndrome. These patients are at risk of developing asymptomatic autoimmune thyroiditis and thyroid dysfunction. Subclinical hypothyroidism and, perhaps, preclinical hyperthyroidism may be found in these patients.

Adult

Efficacy of hepatic computed tomography to detect iron overload in chronic hemodialysis.

The diagnostic efficacy of hepatic computed tomography density (HCTD) in comparison with serum ferritin for the detection of iron overload was investigated in uremic patients on maintenance hemodialysis (HD) and in patients with idiopathic hemochromatosis (IHC). Ten IHC patients, 38 HD patients and 40 healthy subjects underwent the CT scanning of the liver and determination of percent saturation of transferrin, serum ferritin concentration and HLA typing. Liver iron content was determined by histochemical grading and direct measurement of liver iron concentration either in IHC patients or in HD patients. Nineteen HD patients were considered to have iron overload on the basis of liver iron concentration exceeding 3.6 mumol/100 mg dry weight. The mean +/- SD values of HCTD in healthy subjects, IHC patients, HD patients with iron overload and without iron overload were 60.2 +/- 5.6, 79 +/- 5.6, 71.4 +/- 3.6, 58 +/- 3.8 Hounsfield units, respectively. HCTD showed positive correlations with liver iron concentration and serum ferritin either in IHC patients or in HD patients. The analysis of the diagnostic efficacy of HCTD in comparison with serum ferritin for the detection of excessive hepatic iron in HD patients demonstrated that HCTD had higher sensitivity, specificity, positive and negative predictive values. Cut-off points were arbitrarily fixed to 66 Hounsfield units for HCTD, 400 micrograms/liter for serum ferritin and 3.6 mumol/100 mg dry weight for liver iron concentration. Seventeen HD patients who possessed the histocompatibility antigens associated with IHC, namely HLA-A3 and/or HLA-B7 and/or HLA-B14, had liver iron concentration, serum ferritin and HCTD values higher than those of the HD patients without these "hemochromatosis alleles".(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Severe metabolic acidosis and disturbances of calcium metabolism induced by acetazolamide in patients on haemodialysis.

1. To investigate mechanisms of extrarenal buffering in uraemic acidosis, we studied the effects of the carbonic anhydrase inhibitor, acetazolamide, in normal subjects and in patients with end-stage kidney disease on maintenance haemodialysis with virtually no urine output. 2. Acetazolamide (500 mg) was administered daily for 7 days, after pretreatment for 1 month with 1,25-dihydroxyvitamin D (n = 12) or placebo (n = 12); only placebo was administered to a third group (n = 12) of haemodialysis patients. In addition, acetazolamide was administered to normal control subjects (n = 12). 3. Treatment with acetazolamide resulted in a more marked metabolic acidosis in haemodialysis patients than in normal control subjects and the effect in haemodialysis patients was attenuated by prior treatment with 1,25-dihydroxyvitamin D. 4. The administration of acetazolamide to haemodialysis patients led to an increase in serum inorganic phosphorus, bone isoenzyme of alkaline phosphatase and parathyroid hormone, and a reduction in serum calcium, whereas acetazolamide had no effect on these variables in normal subjects. In contrast, in the haemodialysis patients previously treated with 1,25-dihydroxyvitamin D, acetazolamide increased serum inorganic phosphorus, bone isoenzyme of alkaline phosphatase, parathyroid hormone and serum calcium. 5. We hypothesize that the metabolic acidosis induced by acetazolamide in haemodialysis patients may result from interference with the mechanisms of extrarenal buffering. 6. As parathyroid hormone, 1,25-dihydroxyvitamin D and carbonic anhydrase are thought to be involved in bone buffering, we suggest that the marked acidosis seen in haemodialysis patients treated with acetazolamide may be due to impaired parathyroid hormone-mediated bone buffering.

Acetazolamide

Intraocular pressure changes during hemodialysis: prevention of excessive dialytic rise and development of severe metabolic acidosis following acetazolamide therapy.

The response of intraocular pressure (IOP) to hemodialysis was investigated in 55 patients with end-stage kidney disease enrolled in a chronic dialysis program. The mean level of IOP, measured by the Goldman applanation tonometer, before dialysis was slightly lower than that of a control group of 50 healthy subjects (14.9 +/- 2 mm Hg vs 15.6 +/- 1.9 mm Hg. p = .07). During dialysis IOP underwent an excessive rise (7.8 to 12.5 mm Hg) in 10 patients (group 1), remained unchanged (variations below 2 mm Hg) in 41 patients (group 2), and decreased (3.1 to 5.1 mm Hg) in 4 patients (group 3). In group 1 patients, gonioscopy showed a narrow angle between iris and lateral cornea. Conversely, the anterior chamber angle was normal in patients of groups 2 and 3. The effect of a 7-day course of acetazolamide therapy (500 mg per day orally) on IOP was investigated in group 1 patients. Acetazolamide was capable of preventing the excessive IOP rise during dialysis. The mean reduction of such a dialytic rise was 8.1 mm Hg. However, despite this effect, in these patients the IOP level after dialysis still remained significantly higher than that of patients of group 2 (18.1 +/- 1 mm Hg vs 14.9 +/- 0.8 mm Hg. p less than .0001). Acetazolamide therapy precipitated in all patients a severe metabolic acidosis (blood pH fell from 7.38 +/- 0.02 to 7.24 +/- 0.03, p less than .0001; and bicarbonate concentration from 21 +/- 2.5 mmol/liter to 12.3 +/- 2.4 mmol/liter, p less than .0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide

Dialysis for the elderly: survival and risk factors.

We evaluated survival and risk factors in 86 elderly patients (pts) who underwent dialysis at one center throughout the last 10 years. Thirty-five pts received hemodialysis (HD), 32 intermittent peritoneal dialysis (IPD), and 19 continuous peritoneal dialysis (CAPD). Risk factors included: treatment, age, sex, underlying disease, heart failure (HF), peripheral vascular disease (PVD), diabetes mellitus (DM) and malignancy. Median age was 65 years for both HD and CAPD, and 69 for IPD (p less than 0.05). Survival evaluation demonstrated a longer life span for HD vs. IPD (p = 0.02) for CAPD vs. IPD (p = 0.03) and no difference between HD and CAPD pts. Cox analysis showed higher death odds ratio (OR = 2.4) for IPD vs. HD and lower ratio for CAPD vs. IPD (OR = 0.3). Other OR positive risk factors were: HF, PVD, DM and malignancy. The median value of risk factors for each group was higher for both IPD and CAPD vs. HD. Both life span and death OR for CAPD were equal to HD in spite of higher risk factors in CAPD group. The lower survival of the IPD group may be due to its older age. CAPD should represent the elective treatment for elderly uremics while HD or IPD should be reserved for selected patients.

Aged

Rheological abnormalities of erythrocyte deformability and increased glycosylation of hemoglobin in the nephrotic syndrome.

This report is an attempt to gain more complete knowledge of the causes of the tendency to thrombosis in the nephrotic syndrome. Our purpose was to detect some rheological abnormalities in a group of nephrotic patients having normal renal function. Plasma and blood viscosity, erythrocyte filtration flow (EFF) and some indices of the carbohydrate metabolic state (glycosylated hemoglobin A1c; HbA1c, fasting glycemia and oral glucose tolerance test) were investigated in 10 patients with newly diagnosed primary nephrotic syndrome and 10 healthy subjects. EFF was determined in order to avoid variables depending upon plasma, white cells and hematocrit. The mean level of HbA1c was higher in the nephrotic group, in which we found 4 patients with impaired glucose tolerance according to the criteria of the National Diabetes Data Group. EFF was lower in nephrotic patients than in controls and correlated inversely with HbA1c. These findings indicate that nephrotic patients have a reduced red cell deformability which seems to be related to the abnormal carbohydrate metabolism commonly observed in this syndrome.

Adult

Serum reverse T3 assay for predicting glucose intolerance in uremic patients on dialysis therapy.

Sixty patients with end stage chronic renal failure (CRF) enrolled in a dialysis program underwent studies of serum thyroid hormones and carbohydrate metabolic state. The aim of the study was: 1) to evaluate whether the glucose intolerance per se represents a factor for the alteration of circulating thyroid hormones; and 2) to explore the potential usefulness of specific thyroid hormones and particularly reverse T3 (RT3) as indicators for predicting glucose intolerance. Forty-two patients received hemodialysis and 18 were on intermittent peritoneal dialysis (IPD). CRF patients had reduced serum total T4 and T3 levels, slightly decreased RT3 and TBG concentrations and normal TSH values. There was no significant difference in serum thyroid hormone indices between HD and IPD patients. Glucose intolerance was found in 25 patients. Ten had fasting hyperglycemia and diabetic response to oral glucose tolerance test (OGTT), 15 had an impaired glucose tolerance according to the criteria of the National Diabetes Data Group. In CRF patients with glucose intolerance, serum T3 and T3/T4 molar ratio were significantly lower than in those with a normal OGTT response, whereas serum RT3 and RT3/T4 molar ratio were found to be higher. In the whole group of CRF patients these serum thyroid hormones closely correlated with glucose tolerance indices. To investigate the usefulness of serum RT3 assay in predicting glucose intolerance we compared the outcome of the OGTT and serum RT3 values. Using the results of the OGTT as the true diagnosis of glucose intolerance, serum RT3 assay showed a diagnostic specificity of 94.2% and a sensitivity of 100%. In conclusion these results suggest that: 1) the glucose intolerance, which frequently occurs in uremia, may influence circulating thyroid hormones probably leading to a shift in the peripheral tissue conversion of T4 from T3 to RT3; and 2) serum RT3 assay could assume a clinical interest in assessing carbohydrate metabolic state in treated end stage renal failure independently of the type of dialysis therapy.

Adult