PubMed Health⌕ Search

Biomedical subjects

C Vitale

Publications and source records attributed to C Vitale.

At least 55 records · Page 3Linked to original sources
PubMed1996

Effect of superantigens on human thymocytes: selective proliferation of V beta 2+ cells in response to toxic shock syndrome toxin-1 and their deletion upon secondary stimulation.

The effects of toxic shock syndrome toxin-1 (TSST-1) on human thymocytes and their CD4/CD8-defined subsets have been analyzed. Postnatal thymocyte cell suspensions were cultured with 5 ng/ml TSST-1 for different time intervals. A strong cell proliferation of CD3+/TCR+ cells, characterized by selective expansion of cells expressing TCR V beta 2, occurred. In these cultured thymocytes, V beta 2+ cells were detected in all subsets including CD4-CD8+ cells. CD4-CD8+ thymocyte populations (obtained by depletion of CD4+ cells) were further analyzed for their ability to directly respond to TSST-1. An efficient cell proliferation occurred; however, it was completely abrogated upon removal of HLA class II+ cells (representing 10% of fresh thymocytes depleted of CD4+ cells). The HLA class II dependency of TSST-1 mediated functions was further documented at the clonal level. Thus, in the presence of TSST-1, CD4-CD8+ V beta 2+ clones efficiently lysed the HLA class II+ Raji target cells but not the corresponding HLA class II- variant RJ 2.2.5. Analysis of the effect of TSST-1-induced secondary stimulation on cultured (V beta 2+-enriched) thymocytes resulted in a selective depletion of V beta 2+ cells due to apoptotic cell death.

Bacterial Toxins↗
PubMed1995

Bony content of oxalate in patients with primary hyperoxaluria or oxalosis-unrelated renal failure.

Oxalate retention occurs in end-stage renal failure. Regular dialysis treatment does not prevent progressive accumulation of oxalate in cases of ESRF due to primary hyperoxaluria (PH), whereas such accumulation seldom seems to occur in oxalosis-unrelated ESRF. To elucidate this issue we have measured the bony content of oxalate on biopsies of the iliac crest taken from 32 uremic patients, 7 of them with ESRF associated with PH1 (6 cases) or PH2 (1 case). Ten subjects with normal renal function and no evidence of metabolic bone disease were taken as controls. Only trace amounts levels of oxalate were detected in normal subjects and oxalate to phosphate ratio was below 3:10,000. Non-PH dialyzed patients exhibited fivefold increases in oxalate levels, which rose to 5.1 +/- 3.6 mumol/g bony tissue. Calcium oxalate was estimated to represent 0.18% of the hydroxyapatite content of bone. Oxalate amounts were neither related to pre-dialysis plasma levels of oxalate, nor with duration of dialysis treatment, suggesting that accumulation was not progressive disorder. Oxalate levels were slightly higher in patients with a low turnover osteodystrophy compared to those with a high turnover pattern. Dialyzed patients with PH had remarkable increases in oxalate levels, which ranged between 14.8 and 907 mumol/g bony tissue. Oxalate deposition appeared to be progressive in that oxalate levels were significantly related to time on dialysis. In three patients calcium oxalate was a significant fraction of the mineralized bone. The occurrence of calcium oxalate crystals affected the histomorphometric patterns, that were featured by an increase in resorptive areas and a decrease in bone formation rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Cytolytic T lymphocytes displaying natural killer (NK)-like activity: expression of NK-related functional receptors for HLA class I molecules (p58 and CD94) and inhibitory effect on the TCR-mediated target cell lysis or lymphokine production.

Natural killer (NK) cells express surface receptors for defined groups of HLA class I alleles. The specific interaction between these receptors and HLA class I molecules expressed on target cells results in inhibition of NK-mediated target cell lysis. In this report, we analyzed whether similar mechanisms were operating in cytolytic T lymphocytes (CTLs) capable of lysing NK-sensitive target cells. T cell clones were screened for their ability to lyse K562 target cells. The selected clones expressed either gamma delta or alpha beta TCR. The majority of these clones failed to lyse the HLA class I+ R8/15375 cell line; however, upon addition of the previously described A6-136 (IgM) or 6A4 F(ab')2 anti-HLA class I mAbs, target cells were efficiently lysed. Lysis of autologous phytohemagglutinin blasts in the presence of anti-HLA class I mAbs occurred primarily with TCR gamma delta+ CTLs. Recognition of HLA class I molecules on target cells implies the expression of NK-related specific receptors in CTL clones. Indeed, phenotypic analysis of > 300 CTL clones with NK-like activity revealed that 28% expressed p58 molecules (specific for HLA-C alleles) while 30% expressed CD94 molecules (specific for the Bw6 specificity). These receptor molecules were found to function as inhibitory receptors, as revealed by the effect of anti-p58 or anti-CD94 mAbs (of IgG isotype) on the lysis of the Fc gamma R+ K562 target cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Antigens, CD↗
PubMed1995

The clinical significance of assessment of serum calcium oxalate saturation in the hyperoxaluria syndromes.

Estimating calcium oxalate saturation (beta CaOx) in body fluids is proposed as a simple and reproducible procedure to assess the risk of systemic oxalosis in several clinical conditions associated with oxalate retention. beta CaOx was computerized from the measured concentrations of main serum ions. Accurate assay of serum oxalate was crucial for reliability of beta CaOx estimates. However, beta CaOx also depended upon changes of calcium and magnesium concentrations. Patients with end-stage renal failure (ESRF) due to primary or enteric hyperoxaluria had beta CaOx greater than saturation, whereas this happened in only 10 of 25 and two of 24 of those with oxalosis-unrelated ESRF. Bony content of oxalate measured in some of these patients was consistent with these results. In patients with maintained renal function beta CaOx was inversely related to glomerular filtration rate, but the slope was steeper in patients with than in those without hyperoxaluria and beta CaOx reached saturation at earlier stages of renal insufficiency.

Calcium Oxalate↗
PubMed1995

Detection of primary hyperoxaluria type 2 (L-glyceric aciduria) in patients with maintained renal function or end-stage renal failure.

Primary hyperoxaluria (PH) type 1 and type 2 are autosomal recessive defects of oxalate metabolism resulting from glyoxylate accumulation which occurs by two distinct pathways. PH1 is associated to glycolic aciduria; PH2 to L-glyceric aciduria. Because hyperoxaluria leads to nephrolithiasis or nephrocalcinosis in both, they can be differentiated only through detection of the associated acidurias. However, glycolate and L-glycerate assays are not widely available and, in the setting of ESRF, diagnosis is hampered by a number of misleading events. At any stage of the disease diagnosis is crucial because there are differences between the two forms in clinical behaviour, long-term prognosis, and treatment. In this paper we outline diagnostic criteria for identification of PH2 in two patients, one with maintained renal function and one with ESRF on CPD, based on the use of a novel HPLC assay of L-glycerate in different body fluids. With the routine application of this procedure PH2 has been identified in two of 23 patients fulfilling criteria for diagnosis of PH. This suggests that the type 2 variant of PH may occur more frequently than so far suspected, and should be tested for even in the setting of ESRF.

Child, Preschool↗
PubMed1994

[Bartter's syndrome in children and adults. Study of 6 cases].

Six patients (3 children and 3 adults) with the clinical and biochemical features of Bartter's syndrome are presented. Pediatric cases included a more severe form, in one patient, with physical and mental retardation, hypercalciuria and nephrocalcinosis, and a less severe one, including two patients, with milder clinical features, low calcium and high magnesium excretion and hypomagnesiemia. Adult patients were affected by either the mild congenital form (case n. 4) or the acquired variety (cases n.5 and 6). Tubular function was investigated in the 3 adults by assessing clearance measurements during maximal diuresis. There was a defective fractional distal solute reabsorption (FDR) ranging between 0.52 and 0.60. This was well below the results obtained in one patient with psychogenous vomiting (FDR 0.94) and comparable to those in two patients with interstitial nephropathies caused by vesico-ureteral reflux (FDR 0.63 and 0.67 respectively). We concluded that: 1) the etiopathogenetic spectrum of Bartter's syndrome corresponds to different clinical presentation (mild, heavy, congenital or acquired varieties), and alterations in mineral and electrolyte renal handling; 2) reduction in FDR is a feature neither essential nor exclusive of this syndrome.

Adult↗
PubMed1994

Assay of plasma oxalate with soluble oxalate oxidase.

We use oxalate oxidase from barley seedlings for the colorimetric determination of oxalate in plasma. The oxalate is converted to hydrogen peroxide, which, in the presence of peroxidase, is detected by a Trinder-like chromogenic system. Optimization of the assay, including deproteinization and elimination of interferences from reducing substrates, is described. Ascorbate additions (200 mumol/L) did not affect oxalate concentration in plasma, even after long frozen storage. Mean analytical recovery of oxalate averaged 102% +/- 6.9%, imprecision (CV) at 2.0 mumol/L was 7.2%, and the lower limit of quantification (CV = 20%) was 0.6 mumol/L. Results correlated well with those by chromatography (r = 0.999, Sy/x = 0.29 mumol/L, n = 32, range for x, y = 0-140 mumol/L). Plasma oxalate concentrations measured in 32 healthy subjects ranged from 0.6 to 2.9 mumol/L (mean 1.28, SD 0.71 mumol/L), which agrees with those measurable by using indirect radioisotopic dilution methods. Patients with primary hyperoxaluria and chronic renal failure exhibited markedly greater plasma concentrations of oxalate.

Adolescent↗
PubMed1993

Effects of oral and intravenous calcitriol on serum calcium oxalate saturation in dialysis patients.

1. To determine whether the multiple changes in the blood chemistry profile induced by calcitriol may be conducive to secondary systemic oxalosis we have studied nine patients on regular dialysis treatment under three different regimens: (1) oral calcitriol, 0.25 microgram/daily for at least 6 months. (2) off calcitriol, a 1-month withdrawal of the drug, taken as the baseline study period; (3) intravenous calcitriol, 1 microgram three times weekly at the end of dialysis, with tests performed at 1 and 3 months from initiation. 2. Serum concentrations were measured pre- and post-dialysis at the end of each study period. The whole dialysate was used for the determination of the overall calcium and oxalate removal by dialysis. The degree of saturation with calcium oxalate monohydrate was estimated by a computer program. Serum calcitriol concentrations were also assessed. 3. Total and ionized serum calcium did not change on average, although mild hypercalcaemia developed in some patients on intravenous calcitriol. There was an increase in plasma level of oxalate during both oral and intravenous calcitriol treatment, but this was less pronounced during intravenous therapy. Removal of oxalate by dialysis was also greater in patients on oral calcitriol. 4. These increases were probably originated from intestinal absorption and secondary to hyperabsorption of dietary calcium. Consequently, the degree of saturation with calcium oxalate before dialysis rose during calcitriol treatment, irrespective of the route of administration. 5. These results emphasize that, in addition to soft tissue calcification due to calcium phosphates, ectopic calcium oxalate crystallization must also be viewed as a potential risk associated with long-term administration of calcitriol.

Administration, Oral↗
PubMed1993

Thresholds of serum calcium oxalate supersaturation in relation to renal function in patients with or without primary hyperoxaluria.

Systemic oxalosis is a constant feature in patients with primary hyperoxaluria type 1 (PH1) and chronic renal failure (CRF) and is not prevented by regular dialysis (RDT), because removal cannot keep up with retention and overproduction of oxalate. These patients are candidates to kidney and/or liver transplantation, which should be ideally planned prior to the development of oxalosis. However, methods to detect the presence and extent of oxalosis are invasive and poorly reproducible, and only indirect approaches are feasible. Because supersaturation of body fluids is an essential condition for oxalotic deposits to form, we have assessed serum calcium oxalate saturation (beta CaOx) in 12 patients with PH1 and 26 with PH1-unrelated renal diseases and varying degrees of CRF. Nineteen healthy individuals were taken as controls. beta CaOx was closely dependent on oxalate serum levels. Serum oxalate and beta CaOx were increased in patients with CRF as compared to controls, and were inversely related to GFR, assessed as creatinine clearance. However, at any level of GFR, both were always greater in PH1 patients. From the slopes of the regression of beta CaOx over ClCr, saturation was predicted to be obtained at ClCr ranging 24-34 and 8-11 ml/min/1.73 m2 in PH1 and non-PH1 patients respectively. Based on the dependence of beta CaOx on oxalate, saturation was associated with serum oxalate between 44 and 46 mumol/l, irrespective of either the prevailing GFR or the underlying disease. These simple procedures represent a valuable non-invasive tool to define the risk of systemic oxalosis and may assist in timing of transplantation.

Adolescent↗
PubMed1992

Plasma and urine glycolate assays for differentiating the hyperoxaluria syndromes.

To differentiate hyperoxaluria syndromes we measured plasma and urine glycolate by a novel high performance liquid chromatographic procedure. Mean glycolate level was 7.9 +/- 2.4 mumol./l. in plasma and 422 +/- 137 mumol./24 hours in urine from 19 control subjects. Renal clearance was about 50% the glomerular filtration rate irrespective of the underlying disease. There was close correlation between glycolate and oxalate in plasma. Plasma glycolate was normal in all but 8 patients who had primary hyperoxaluria 1. Plasma assay detected the disease more efficiently than urine assay. Pyridoxine decreased oxalate biosynthesis in 2 of the 4 patients treated with it and glycolate assay confirmed this behavior. Glycolate excretion was significantly high in 3 of 8 patients of primary hyperoxaluria 1 patients. Idiopathic stone formers had mild increases in glycolate excretion but this was not related with oxalate excretion. Glycolate levels were normal in 5 patients with enteric hyperoxaluria. We conclude that glycolate assay is essential for identifying patients with primary hyperoxaluria 1 and may represent a valuable tool for differentiating hyperoxaluria.

Adolescent↗
PubMed1992

Oxalate balance studies in patients on hemodialysis for type I primary hyperoxaluria.

Primary hyperoxaluria type I (PH1) always leads to end-stage renal failure (ESRF) due to deposition of calcium oxalate in the kidney. Regular dialysis therapy (RDT) can not overcome the excess production of oxalate, hence, systemic oxalate deposition occurs. The extent of tissue deposition and the rate at which oxalate accumulates influence the quality of life and survival of the patients. Therefore, an estimate of the oxalate balance needs to be made for patients on RDT. In this study, we suggest a simple model by which some of the main parameters of oxalate turnover can be assessed without using radioactive materials. Levels of oxalate, glycolate, and urea, and degrees of calcium oxalate saturation, were assessed on plasma ultrafiltrates from two patients with PH1, sampled before, at the end of a dialysis session, and over the entire interdialytic interval. In patients with PH1, oxalate increased linearly during the early phases and then the curve flattened at a concentration corresponding to approximately threefold saturation. The initial phase of the relationship was used to estimate generation rate of oxalate. The delayed phase was ascribed to the deposition of newly generated oxalate out of its miscible pool. Conversely, the relationship for glycolate and urea remained linear. This was also different from the values obtained in four patients with oxalosis-unrelated ESRF, whose oxalate levels increased linearly over the entire interdialytic interval. In the two patients with PH1, the overall oxalate generation was assessed at 4 to 7 mmol/d. The difference between generation and dialysis removal indicated that tissue deposition was greater than 50 mumol/kg body weight/d.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Plasma profiles and dialysis kinetics of oxalate in patients receiving hemodialysis.

Regular dialysis treatment (RDT) does not obviate hyperoxalemia of chronic renal failure (CRF). However, there is emerging evidence suggesting that current dialysis prescription is not always associated to progressive oxalate accumulation. In view of the controversy still concerning this issue, we have investigated on plasma profiles and dialysis kinetics of oxalate in patients on RDT. Oxalate was determined by ion chromatography on serum ultrafiltrates and on the whole dialyzate in 23 stable patients on RDT for end-stage renal failure unrelated to primary hyperoxaluria. Nine patients were on traditional hemodialysis (HD) and 14 on soft hemodiafiltration (HDF). Dialysis prescription was set so as to obtain similar KT/V of urea. Mean dialyzer clearance of oxalate (KdOx) was calculated by standard procedures and was compared to urea (KdUrea) and creatinine (KdCr) clearances. Oxalate removal was measured on the whole spent dialyzate. Distribution volume of oxalate (VOx) was estimated by assuming a single-pool model and was used to estimate the oxalate appearance rate (OxAR). Plasma profiles showed that dialysis patients were virtually always hyperoxalemic. However, the threshold of supersaturation for calcium oxalate was exceeded in only 13 of 138 (9.4%) assayed ultrafiltrates, 13% on HD and 7.1% on HDF. Dialysis reduced plasma oxalate by more than 60%. There was a postdialysis oxalate rebound averaging 9.6% at 30 min from the end of dialysis. Plasma oxalate predialysis was independent of sex, age and time on dialysis. KdOx was mildly higher on HDF than on HD, and was lower than both KdUrea and KdCr, irrespective of the dialysis technique.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Glycolate determination detects type I primary hyperoxaluria in dialysis patients.

The detection of type I primary hyperoxaluria is based on the finding of exceedingly high oxalate excretion which is associated with increased glycolate excretion. The differential diagnosis of this disease may become a difficult task once end-stage renal disease (ESRD) and anuria have supervened. The various procedures thus far proposed to obviate this circumstance are complex, inaccurate or not reproducible. In this paper we propose the accurate liquid chromatographic determination of glycolate in blood and dialysate as a means to detect type I primary hyperoxaluria in patients on maintenance hemodialysis (RDT). The method is based on the enzymatic conversion of glycolate to glyoxylate coupled with alpha-keto acid derivatization with phenylhydrazine. The resulting phenylhydrazone is then resolved by high-performance liquid chromatograph (HPLC). With this method, plasma glycolate in 12 healthy controls was 7.8 +/- 1.7 mumol/liter, almost twentyfold less than previously reported. Five dialysis patients with high serum oxalate, of whom four with primary hyperoxaluria and one with Crohn's disease and presumed enteric oxalate hyperabsorption, were checked by this method and compared to nine patients with oxalosis-unrelated ESRD. The patients with hyperoxalemia were also evaluated for their response to pyridoxine therapy. The measurement of glycolate in blood drawn prior to and at the end of the dialysis session as well as in the dialysate soundly discriminated the patients with type I hyperoxaluria from all the other dialysis patients. Glycolate measurement was shown to be much more powerful than oxalate in that patients with oxalosis-induced ESRD exhibited an almost two hundred and fiftyfold increase compared to the oxalosis-unrelated patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗