Behçet's disease and coeliac disease.
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Biomedical subjects
Publications and source records attributed to G Triolo.
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Nineteen of 50 sera from children with type 1 (insulin-dependent) diabetes mellitus showed anti-platelet reactivity. This reactivity was significantly associated with the presence of proteoglycan cross-reactive anti-ssDNA antibodies. As well as DNA-anti-DNA interaction, increasing salt concentration of the dilution buffer caused a decrease in the binding of positive sera to platelets. Purified ssDNA inhibited also the anti-platelet reactivity of anti-ssDNA positive sera. The addition of purified IgG from anti-ssDNA positive but not from anti-ssDNA negative sera to washed platelets caused an increased collagen-induced platelet aggregation similar to that obtained with the addition of polycationic agents. It may be suggested that ionic interaction between anti-negative charged molecule antibodies (such as anti-ssDNA antibodies) and platelet surface negative charges may be a pathophysiological mechanism contributing to the altered platelet function observed in diabetes.
In recent years, the availability of large epidemiological series allowed identification of biochemical outcome markers in the dialysis population. Interest towards albumin and cholesterol levels is motivated by their easy availability and by the presence of a strong short-term effect on mortality and morbidity. The aim of the study was an analysis of the relationship between albumin and cholesterol levels at start of dialysis and mortality (gross mortality and Kaplan Meier survival curves). Data were obtained from the Piedmont Regional Registry of Dialysis and Transplantation (Northern Italy Region, about 4,400,000 inhab, 20 Dialysis Centers, open acceptance since mid '70, yearly information on 100% of patients) in the period 1981-1990 (4734 patients on file). Only non diabetic patients with follow-up > = 1 month, who started treatment in the Region, were selected. Patients with renal function recovery were excluded. Albumin levels were dichotomized at 3.5 g/dl. Cholesterol was stratified into 3 levels (< 150, 150-250, > or = 300 mg/dl). The choice of dividing the study into 2 periods (1980-1985 vs 1986-1990) is due to the fact that 1984 has been the year of switch from acetate to bicarbonate dialysis. Prevalence of albumin and cholesterol under the normal range (22% and 15%) is low and rises with age and presence of high risk conditions. A a good correlation with the risk of death of these biochemical markers (stronger for albumin at least in the short term) was observed. No correlations are found with risk of death and elevated cholesterol levels (low number of cases).(ABSTRACT TRUNCATED AT 250 WORDS)
Ninety patients on dialysis, 241 cadaveric kidney donors and 27 cadaveric kidney recipients with a follow-up of 2 years, have been investigated as for anti-HCV positivity by means of 3 tests. As for patients on dialysis and cadaveric donors, the prevalence was 32 and 4%, respectively. As for transplanted patients, it must be noted that 4 negative recipients from positive donors seroconverted, but without any change in hepatic enzymes, while in 2 or 9 anti-HCV-positive recipients, hepatic enzymes increased after transplantation. Seroconversion in patients transplanted from a negative donor was not significantly different. We conclude that, according to their experience, anti-HCV positivity in the donors is not associated with a significant risk of infection in recipients of cadaveric grafts.
Renal transplantation modifies the dyslipidemia characteristic of chronic renal failure (CRF). The change in lipoprotein and lipid values of 51 transplant recipients, on cyclosporine and corticosteroid treatment, was studied during 2 years after transplantation to examine the short- and medium-term variations of lipid metabolism. Compared with control values of (all in mg/dL) triglycerides (Tg) 111 +/- 44, very-low-density lipoprotein (VLDL) Tg 69 +/- 18, total cholesterol (Chol) 201 +/- 32, VLDL-Chol 32 +/- 9, low-density lipoprotein (LDL) Chol 118 +/- 28, and high-density lipoprotein (HDL) Chol 50 +/- 10, uremic patients pretransplantation exhibited values of Tg 200 +/- 82 (P less than .001), VLDL-Tg 133 +/- 70 (P less than .001), Chol 193 +/- 51 (NS), VLDL-Chol 52 +/- 16 (P less than .001), LDL-Chol 100 +/- 37 (P less than .007), HDL-Chol 40 +/- 16 (P less than .001), which changed to Tg 118 +/- 18 (P less than .001), VLDL-Tg 64 +/- 45 (P less than .001), Chol 223 +/- 48 (P less than .006), VLDL-Chol 26 +/- 33 (P less than .001), LDL-Chol 134 +/- 43 (P less than .001), at HDL-Chol 63 +/- 21 (P less than .001) at 3 months and Tg 135 +/- 76, VLDL-Tg 81 +/- 62, Chol 218 +/- 55, VLDL-Chol 22 +/- 20, LDL-Chol 139 +/- 46, and HDL-Chol 58 +/- 18 at 24 months without evidence of a significative variations in the 3- to 24-month posttransplant period.(ABSTRACT TRUNCATED AT 250 WORDS)
There is evidence from several laboratories of an increased prevalence of circulating immuno-complexes (CIC) in diabetic patients. It has also been suggested that CIC are pathogenetically related to chronic diabetic complications. The aim of this study was to assess peripheral nerve function in children with Type 1 diabetes and to evaluate the relationship between the neurophysiological abnormalities and the possible presence of CIC. The investigation was carried out in 25 Type 1 diabetic patients ranging in age from 7-19 years and in 20 normal controls. Neurophysiological assessment was performed to evaluate motor and sensory conduction velocity on median and tibial nerves. IgG-CIC were detected by the solid-phase C1q-binding and anti-C3 enzyme immuno-assay. The results of this study showed a greater slowing of median motor and sensory and tibial sensory conduction velocities in patients with CIC with respect to the patients without CIC, suggesting a possible role of immunological factors in the pathogenesis of diabetic neuropathy.
Antibody directed against insulin carries idiotypic determinants that may induce an auto-anti-idiotype (anti-Id) antibody response. We describe a solid-phase enzyme immunoassay which allows specific detection of IgG anti-Id directed against anti-insulin antibodies. Among 36 patients with type 1 diabetes, IgG anti-idiotype was detected in 21 (58%). An inverse significant correlation was found between titers of anti-idiotype and anti-insulin antibodies. These findings suggest that anti-idiotype antibodies may function to regulate the immune response to insulin. Whatever the mechanism of action of the anti-idiotype antibodies, we detected by ELISA, the clinical consequences and the theoretical implications of this determination may be important.
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An ELISA was used to measure the fluid-phase complement complex in the plasma of 54 patients with insulin-dependent (type I) diabetes mellitus. Sixty-seven per cent of the diabetic patients had increased levels of SC5b-9. In individual diabetic patients, increased SC5b-9 was found to be significantly associated with the occurrence of anti-heparan sulphate cross-reactive anti-ssDNA antibodies and in some cases with circulating immune complexes. There was a significant correlation between levels of SC5b-9 and those of urinary albumin excretion rate (AER) (r = 0.39, P less than 0.01). Levels of AER were 8.4 +/- 2.26 micrograms/min and 2.04 +/- 0.35 micrograms/min in the SC5b-9 positive and negative patients, respectively (P less than 0.01). A relationship was also found between SC5b-9 and plasma von Willebrand Factor (r = 0.45, P less than 0.02), von Willebrand factor was 189.2 +/- 19.3% and 132.3 +/- 19.6% in SC5b-9 positive and negative patients, respectively (P less than 0.05). It may be that the abnormalities found in this study play a role in the pathogenesis of the late diabetic vascular complications.
Sera of 43 patients with type 1 (insulin-dependent) diabetes and from 42 normal subjects were examined for the presence of Fc-gamma receptor-blocking IgG immune complexes, detected by EA rosette inhibition, and for the presence of anti-ssDNA antibodies by ELISA. Forty-four percent of diabetic patients had levels of inhibition above the upper limit of normality in comparison to 7% of normal controls. Anti-ssDNA antibodies were found in the sera of 14 out of 43 diabetic patients. Ten out of 14 anti-ssDNA positive patients (71.5%) had inhibition levels above the upper limit of normality in comparison to 9 out of 29 (31%) of the anti-ssDNA negative population. The difference was statistically significant (P less than 0.005). Levels of EA rosette inhibition were found to be high in patients with duration of diabetes of less than 2 years and correlated with high prevalence of anti-ssDNA antibodies. The percentage of EA rosette inhibition was found not to correlate with the levels of C1q-binding immune complexes, suggesting that immune complexes detected by EA rosette inhibition may belong to a pool of noncomplement-fixing immune complexes. The possible role of immune complexes with autoantibodies anti-ssDNA in the mechanism triggering and perpetuating autoimmune phenomena in diabetes is discussed.
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The outcome of renal transplantation in CAPD patients is still controversial since age and clinical differences often make comparison with hemodialysis patients difficult. The aim of this study was to analyse two homogeneous groups of patients, on CAPD and on hemodialysis. 18 CAPD (Group A) and 18 hemodialysis patients (Group B) were selected for a case-control analysis, matched for age, presence of acute tubular necrosis and Cyclosporine A regimen. Group A and B were not different for male/female ratio, donor age, HLA-Dr mismatches, arterial pressure, cold ischemia, or follow-up. Patient, graft survival and number of rejection episodes did not differ significantly at 1 year; serum creatinine at 6 and 12 months and CyA doses at 1 and 6 months were not different; hospitalization rates for first and subsequent admissions did not differ. Infection-free patients were 9/18 in Group A and 15/18 in Group B, with 12 episodes in Group A and 3 in Group B. Post transplant cholesterol levels showed a trend to increase in both groups and triglycerides levels to a decrease; differences in pre and post transplant in body weight were not significant at 12 months. In conclusion, the outcome of transplantation in CAPD patients is not significantly different from that in hemodialysis patients with similar clinical characteristics.
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C3 fixing IgA immune complexes were found to be elevated in 25% of patients with type 2 (non insulin-dependent) diabetes mellitus as compared to healthy subjects (2%). Immune complexes containing both IgA and IgG were found in 42% of the diabetic population but not in controls. The presence of C3-IgA and/or IgA/IgG immune complexes correlated with the occurrence of antiglobulins antibodies of IgA class in particular with autoantibodies reactive with the Fab2 portion of IgG. These immunopathological findings were more frequent in patients that exhibited microvascular complications and in particular in patients with proliferative retinopathy. These and our previous results strongly suggest a role of IgA system abnormality in the pathogenesis of diabetic vascular complications.
Serum levels of type III procollagen peptide (P-III-P) were investigated in 19 patients with type 1 (insulin-dependent) and in 48 (25 orally treated, 23 insulinized) patients with type 2 (non insulin-dependent) diabetes mellitus. Among patients with type 2 diabetes, 16 orally treated and 14 insulin-treated subjects had macrovascular complications. P-III-P levels were not correlated with the duration of diabetes and with glucose control, nor were there any significant sex and age differences in the levels. P-III-P values were significantly higher in the sera of insulin-treated non insulin-dependent diabetic patients with macroangiopathy. These high values (18.5 +/- 10.8 ng/ml) were in contrast with normal values in healthy subjects (8.5 +/- 2.5, P less than 0.001), insulin-dependent diabetics (9.9 +/- 3.4 ng/ml, P less than 0.01), non insulin-dependent diabetics treated with oral agents (8.2 +/- 2.6 ng/ml, P less than 0.001) and insulin-treated non insulin-dependent patients without macroangiopathy (8.2 +/- 4.9 ng/ml, P less than 0.001). Although this study does not demonstrate that an increase in type III collagen synthesis is responsible for the pathogenesis of macroangiopathy, it suggests that insulin-dependent fibroblast sensitization may play a role in the acceleration and progression of macroangiopathy.
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Anti-single-stranded-DNA antibodies cross-reactive with heparan sulfate were detected in serums of patients with type I (insulin-dependent) diabetes mellitus. The results suggested that heparan sulfate, the major glycosaminoglycan constituent of the glomerular basement membrane, may serve as a target antigen in vivo for cross-reactive anti-DNA antibodies. These polyreactive antibodies, directed toward repeating negatively charged units, may neutralize the heparan sulfate-associated polyanionic sites in the glomerulus, leading to an abnormal permeability of anionic plasma proteins.