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Biomedical subjects

U Di Mario

Publications and source records attributed to U Di Mario.

At least 145 records · Page 8Linked to original sources
PubMed1981

Circulating immune complexes and autoantibodies in lung cancer.

The sera of 80 newly diagnosed lung-cancer patients have been examined for immune complexes and autoantibodies. Control subjects consisted of 20 bronchitic patients and 150 normal blood donors. Immune-complex measurements used 4 established and sensitive techniques (Raji cell assay, fluid and solid-phase C1q assays and conglutinin-binding assay) and a 5th newly devised technique based on the binding of polyethylene-glycol-precipitated immune-complex-rich serum fractions to Staphylococcus aureus. Using the Raji cell assay and the S. aureus binding assay to measure immune complexes, both newly diagnosed lung cancer patients and bronchitic patients had significantly higher prevalences of immune complexes than normal controls, but the two groups of patients did not differ significantly in either prevalence or quantity of immune complexes. When techniques which depend solely upon complement fixation (C1q assays and conglutinin binding) were used, only meagre quantities of immune complexes were found, and in at most 15% of newly diagnosed lung-cancer patients. The presence of autoantibodies in newly diagnosed cancer patients and controls appeared to correlate with the increase in the detectable prevalence of immune complexes.

Adolescent↗
PubMed1981

The detection of circulating immune complexes in normal subjects using four different methods.

336 estimations of circulating immune complexes have been performed on the sera of blood donors by four different methods: the solid phase C1q binding test, the fluid phase C1q binding assay, the conglutinin binding test and the Raji cell radio-immune assay. Between 68 and 105 subjects were used in the analysis of each method. With the first three methods, immune complex levels showed a peaked asymmetric distribution with a positive tail including about 10% of subjects, whereas using the fourth method immune complex values were widely spread. No difference in immune complex values between males and females was found. There was a significant trend for the prevalence of immune complexes to increase with age when methods were used which detect complexes through C3 binding. In a further 13 subjects tested at regular intervals during a period of 24 hours, using the fluid phase C1q binding test, significant variations in immune complex levels were found but no consistent pattern of variation at different hours of the day or after meals could be seen. In studies of immune complexes on small groups of patients it is advisable to test multiple samples from te same subjects taken at different times, whereas when large series of patients are being studied results should be compared to those obtained with age matched controls.

Adult↗
PubMed1981

New evidence of circulating immune complexes in Crohn's disease using two sensitive methods.

Circulating immune complexes (AgAb) were studied in 183 serum samples from 119 patients with Crohn's Disease. AgAb were studied by the solid phase C1q binding test in all sera and also by the conglutinin binding assay in 161 sera. A significantly higher prevalence of circulating AgAb was observed in Crohn's disease patients in comparison with the control population. About one half of the sera were AgAb positive when the results of both tests were combined whereas AgAb were found in about one third of the sera by each individual method. Complexes revealed by the C1q-SP appeared to be related to the disease activity and to the occurrence of complications. Such a correlation was not observed as far as conglutinin results are concerned. Data emerging from the present investigation indicate that circulating AgAb may be present in Crohn's disease and suggest that the AgAb material is heterogeneous. They also suggest the possibility that AgAb represent a secondary phenomenon.

Antigen-Antibody Complex↗
PubMed1980

Inhibition of allogeneic lymphocyte E-rosettes induced by sera from newly diagnosed type I diabetics.

Sera from 64 juvenile onset insulin-dependent diabetics (Type I diabetics) and 30 normal subjects were tested for their ability to inhibit sheep red blood cell rosette formation (E-rosette) by normal allogeneic lymphocytes. Inhibition of E-rosette formation by greater than 20% was found with 16 (66%) sera from newly diagnosed patients, 3 (16%) sera from patients with duration of disease between 2 and 12 months and with 4 (18%) sera from diabetics with duration of disease between 1 and 7 years. On the other hand, only 2 (6%) control sera showed inhibitory effect. No relationship between E-rosette inhibition and islet-cell antibodies presence, anti-lymphocyte antibodies occurrence, anti-HLA activity, blood glucose levels, respectively, was found. Investigation of the properties of this inhibitory factor suggests that it is different from other substances that reportedly inhibit E-rosette formation.

Adolescent↗
PubMed1980

Immune complexes in type I diabetics with persistent islet cell antibodies.

The sera of 33 type I diabetics found to have pancreatic IgG antibodies to the cytoplasm of pancreatic islet cells (ICAb) at three or more years after diagnosis were tested for immune complexes (AgAb), insulin antibodies and thyroid and gastric cytoplasmic antibodies, and the subjects were HLA typed. Sera from 69 insulin treated diabetics of comparable duration of disease and without ICAb at the time of study were also included in the investigation. The prevalence of AgAb in patients with persistent ICAb was found to be 52% in comparison with 19% of ICAb negative diabetics (p < 0.001) and 10% of normal blood donors (p < 0.0005). AgAb positivity was increased, but not significantly, in HLA-B8 positive compared to B8 negative ICAb persisters. There was a significant negative correlation between AgAb levels and insulin antibody titres. Circulating AgAb were not significantly correlated with the presence of either thyroid or gastric cytoplasmic antibodies.

Antibodies↗
PubMed1979

Gastric carcinoma associated with severe hypoglycemia sensitive to diazoxide.

A case of carcinoma of the stomach associated with severe hypoglycemia is reported. Diagnosis of insulinoma was excluded on the basis of history as well as laboratory tests. Postmortem examination revealed widespread small metastases to various organs; no metastasis was found in the pancreas; the histology of this gland did not show any pathological finding. No impairment in pituitary, thyroid, adrenal and liver function was detected. Fasting blood sugar ranged from 18 to 56 mg/100 ml. An oral glucose tolerance test showed a diabetic pattern with low insulin. Tolbutamide, glucagon and glucose injected i.v. gave only a moderate rise in plasma insulin levels; plasma glucagon response to arginine was subnormal. The determination of NSILA-s and gastrin in the serum of this patient gave normal values. Diazoxide infusion induced an increase in blood glucose and subsequent treatment with diazoxide relieved hypoglycemia for some months. The occasional detection of an islet cell antibody by immunofluorescence in this case is not easily understandable, but it might partly account for the carbohydrate intolerance. An impairment in gluconeogenesis dependent upon some substrate deficiency might account for the hypoglycemia in this patient.

Adenocarcinoma↗
PubMed1979

Increased lymphocyte transformation by insulin induced hypoglycaemia in normal subjects.

To study the effect of carbohydrate metabolism on lymphocyte reactivity, we performed phytohaemoagglutinin and pokeweed mitogen induced lymphocyte transformation after insulin induced hypoglycaemia in normal subjects. A statistically significant increase of PHA-LT and a slight increase of PKW-LT were detected 30 minutes following insulin administration. These data suggest a stimulating effect of insulin induced hypoglycaemia on T lymphocyte reactivity and this finding has clinical importance in regard to the management of diabetic patients.

Adult↗
PubMed1978

Immune complexes in newly diagnosed insulin-dependent (type I) diabetics.

Soluble immune complexes (AgAb) and islet cell antibodies (ICAb) were studied in 110 insulin dependent diabetics (IDD) within a week of diagnosis and in about a third of the patients after 1, 3, 6 and 12 months. AgAb were studied by the solid phase Clq binding test in all the patients and also by the Raji cell radioimmunoassay in 52 sera at diagnosis. Diabetics at diagnosis showed a significantly higher incidence of AgAb in comparison with the control population. AgAb positivity declined with increasing time from diagnosis to reach the normal range within 3 months. Both the Clq and the Raji methods revealed a significant correlation at diagnosis between the occurrence at AgAb and the presence of ICAb. The possibility exists that AgAb, perhaps comprised of pancreatic antigen and ICAb, may be involved in the pathogenesis of type I diabetes.

Antibodies↗
PubMed1978

Immune complexes and diabetic microangiopathy.

Soluble immune complexes (AgAb) as detected and quantitated by the solid phase Clq assay (Clq-SP) were found to be increased in (a) long-duration diabetics with proliferative retinopathy and (b) short duration diabetics with early onset of retinopathy irrespective of whether they were treated with insulin or oral hypoglycaemic agents (OHA), in comparison to a normal population. No such increases were observed in diabetics of comparable duration without retinopathy. The trend for long-term diabetics to show an increased prevalence of AgAb according to the severity of retinopathy was statistically significant. Detection and quantitation of AgAb by the Raji cell assay (RAJI) gave comparable results although the differences were less pronounced and fell short of statistical significance. AgAb as detected by either method in insulin-treated diabetics could not be correlated with insulin antibodies. These findings suggest that AgAb, not necessarily comprised of insulin and anti-insulin antibodies, may contribute to the pathogenesis of diabetic microangiopathy.

Antibodies↗
PubMed1975

[Clucagon].

Only in 1969 reliable information about glucagon and its different forms was acquired. Some factors are already known to increase or diminish the production both of pancreatic glucagon (nesidioglucagon) and of enteroglucagon. There are various methods for their study. In the present report some results are dealt with that may be of clinical interest, and the possibility of measuring those two kinds of hormones is pointed out as a diagnostic help in reactive and functional hypoglycemic syndromes. Information about glucagon in clinical medicine, however, is still -- on the whole -- scarce and insufficient to throw light on its several physiological and physiopathological aspects.

Blood Glucose↗
PubMedDate not supplied

High glucose modifies heparansulphate synthesis by mouse glomerular epithelial cells.

BACKGROUND: Alterations in proteoglycan metabolism are involved in the pathogenesis of diabetic nephropathy. The aim of this study is to evaluate the effects of high glucose on proteoglycan production and to find a reliable in vitro model for the study of diabetic nephropathy. METHODS: A clone of mouse glomerular epithelial cells was cultured in media containing elevated (30 mmol) and physiological (5 mmol) glucose, or iso-osmolar (30 mmol) mannitol concentrations. We evaluated the synthesis of 35SO4-labeled molecules and the amount of proteoglycans by Sepharose CL6B and DEAE-Sephacel chromatographies. RESULTS: A clear decrease (56%) in total cell-layer proteoglycan synthesis was induced by 30 mmol glucose, in comparison with normal glucose. A reduction of 25% in medium associated proteoglycan synthesis was observed in high glucose cultured cells. After Sepharose CL6B, in cells cultured in high glucose, cell layer heparansulphate proteoglycan-I (Kav 6B 0. 04) synthesis was reduced by about 81%, heparansulphate proteoglycan-II (Kav 6B 0.21) by about 87% and heparansulphate glycosaminoglycan (Kav 0.4-0.8) by about 91%, respectively. In mannitol-incubated cells the reductions observed were less evident and not significantly different from those in normal glucose. CONCLUSIONS: These results indicate that (1) glomerular epithelial cells play a central role in proteoglycan synthesis, (2) high glucose modifies the amount and influences the different species production of these macromolecules, while osmotic forces seem to be only partially involved in these effects, and (3) this cellular clone of glomerular epithelial cells can represent a reliable in vitro model for the study of the mechanisms involved in diabetic nephropathy.

Animals↗
PubMedDate not supplied

The circulating insulin-like growth factor system in children with coeliac disease: an additional marker for disease activity.

BACKGROUND: Chronic undernutrition resulting from coeliac disease (CD) could be associated with changes in the circulating insulin-like growth factor (IGF) system, which may participate in the pathogenesis of growth retardation occurring in these patients. METHODS: We performed a cross-sectional study in CD subjects attempting to (1) document the pattern of serum IGF-I and IGF binding protein (IGFBP) 1 and 3 at diagnosis and (2) assess the response of circulating IGF system to dietary treatments, in comparison with the response of clinical and laboratory findings utilized for the diagnosis of CD. Thirty-two prepubertal CD children were divided into three groups based on the dietetic treatment: at diagnosis (D, n=18); on gluten-free diet for at least 6 months (GFD, n=7); and on gluten challenge for at least 3 months (CH, n=7). Six postpubertal CD patients were also studied at diagnosis. RESULTS: In prepubertal children IGF-I levels were significantly reduced (by 29%) in D vs sex- and age-matched normal control (NC) subjects, with reductions being more pronounced before 3 years of age. Likewise, serum IGFBP-3 concentrations were decreased by 22%, whereas circulating IGFBP-1 levels were increased by 60%, compared with NC, with more marked IGFBP changes in older children. Similar alterations were observed in postpubertal patients. Changes in the circulating IGF system disappeared in GFD subjects and reappeared in CH children, as positivity of disease-specific antibodies. Body mass index (BMI) also improved in GFD subjects, but did not decrease in CH children. Changes in IGF-I and IGFBPs did not correlate with each other. Levels of IGF-I, but not of IGFBPs, maintained the relation with age and correlated significantly with BMI and positivity of antibodies. CONCLUSIONS: These results demonstrate that CD patients show significant changes in serum IGF-I, in younger children, and IGFBPs (particularly IGFBP-1), in older children and adolescents, correlating with clinical course and response to dietary treatments. The alteration in the circulating IGF system could be implicated in the pathogenesis of growth retardation occurring in CD and may provide an additional tool in monitoring of the disease.

Autoantibodies↗
PubMedDate not supplied

Autoantibody negative new onset type 1 diabetic patients lacking high risk HLA alleles in a caucasian population: are these type 1b diabetes cases?

BACKGROUND: In Caucasians, a small number of Type 1 diabetic patients do not show evidence of humoral islet autoimmunity at disease onset, at least with common screening procedures. In African- and Hispanic-American diabetic children at time of diagnosis, many show no evidence of autoimmunity but have an atypical clinical form of the disease. According to the recent American Diabetes Association classification, this subgroup of autoantibody negative patients is referred to as Type 1b diabetic subjects. In the present study, a homogeneous Caucasian Type 1 diabetic clinic-based cohort has been evaluated at diagnosis using a large panel of diabetes-related antibodies and then characterized for various genetic features in order to identify newly diagnosed Type 1 diabetics who are potentially autoantibody negative, i.e. possibly referrable to as idiopathic Type 1b diabetes. METHODS: Newly diagnosed Type 1 diabetic patients of Italian origin (n=141, mean age 12.0+/-7.6 years) were tested for anti-islet cell, anti-insulin, anti-65 kDa isoform of glutamic acid decarboxylase and anti-amino acid residues 256-979 of the tyrosine-phosphatase IA-2 molecule autoantibodies (Step 1). Only those patients found to be autoantibody negative were tested for anti-disialo-ganglioside GD3, anti-thyroid peroxidase, anti-thyroglobulin, anti-21-OH hydroxylase, anti-gastric parietal cell and anti-transglutaminase antibodies (Step 2). Sera negative for the presence of these six autoantibodies as well were characterized in terms of HLA DRB1, DQB1 and CTLA-4. RESULTS: Six out of 141 subjects (3.5%) were autoantibody negative in the first step of the study and five out of six in the second. These five autoantibody negative patients underwent genetic analysis. Three of them had at least one Type 1 diabetes-related high risk HLA haplotype (3/141, 2.1%) while the remaining two cases showed neutral (DR5-DQB1*0301/DR5-DQB1*0301) or strongly protective (DR2-DQB1*0602/DR2-DQB1*0602) HLA genotypes, respectively (2/141, 1. 4%). CONCLUSIONS: Clinically defined Type 1 diabetic patients with no sign of autoimmunity do exist in a Caucasian population. These patients (2 out of 141) that cannot be classified as Type 1a diabetic patients lack clinical characteristics of Type 1b diabetes and have to be reconsidered for a more appropriate ADA classification. These data suggest the need of further large population-based studies to understand if Type 1b diabetes really occurs in a Caucasian population. The patient with a strongly protective HLA genotype is particularly interesting considering that among Caucasians only a few sporadic cases with Type 1 diabetes and DQB1*0602, have been reported, none of whom was homozygous at DQB1 locus.

Abatacept↗