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M A Avanzini

Publications and source records attributed to M A Avanzini.

46 records · Page 3Linked to original sources
PubMed1986

Role of IgE in the pathogenesis of milk allergy in infancy: reassessment by a new ELISA technique.

An ELISA technique using labelled antigen for the determination of cow's milk specific IgE in serum is described. The use of labelled antigen, rather than labelled antibody as in the RAST, permits avoidance of interference by antibodies other than IgE, such as IgG, at times responsible for a negative RAST. The results obtained with the 2 techniques in 43 infants with a positive cow's milk challenge showed a positive RAST in 28%, a positive ELISA in 35% and a positive RAST or ELISA in 42%. These findings suggest that the use of both ELISA and RAST permits in vitro diagnosis of cow's milk allergy in more patients than either test alone.

Animals↗
PubMed1986

IgG2 deficiency and intractable epilepsy of childhood.

Twelve children with intractable childhood epilepsy (ICE) were treated with high-dose intravenous immunoglobulins every 21 days for 6 months after immunologic and neurologic evaluations had been carried out. 50% (6/12) were found to have a deficiency of serum IgG2 and all but 1 of these responded to treatment with marked reduction in the daily number of seizures assessed both clinically and electroencephalographically. The response to treatment was, in fact, significantly higher in the children with IgG2 deficiency than in the others. IgG4 deficiency, observed in 5 children, did not affect treatment response. It is suggested that IgG2 deficiency may predispose to some form of viral encephalitis which may trigger an immune mechanism leading to the ICE.

Child↗
PubMed1984

An avidin-biotin ELISA for the measurement of serum and secretory IgD.

This paper describes an improved microtiter solid-phase enzyme immunoassay for the determination of serum and secretory IgD. Use of the interaction between biotinylated anti-human IgD and horseradish peroxidase(HRP)-avidin conjugate permits quantitation of human IgD in the range of 1-64 ng/ml. IgD was detected in all samples of serum, saliva and nasal secretions of 28 normal adults. In only one subject both serum and secretory IgD were undetectable. The mean concentration of serum IgD determined by this assay is similar to that reported by other authors using radioimmunoassay. The assay described is not only rapid and inexpensive but at least as sensitive as the radioimmunoassays usually employed for quantitation of IgD.

Adult↗
PubMed1984

Immunofluorescence and enzyme histochemistry on consecutive sections from glycol-methacrylate-embedded bone marrow, lymph node and kidney specimens.

We describe an immunohistochemical technique adapted to tissues embedded in glycol-methacrylate (GMA). 1-micron-thick GMA sections from kidney, lymph node and bone marrow biopsies were trypsinized and then incubated with F(ab)2 antisera. GMA sections presented some distinct advantages with respect to compared paraffin and cryostatic sections: (1) reduction of background fluorescence, (2) higher resolution of morphologic details, (3) possibility of studying undecalcified bone marrow specimens and (4) possibility of coupling histochemistry with immunofluorescence on consecutive sections. Moreover, in a case of lymphoplasmacytoid lymphoma specific immunostaining for membrane IgM was obtained on GMA sections.

Acid Phosphatase↗
PubMedDate not supplied

Celiac disease and type I (insulin-dependent) diabetes mellitus in childhood: follow-up study.

To ascertain the specificity of IgA and IgG antigliadin (IgA-AGA, IgG-AGA), IgA-antireticulin (R1-ARA), and antiendomysial (AEA) antibodies for the diagnosis of celiac disease, we evaluated 133 type I diabetic children aged 1.4-28.4 years (mean 14.1 +/- 6.6), with diabetes from onset to 20.5 years. Fifty-three patients were considered at onset and 49 of these also during follow-up. IgA-AGA and IgG-AGA were determined by enzyme-linked immunosorbent assay (ELISA), R1-ARA and AEA by indirect immunofluorescence. IgA-AGA were positive in 20 of 133 (15%), IgG-AGA were positive in seven of 133 (5.26%), while R1-ARA and AEA were positive in three patients. At the onset of disease we found elevated IgA-AGA in 17 of 53 (32%) patients, IgG-AGA in four (7.55%) patients, three of them with IgA-AGA as well; R1-ARA and AEA were present in three (5.66%) patients, all with high IgA-AGA levels. During 1-10 year follow-up IgA-AGA decreased to within the normal range in 13 patients, with elevated IgA-AGA at onset but without R1-ARA and AEA; in four patients with high IgA-AGA at onset, IgA-AGA remained constantly elevated as did R1-ARA and AEA in three of them; and two patients, without IgA-AGA, R1-ARA, and AEA at onset, became positive for all three antibodies. Intestinal biopsy confirmed a diagnosis of celiac disease in five of these with IgA-AGA, R1-ARA, and AEA, but not in one patient with persistent IgA-AGA but no AEA and R1-ARA, suggesting that R1-ARA and AEA are more reliable markers for the screening of celiac disease in type I diabetic patients.

Adolescent↗
PubMedDate not supplied

Deficiency of INFgamma producing cells in adenoids of children exposed to passive smoke.

Exposure to passive smoke is a very common event associated with increased susceptibility to respiratory tract infections. Many related adverse effects result from the ability of cigarette smoke extracts to interfere with the immune system, but the mechanism is not yet completely understood. The aim of the present study is to evaluate the intracellular cytokine profile in adenoids and peripheral blood cells of children exposed to passive smoke. Children undergoing adenoidectomy exposed or not exposed to passive smoke were studied. The intracellular cytokine profile of lymphocyte subsets in adenoids and in peripheral blood were evaluated by flow cytometry analysis. Children exposed to tobacco smoke showed a significantly lower percentage of INF-gamma producing CD4+ and CD8+ cells in adenoids. Moreover a significant correlation was observed between the quantity of exposure and reduction in Th1 (CD4+INFgamma+ and CD8+INFgamma+) cells in adenoids. This reduction may be a contributing factor in the increasing susceptibility to respiratory tract infection in children exposed to tobacco smoke.

Adenoids↗
PubMedDate not supplied

Elevated IgA anti-gliadin antibodies in juvenile chronic arthritis.

Increased intestinal permeability secondary to treatment with non-steroidal anti-inflammatory drugs (NSAIDs) and raised levels of anti-gliadin antibodies (AGA) have been reported in adults with rheumatoid arthritis. We have therefore retrospectively investigated the presence of serum AGA of the IgA and IgG classes in 70 patients with juvenile chronic arthritis (JCA). Serum IgA (but not IgG) AGA were found to be higher in JCA patients than in controls (6.2 +/- 8.7 vs 2.1 +/- 1.5 AU/ml; p less than 0.0001). This finding was observed independently of the JCA onset subtype or disease activity; however, lower levels of IgA AGA were found in patients with pauciarticular JCA and in those in remission. No significant differences in IgA AGA serum levels were observed between untreated patients and patients treated with NSAIDs. Five patients who presented the highest levels of IgA AGA were further studied a second time; serum IgA AGA were found to be markedly reduced or normalized and no clinical or laboratory evidence of coexistent coeliac disease was observed. In conclusion, our results suggest that the elevation of IgA AGA seen in our patients is secondary to non-specific immune stimulation rather than to an NSAID-induced increase in intestinal permeability.

Adolescent↗