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At least 19 recordsLinked to original sources
PubMed1979

IgA synthesis by peripheral blood mononuclear cells from normal and selectively IgA deficient subjects.

IgA secretion and intracellular IgA synthesis by PWM-stimulated peripheral blood lymphocytes from normal and IgA deficient subjects were measured by radioimmunoassay. Cultured lymphocytes from eleven out of twelve IgA deficient subjects had impaired or undetectable IgA production. Measurement of intracellular IgA showed that the defect was more basic than simply defective secretion by IgA plasma cells. Co-culture of lymphocytes from IgA deficient and normal subjects revealed defects in both the B and T cell populations of IgA deficient subjects. In one subject the defect was in the T cells, in another the B cells, and in two others both T and B cells were defective.

Animals↗
PubMed1976

Virus antibody levels in IgA deficiency.

IgA-deficient blood donors and their age- and sex-matched controls were compared for the occurrence of complement-fixing antibodies in serum against several viruses. The level in the IgA-deficient persons was slightly higher against several respiratory pathogens (adenoviruses, type B influenza virus, parainfluenza virus, and respiratory syncytial virus) that give rise to localized infections, and against coxsackie B group of viruses. No corresponding difference was observed in mumps, varicella, and cytomegalovirus infections, where viraemia is a characteristic feature, or in Mycoplasma pneumoniae infection.

Adenoviruses, Human↗
PubMed1978

Distribution of IgA 1 and IgA 2 plasma cells in various normal human tissues and in the jejunum of plasma IgA-deficient patients.

The distribution of IgA 1 and IgA 2 plasma cells was studied in normal human tissues. IgA 2 is a minor constituent in peripheral lymph nodes as well as in serum and in bone marrow plasma cells. An increased proportion of IgA 2 plasma cells was observed in gastric and intestinal mucosa, as well as in bronchial mucosa and salivary and mammary glands. Tonsils and mesenteric lymph nodes exhibit values intermediate between those of central and peripheral lymphoid systems. In patients with plasma IgA-deficiency, IgA 2 is the predominant intestinal IgA plasma cells. This may explain the frequent association of an asymptomatic condition and plasma IgA deficiency.

Adolescent↗
PubMed1975

Selective IgA deficiency in blood donors.

The frequency of selective deficiency of serum IgA was determined in a population of 64,588 new Finnish blood donors by Ouchterlony's double diffusion with 10 mug/ml as the limit of detection. The incidence was 1:396. Those found IgA-deficient were retested by hemagglutination inhibition and by radioimmunoassay. The calculated incidences of IgA levels below 0.5 and 0.015 mug/ml were 1:500 and 1:800, respectively. Statistically significant compensatory elevation of serum IgG was observed in the IgA-deficient donors. The IgM levels were not changed. Among 9,920 hospital patients, the incidence of IgA deficiency was 1:660. The age structure of the IgA-deficient patients was similar to that of the IgA-deficient healthy blood donors but lower than that of hospital patients in general. No difference was observed between the clinical history of IgA-deficienct blood donors and of the controls.

Adolescent↗
PubMed1978

Immunoglobulin abnormalities in relatives of IgA deficient epileptics.

Serum levels of IgA were found to be reduced in some patients with epilepsy. Further studies revealed that only epileptics with constitutional factors for seizures showed, if ever, IgA deficiency, particularly those treated with hydantoins (up to 25%). In order further to substantiate the association of immunoglobulin alterations with epilepsy nine families in whom the disease was clustered were investigated. An IgA deficiency was detected in 16 of the 19 epileptics (three without hydantoin medication), but in none of their 45 non-epileptic relatives. However, four of the relatives had a low IgM. Seven other families were tested in each of which only one IgA deficient epileptic was known. No other family members were found with a low IgA, but 24 of 58 such relatives had increased IgM serum concentrations. The association of IgA deficiency and epilepsy with IgM imbalances in relatives of IgA deficient epileptics gives additional support for the hypothesis that immune imbalances and certain forms of epilepsy might be linked.

Epilepsy↗
PubMed1978

Gammaglobulin treatment and anti-IgA antibodies in IgA-deficient patients.

Antibodies to IgA may cause severe anaphylactic reactions during blood transfusions. Tests for anti-IgA antibodies were carried out on six patients with IgA deficiency (five of whom also had hypogammaglobulinaemia) who had received continuous gammaglobullin treatment for chronic or recurrent infections for three to eight years. Three patients had minute amounts of IgA, and three had none (less than 0.01 microgram/ml). Only one patient had anti-IgA. Her antibody titre did not change during treatment. No patient had any untoward effects of treatment, which relieved the symptoms of infection in every case. IgA determinations should be performed by more accurate methods than radial immunodiffusion when evaluating the risks of giving gammaglobulin to patients with hypogammaglobulinaemia and IgA deficiency. Probably the stimulus provided by intramuscular gammaglobulin in such patients is insufficient for the formation of anti-IgA antibody.

Adult↗
PubMed1977

Epilepsy and IgA deficiency--the effect of sodium valproate.

IgA deficiency (less than 80 IU/ml serum) occurred in 29% of 41 epileptic patients on anticonvulsant therapy. Sodium valproate users had significantly lower mean IgA levels (102 IU/ml) than non-users (151 IU/ml) and had a significantly higher incidence of IgA deficiency (50%) than non-users (16%). The occurrence of IgA deficiency did not appear to be related to age, sex, number of drugs used or to serum anticonvulsant levels.

Adult↗
PubMed1975

Anti-IgA antibodies in two brothers with selective serum IgA deficiency.

A selective serum IgA deficiency with anti-IgA antibodies at high titer were found in a patient who suffered severe transfusion reactions. The same abnormalities were detected in his brother, a 72-year-old-man in good general condition. Anti-IgA antibodies were found in the IgG fraction and were directed against alpha-chains. A deficiency of isoagglutinins and an absence of heteroagglutinins in the propositus' serum could be shown.

Aged↗
PubMed1978

The occurrence of systemic lupus erythematosus in two kindreds in association with selective IGA deficiency.

The families of two patients with SLE and IgA deficiency were examined. A study of the first patient's family revealed that IgA deficiency was determined by an incompletely penetrant autosomal dominant gene not linked to the HLA locus. Antinuclear antibodies, found in consanguineous and nonconsanguineous relatives were not related to the presence of IgA deficiency or any HLA haplotype. The second patient and his father with antinuclear, anti RBC, and antithyroid auto-antibodies shared an HLA haplotype not present in other sibs. IgA deficiency was not inherited in this family but may have influenced the expression of disease in the propositus or could have resulted from the disease itself.

Adolescent↗
PubMed1978

Immunopathology of juvenile-onset diabetes mellitus. I. IgA deficiency and juvenile diabetes.

There is an increased prevalence (P less than 0.001) of IgA deficiency in children with juvenile-onset insulin-dependent diabetes mellitus (9/366) but not in adults with insulin-dependent diabetes (0/421). The juvenile diabetics with IgA deficiency have other immune-associated diseases, such as thyroiditis and chronic active hepatitis, and have a history of infections. Four of the nine IgA-deficient diabetics we studied have autoantibodies to endocrine organs. Seven of eight have the HLA-B8, a proportion significantly (P less than 0.05) greater than control populations. Based on the clinical findings of IgA deficiency and multiple autoantibodies in patients with ataxia-telangiectasia and chronic mucocutaneous candidiasis, diseases associated with thymus deficiency, we suspect that thymus deficiency and autoimmunity may play a role in the pathogenesis of some types of juvenile-onset diabetes mellitus. In addition, an excess morbidity of the IgA-deficient juvenile diabetic population may explain the lack of IgA deficiency in older insulin-dependent diabetic individuals.

Adolescent↗
PubMed1975

Clinical and immunologic features of selective IgA deficiency.

Selective absence of serum and secretory IgA is probably the most common form of human immunodeficiency. High frequencies of recurrent sinusitis, otitis media, pneumonia, and atopy were noted among a group of 75 such patients, all but 4 of whom were Caucasian. Seven instances of familial absence of IgA were detected among 106 relatives of 34 of the group; in 1 family 1 member from each of 3 successive generations was affected. Two IgA-deficient children were later found to have normal amounts of serum IgA. Despite their humoral deficit, B lymphocytes bearing surface IgA were detected in 9/9 IgA-deficient patients in immunofluorescence studies of their peripheral blood lymphocytes. Although in vitro lymphocyte responses to 2 putative T-cell mitogens and to allogenic cells were normal, results of spontaneous rosette formation studies with sheep erythrocytes raise the possibility of a lymphocyte subpopulation deficit in this condition.

Absorption↗
PubMed1979

Circulating immune complexes in IgA deficiency.

Circulating immune complexes (IC) were demonstrated in patients with serum IgA deficiency. Sixteen of thirty-one IgA deficient patients had serum IC detected by solid phase C1q radioimmunoassay for IgG class complexes. The presence of cryoglobulins (thirteen out of thirty-one patients) and increased polyethylene glycol precipitation (ten out of thirty patients) provided additional evidence for the presence of IC. Fourteen patients were asymptomatic but seven had clinical evidence of disease which could have been IC mediated: two with glomerulonephritis, three with polyarthritis, one with vasculitis and one with thyroiditis. Serum IC remained detectable in multiple samples over several months but this correlated poorly with the presence or absence of disease. Serum antibody to IgA was detected in fifteen out of thirty-one patients. There was no direct relationship between the presence of IC and the level of serum anti-IgA antibody; however, this antibody was shown to be present in the IC isolate in eight patients. It is proposed that a considerable portion of the IC load in IgA deficiency results from defective antigen exclusion at the level of the mucosa.

Adolescent↗
PubMed1978

Serum IgE levels in patients with selective IgA deficiency.

In this study serum IgE levels were measured by a double-antibody radioimmunoassay in 31 patients with serum IgA concentration less than 0.01 mg/ml who were followed in the arthritis and allergy clinics. On a group basis there was no significant difference in mean serum IgE levels between the IgA deficient patients and normal subjects of the same age. However, in the absence of atopic disease, IgA deficient patients had significantly lower serum IgE levels. When atopy was associated with IgA deficiency IgE levels were the same as in the normal subjects but significantly lower than those of atopic non-IgA deficient patients. IgE levels in those with recurrent respiratory tract infection were not different. Adults with anti-IgA antibodies had significantly lower IgE values. IgE levels in patients with RA, JRA or SLE were not significantly different. Selective IgA deficient patients may have a relative deficiency of serum IgE depending on the comparison group.

Adolescent↗
PubMedDate not supplied

Selective IgA deficiency. Immunologic and cytogenetic studies.

24 cases of selective IgA deficiency were found among 2,650 children studied in an immuno-Allergy service. The population studied must therefore be considered highly selected. The Amman and Hong criteria were used as a basis for diagnosis (Table 1). Even though they are currently being revised, they are still on some practical value. Statistically, the incidence of selective IgA deficiency in this study is higher (0.905%) than in other publications. Respiratory symptoms were the most important. Only one case presented digestive symptoms (resembling coeliac disease), and no cases with autoimmune disease were found, although the possibility of its occurrence later on cannot be dismissed. A cytogentic analysis was performed in 8 cases and interesting results were found. Five cases showed an increase in heterochromatic material in the paracentric region (1qh+, 2qh+, 16qh+ and Yqh+). These polymorphic variations are present in the general population without any apparent clinical significance, even though their presence in several clinical has been described. However, in this study the frequency seems higher than in the general population. In 2,051 cases studied for other reasons, the frequency of occurrence of polymorphic traits was 3.12%, while in the cases studied by us the incidence amounted to 62.5%, a highly significant proportion. Our data do not try to establish a relationship between the chromosomal alterations and the etiology of the IgA deficiency, even through some relationship may in the future be found to exist.

Child↗
PubMed1978

Human antibodies to immunoglobulin A (IgA). A radioimmunological method for differentiation between anti-IgA antibodies and IgA in the serum of IgA deficient individuals.

In the sera of 12 out of 27 individuals with IgA deficiency (serum level below 0.02 mg IgA/ml) class-specific anti-IgA antibodies were demonstrated by haemagglutination. These sera showed false-positive results in a solid-phase inhibition radioimmunoassay (RIST) (apparent IgA concentration between 0.6 and 13.7 microgram IgA/ml) indicating that the RIST is not an appropriate test for the analysis of serum of IgA deficient individuals. A modification of the RIST is proposed (titration RIA) that permits differentiation between low levels of IgA and class-specific anti-IgA antibodies. With this test IgA deficient individuals could be classified as those with low but detectable levels of IgA and those with class-specific anti-IgA antibodies. A computer procedure was developed to calculate both the amount and the avidity (K) of the anti-IgA antibodies and to simulate the assay system. The K value calculated from experimental points proved to be an overestimation of the K value which fitted most adequately in the simulation. The comparison of the results with clinical findings indicated a possible correlation between the amount and the avidity of the anti-IgA antibodies and the appearance of anaphylactic reactions after transfusion of IgA.

Antibodies↗
PubMed1978

Case report. Cervical carcinoma with selective IgA deficiency.

A patient with cervical carcinoma was found to have selective IgA deficiency. The intact cell-mediated immunity, normal levels of IgG and IgM, and the absence of serum and salivary IgA established the diagnosis. Contrary to those of normal persons, salivary IgM was elevated and salivary IgA was not detectable in this patient. The patient had no signs attributable to IgA deficiency, but she always had dryness of the mouth. The association between cervical carcinoma and selective IgA deficiency was discussed.

Carcinoma, Squamous Cell↗