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Serologic Testing for Celiac Disease in Graves' Hyperthyroidism: Should We Act Early?

BACKGROUND: The general practice is to screen patients with autoimmune thyroid disease for celiac disease (CD); however, optimal timing for … A (n = 2/35, 6%) and IgA-tTG (n = 2/35, 6%). No patient had multiple antibodies positive. Selective IgA deficiency was not detected in patients and controls. When patients were euthyroid, baseline positive IgA-AGA, IgG-AGA, and IgA-EmA became negative, while positive anti-tTG persisted in two patients. Endoscopic duodenal biopsy showed a normal villi/crypts rati …

Профиль иммуноглобулинов кори.

Профиль иммуноглобулинов проводился в 60 случаях заболевания корью (30 случаев с осложнениями и без них), а также в 30-летнем и половом возрасте. Уровни антителных титра и иммуноглобулинов (IgG, IgM и IgA) были определены соответственно путем ингибирования гемагглютинации и с помощью методов однорадиального иммунодифилирования. Несмотря на то, что в сложных случаях по сравнению с мерами контроля были выявлены более высокие уровни IgG и IgM, в этих случаях были отмечены более низкие уровни IgA. Поскольку большинство осложнений, связанных с корью, являются вторичными бактериальными инфекциями му

Совпадение в аннотации оригинала
Immunoglobulins profile was carried out in 60 cases of measles (30 each with and without complications) and 30 age and sex matched controls. … e been selected for a relatively severe form of the disease due to either a pre-existing or induced IgA deficiency.

Periodontal disease mechanisms in immunocompromised patients.

Deficiency in the number and function of phagocytes is associated with gingival inflammation and periodontitis. A hereditary deficiency in membrane glycoproteins involved in granulocyte adherence causes impaired chemotaxis, reduced phagocytosis and periodontal problems. Virus infections of antigen-presenting cells interfere with immune responses and lead to seriously increased susceptibility to infections with bacteria which cause no problems in normal patients. Increased levels of IgG antibodies may limit penetration of antigens in the tissues, but at the cost of local inflammation and tissue

B cells regulate T cell transfer colitis by partially reconstituting luminal IgA and modulating the colonic microbiota.

Loss of immune tolerance to commensal microbial antigens is a central driver of inflammatory bowel disease. While regulatory T cells are well recognized in maintaining intestinal homeostasis, the contribution of B cells-particularly IgA-secreting cells-remains incompletely defined. In the T cell transfer colitis model, cotransfer of splenic B cells attenuates disease, an effect largely attributed to IL-10-producing regulatory B cells (Bregs). However, alternative B cell-dependent mechanisms have not been fully explored. Here, we investigated whether splenic B cells regulate T cell transfer col

Trueness Evaluation and Verification of Interassay Agreement of 11 Serum IgA Measuring Systems: Implications for Medical Decisions.

BACKGROUND: To identify an IgA deficiency, the availability of reliable IgA lower reference limits is essential, especially in pediatrics. In this study, we reported the results of an intercomparison study aimed to verify the status of standardization of IgA measurements using 11 commercially available measuring systems (MSs). METHODS: After confirming its commutability, the ERM-DA470k/IFCC reference material was used for the trueness evaluation of IgA MSs. Furthermore, the interassay agreement was verified using 18 patient pools. By combining the bias, if any, between the obtained mean of ER…

Inflammatory epidermolysis bullosa acquisita with coexistent IgA antibodies to plectin.

We present a case of inflammatory epidermolysis bullosa acquisita (EBA) with IgA antibodies to plectin. Analysis of lesional skin biopsies by electron microscopy revealed the split level to be in the sublamina densa zone, corresponding to the diagnosis of EBA. Direct immunofluorescence of perilesional skin demonstrated u-serrated depositions of IgG and IgA that under immunoelectron microscopy were shown to be located in the sublamina densa. In contrast, indirect immunofluorescence on salt-split skin revealed circulating IgA antibodies that stained the roof rather than the floor of the blister.

[Antigliadin and antireticulin antibodies in juvenile insulin-dependent diabetes mellitus].

A total of 203 patients with insulin-dependent diabetes mellitus (IDDM) were screened for coeliac disease (CD) by means of serum IgA and IgG antigliadin (AGA) (ELISA) and total anti reticulin antibody (ARA) IFL assay. As suggested by Savilhati, the combination of the IgA and IgG AGA test with IgA titration in serum (to find IgA deficient individuals) identifies almost 100% of CD patients. In this study ARA antibody assay was performed and two new suspect coeliac cases were found among IgA AGA negative children. Together the ARA and AGA tests give a 3% overall prevalence of CD in IDDM. The conf

Disease modification in immunoglobulin A nephropathy.

With the rapidly expanding therapeutic landscape in IgA nephropathy, that incorporates new drugs with varied mechanisms of action, many of which may lead to modification of the fundamental pathophysiology of the world's commonest glomerular disease, thoughts are now turning to how we should define disease modification in IgA nephropathy. In the absence of validated biomarkers that reflect the pathogenic cascade we currently have to rely on proteinuria and eGFR, some would also advocate for inclusion of haematuria, and others for galactose-deficient IgA. In this review the approach to defining

Adaptive immune response to Shigella flexneri 2a cydC in immunocompetent mice and mice lacking immunoglobulin A.

Shigella flexneri cydC, which is deficient in cytochrome bd, was rapidly cleared from the lungs of intranasally inoculated mice and was Sereny negative, yet it induced 93% protection against challenge with wild-type S. flexneri. Mice that lack immunoglobulin A (IgA) were fully protected, suggesting that IgA may not be required for adaptive immunity in this model system.

Kabuki syndrome with trichrome vitiligo, ectodermal defect and hypogammaglobulinemia A and G.

We report a unique combination of symptoms in a case of Kabuki syndrome (KS), a multiple malformation/mental retardation syndrome that has a prevalence of 1:32,000 to 1:86,000. The patient was a mentally delayed 12-year-old male with trichrome vitiligo, ectodermal defect, and hypogammaglobulinemia A and G. This unique combination of signs, described here for the first time, indicates that KS comprises multiple deficits that affect not only the brain, but ectoderm-derived structures and the immune system as well. Our report may provide important clues for understanding the pathogenesis of the K

Discoid lupus erythematosus associated with a primary immunodeficiency syndrome showing features of non-X-linked hyper-IgM syndrome.

Hyper-IgM (HIM) syndrome is a rare primary immunodeficiency disorder. Approximately 120 cases have been described in the literature world-wide. Features of HIM include low serum IgG, a very low IgA with normal or high IgM levels. Autoimmune phenomena are recognized associations but connective tissue disorders have so far not been described in HIM patients. We report the case of a 19-year-old Indian woman with an immunodeficiency syndrome characteristic of non-X-linked HIM who developed discoid lupus erythematosus. Anti-double-stranded DNA antibodies were negative. Antibodies to extractable nuc

Ataxia telangiectasia with generalized skin pigmentation and early death.

A female infant with clinical and laboratory features of ataxia telangiectasia (AT) showed two clinical features exceptional for the disease, i.e. generalized skin pigmentation and an unusually early death at the age of 15 months. Her clinical features supportive of the diagnosis of AT included growth and developmental retardation and muscle weakness. Findings indicating immunodeficiency included recurrent pulmonary infections, failure of PHA stimulation of PB lymphocytes, decreased levels of serum IgM and IgA and on autopsy, an atrophic thymus without Hassall's corpuscles. Her cultured skin f

Hepatic pIgR-mediated secretion of IgA limits bacterial translocation and prevents ethanol-induced liver disease in mice.

OBJECTIVE: Alcohol-associated liver disease is accompanied by microbial dysbiosis, increased intestinal permeability and hepatic exposure to translocated microbial products that contribute to disease progression. A key strategy to generate immune protection against invading pathogens is the secretion of IgA in the gut. Intestinal IgA levels depend on the polymeric immunoglobulin receptor (pIgR), which transports IgA across the epithelial barrier into the intestinal lumen and hepatic canaliculi. Here, we aimed to address the function of pIgR during ethanol-induced liver disease. DESIGN: pIgR a

The Evolutionary Scenario of Pediatric Unclassified Primary Antibody Deficiency to Adulthood.

BACKGROUND: Unclassified primary antibody deficiency (unPAD) is a relatively novel inborn error of immunity (IEI) condition that can vary wi … 23 (13%), 2/23 (9%), and 1/23 (4%) were reclassified as common variable immunodeficiency, selective IgA deficiency, and isolated IgM deficiency, respectively. Low IgA, low specific antibody response to pneumococcus, and lower respiratory tract infections at diagnosis were independently associated with IEI persistence. CONCLUSIONS: Long-term monitoring of unPAD …

Quantitation of exocrine IgA in human serum in health and disease.

Exocrine IgA in serum was estimated by a sensitive haemagglutination-inhibition technique using a specific anti-secretory piece antiserum and colostral IgA coated cells. The mean level in healthy individuals was 5·2 μg/ml. Decreased levels are found in cord sera and the sera of IgA deficient individuals. Normal levels were found in the sera of patients with renal disease and slightly elevated levels in the sera of a group of patients with neoplastic disease. Elevated levels were found in the sera of lactating women, patients with acute chest infection, and patients with sero-positive rheumatoi

Krüppel-like factor 2 controls IgA plasma cell compartmentalization and IgA responses.

Krüppel-like factor 2 (KLF2) is a potent regulator of lymphocyte differentiation, activation and migration. However, its functional role in adaptive and humoral immunity remains elusive. Therefore, by using mice with a B cell-specific deletion of KLF2, we investigated plasma cell differentiation and antibody responses. We revealed that the deletion of KLF2 resulted in perturbed IgA plasma cell compartmentalization, characterized by the absence of IgA plasma cells in the bone marrow, their reductions in the spleen, the blood and the lamina propria of the colon and the small intestine, concomita

Most probable origin of coeliac disease is low immune globulin A in the intestine caused by malfunction of Peyer's patches.

Coeliac disease frequency increases by obscure reasons and affects in some Western countries as much as 1% of the populations. The second one of monozygotic twins does not develop the disease in 100% but only in 20-50%. To unravel these mysteries, literature was searched to determine the disease background and find suggestions for research and prevention. The causal antigen of coeliac disease is gluten of wheat that is neutralised in the intestine by secretory immune globulin A (sIgA). SIgA is secreted by the secondary (lymphoid) immune system that develops in a newborn infant after the primar

Primary immunodeficiency syndrome in Spain: first report of the National Registry in Children and Adults.

The Spanish Registry for Primary Immunodeficiency Diseases (REDIP) was organized in 1993. One thousand sixty-nine cases of primary immunodeficiency diseases (PID) were registered in patients diagnosed between January 1980 and December 1995. PID diagnosis was made according to the World Health Organization criteria. The most frequent disorders were IgA deficiency (n = 394) and common variable immunodeficiency (n = 213), followed by severe combined immunodeficiency (n = 61), C1 inhibitor deficiency (n = 52), X-linked agammaglobulinemia (n = 49), IgG subclass deficiency (n = 48), and chronic gran…