ELEVATED SERUM IgA GLOBULIN IN ANAPHYLACTOID PURPURA

PEDIATRICS ◽  
1971 ◽  
Vol 47 (6) ◽  
pp. 1023-1028
Author(s):  
Carl W. Trygstad ◽  
E. Richard Stiehm

Serial determinations of serum levels of IgA, IgD, IgG, and IgM globulin were performed on 27 children with anaphylactoid purpura and two children with acute poststreptococcal glomerulonephritis. Ten of 20 children with anaphylactoid purpura seen within 3 months of the onset of the skin rash had significant elevations of their serum IgA globulin. The other immunoglobulin levels were normal in the remaining children and those with acute poststreptococcal glomerulonephritis. The selective elevation of serum IgA globulin may be related to the pathogenesis of anaphylactoid purpura.

PEDIATRICS ◽  
1967 ◽  
Vol 40 (6) ◽  
pp. 1028-1030
Author(s):  
WARREN F. DODGE ◽  
BENJAMIN H. SPARGO ◽  
LUTHER B. TRAVIS

Additional cases of acute glomerulonephritis in sibling contacts were observed in from one fourth (proven by renal biopsy) to one half (proven and suspected) of the index case sibships examined. These data suggest that the occurrence of acute glomerulonephritis in family contacts of children with sporadic acute poststreptococcal glomerulonephritis is so common as to warrant close observation of the other siblings.


2017 ◽  
Vol 18 (3-4) ◽  
pp. 75
Author(s):  
H. Alatas ◽  
I.G.N. Wila Wirya ◽  
T. Tambunan

Seventy children who were hospitalized for kidney diseases in the Nephrological ward Department of Child Health, University of Indonesia, Jakarta were used in this study. Thirty seven patients sufferfng from acute poststreptococcal Glomerulonephritis (A.G.N.), 3 patients with Membranoproliferative Glomerulonephritis (M.P.G.N.) and 30 patients with Nephrotic Syndrome due to other causes were examined for complement concentration. A total of 80 samples were examined for C3 and 25 samples for C4 concentration using the immunediffusion plates. Almost all patients with A.G.N. and M.P.G.N. showed depression of C3. C4 concentration was normal except in 2 patients, 1 with A.G.N. and the other With M.P.G.N. This suggest activation of complement at the C3 level by the alternating pathway in most of the patients. C3 concentration in A.G.N. patients returned to normal after 8-10 weeks. In MPGN the depression was persistent in 2 patients, while in 1 patient it returned to normal level after 3 months of Immunosuppressive treatment.


1985 ◽  
Vol 69 (2) ◽  
pp. 113-121 ◽  
Author(s):  
C. A. Ollis ◽  
S. Tomlinson ◽  
D. S. Munro

Graves’ disease is the commonest form of hyperthyroidism in which excessive production of thyroid hormones by the hyperplastic overactive thyroid gland produces elevated serum levels of the thyroid hormones tri-iodothyronine (T3) and thyroxine (T4). Many of the manifestations of Graves’ disease, increased basal metabolic rate, increased heart rate, heat intolerance, sweating and nervousness, can be attributed to the peripheral actions of the excess thyroid hormones. The pathogenesis of many of the other dramatic features of Graves’ disease, such as the eye involvement or localized skin changes, is not fully understood, but circulating immunoglobulins with thyroid stimulating activity are almost certainly linked to excess thyroid hormone production and thereby cause the hyperthyroidism.


2000 ◽  
Vol 191 (12) ◽  
pp. 2171-2182 ◽  
Author(s):  
Abdalla Rifai ◽  
Kim Fadden ◽  
Sherie L. Morrison ◽  
Koteswara R. Chintalacharuvu

Human immunoglobulin (Ig)A exists in blood as two isotypes, IgA1 and IgA2, with IgA2 present as three allotypes: IgA2m(1), IgA2m(2), and IgA2m(n). We now demonstrate that recombinant, chimeric IgA1 and IgA2 differ in their pharmacokinetic properties. The major pathway for the clearance of all IgA2 allotypes is the liver. Liver-mediated uptake is through the asialoglycoprotein receptor (ASGR), since clearance can be blocked by injection of excess galactose-Ficoll ligand and suppressed in ASGR-deficient mice. In contrast, only a small percentage of IgA1 is cleared through this pathway. The clearance of IgA1 lacking the hinge region with its associated O-linked carbohydrate was more rapid than that of wild-type IgA1. IgA1 and IgA2 that are not rapidly eliminated by the ASGR are both removed through an undefined ASGR-independent pathway with half-lives of 14 and 10 h, respectively. The rapid clearance of IgA2 but not IgA1 through the liver may in part explain why the serum levels of IgA1 are greater than those of IgA2. In addition, dysfunction of the ASGR or altered N-linked glycosylation, but not O-glycans, that affects recognition by this receptor may account for the elevated serum IgA seen in liver disease and IgA nephropathy.


2018 ◽  
Vol 5 (5) ◽  
pp. 1933
Author(s):  
Shyamali Datta ◽  
Bijan Kumar Datta ◽  
Avirupa Kansha Banik ◽  
Nilanjan Datta

Background: In the critical phase of immunological immaturity of the newborn, particularly for the immune system of mucous membranes, infants receive large amounts of bioactive components through colostrum and breast milk. Breastfeeding provides unsurpassed natural nutrition to the newborn and infant. Study was done to know the effects of breast milk feeding versus formula feeding in early infancy on the development of serum IgA, IgM and IgG.Methods: The present study investigated 100 cases of failure of breast feeding. The cases included both complete and partial failure. Values of immunoglobulin levels (IgA, IgM and IgG) in the serum of eleven breast fed and eleven artificially fed infants (all aged one month) were determined using Tripartigen plates.Results: Mean level of IgA in artificially fed infants was 20.72±3.82µg/100 ml. The diameter of precipitin ring using sample number 7 was 3.9 mm. The mean level of IgA in breast fed infants was 25.94±3.89 µg/100 ml.  The mean level of IgM in artificially fed infants was 31.690±3.504 µg/100 ml. The mean level of IgM in breast fed infants was 36.81±5.13 µg/100 ml. The mean level of IgG in artificially fed infants was 480.25±52.23 µg /100 ml. The mean level of IgG in breast fed infants was 517.59±56.72 µg /100 ml.Conclusions: It is evident from the results of immunoglobulin estimation (Ig A, Ig M and IgG) in infants with artificial milk and in infants with breast milk (vide table 5, 6, 7, 8, 9 and 10) that though the mean serum levels (Ig A, Ig M and IgG) in breast fed infants were slightly higher than that of artificially fed infants. There was no statistically significant difference in the serum immunoglobulin levels between these two groups.


2009 ◽  
Vol 36 (5) ◽  
pp. 976-983 ◽  
Author(s):  
YOHEI IWATA ◽  
AYUMI YOSHIZAKI ◽  
FUMIHIDE OGAWA ◽  
KAZUHIRO KOMURA ◽  
TOSHIHIDE HARA ◽  
...  

Objective.To determine serum concentrations of pentraxin 3 (PTX3) and its clinical associations in patients with systemic sclerosis (SSc).Methods.Serum PTX3 levels from 45 patients with diffuse cutaneous SSc (dSSc), 46 with limited cutaneous SSc (lSSc), and 20 healthy controls were examined by ELISA. PTX3 expression in the sclerotic skin from SSc patients was evaluated immunohistochemically. Normal and SSc fibroblasts were cultured and PTX3 levels in the culture medium were also examined by ELISA.Results.Serum PTX3 levels were elevated in patients with SSc relative to controls. PTX3 levels in dSSc patients were significantly higher than in controls and lSSc patients. PTX3 expression in the sclerotic skin from SSc patients was more intense relative to normal skin. Elevation of serum PTX3 levels was associated with more frequent presence of pulmonary fibrosis, cardiac disease, and pitting scar/ulcer and increased serum immunoglobulin levels and erythrocyte sedimentation rates. PTX3 levels correlated positively with modified Rodnan total skin thickness score, and negatively with percentage vital capacity and percentage DLCO in patients with SSc. PTX3 levels also correlated positively with serum levels of 8-isoprostane, a marker of oxidative stress, and hyaluronan, recently identified as an endogenous ligand for Toll-like receptors. PTX3 production from cultured SSc fibroblasts was increased by stimulation with hyaluronan.ConclusionThese results suggest that elevated serum PTX3 levels are associated with the disease severity of SSc.


Author(s):  
Bianca Mages ◽  
Thomas Fuhs ◽  
Susanne Aleithe ◽  
Alexandra Blietz ◽  
Constance Hobusch ◽  
...  

AbstractIn the setting of ischemic stroke, the neurofilament subunit NF-L and the microtubule-associated protein MAP2 have proven to be exceptionally ischemia-sensitive elements of the neuronal cytoskeleton. Since alterations of the cytoskeleton have been linked to the transition from reversible to irreversible tissue damage, the present study investigates underlying time- and region-specific alterations of NF-L and MAP2 in different animal models of focal cerebral ischemia. Although NF-L is increasingly established as a clinical stroke biomarker, MAP2 serum measurements after stroke are still lacking. Therefore, the present study further compares serum levels of MAP2 with NF-L in stroke patients. In the applied animal models, MAP2-related immunofluorescence intensities were decreased in ischemic areas, whereas the abundance of NF-L degradation products accounted for an increase of NF-L-related immunofluorescence intensity. Accordingly, Western blot analyses of ischemic areas revealed decreased protein levels of both MAP2 and NF-L. The cytoskeletal alterations are further reflected at an ultrastructural level as indicated by a significant reduction of detectable neurofilaments in cortical axons of ischemia-affected areas. Moreover, atomic force microscopy measurements confirmed altered mechanical properties as indicated by a decreased elastic strength in ischemia-affected tissue. In addition to the results from the animal models, stroke patients exhibited significantly elevated serum levels of MAP2, which increased with infarct size, whereas serum levels of NF-L did not differ significantly. Thus, MAP2 appears to be a more sensitive stroke biomarker than NF-L, especially for early neuronal damage. This perspective is strengthened by the results from the animal models, showing MAP2-related alterations at earlier time points compared to NF-L. The profound ischemia-induced alterations further qualify both cytoskeletal elements as promising targets for neuroprotective therapies.


Author(s):  
Pooja Madki ◽  
Mandya Lakshman Avinash Tejasvi ◽  
Geetha Paramkusam ◽  
Ruheena Khan ◽  
Shilpa J.

Abstract Objectives The aim of the present study is to evaluate the role of immunoglobulins (IgA, IgG, and IgM) and circulating immune complexes (CIC) as tumor marker in oral cancer and precancer patients. Materials and Methods The present study was performed on 45 individuals subdivided into three groups, that is, oral precancer, oral cancer and healthy individuals, and levels of immunoglobulins, and CIC was estimated by turbidometry and ELISA method. Results In the present study, the mean serum IgA levels in oral precancer were 161.00 ( ±  118.02) mg/dL, oral cancers were 270.67 ( ±  171.44) mg/dL, and controls were 133.73 ( ±  101.31) mg/dL. Mean serum levels of IgG in oral precancer were 1,430.87 ( ±  316) mg/dL, oral cancers were 1,234.27 ( ±  365.42) mg/dL, and controls were 593.87 ( ±  323.06) mg/dL. Conclusion We found that the levels of serum IgG and IgA were elevated consistently in precancer and cancer group, and Serum IgM levels were increased only in precancer. Also, significant increase in serum CIC levels were seen in oral precancer and cancer group on comparison with control.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Danielle Perez-Bercoff ◽  
Hélène Laude ◽  
Morgane Lemaire ◽  
Oliver Hunewald ◽  
Valérie Thiers ◽  
...  

AbstractAPOBEC3 (A3) enzymes are best known for their role as antiviral restriction factors and as mutagens in cancer. Although four of them, A3A, A3B, A3F and A3G, are induced by type-1-interferon (IFN-I), their role in inflammatory conditions is unknown. We thus investigated the expression of A3, and particularly A3A and A3B because of their ability to edit cellular DNA, in Systemic Lupus Erythematosus (SLE), a chronic inflammatory disease characterized by high IFN-α serum levels. In a cohort of 57 SLE patients, A3A and A3B, but also A3C and A3G, were upregulated ~ 10 to 15-fold (> 1000-fold for A3B) compared to healthy controls, particularly in patients with flares and elevated serum IFN-α levels. Hydroxychloroquine, corticosteroids and immunosuppressive treatment did not reverse A3 levels. The A3AΔ3B polymorphism, which potentiates A3A, was detected in 14.9% of patients and in 10% of controls, and was associated with higher A3A mRNA expression. A3A and A3B mRNA levels, but not A3C or A3G, were correlated positively with dsDNA breaks and negatively with lymphopenia. Exposure of SLE PBMCs to IFN-α in culture induced massive and sustained A3A levels by 4 h and led to massive cell death. Furthermore, the rs2853669 A > G polymorphism in the telomerase reverse transcriptase (TERT) promoter, which disrupts an Ets-TCF-binding site and influences certain cancers, was highly prevalent in SLE patients, possibly contributing to lymphopenia. Taken together, these findings suggest that high baseline A3A and A3B levels may contribute to cell frailty, lymphopenia and to the generation of neoantigens in SLE patients. Targeting A3 expression could be a strategy to reverse cell death and the generation of neoantigens.


Antibodies ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 57 ◽  
Author(s):  
Patrícia de Sousa-Pereira ◽  
Jenny M. Woof

Immunoglobulin A (IgA) plays a key role in defending mucosal surfaces against attack by infectious microorganisms. Such sites present a major site of susceptibility due to their vast surface area and their constant exposure to ingested and inhaled material. The importance of IgA to effective immune defence is signalled by the fact that more IgA is produced than all the other immunoglobulin classes combined. Indeed, IgA is not just the most prevalent antibody class at mucosal sites, but is also present at significant concentrations in serum. The unique structural features of the IgA heavy chain allow IgA to polymerise, resulting in mainly dimeric forms, along with some higher polymers, in secretions. Both serum IgA, which is principally monomeric, and secretory forms of IgA are capable of neutralising and removing pathogens through a range of mechanisms, including triggering the IgA Fc receptor known as FcαRI or CD89 on phagocytes. The effectiveness of these elimination processes is highlighted by the fact that various pathogens have evolved mechanisms to thwart such IgA-mediated clearance. As the structure–function relationships governing the varied capabilities of this immunoglobulin class come into increasingly clear focus, and means to circumvent any inherent limitations are developed, IgA-based monoclonal antibodies are set to emerge as new and potent options in the therapeutic arena.


Sign in / Sign up

Export Citation Format

Share Document