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Circulating Antibodies (circulating + antibody)

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Medical Sciences	100%

Selected Abstracts

A new ELISA assay for diagnosis of acquired von Willebrand Syndrome

HAEMOPHILIA, Issue 3 2003
C. Siaka
Summary. The pathophysiology of acquired von Willebrand syndrome (AVWS), a rare bleeding disorder, is not fully understood. Circulating antibodies to Von Willebrand factor (VWF) are found in patients with AVWS associated with lymphoproliferative disorders but these autoantibodies are difficult to detect with routine laboratory tests and neutralisation assays. We have developed a simple enzyme-linked immunosorbent assay (ELISA) to detect serum antibody binding to VWF protein immobilized on polystyrene plates. Ten patients with AVWS were studied, eight of whom also had lymphoproliferative disorders. We found antibodies in eight patients; all of them were positive for IgG and five were also positive for IgM. This simple method appears to be more sensitive than functional assays, which failed to identify two of the patients who were positive with the ELISA. In conjunction with other tests, this ELISA method may be useful for demonstrating the immunological mechanism underlying some cases of AVWS. Such patients would qualify for intravenous immunoglobulin therapy, which can correct the clotting disorder. [source]

Helicobacter pylori Infection and Gastric Autoimmune Diseases: Is There a Link?

HELICOBACTER, Issue 6 2003
Fabio Presotto
ABSTRACT Background.,Helicobacter pylori is thought to be involved in atrophic body gastritis. We explored the prevalence of H. pylori infection in asymptomatic subjects with gastric parietal cell antibodies, as well as in patients with pernicious anemia, to evaluate a possible role of H. pylori gastric infection in gastric autoimmunity. Patients and Methods., We studied 79 consecutive asymptomatic subjects with parietal cell antibodies, 24 patients with pernicious anemia, and 66 parietal cell antibody-negative controls. All patients underwent gastric biopsies for histology and detection of H. pylori. Red blood cell count and volume, serum levels of gastrin, pepsinogen I, iron, folic acid, vitamin B12, and circulating antibodies to H. pylori and to intrinsic factor were also determined. Results., We found an atrophic body gastritis in 14 of the 79 asymptomatic subjects with parietal cell antibodies (18%) and in 2 of the 66 controls (3%) (p = .01). Mean levels of gastrin were increased (p < .0001), while those of pepsinogen were reduced (p < .001) compared with controls. H. pylori was identified at the gastric level and/or circulating anti- H. pylori antibodies were detected in 46 parietal cell antibody-positive subjects (58%) compared with 26 controls (39%) (p = .03). In patients with pernicious anemia we found an atrophic body gastritis in 18 of 24 cases (75%) (p < .001 vs. controls). Mean levels of gastrin were markedly increased (p < .0001) and those of pepsinogen I decreased (p < .0001) relative to controls. Only five of these patients (21%) had evidence of H. pylori infection compared with 46 of the parietal cell antibody-positive subjects (58%) (p = .003) and 26 of the controls (39%). Considering all patients with gastric autoimmunity (i.e. with parietal cell antibodies and/or with pernicious anemia), H. pylori was found in 44 of 72 of those without atrophy (61%) but in 6 of 31 with gastric body atrophy (19%) (p < .001), indicating that H. pylori infection is greatly reduced when gastric acid secretion decreases. Conclusions., The frequent detection of H. pylori infection in subjects with early gastric autoimmunity, indicated by the presence of parietal cell antibodies, suggests that H. pylori could have a crucial role in the induction and/or the maintenance of autoimmunity at the gastric level. [source]

Biostability and pharmacokinetics of LJP 920, an octameric Gal (,1,3) Gal conjugate for the inhibition of xenotransplantation rejection

JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 7 2001
Lee Jia
Antibodies to an ,-galactosyl saccharide structure present in human serum are associated with hyperacute rejection and delayed xenograft rejection after pig-to-primate xenotransplantation. To overcome this major barrier to the xenotransplantation, LJP 920, a galactosyl ,1,3 galactose (Gal (,1,3) Gal) coupled to a non-immunogenic platform at a valency of eight Gal (,1,3) Gal molecules/platform, was synthesized to clear circulating antibodies and to inhibit their production by B cells that produce these antibodies. Herein we report on the stability of LJP 920 in biological media and its pharmacokinetic profile. Incubation of LJP 920 with mouse serum or liver microsomes at 37°C for 2 days showed no indication of degradation of the conjugate as detected by a reversed-phase HPLC method, indicating that the conjugate is not subject to enzymatic metabolism. After intravenous administration of LJP 920 to mice at the doses of 20 and 100 mg kg,1, LJP 920 serum concentration decreased rapidly, showing a biphasic pattern, with a distribution half-life of 3 min and an elimination half-life of more than 30 min, respectively. The serum-to-erythrocyte concentration ratio of LJP 920 was 33- and 36-fold excess at 0.5 and 5 min, respectively, after intravenous administration (100 mg kg,1). Both Cmax and AUC values increased in a dose-proportional manner. LJP 920 displayed a great distribution to well-perfused tissues. It was eliminated mainly through renal excretion in the unchanged form, which accounted for 23% of the total amount within 8 h of dosing. [source]

The role of B cells and alloantibody in the host response to human organ allografts

IMMUNOLOGICAL REVIEWS, Issue 1 2003
Attapong Vongwiwatana
Summary:, Some human organ transplants deteriorate slowly over a period of years, often developing characteristic syndromes: transplant glomerulopathy (TG) in kidneys, bronchiolitis obliterans in lungs, and coronary artery disease in hearts. In the past, we attributed late graft deterioration to ,chronic rejection', a distinct but mysterious immunologic process different from conventional rejection. However, it is likely that much of chronic rejection is explained by conventional T-cell-mediated rejection (TMR), antibody-mediated rejection (AMR), and other insults. Recently, criteria have emerged to now permit us to diagnose AMR in kidney transplants, particularly C4d deposition in peritubular capillaries and circulating antibody against donor human leukocyte antigens (HLA). Some cases with AMR develop TG, although the relationship of TG to AMR is complex. Thus, a specific diagnosis of AMR in kidney can now be made, based on graft damage, C4d deposition, and donor-specific alloantibodies. Criteria for AMR in other organs must be defined. Not all late rejections are AMR; some deteriorating organs probably have smoldering TMR. The diagnosis of late ongoing AMR raises the possibility of treatment to suppress the alloantibody, but efficacy of the available treatments requires further study. [source]