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Y Shoenfeld

Publications and source records attributed to Y Shoenfeld.

At least 415 records · Page 23Linked to original sources
PubMed1996

Guillain-Barré as an autoimmune disease.

Guillain-Barré syndrome (GBS) entails a demyelinating process of the peripheral nervous system. The etiopathogenesis of the syndrome is still a matter of debate although considerable progress has been accomplished in the recent years. Abundant evidence has been put forward so as to support the role of the immune system in initiating and perpetuating the ongoing damage culminating in the emergence of the clinically overt syndrome. As such, data on the involvement of the humoral immune pathways add to the information already presented with regard to cell-mediated mechanisms participating in disruption of peripheral nerve. The following review will focus on the current knowledge of these complex mechanisms and the relative significance of each in the pathogenesis of GBS.

Animals↗
PubMed1996

Treatment of systemic lupus erythematosus and antiphospholipid syndrome: from experimental models to patients' bedside.

Animal models are of great value in the evaluation of novel and experimental treatments that cannot be tested directly on patients. In this article, we summarize the spectrum of murine models for systemic lupus erythematosus and antiphospholipid syndrome, focusing on animal models based on idiotypic immunization. Several therapeutic modalities that have been tested in those models had promising potential for application in human patients.

Animals↗
PubMed1996

Libman-Sacks endocarditis in the antiphospholipid syndrome: immunopathologic findings in deformed heart valves.

OBJECTIVE: To examine the potential immunologic mechanism and involvement of antiphospholipid antibodies in the pathogenesis of heart valve lesions in patients with the antiphospholipid syndrome (APS). METHODS: Immunoperoxidase and immunofluorescence staining methods were used to evaluate 13 heart valve specimens derived from eight patients with the APS, either primary or secondary to systemic lupus erythematosus. Primary antibodies to human immunoglobulins, complement components, serum albumin and a monoclonal anti-idiotypic antibody to human anticardiolipin antibodies (aCL) were employed. Various tissue specimens from a patient with the APS as well as deformed and normal valves from subjects without the APS were used as controls. RESULTS: Linear subendothelial deposition consisting of immunoglobulins with complement components but not of a non-specific serum protein was found in deformed valves from patients with the APS. None of the control valves or tissues disclosed similar deposition. The same pattern and location of staining was obtained by the anti-idiotypic antibody to aCL. A significant amount of IgG immunoglobulins that bound to cardiolipin was eluted from a valve of a patient with secondary APS. CONCLUSION: Deposits of immunoglobulins including aCL, and of complement components, are common in affected valves of patients with primary and secondary APS. Such deposits may be involved in the pathogenesis of valvular lesions.

Adult↗
PubMed1996

Modulation of experimental systemic lupus erythematosus with linomide.

OBJECTIVE: The objective of this study was to assess the beneficial effects of an early administration of low dose linomide, a new immunomodulator, in an animal model of experimental systemic lupus erythematosus (SLE). METHODS: Experimental SLE was induced in naive BALB/c mice, by immunization with anti-DNA mAb (MIV-7). Control Mice immunized with irrelevant human IgM served as controls. The immunized mice were treated with linomide (0.1 mg/ml in the drinking water), four weeks prior to the first immunization, at an early stage of the disease induction (one month after boost injection), or at a later stage (3 months following boost immunization). The treatment duration was 3 months in all schedules. The follow-up studies continued for 8 weeks after discontinuation of the treatment. The presence in the serum of autoantibodies against ssDNA, dsDNA histones, phospholipids and an irrelevant autoantigen-pyruvate dehydrogenase, was determined by enzyme-linked immunosorbent assay (ELISA). The clinical parameters assessed included erythrocyte sedimentation rate, peripheral blood cell counts and proteinuria. RESULTS: There was a 50-64% decrease in autoantibody levels in the sera of mice immunized with anti-DNA (MIV-7) mAb at the early stage of experimental SLE in mice which received linomide for a period of 3 months. No effect of linomide was noted in mice which received the drug during the later stages of experimental SLE when the disease was fully developed. Linomide had a preventive effect on the induction of experimental SLE in naive mice, when the treatment was initiated before the induction of the disease. This effect was abolished following cessation of the treatment. CONCLUSIONS: Linomide proved to be effective at the early stages of induction of the experimental SLE. However, the autoantibody levels rose following discontinuation of the therapy.

Adjuvants, Immunologic↗
PubMed1996

Immunomodulation of experimental APS: lessons from murine models.

During the last few years several murine models for APS have been described. These include spontaneous occurring disease, or APS induced by immunization with pathogenic autoantibodies. Employing those models, several treatment modalities, in different stages of the disease, were studied. Treatments which showed promising potential for application in patients with APS include immunomodulation with specific anti-idiotypic or anti-CD4 antibodies, treatment with IL-3, high-dose intravenous immunoglobulins, ciprofloxacin or bromocriptine, as well as antithrombotic and anticoagulant treatments using aspirin and/or low-molecular-weight heparin. Bone-marrow transplantation was also found to improve clinical and serological manifestations of the disease. These studies might promote the handling of controlled clinical trials assessing their efficacy in APS patients.

Animals↗
PubMed1996

Immune network and autoimmunity.

The concept of autoimmunity is regarded as the inability of the immune system to distinguish between self and non-self. This oversimplification of the concept is far from explaining the complex and perplexing mechanisms that are postulated to lead to its development. The transition from autoimmune state, in which no corresponding clinical manifestation exist, to an autoimmune disease, is further complicated by the evidence of multiple factors that participate in the evolution of the disease state. This article is written in a stepwise manner, initially reviewing the basic elements of the immune system, which are essential to understanding the fundamental processes underlying the occurrence of autoimmunity. Subsequently, a description of the factors involved in the etiopathogenesis and the presumed triggering events leading to the emergence of autoimmune diseases are described, with special emphasis on the important role of the idiotypic network, either in the maintenance of the normal immune response, or in the breakdown of self-tolerance eventuating in the autoimmune disease.

Animals↗
PubMed1996

Catalytic antibodies: generation, nature, and possible role as chemical warfare scavengers.

Nearly three decades have passed since the idea was proposed that antibodies may provide catalytic activity as enzymes. Since then the term "catalytic antibodies" has gained more and more popularity. Numerous antibodies enhancing the rate of reactions have been described. This review will address the basic biological considerations involved in the genesis of catalytic antibodies and explore their possible role in the future providing protection in chemical warfare.

Antibodies, Catalytic↗
PubMed1996

Comparison of clinical and laboratory parameters for systemic lupus erythematosus activity in Israelis versus Europeans.

The clinical activity of systemic lupus erythematosus (SLE) may be influenced by ethnic and environmental factors. The Consensus group on Activity Criteria for SLE attempted in a multicenter study to determine well-accepted criteria for disease activity. Of the 704 randomly assigned patients, 41 (5.8%) were from Israel. A detailed history including epidemiological, clinical and laboratory data was recorded. Significant differences were found between Israeli and European patients in the occurrence of Raynaud's phenomenon [12 (30%) vs. 358 (51%), respectively (P < 0.05)] and skin vasculitis [6 (15%) vs. 216 (34%), respectively (P < 0.05)]. In addition to those clinical differences, significant differences were also found in the occurrence of VDRL, low complement levels and lupus anticoagulant. Additional differences were found in some laboratory data, indicating differences in the sensitivity of the various laboratories. We conclude that the differences between the Israeli and European groups in the clinical data can be attributed mainly to environmental factors (weather, viruses), and in the laboratory data to ethnic differences (e.g., HLA) and to the different diagnostic methods used.

Adult↗
PubMed1996

Low dose aspirin in patients with ischemic heart disease may precipitate secondary myocardial infarction.

We conducted a retrospective case-control study to compare the frequency of myocardial infarction (MI) or unstable angina (UA) precipitated by aspirin-induced upper gastrointestinal (GI) bleeding among patients with and without ischemic heart disease(IHD), and to determine whether the risk of MI or UA is related to the hemoglobin level on admission. Of the 51 patients admitted to the hospital between 1987 and 1994 because of aspirin-induced upper GI bleeding, 33 had ischemic heart disease. The prevalence of MI and UA inpatients with IHD and aspirin-induced upper GI bleeding was significantly higher than in patients without IHD (42% vs. 5.5% respectively) (P < 0.005). Of the patients with upper GI bleeding and a hemoglobin concentration of 5-8 g/dl, 75% had either MI or UA in comparison to 50% and 18% of the patients with hemoglobin concentrations of 8-10 and 10-14 g/dl respectively. We conclude that low dose aspirin therapy may precipitate MI or UA, especially in patients with IHD, by inducing upper GI bleeding. Patients with IHD who use low dose aspirin to prevent MI should be instructed how to identify emerging symptoms of peptic ulcer as well as the initial signs of upper GI bleeding. Early diagnosis and treatment of these patients might prevent the induction of secondary MI or UA.

Aged↗
PubMed1996

No correlation between prolactin levels and clinical activity in patients with systemic lupus erythematosus.

OBJECTIVE: To assess the frequency of hyperprolactinemia and its possible clinical significance in patients with systemic lupus erythematosus (SLE). METHODS: Concentrations of prolactin (PRL) were determined in 63 consecutive patients with SLE by an immunoradiometric assay. Antinuclear antibodies, anti-DNA, ribonucleoprotein, Sm, Ro, La, and anticardiolipin antibodies were determined by standard techniques. PRL concentrations were correlated with SLE clinical and serological activity. RESULTS: Elevated serum concentration of PRL (> 20 ng/ml) were found in 10 of 63 (15.9%) patients [21 to 57 ng/ml, mean (SD) 35.6 (13.4)]. No direct correlation between PRL levels and clinical disease activity of SLE was found (Pearson correlation r = -0.186, NS). In addition, hyperprolactinemia was not associated with serological activity. CONCLUSION: Mild hyperprolactinemia is present in a subset of patients with SLE but its clinical significance is still uncertain.

Adolescent↗
PubMed1996

Anti-topoisomerase-I and clinical findings in systemic sclerosis (scleroderma).

The relationship between anti-topoisomerase-I antibodies and clinical findings was studied in 191 patients with definite systemic sclerosis. This was done by performing ELISA to detect antibodies to recombinant topoisomerase-I. Antibodies to topoisomerase-I were found in 72 patients (37%) with systemic sclerosis, which is a higher percentage than reported in most previous reports on a large unselected population. In 43 patients the presence of antibodies to recombinant topoisomerase-I was confirmed using both the immunodiffusion method and ELISA, with similar results. When classified into diffuse versus limited disease, a significant difference in antibody prevalence was demonstrated (P < 0.005), thus indicating that anti-topoisomerase-I antibody detection with ELISA may assist in early identification of systemic sclerosis subtypes.

Autoantibodies↗
PubMed1996

[Septic arthritis in an HIV-positive hemophiliac].

Despite the high frequency of bacterial infections in HIV-positive patients, septic arthritis is rare, but it is increasing in HIV-positive hemophiliacs. We describe an HIV-positive male hemophilic, aged 38, with septic arthritis who was treated unsuccessfully with antibiotics for 4 days. Synovial fluid was then aspirated and from the culture grew Salmonella (Group D). He was treated according to the in-vitro sensitivity of the organism and gradually improved. It is important to include septic arthritis in the differential diagnosis of HIV-positive hemophiliacs with arthritis and fever. Synovial fluid should be cultured early in the course of the disease to isolate the pathogen so that antibiotic therapy can be started in accordance with in-vitro sensitivity.

Adult↗