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Biomedical subjects

Yehuda Shoenfeld

Publications and source records attributed to Yehuda Shoenfeld.

At least 37 records · Page 2Linked to original sources
PubMed2006

Mechanisms of disease: atherosclerosis in autoimmune diseases.

Atherosclerosis is a pathologic process affecting blood vessels, which leads to the development of cardiovascular disease. The immune system is involved in atherogenesis and in the pathogenesis of atherosclerosis. Several autoimmune rheumatic conditions, including rheumatoid arthritis, systemic lupus erythematosus and antiphospholipid syndrome, are characterized by enhanced atherosclerosis and consequently higher cardiovascular morbidity and mortality rates. Enhanced atherosclerosis, in these diseases, can manifest as overt cardiovascular diseases, but could be detected at an earlier stage by identification of abnormal endothelial function and arterial intima-media thickening. Both classical and nonclassical risk factors are presumed to contribute to atherosclerosis progression in rheumatic diseases. As atherosclerosis can be considered to be an immune-mediated process, several experimental strategies exist for its immunomodulation, including induction of immune tolerance. In this article, we briefly review the contribution of autoimmune elements, such as autoreactive lymphocytes and autoantibodies to atherosclerosis and discuss the nature of atherosclerosis in autoimmune rheumatic diseases.

Animals↗
PubMed2006

Autoimmunity to protective molecules: is it the perpetuum mobile (vicious cycle) of autoimmune rheumatic diseases?

Apoptotic defects and impaired clearance of cellular debris are considered key events in the development of autoimmunity, as they can contribute to autoantigen overload and might be involved in the initiation of an autoimmune response. The C1q protein and mannose-binding lectin are activators of the complement system. The pentraxins are a group of highly conserved proteins including the short pentraxins, C-reactive protein and serum amyloid P, and the long pentraxin family member, pentraxin 3, all of which are involved in innate immunity and in acute-phase responses. In addition to their role in innate immunity and inflammation, each of these proteins participates in the removal of damaged and apoptotic cells. In this article, we discuss the clinical significance of different levels of these proteins, their role in the induction of or protection against autoimmunity, and the presence of specific autoantibodies against them in various autoimmune diseases.

Animals↗
PubMed2006

Long term safety of IVIg therapy in multiple sclerosis: 10 years experience.

Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system. The majority of MS patients have a relapsing-remitting course with progressive neurological disability that accumulates over the years. Intravenous Immunoglobulin (IVIg) has demonstrated benefit in the treatment of some patients with relapsing-remitting MS. Concerns about adverse events of IVIg, mainly acute renal failure and thromboembolic events have been raised in the medical literature. We examined the adverse events profile of IVIg treatment in a large cohort of 293 relapsing-remitting MS patients treated with an initial loading dose of IVIg (0.4 g/Kg body weight/day, for 5 consecutive days) and additional booster dose infusions (0.4 g/Kg body weight/booster dose, every 6 weeks) as a maintenance treatment. A total of 9281 IVIg infusions were administered within a mean treatment period of 3.8 +/- 3.5 years (3 months-10 years). The main adverse event during the loading dose period was headache, occurring in 12.6% of the patients. The annual rate of any adverse event during the IVIg maintenance period was 4.4% during the first year and had a trend to decrease with every passing year of treatment. Adverse events during the loading dose did not predict adverse events during the maintenance phase. No severe adverse events were recorded. We conclude that IVIg is a safe therapy in MS either for short or for long-term periods.

Adult↗
PubMed2006

Immunomodulation of experimental pulmonary fibrosis by intravenous immunoglobulin (IVIG).

OBJECTIVES: To assess the immunomodulatory effect of intravenous immunoglobulin (IVIG) using an experimental model of bleomycin-induced pulmonary fibrosis. METHODS: Pulmonary fibrosis was induced in C57BL/6 mice by direct intratracheal injection of bleomycin. Mice were treated with IVIG 1 week prior to (prevention protocol), or 10 days following bleomycin injection, when the disease was in progress. The controls used in the study included mice given phosphate buffered saline (PBS) and mice subjected to a commercial individual-IgG. Collagen-I deposits in the affected lungs were detected by Sirius red staining of paraffin embedded lung sections. The collagen-I content was measured by employing the hydroxyproline assay. RESULTS: Prevention of bleomycin-induced pulmonary fibrosis by IVIG has been demonstrated by reduced expression of collagen-I protein in the affected lungs. The hydroxyproline levels in the lungs of the IVIG-treated mice were 214.33 +/- 13.56 microg/1 g tissue, compared to the higher levels in lungs of IgG treated mice (342.44 +/- 35.60 microg/1 g tissue) or untreated controls 328.00 +/- 45.55 microg/1 g tissue, (p < 0.0001). Effective treatment of bleomycin-induced pulmonary fibrosis by IVIG has been demonstrated by the reduced expression of collagen-I protein in the affected lungs, detected by sirius red histological staining. The hydroxyproline levels in the lungs of the IVIG-treated mice were 261.00 +/- 18.81 microg/1 g tissue, in comparison to the higher levels in the lungs of the IgG treated mice (342.43 +/- 32.89 microg/1 g tissue) and of untreated controls (344.33 +/- 49.85 microg/1 g tissue), (p < 0.001). CONCLUSIONS: Based on these preliminary studies, we conclude that IVIG may have a beneficial effect in the down regulation of collagen-I levels in the lungs of mice with bleomycin-induced pulmonary fibrosis.

Animals↗
PubMed2006

International multicenter evaluation of autoantibodies to ribosomal P proteins.

Autoantibodies to the ribosomal phosphoproteins (Rib-P) are a serological feature of patients with systemic lupus erythematosus (SLE). The reported prevalence of anti-Rib-P antibodies in SLE ranges from 10 to 40%, being higher in Asian patients. The variation in the observed frequency may be related to a number of factors but is dependent in large part on the test system used to detect the autoantibodies. An association of anti-Rib-P with central nervous system involvement and neuropsychiatric manifestations of SLE has been controversial. In the present international multicenter study, we evaluated the clinical accuracy of a new sensitive Rib-P-specific enzyme-linked immunosorbent assay based on recombinant Rib-P polypeptides. The results showed that 21.3% of 947 SLE patients, but only 0.7% of 1,113 control patients, had a positive test result (P < 0.0001). The sensitivity, specificity, positive and negative predictive values, and diagnostic efficiency were determined to be 21.3%, 99.3%, 95.6%, 62.2%, and 65.3%, respectively. When evaluated in the context of participating centers, the prevalence of anti-Rib-P antibodies was found in descending frequency, as follows: China (35%) > Poland (34%) > Japan (28%) > United States (26%) > Germany (Freiburg; 23.3%) > Denmark (20.5%) > Germany (Berlin; 19%) > Mexico (15.7%) > Israel (11.7%) > Brazil (10%) > Canada (8%). The substantial data from this study indicate that the prevalence of anti-Rib-P antibodies may not be restricted to the genetic background of the patients or to the detection system but may depend on regional practice differences and patient selection. We confirm previously reported associations of antiribosomal antibodies with clinical symptoms and serological findings. Remarkably, we found a lower occurrence of serositis in Rib-P-positive lupus patients.

Autoantibodies↗
PubMed2006

Predicting and preventing autoimmunity, myth or reality?

Many autoimmune diseases are chronic conditions that progress over the course of years, and are characterized by the presence of autoantibodies that precede the overt disease by months or years. As examples, the presence of two islet cell antibodies (ICA) are associated with a 50% risk of developing diabetes mellitus in 5 years, anticyclic citrullinated (anti-CCP) antibodies are found in the sera of rheumatoid arthritis (RA) patients a median of 4.5 years before the overt disease, and in systemic lupus erythematosus (SLE), patients accrue antibodies throughout a foreseen course during the 3-4 years prior to the clinical symptoms. This ability to predict autoimmune diseases, or rather their clinical manifestations, leads to the prospect of screening healthy individuals for autoantibodies. The importance of such a notion lies not only in the ability to prevent life-threatening manifestations, such as Addisonian's crisis and thyroid storm, but also in the ability to treat and even prevent overt autoimmune diseases. Among such documented treatment modalities are administration of aspirin in antiphospholipid syndrome, ursodeoxycholic acid in primary biliary cirrhosis (PBC), vitamin D in SLE and autoimmune thyroid diseases (AITD), and more. Although additional studies are still needed to fully assess these notions, as well as the appropriate screening strategies to apply them, one cannot ignore the prospect of predicting and preventing autoimmunity.

Abortion, Habitual↗
PubMed2006

BCG immunotherapy--from pathophysiology to clinical practice.

Treatment with Bacillus Calmette-Guérin vaccine is mainly in use for superficial bladder cancer, for which it is given intravesically. Overall, this therapy is safe with only minor side effects. Arthritis secondary to such therapy has been rarely reported and usually responds well to NSAID treatment. The mechanisms leading to such a complication, as well as the clinical data, are discussed.

Adjuvants, Immunologic↗
PubMed2006

[Chronic fatigue syndrome].

BACKGROUND: Chronic fatigue syndrome (CFS) is characterized by severe fatigue and other non-specific symptoms. It causes disturbance of normal function. Uncertainty about etiology and the appropriate treatment, combined with high prevalence of psychiatric comorbidity, cause a problem in the perception of the disease by the patient, physician and society. OBJECTIVES: This review recapitulates the updated information regarding CFS. It addresses the following aspects: definitions, diagnosis, demographic figures, etiology and treatment options. Since much about CFS is yet to be known, a large amount of work has recently been performed on this subject. Current perceptions, as recognized today, are also presented. METHODS: A literature search was performed using Medline. RESULTS: Accurate diagnosis of CFS patients is low despite the disabling fatigue. CFS patients present certain demographic characteristics and the illness etiology is as yet unclear. Nonetheless, many possible directions exist with inconclusive evidence about certain suspected causes. There are no treatment guidelines available. Different treatment approaches were investigated without consensus on the results. CONCLUSIONS: CFS is an illness that should be taken seriously by the medical establishment. Conscious awareness of the malady might reduce rates of undiagnosed patients. The different etiologic factors showing some degree of involvement in CFS, might suggest that this syndrome is a multi-factorial condition. Despite the fact that there is no distinct undisputed treatment, there are 2 treatments (cognitive behavioral therapy and graded exercise therapy) that might be effective.

Demography↗
PubMed2006

Darier's disease.

Explore the source record for details and available documents.

Calcium-Transporting ATPases↗
PubMed2005

Juvenile idiopathic arthritis.

One of the most enigmatic problems in rheumatology has been juvenile idiopathic arthritis (JIA). Firstly, the classification has often depended on clinical features that have variations between patients. Secondly, there are different classification schemes in usage and there are few objective serologic tests that help to resolve the differences between the criteria sets. Thirdly, only recently have significant advances been made in understanding the immunology and immunopathology of JIA and, in particular, new treatment options. In this review, we will define the historical basis of JIA and emphasize not only the clinical features, but also the immunological characteristics, the pathogenesis, and treatment options. We will also discuss, in particular, quality of life, psychosocial functioning, socioeconomic outcomes and the difficult area of mortality. Finally, this review will attempt to bridge genetic observations with clinical presentation. JIA represents a relatively common syndrome of pediatric onset rheumatologic disease and a better understanding of the clinical definition, the relationship to autoimmunity, and novel treatments with biologic agents are critical for improved patient care.

Adolescent↗
PubMed2005

The infectious etiology of the antiphospholipid syndrome: links between infection and autoimmunity.

Like many other autoimmune diseases, the antiphospholipid syndrome (APS) is considered as of a multifactorial etiology, mainly genetic susceptibility coinciding with environmental triggers, of which infectious agents are considered most prominent. Different clinical and experimental studies of the beta2 glycoprotein I (beta 2 GPI) molecule, one of the target autoantigens in APS, have linked infection to the development of APS. Using a peptide phage library, it has been shown that target epitopes of beta 2 GPI share similarities with common infectious pathogens. Also, circulating anti-beta 2 GPI antibodies have been identified in the sera of patients with different infectious conditions, and have been associated with various clinical APS manifestations. Molecular mimicry as a key mechanism linking infection and APS has been demonstrated in experimental models. In these studies, APS was induced by immunization of mice to various microbial pathogens. Anti-beta 2 GPI titers were found to be especially high following immunization with Haemophilus influenzae, Neisseria gonorrheae or tetanus toxoid. These findings contribute greatly to the understanding of APS pathogenesis, as well as create new directions for therapy modalities, namely specific peptide toleragens and antimicrobial treatment.

Animals↗