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Yehuda Shoenfeld

Publications and source records attributed to Yehuda Shoenfeld.

At least 109 records · Page 6Linked to original sources
PubMed2005

[Intravenous immunoglobulin (IVIG) as treatment for recurrent pregnancy loss (RPL)].

Miscarriages are the most common complication in human pregnancies. Recurrent pregnancy loss (RPL) could occur for several reasons, such as: immunological abnormalities of the pregnant women and chromosomal abnormalities of the embryo. There are several autoimmune characteristics for RPL, such as autoantibodies, and sometimes RPL are a symptom of an autoimmune disease. It is unclear whether the autoantibodies are the cause, the consequence or an artifact of the RPL. Intravenous immunoglobulin (IVIG) is a preparation made of purified plasma of thousands of healthy donors. Currently, IVIG is provided as a treatment for several autoimmune diseases. There are reports on a beneficial effect of IVIG for women with RPL of unknown reason. Some reports indicate a beneficial effect of IVIG independent of aspirin, as well as in artificial fertilization. Nevertheless, the efficacy of IVIG has yet to be established. Perhaps a certain sub-group should be defined of women who suffer from RPL and have greater odds for successful IVIG treatment. A sub-group analysis showed that, in secondary RPL, IVIG is more successful when provided after embryo implantation, whereas, in primary RPL, IVIG is better when provided prior to conceiving. Apart from the miscarriage type (secondary or primary) other factors that might influence the IVIG-treatment success were found: the number of previous miscarriages, the age of the pregnant women and the way IVIG is administrated. The mechanisms of action of IVIG in RPL are multiple, complex and not fully understood. IVIG therapy regulates the immune system in several mechanisms, in a way that might increase the survival rate of the embryo in the uterus and might decrease the odds of a miscarriage. For example, one of the main mechanisms of IVIG in RPL is down-regulation of natural killer cells (NK cells) activity and expression. This finding is of great importance because it has been reported that women who have never given birth and have high levels of NK cells in their peripheral blood have higher chances of pregnancy loss. In conclusion, IVIG is an immunomodulator that exerts its beneficial effects in multiple mechanistic ways acting together synergistically. IVIG is a potential treatment for women with RPL as a result of immunological abnormalities.

Abortion, Habitual↗
PubMed2005

[Accelerated atherosclerosis in rheumatoid arthritis].

Cardiovascular manifestations are frequent in rheumatoid arthritis (RA) and significantly contribute to morbidity and mortality in this disorder. Premature atherosclerosis is responsible for these complications, as supported by autopsy studies. Moreover, a high prevalence of sub-clinical atherosclerosis--evaluated by imaging and instrumental parameters--has been reported. Traditional risk factors cannot completely account for accelerated atherosclerosis in RA. The presence of RA by itself and the immunosuppressive therapy (especially corticosteroids) represent non-traditional risk factors for premature atherosclerosis. Additional factors playing a synergistic role in the atherosclerotic process are systemic chronic inflammation frequently associated with RA and both humoral and cellular specific autoimmune responses. Herein we review and discuss atherosclerosis in rheumatoid arthritis, with special emphasis on clinical presentations, pathogenesis and therapy.

Arteriosclerosis↗
PubMed2005

[Dermatological manifestations in the antiphospholipid syndrome].

Antiphospholipid syndrome is regarded as a systemic disease. A total of 41% of the patients are presented with one form of the diverse skin findings at diagnosis. Due to the high prevalence of skin affliction it was recently suggested to include this syndrome in the diagnostic criteria of APS. The importance of these findings also entails the fact that in 25% of the patients the skin manifestations precede thromboembolic phenomena. The findings entail livedo reticularis, anetoderma, skin necrosis and others. This article discusses their prevalence and their relationships to other clinical manifestations in APS and how to approach them therapeutically.

Antiphospholipid Syndrome↗
PubMed2005

Measurement of electrical skin impedance of dermal-visceral zones as a diagnostic tool for inner organ pathologies: a blinded preliminary evaluation of a new technique.

BACKGROUND: As complementary and alternative medicine is gaining popularity among health consumers, diagnostic screening tools based on neuroreflexology are also being developed. These techniques, which are based on the rationale that measurement of electrical impedance of specific dermatomes reflects corresponding internal organ pathologies, have not yet been the subject of conventional scientific research. OBJECTIVES: To determine the effectiveness of a neuroreflexology-based screening test, specifically the Medex device (Medex Screen Ltd.), for diagnosing patients undergoing conventional internal organ assessment, in a hospital setting. METHODS: Patients admitted to an internal medicine department, who met the inclusion criteria and agreed to participate, underwent conventional medical evaluation that included past medical history and physical examination. Another examination was conducted by a second physician using the Medex device to determine internal organ pathologies. A third researcher compared the actual "conventional" diagnosis with the Medex device output using standard statistical analysis. RESULTS: Overall, 150 patients participated in the study. Correlation was significant for all categories (P < 0.01) except for blood and lymphatic disease. A high sensitivity (>70%) was measured for cardiovascular, respiratory, gastrointestinal and genitourinary diseases. The highest measure of agreement, as represented by the Cohen-Kappa factor, was found for respiratory disease (0.57). CONCLUSIONS: Although the exact mechanism is not entirely clear, measurement of electroskin impedance of dermal-visceral zones has the potential to serve as a screening tool for inner organ pathologies. Further research should be conducted to create more evidence to support or dispute the use of this technique as a reliable diagnostic tool.

Complementary Therapies↗
PubMed2005

Low levels of heat shock proteins-60 and -65 autoantibodies in Sjögren's syndrome.

BACKGROUND: Heat shock proteins are highly conserved immunodominant antigens found in various species. Humoral immune responses to mycobacterial HSP65 and human HSP60 have been established in a number of human autoimmune diseases. OBJECTIVE: To assess the prevalence of antibodies to HSP60 kDa and HSP65 kDa in patients with Sjögren's syndrome as compared to normal subjects. METHODS: Thirty-seven patients with SS were compared with normal controls. The antibodies against human HSP60 were measured by the Anti-Human (IgG/IgM) HSP60 ELISA kit. IgGs and IgMs to mycobacterial HSP65 were determined using an enzyme-linked immunosorbent assay with mycobacterial recombinant HSP65 antigens. RESULTS: The levels of both anti-HSP60 and -HSP65 were lower in patients compared with controls. IgG autoantibodies to HSP60 were significantly different between groups: 162 +/- 55.1 ng/ml in controls versus 112.3 +/- 30.6 ng/ml in SS patients (P < 0.001). The levels among controls of anti-HSP65 IgM isotype were also significantly higher than among the SS patients: 111.6 +/- 33.4 U/ml versus 96.1 +/- 8.9 U/ml (P= 0.01). CONCLUSIONS: The results of the present study show that the levels of different isotypes of anti- HSP60 and HSP65 antibodies were lower in patients with SS than in normal subjects. Additional studies in larger patient populations are required to evaluate the prevalence of these autoantibodies in SS patients.

Autoantibodies↗
PubMed2004

From animal models to human genetics: research on the induction and pathogenicity of autoantibodies.

The revolutionary techniques of modern molecular and cellular biology enhance almost daily our knowledge of immunity and autoimmunity in men and experimental animals. Our fragmentary puzzle of the immune system is going to form a fascinating picture of a masterpiece of evolution. Although many of these aspects were achieved by analysis of human body fluids and tissues, the etiopathogenesis of autoimmune diseases cannot readily be analyzed without appropriate animal models. Therefore, the 7th Dresden Symposium on Autoantibodies has focused on experimental autoimmune models. The 295 attendants of the symposium listened to and discussed about the pathogenesis and therapy of autoimmunity in experimental mouse models, natural and pathogenic autoantibodies, molecular mechanisms of xenobiotic-induced autoimmunity, the genetic background of autoimmune diseases, novel autoantibodies and their pathogenic and/or clinical relevance, autoantibodies in systemic and neurological diseases, the occurrence and measurement of therapy-induced antibodies and methodical aspects as well as novel diagnostic strategies including multiplex assays for autoantibody profiling. Those who are interested to read the full length articles are referred to the book published in parallel to this meeting ([Conrad K, Bachmann MP, Chan EKL, Fritzler MJ, Humbel RL, Sack U, Shoenfeld Y, editors. From animal models to human genetics: research on the induction and pathogenicity of autoantibodies, Report on the 7th Dresden Symposium on Autoantibodies held in Dresden on September 1-4, 2004. Germany: Pabst Science Publishers; 2004.]; www.pabst-publishers.de).

Animals↗
PubMed2004

Suppression of early atherosclerosis in LDL-receptor deficient mice by oral tolerance with beta 2-glycoprotein I.

BACKGROUND: Atherosclerosis is considered analogous to chronic inflammatory diseases. Beta 2-glycoprotein I (beta 2GPI) is a phospholipid binding protein shown to serve as a target for prothrombotic antiphospholipid antibodies. It has recently been demonstrated to drive an immune mediated reaction and enhance murine atherosclerosis. Oral tolerance is a method in which feeding a given antigen, downregulates the respective immune responses towards it, and attenuates concomitant organ specific disorders. Herein, we tested the hypothesis, that inhibiting cellular immunity to beta 2GPI would result in suppression of fatty streak formation in mice. METHODS AND RESULTS: LDL receptor deficient mice were fed different doses of human or bovine beta 2GPI or BSA and than switched to an atherogenic diet. To determine the effect of feeding on lymph node proliferative indices, separate groups of mice were fed beta 2GPI and then immunized with the respective antigen. Feeding either human or bovine beta 2GPI was effective in attenuating atherosclerosis as compared to control fed animals. Oral feeding with of beta 2GPI inhibited lymph node cell reactivity to beta 2GPI in mice immunized against the human protein. Oral tolerance was also capable of reducing reactivity to oxidized LDL in mice immunized against oxLDL. IL-4 and IL-10 production was upregulated in lymph node cells of beta 2GPI-tolerant mice immunized against beta 2GPI, upon priming with the respective protein. CONCLUSION: Thus, oral administration of beta 2GPI is an effective means of suppressing atherogenesis in mice and should further be investigated.

Administration, Oral↗
PubMed2004

CD4+CD28- T lymphocytes contribute to early atherosclerotic damage in rheumatoid arthritis patients.

BACKGROUND: Peripheral blood expansion of an unusual CD4+ T-cell subset lacking surface CD28 has been suggested to predispose rheumatoid arthritis (RA) patients to develop more aggressive disease. However, the potential association between CD4+CD28null T cells and early atherosclerotic changes in RA has never been investigated. METHODS AND RESULTS: The number of circulating CD4+CD28null cells was evaluated in 87 RA and 33 control subjects who also underwent evaluation of carotid artery intima-media thickness (IMT) and endothelial function via flow-mediated vasodilation (FMV). Patients had higher IMT and lower FMV compared with control subjects. The frequency of CD4+CD28null cells was significantly higher in patients than in control subjects. Twenty patients with persistent expansion of circulating CD4+CD28null cells had more marked increase of carotid artery IMT and stronger decrease of brachial artery FMV. Blockade of tumor necrosis factor-alpha led to a partial reappearance of the CD28 molecule on the CD4+ cell surface. CONCLUSIONS: Circulating CD4+CD28(null) lymphocytes are increased in RA. Patients with persistent CD4+CD28null cell expansion show preclinical atherosclerotic changes, including arterial endothelial dysfunction and carotid artery wall thickening, more significantly than patients without expansion. These findings suggest a contribution of this cell subset in atheroma development in RA. Moreover, the demonstration that tumor necrosis factor-alpha blockade is able to reverse, at least in part, the CD28 deficiency on the CD4+ cell surface may be of interest for possible innovative therapeutic strategies in cardiovascular diseases.

Aged↗
PubMed2004

Systemic lupus erythematosus in a multiethnic US cohort (LUMINA). XXIII. Baseline predictors of vascular events.

OBJECTIVE: To determine the baseline (time 0) risk factors associated with the subsequent occurrence of vascular events in a multiethnic US cohort (LUMINA [LUpus in MInorities: NAture versus nurture]) of patients with systemic lupus erythematosus (SLE). METHODS: Five hundred forty-six LUMINA patients were assessed at time 0 for traditional and nontraditional (disease-related) risk factors for vascular events. These were defined as 1) cardiovascular (myocardial infarction and/or definite or classic angina and/or the undergoing of a vascular procedure for myocardial infarction [coronary artery bypass graft]), 2) cerebrovascular (stroke), and 3) peripheral vascular (arterial claudication and/or gangrene or significant tissue loss and/or arterial thrombosis in peripheral arteries). The observation time (followup time in the cohort) was the interval between time 0 and the last visit. The unit of analysis was the patient and not each vascular event. Variables at time 0 and vascular events were examined by univariable and multivariable (logistic and Cox proportional hazards regression) analyses. Age, sex, ethnicity, followup time, and all known risk factors for the occurrence of vascular events were included in the model. RESULTS: Thirty-four patients (6.2%) developed one or more vascular event after time 0. The overall median duration of followup in the cohort was 73.8 months (range 10.8-111.3 months). Vascular events (13 cardiovascular, 18 cerebrovascular, 5 peripheral vascular) occurred in 7 Hispanics from Texas (6.5%), 1 Hispanic from Puerto Rico (1.2%), 15 African Americans (7.5%), and 11 Caucasians (7.1%). The mean total number of traditional risk factors was significantly higher in patients who developed vascular events than in those who did not (7.1 versus 5.6). Independent predictors of vascular events were older age, current smoking status, longer followup time, elevated serum levels of C-reactive protein (CRP), and the presence of any antiphospholipid antibody. The same variables were identified when time-dependent analyses were performed, although azathioprine use was also found to be a contributing factor. CONCLUSION: Smoking, previously not reported in SLE, emerged as a predictor of vascular events and should be strongly discouraged. Antiphospholipid antibodies and CRP support the role of inflammation and autoimmunity in the development of accelerated atherosclerosis in SLE. Ethnicity was not associated with vascular events in our patients.

Adult↗