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Biomedical subjects

Y Shoenfeld

Publications and source records attributed to Y Shoenfeld.

At least 379 records · Page 21Linked to original sources
PubMed1997

Atherosclerosis in LDL-receptor knockout mice is accelerated by immunization with anticardiolipin antibodies.

Atherosclerosis is a process initiated by accumulation of macrophages in distinct areas of endothelial cell damage and uptake of large amounts of lipids. Recently, it has been shown that the immune system plays an active part in the progression of the atherosclerotic plaque although its precise role has not yet been elucidated. Anticardiolipin antibodies (aCL) are generally found in the sera of patients with the antiphospholipid syndrome (APS) and are associated with a prothrombotic state. Several authors have demonstrated that aCL can activate platelets and endothelial cells as well as increase oxidized low density lipoprotein (LDL) uptake by macrophages. In the present study we sought to assess the effect of immunization with aCL (Ab1, leading to the production of mouse aCL-Ab3) on the progression of atherosclerosis. Two groups of 8-weeks old female LDL-receptor knockout mice (n = 13 per group) were immunized with IgG purified from the serum of an APS patient or with normal human IgG, respectively. The aCL immunized mice developed high titres of 'self' aCL (detected using the standard aCL ELISA) as compared with the normal human IgG immunized mice, whereas no differences were noted between both study groups with respect to the serum lipid levels. The extent of fatty streak formation was significantly higher in the aCL immunized mice in comparison with the human IgG injected mice (mean aortic lesion size of 5308 +/- 471 microns2 vs 1027 +/- 184 microns2, respectively, P < 0.01). The immunohistochemical analysis of the atherosclerotic plaques from both mouse groups did not display differences in cellular composition. The results of the study show that mouse aCL induced by immunization with human aCL from an APS patient enhance atherogenesis in LDL-RKO mice and imply that these antibodies may play a role in atherosclerosis development in patients with the APS.

Animals↗
PubMed1997

Aspirin for prevention of myocardial infarction. A double-edged sword.

BACKGROUND: The use of low dose aspirin is associated with upper gastrointestinal bleeding, especially in the elderly. Anemia is one of the risk factors of acute myocardial infarction especially in patients with ischemic heart disease. METHODS AND RESULTS: We present a series of fifteen patients treated with low dose aspirin for secondary prevention of ischemic heart disease who had upper GI bleeding and were admitted to our hospital because of unstable angina or myocardial infarction. Nine patients had acute myocardial infarction and six patients had unstable angina. The mean age of the patient was 72 +/- 9 years. Only two patients had a previous history of duodenal ulcer before their admission. The duration of aspirin therapy ranged from a few days to more than a year. Weakness, abdominal pain and melena were present in most of the patients between 2-7 days before the appearance of chest pain, and syncope was the chief complaint in 5 patients. CONCLUSIONS: We conclude that aspirin which is given to patients in order to prevent myocardial infarction might cause myocardial infarction as a sequella of upper gastrointestinal bleeding. Lack of patient education was the primary cause of the delayed diagnosis of this complication. Instruction of patients treated by aspirin to seek medical advise because of symptoms of gastrointestinal bleeding could prevent acute myocardial infarction in patients treated by aspirin who have upper gastrointestinal bleeding.

Aged↗
PubMed1997

Magnesium fortification of water. A possible step forward in preventive medicine?

Magnesium is an essential cation for more than 300 enzymes in our body. Among them, it is a cofactor for ATP metabolism. Diverse clinical manifestations have been reported in conjunction with Mg++ deficiencies, including sudden death, accelerated atherosclerosis, asthma, neurologic and even psychiatric clinical entities. Limited previous studies with Mg++ supplementation have shown to be of a large preventive advantages. We summarize the current literature concerning Mg++ supplementation and recommend to do so on national basis adding magnesium to the water supplies of large areas.

Humans↗
PubMed1996

[Playing with fire...].

Cigarette smoking is the most common cause of domestic fires leading to death from burns. A 63-year-old woman is described, who smoked more than 250 pack-years and developed chronic obstructive pulmonary disease, cor pulmonale, acute myocardial infarction and 2 strokes. She continued to smoke even after tracheostomy and constant oxygen therapy was instituted. She had been admitted for acute respiratory failure following 2nd and 3rd degree burns of her right cheek, neck, arm, forearm, and thigh. We draw attention of physicians and nursing staff to the potential danger of smoking during oxygen therapy. Patients who want to smoke despite oxygen therapy should have noninflammable linens and there should be smoke detectors in rooms of patients who smoke.

Acute Disease↗
PubMed1996

Analysis of different glycosylation states in IgG subclasses.

Altered IgG glycosylation affects certain immunological activities of human IgG. Enzyme-linked lectin assays (ELLA) were developed for detecting the glycosylation on IgG and its individual subclasses in sera from healthy controls. Biotinylated Sambucus nigra, Ricinus communis agglutinin I and Bandeiraea simplicifolia II were used to detect the terminal sialic acid (SA), galactose (Gal) and N-acetylglucosamine (GlcNAc) sugar residues, respectively on the captured IgG. A mild oxidation step of the anti-IgG-coated plates obviated background reaction with the lectins. Terminal glycosylation varied significantly with age. The old age group (> 65 years) had less SA in IgG1, and IgG2, when compared to young (0-19 years) and adult (20-39 years) groups, respectively. Also the old age group had less Gal in IgG2, IgG3 and IgG4 subclasses compared to the adult group, and to the young group in the case of IgG3. This ELLA system may be a valuable tool in the detection of glycosylation disorders in patients' sera.

Adult↗
PubMed1996

Pathogenic role of anti-endothelial cell antibodies in vasculitis. An idiotypic experimental model.

Idiotypic manipulation of naive mice has previously been used for induction of systemic autoimmune diseases (e.g., antiphospholipid syndrome, systemic lupus erythematosus, and Wegener's granulomatosis). The aim of this study focused on the utilization of this technique to induce the production of anti-endothelial cells Abs (AECA) and autoimmune vasculitis in a murine model. AECA were derived from a Wegener's granulomatosis patient's plasma. IgG was purified by absorption on a proteinase-3 affinity column resulting in the depletion of anti-neutrophil cytoplasmic Ab activity. The absorbed IgG fraction displayed a high titer of AECA as evidenced by a cyto-ELISA against unfixed human umbilical vein endothelial cells. BALB/c mice were actively immunized with the purified AECA. Three months after a boost injection with the human AECA, mice developed endogenous AECA (AB), but not Abs to proteinase-3, cardiolipin, or DNA. Histologic examination of lungs and kidneys revealed both lymphoid cell infiltration surrounding arterioles and venules; as well as deposition of Igs at the outer part of blood vessel walls. This experimental animal model of vasculitis, a product of our method of idiotypic manipulation, provides the first direct proof for the pathogenicity of AECA.

Animals↗
PubMed1996

Heart valve involvement (Libman-Sacks endocarditis) in the antiphospholipid syndrome.

The antiphospholipid syndrome (APS) is defined by the presence of anti-phospholipid antibodies (aPLs) and venous or arterial thrombosis, recurrent pregnancy loss, or thrombocytopenia. The syndrome can be either primary or secondary to an underlying condition, most commonly systemic lupus erythematosus (SLE). Echocardiographic studies have disclosed heart valve abnormalities in about a third of patients with primary APS. SLE patients with aPLs have a higher prevalence of valvular involvement than those without these antibodies. Valvular lesions associated with aPLs occur as valve masses (nonbacterial vegetations) or thickening. These two morphological alterations can be combined and are thought to reflect the same pathological process. Both can be associated with valve dysfunction, although such association is much more common with the latter alteration. The predominant functional abnormality is regurgitation; stenosis is rare. The mitral valve is mainly affected, followed by the aortic valve. Valvular involvement usually does not cause clinical valvular disease. The presence of aPLs seems to further increase the risk for thromboembolic complications, mainly cerebrovascular, posed by valve lesions. Superadded bacterial endocarditis is rare but may be difficult to distinguish from pseudoinfective endocarditis. The current therapeutic guidelines are those for APS in general. Secondary antithrombotic prevention with long-term, high-intensity oral anticoagulation is advised. The efficacy of aspirin, either alone or in combination, is yet to be assessed. Corticosteroids are not beneficial and may even facilitate valve damage. Immunosuppressive agents should only be used for the treatment of an underlying condition. Current data suggest a role for aPLs in the pathogenesis of valvular lesions. aPLs may promote the formation of valve thrombi. These antibodies may also act by another mechanism, as indicated by the finding of subendothelial deposits of immunoglobulins, including anticardiolipin antibodies, and of colocalized complement components in deformed valves from patients with APS.

Antiphospholipid Syndrome↗
PubMed1996

[Satisfaction among patients of a homeopathic clinic].

The use of unconventional medicine has been increasing in recent decades. We surveyed 102 patients treated in the homeopathic clinic of a large medical center (42 men and 62 women aged 1-71 years, mean 22.7), and compared them with 72 patients treated in the outpatient clinics (42 men and 32 women mean 38 years). The majority of respondents were children and young adults suffering mainly from chronic illnesses, in whom conventional treatment had been ineffective. Although standard medical insurance does not cover complementary medical treatment, the great majority of homeopathic patients maintained their insurance and continued follow-up with their conventional physician. Medical conditions diagnosed at the homeopathy clinic were different from the general distribution of medical conditions and causes of death in Israel. The 3 most frequent medical conditions treated were allergy, recurrent upper respiratory tract infections and dermatological problems. We assume that the public prefers to treat life-threatening diseases by conventional means, turning to homeopathic treatment only in the case of conditions that reduce the quality of life. More than 80% of the responders were greatly satisfied by the approach of the therapist and half felt that their principal medical condition was improved. There was no difference between reports of satisfaction by the patients of our homeopathic and conventional outpatient clinics. We believe that homeopathic medicine complements conventional medicine, and is not an alternative. We hope that this study will contribute to defining legislation regarding the status of homeopathic health services.

Adolescent↗
PubMed1996

Anti-endothelial cell IgG antibodies from patients with Wegener's granulomatosis bind to human endothelial cells in vitro and induce adhesion molecule expression and cytokine secretion.

OBJECTIVE: To elucidate the role of anti-endothelial cell antibodies (AECA) in vascular inflammation in patients with Wegener's granulomatosis (WG). METHODS: IgG fractions from 3 AECA-positive WG patients, IgG from 3 AECA-negative WG patients, and IgG from healthy donors were tested for their ability to: a) bind to endothelial cells and to display complement-dependent or antibody-dependent cellular cytotoxicity, b) modulate cell membrane expression of adhesion molecules, as evaluated by cytofluorometry and by immunoenzymatic assay, and c) induce the secretion of interleukin-1 beta (IL-1 beta), IL-6, IL-8, and monocyte chemotactic protein 1 (MCP-1). RESULTS: We found that AECA IgG from WG patients do not display any significant cytotoxicity but are able to up-regulate the expression of E-selectin, intercellular adhesion molecule 1 and vascular cell adhesion molecule 1 and to induce the secretion of IL-1 beta, IL-6, IL-8, and MCP-1. CONCLUSION: AECA in patients with WG could play a potential pathogenetic role by activating endothelial cells, and thus facilitating leukocyte recruitment and adhesion to endothelial surfaces, rather than by displaying a cytotoxic activity.

Autoantibodies↗