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Biomedical subjects

Y Shoenfeld

Publications and source records attributed to Y Shoenfeld.

At least 487 records · Page 27Linked to original sources
PubMed1995

[Cerebral infarction in Crohn's disease].

Thromboembolic complications in Crohn's disease are not rare. Most of them are disseminated vascular thrombosis or pulmonary emboli. Cerebral artery thrombosis is a rare complication of Crohn's disease. We describe a 27-year-old woman who had Crohn's disease for 8 years, with exacerbation 3 months before admission. She had bloody diarrhea, abdominal pain, weight loss, weakness, and anemia. Hemoglobin was 6.3 g/dl and she received 3 packed cell transfusions the day of admission. Her hemoglobin level rose to 13 g/dl. 2 days after admission she had generalized tonic-clonic convulsions, followed by hemiparesis. EEG and CT examinations showed right temporal lobe infarction. Many studies report a hypercoagulable state in Crohn's disease, which results in a thromboembolic tendency that is potentially fatal.

Adult↗
PubMed1995

Induction of Goodpasture antibodies to noncollagenous domain (NC1) of type IV collagen in mice by idiotypic manipulation.

The characteristic pathogenic autoantibodies in Goodpasture's syndrome (GPS) are directed to the noncollagenous domain (NC1) of basement membrane type IV collagen. To examine whether immunization with anti-NC1 antibodies could lead to GPS-like pathology, naive BALB/c mice were immunized intradermally with a mouse IgG anti-NC1 monoclonal antibody or IgG serum fraction derived from patients with GPS. Mice immunized with normal mouse or human IgG and nonimmunized mice served as controls. Anti-NC1 antibodies of IgG isotype were detected in the sera of mice injected with anti-NC1 antibodies, but not in the sera of control mice. The presence of circulating anti-NC1 antibodies coincided in some of the mice erythrocyturia or proteinuria and pathological changes in the kidneys. No pathologic alterations were seen in the control mice. The results show that specific idiotypic manipulation can induce anti-NC1 antibodies and pathological changes resembling human GPS.

Animals↗
PubMed1994

[Thromboembolic events in heparin-induced thrombocytopenia].

Thrombocytopenia following heparin treatment appears in 5% of patients so treated. In 20% of such patients paradoxical thromboembolic phenomena may be associated with the thrombocytopenia. This process is most probably mediated via an antibody reaction against a heparin-platelet complex. We present a 70-year-old woman with recurrent episodes of lower extremity thrombophlebitis associated with thrombocytopenia following treatment with heparin for pulmonary embolism.

Aged↗
PubMed1994

Induction of tissue factor-like activity in monocytes by anti-cardiolipin antibodies.

Anti-cardiolipin Abs (ACLA) are present in the sera of patients with antiphospholipid syndrome (APLS) and are associated with high incidence of thromboembolic phenomena, fetal loss, thrombocytopenia, and prolongation of the phospholipid-dependent coagulation assays (lupus anticoagulant). Recently, it has been shown that APLS can be induced experimentally by using ACLA. However, the pathophysiology of thrombus formation in this syndrome is unknown. Monocytes generate a potent procoagulant activity (PCA) after stimulation with various substances. Increased PCA has been found in monocytes from patients with diseases that are associated with high incidence of thromboembolic phenomena. In the present study, we report that the monoclonal ACLA that were shown previously by us to induce APLS stimulate mononuclear cells to generate a potent PCA. The PCA resembled tissue factor (TF) in that it accelerated clotting through the extrinsic coagulation pathway, was abolished by phospholipase C, and was inhibited by anti-TF mAbs. The induction of TF-like activity by ACLA in monocytes was dose- and time-dependent. It was induced in monocytes and monocytic cell lines, but not in lymphoid or myeloid cells, and did not require T lymphocytes for expression. The generation of PCA was dependent on protein synthesis inasmuch as it was prevented by adding puromycin to the system and was not affected by cytarabine. The TF-like activity that is induced by ACLA in monocytes may activate coagulation and thereby play a major role in the pathogenesis of thrombus formation in APLS.

Adult↗
PubMed1994

[CA 125 in diagnosis and prognosis of epithelial ovarian cancer].

In 59 women with epithelial ovarian cancer serum CA 125 was determined and they were then followed for 3 years. In those with active disease, mean serum CA 125 (289 units/ml) and positivity rate (85%) were significantly higher than in those without evidence of disease (44 units/ml and 17%, p = 0.001 and p < 0.001, respectively). Actuarial 3-year survival curves were calculated according to CA 125 serum level. 91% of those with CA 125 lower than 35 units/ml survived 3 years, as compared to 40% of those with CA 125 levels higher than 35 units/ml (p < 0.01). In ovarian cancer CA 125 serum level correlates with the state of the disease and can be used in the prediction of 3-year survival.

Actuarial Analysis↗
PubMed1994

Suppression of experimental antiphospholipid syndrome and systemic lupus erythematosus in mice by anti-CD4 monoclonal antibodies.

OBJECTIVE: To investigate whether anti-CD4 antibodies can suppress experimental antiphospholipid syndrome (APS) and systemic lupus erythematosus (SLE) induced by an anti-DNA monoclonal antibody (MAb). METHODS: BALB/c mice were treated with anti-CD4 MAb either before or 2 months after induction of experimental APS and SLE. Control mice were treated with rat IgG or phosphate buffered saline. Serologic and clinical manifestations of the disease were determined. RESULTS: Treatment of mice with anti-CD4 before or 2 months after disease induction prevented the development of experimental APS and SLE. The treated mice did not develop leukopenia or proteinuria, and had fewer episodes of fetal resorption. Similarly, the treated mice did not develop elevated erythrocyte sedimentation rate, prolonged activated partial thromboplastin time, or thrombocytopenia, and had significantly lower levels of antibodies to double-stranded DNA, histones, MIV-7, cardiolipin, and phosphatidylserine. Levels of CD4+ cells in the lymph nodes declined temporarily after the treatment and then returned to normal. CONCLUSION: Anti-CD4 antibodies can prevent experimental APS and SLE. These results may suggest a role for anti-CD4 treatment in human autoimmune diseases.

Animals↗
PubMed1994

Immunization with anticardiolipin cofactor (beta-2-glycoprotein I) induces experimental antiphospholipid syndrome in naive mice.

Beta-2-GPI is a 50 kDa glycoprotein which is known to be a serum co-factor, with a role in determining the binding of pathogenic anticardiolipin antibodies to phospholipids. Immunization of naive mice with beta-2-GPI resulted in elevated levels of antibodies directed against negatively charged phospholipids (cardiolipin, phosphotidylserine, phosphatidylinositol). The presence of increased titres of antiphospholipid antibodies in the sera of the mice was later followed by prolonged activated partial thromboplastin time (APTT), thrombocytopenia, and when the mice were mated, by a high percentage of fetal resorptions in the uterus. These data point to the ability of beta-2-GPI to induce pathogenic anti-cardiolipin antibodies following active immunization.

Animals↗
PubMed1994

Immunosuppressive acidic protein serum levels in breast cancer patients in a reference to CA 15-3 levels.

Immunosuppressive acidic protein (IAP) has been described as a tumor marker in a number of malignant diseases. To evaluate the clinical importance of IAP in breast cancer patients, IAP serum level was determined in 75 breast cancer patients, using single radial immunodiffusion. Serum samples were also tested for CA 15-3. Cut off value for IAP was determined according to IAP serum level in 50 patients with benign, non inflammatory, diseases, and was set as 725 microgram/ml. Mean IAP serum level (623 mcg/ml) and positivity rate (20%) in 24 breast cancer patients with active disease were similar to those in 51 breast cancer patients with no evidence of disease (590 mcg/ml and 18%). The mean CA 15-3 serum level and positivity rate were significantly higher in patients with active disease (200 units/ml, 67%), compared to patients with no evidence of disease (18.3 units/ml, 6%). In our experience IAP was not found to be an effective tumor marker in breast cancer.

Adult↗
PubMed1994

Vitiligo- and melanoma-associated hypopigmentation: a similar appearance but a different mechanism.

The significance of the association between the appearance of hypopigmentation in patients with melanoma and the prognosis is still not clear. It was postulated that, in melanoma, an immune response is responsible for the destruction of the malignant as well as the normal pigmented cells, and that the eventual development of vitiligo-like patches in melanoma patients improves their prognosis. We studied the level of anti-melanoma antibodies in the sera of patients with melanoma with hypopigmentation and compared it to the titer in patients with melanoma only, to the titer of patients with vitiligo, and to that of healthy subjects. Only IgG-type antibodies were found in the sera of patients with vitiligo, with melanoma, or with melanoma with hypopigmentation. No significant differences in the titer of anti-melanoma antibodies could be found between the patients with melanoma when subgrouped according to the initial stage and the status of the disease at the time when the test was carried out. Statistically significantly (P < 0.001) higher titers of antibodies were detected in the sera of patients with vitiligo in comparison to the lower titers in the other groups. Our results point to a similar immunobiological status, which probably does not give any advantage to patients with melanoma with hypopigmentation compared to patients without it. The appearance of hypopigmentary plaques in melanoma patients should be regarded, in our opinion, as a concomitant immunological phenomenon of the disease.

Adolescent↗