J. Pinkhas
Tel Aviv University
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Publication
Featured researches published by J. Pinkhas.
Journal of the American Geriatrics Society | 1980
Yehuda Shoenfeld; R. Mor; A. Weinberger; I. Avidor; J. Pinkhas
The prevalence of ear lobe crease (ELC) was determined in 421 patients with myocardial infarction (MI) and in 421 controls. A higher prevalence (p < 0.05) of ELC was found in MI patients (77 percent) in comparison to controls (40 percent), regardless of age. In addition, a higher prevalence was found in patients in whom MI was combined with diabetic retinopathy or hypertension, and in Ashkenazi Jews compared to non‐Ashkenazi Jews. Ear lobe biopsies in 12 subjects revealed tears of the elastic fibers in all subjects with ELC, and prearteriole wall thickening in subjects with MI and/or ELC, but not in the 2 subjects with neither MI nor ELC. The early appearance of ELC may imply the existence of coronary heart disease with or without coronary risk factors.
Respiration | 1980
Shlomo Berliner; A. Neeman; Yehuda Shoenfeld; M. Eldar; I. Rousso; U. Kadish; J. Pinkhas
A patient with ulcerative colitis developed eosinophilic pneumonia, sinus tachycardia, skin rashes, headache and insomnia following treatment with Salazopyrin. The pneumonia as well as the other side effects resolved spontaneously following discontinuation of the drug and reappeared when Salazopyrin was readministered.
Cancer | 1984
Yehuda Shoenfeld; Shlomv Berliner; Arie Ayalone; Matei Shaklai; Meir Djaldetti; Albert I. Pick; J. Pinkhas
Monoclonal IgG components were found in the serum of 5 of 40 patients with chronic myelocytic leukemia (12.5%), as well as in 2 of 15 patients with acute myelocytic leukemia (13.3%). These findings may represent an involvement of the lymphoplasmacytic system in myeloproliferative disorders. The significance of this association is discussed.
Respiration | 1979
M. Eldar; Yehuda Shoenfeld; R. Zaizov; R. Fogel; J. Asherov; E. Liban; J. Pinkhas
A 16-year old patient with Fanconis anemia developed pre-leukemia and pulmonary infiltration which was found upon autopsy to be pulmonary alveolar proteinosis. The question whether the pulmonary alveolar proteinosis was due to the marked leukopenia and an eventual defective phagocytic ability of the leukocytes is raised.
Respiration | 1978
Yehuda Shoenfeld; Albert I. Pick; A. Weinberger; Mina Ben-Bassat; J. Pinkhas
A patient with multiple myeloma in whom recurrent right pleural effusion was the presenting sign of the disease is reported. An IgA (k) monoclonal component was found in both the pleural effusion and the serum. The bone marrow specimen was interpreted as typical for multiple myeloma and the pleural fluid contained numerous plasma cells. Treatment with cyclophosphamide was followed by clinical improvement and the disappearance of the pleural effusion.
Immunology Letters | 1985
Yehuda Shoenfeld; Nechama I. Smorodinsky; Gad Lavie; Bilha Hazaz; Henri Joshua; J. Pinkhas
Seven of 60 human monoclonal anti-DNA autoantibodies derived from 3 patients with SLE were shown to bind to Raji cells by radioimmunoassay. The binding of the lupus autoantibodies to the Raji cells in solution was not affected by prior incubation of the cells with DNase. Preincubation of the monoclonal autoantibodies with polynucleotides and cardiolipin, resulted in significant inhibition which correlated with the direct binding characteristics of these antibodies. Previous results with mouse IgG monoclonal anti-DNA antibodies supported by our results with human IgM anti-DNA autoantibodies suggest caution in interpreting analyses of immune complexes of sera containing anti-DNA antibodies entailing Raji cells.
Scandinavian Journal of Rheumatology | 1983
Shlomo Berliner; Yehuda Shoenfeld; Y. Sidi; M. Santo; A. Weinberger; D. Luria; Bilha Hazaz; M. Pecht; R. Zaizov; J. Pinkhas
After 3 years of treatment with azathioprine and prednisone, immunoblastic lymphoma appeared in a patient with systemic lupus erythematosus. An increased incidence of immunological aberrations and malignancies was found in her family and their relation to the pathogenesis of this patients diseases is discussed.
Rheumatology International | 1986
A. Levy; A. Weinberger; C. Mor; J. Pinkhas
SummaryTwo patients with cutaneous polyarteritis nodosa with nodules in the lower extremities and another patient with an unusual presentation of polyarteritis nodosa involving only the arteries of the breast are reported.
Scandinavian Journal of Rheumatology | 1984
Shlomo Berliner; A. Weinberger; R. Zamir; Bilha Hazaz; J. Pinkhas
The coexistence of cryoglobulinemia and C4 deficiency was found in one family. Twelve subjects were examined, most of them being asymptomatic. Cryoglobulins were found in 9 members and its type was defined in 6 of them, 3 having mixed IgM-IgG and 3 having monoclonal IgM cryoglobulins. The concentration of the third component of the complement system was normal in 10 subjects, while the concentration of the fourth one was found to be below the lower limit of normal in 9 subjects. Only C4 deficiency--and not cryoglobulinemia--was HLA-linked. There was no evidence of HBs antigenemia. The results of this study are discussed in the light of the pertinent literature.
Respiration | 1983
Dan Aderka; G. Shavit; Doron Garfinkel; M. Santo; S. Gitter; J. Pinkhas
In a hypothyroid patient who suffered also from chronic obstructive lung disease and mild congestive heart failure, treatment with 1 g/day theophylline administered orally, was followed by a life-threatening theophylline intoxication manifested by repeated epileptic fits and ventricular fibrillation, successfully reverted to sinus rhythm. The plasma theophylline was 34.7 micrograms/ml when the life-threatening arrhythmia occurred. Pharmacokinetic studies conducted during the hypothyroid state revealed a markedly prolonged theophylline plasma half-life of 29.5 h. 2 months later, after reestablishment of an euthyroid state, theophylline plasma half-life was shortened to normal, i.e. 5.7 h and the theophylline plasma level was 13.5 micrograms/ml, while the daily intake was 1 g. We conclude that hypothyroidism may predispose to theophylline intoxication, probably because of the decreased activity of the hepatic microsomal drug-metabolizing enzymes, responsible for the degradation of theophylline.