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עמוד בית
Wed, 15.05.24

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January 2008
Y. Shoenfeld, B. Gilburd, M. Abu-Shakra, H. Amital, O. Barzilai, Y. Berkun, M. Blank, G. Zandman-Goddard, U. Katz, I. Krause, P. Langevitz, Y. Levy, H. Orbach, V. Pordeus, M. Ram, Y. Sherer, E. Toubi and Y. Tomer
Y. Shoenfeld, G. Zandman-Goddard, L. Stojanovich, M. Cutolo, H. Amital, Y. Levy, M. Abu-Shakra, O. Barzilai, Y. Berkun, M. Blank, J.F. de Carvalho, A. Doria, B. Gilburd, U. Katz, I. Krause, P. Langevitz, H. Orbach, V. Pordeus, M. Ram, E. Toubi and Y. Sherer
Y. Sherer, S. Kuechler, J. Jose Scali, J. Rovensky, Y. Levy, G. Zandman-Goddard and Y. Shoenfeld

Background: Systemic lupus erythematosus is an autoimmune disease with diverse clinical manifestations that cannot always be regulated by steroids and immunosuppressive therapy. Intravenous immunoglobulin is an optional immunomodulatory agent for the treatment of SLE[1], but the appropriate indications for its use, duration of therapy and recommended dosage are yet to be established. In SLE patients, most publications report the utilization of a high dose (2 g/kg body weight) protocol.

Objectives: To investigate whether lower doses of IVIg are beneficial for SLE patients.

Methods: We retrospectively analyzed the medical records of 62 patients who received low dose IVIg[2] (approximately 0.5 g/kg body weight).

Results: The treatment was associated with clinical improvement in many specific disease manifestations, along with a continuous decrease in SLEDAI scores (SLE Disease Activity Index). However, thrombocytopenia, alopecia and vasculitis did not improve following IVIg therapy.

Conclusions: Low dose IVIg is a possible therapeutic option in SLE and is associated with lower cost than the high dose regimen and possibly fewer adverse effects.






[1] SLE = systemic lupus erythematosus

[2] IVIg = intravenous immunoglobulin


March 2006
T. Berlin, A. Lubina, Y. Levy and Y. Shoenfeld
December 2004
October 2004
Y. Levy, O. Shovman, C. Granit, D. Luria, O. Gurevitz, D. Bar-Lev, M. Eldar, Y. Shoenfeld and M. Glikson

Background: The appearance of pericarditis following insertion of a permanent pacemaker is not widely acknowledged in the literature.

Objectives: To describe our experience with pericarditis following 395 permanent pacemaker implantations over 2 years.

Methods: We retrospectively reviewed the medical records of 395 consecutive patients in whom new pacing systems or pacemaker leads had been implanted over a 2 year period. We searched the records for pericarditis that developed within 1 month after pacemaker implantation according to the ICD-9 code. The incidence, clinical picture, response to treatment and relationship to lead design and location were studied.

Results: Eight cases (2%) of pericarditis following implantation were detected. Clinical manifestations in all patients were similar to those of post-pericardiotomy syndrome and included chest pain (n=7), friction rub (n=1), fever (n=2), fatigue (n=2), pleural effusion (n=2), new atrial fibrillation (n=2), elevated erythrocyte sedimentation rate (n=4) and echcardiographic evidence of pericardial effusion (n=8). All affected patients had undergone active fixation (screw-in) lead implantation in the atrial position. The incidence of pericarditis with screw-in atrial leads was 3% compared to 0% in other cases (P < 0.05).

Conclusions: Pericarditis is not uncommon following pacemaker implantation with active fixation atrial leads. Special attention should be paid to identifying pericardial complications following pacemaker implantation, especially when anticoagulant therapy is resumed or initiated. The use of passive fixation leads is likely to reduce the incidence of pericarditis but this issue should be further investigated.

January 2003
November 2002
Alexander Gorshtein, MD, Yair Levy, MD and Yehuda Shoenfeld, MD
May 2002
Tatiana Fadeeva, MD, Yair Levy, MD, Gisele Zandman-Goddard, MD, Segal Tal, MD and Marina Perelman, MD
April 2002
September 2001
December 2000
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