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עמוד בית
Mon, 29.04.24

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October 2002
Judith Barash, MD, Doron Dushnitzky, MD, Dalia Sthoeger, MD, Rita Bardenstein, MSc and Yigal Barak, MD,

Background: Human parvovirus B19 is responsible for a variety of clinical syndromes, such as erythema infectiosum, non-immune hydrops fetalis, transient aplastic anemia, and arthropathies. HPV is also suspected of playing a role in the pathogenesis of various chronic inflammatory and autoimmune diseases, such as systemic lupus erythematosus, rheumatoid arthritis, Kawasaki disease and multiple sclerosis.

Objectives: To study the age distribution and clinical presentation of patients hospitalized for human parvovirus B19 infection.

Method: We reviewed the case records of all pediatric patients with serologic evidence of HPV infection who were admitted during a 20 month period to a major community hospital

Results: Of 128 children tested for HPV, 48 had evidence of acute infection based on the presence of immunoglobulin M antibodies; 8 patients who also had positive IgM for other viruses were excluded, thus 40 case records were studied. The mean age of the patients was 5.21 years, but 22 patients were under 4: The clinical presentations included 25 patients with fever, either recurrent or prolonged, accompanied in some by enlarged spleen, liver and lymph nodes, skin rash and arthropathy; the remaining patients were investigated for anemia, skin rash, joint complaints and hepatitis. In addition; HPV infection was documented in several well-defihed clinical conditions, such as SLE, vasculitic skin lesions, acute lymphoblastic leukemia, pure red cell aplasia, and optic neuritis.

Conclusions: In a group of 40 pediatric patients exhibiting anti-HPV IgM antibodies, a younger age and less common clinical presentations were observed, furthermore 5 patients had clinical syndromes in which the causative role of HPV infection was not clear.

July 2002
Stephen A. Berger, MD and Itzhak Shapira, MD
June 2002
Oren Shibolet, MD, Olga Schatz, MD, Michal Krieger, MD, Alexander Maly, MD and Yoseph Caraco, MD
May 2002
Tatiana Fadeeva, MD, Yair Levy, MD, Gisele Zandman-Goddard, MD, Segal Tal, MD and Marina Perelman, MD
January 2002
Manfred S. Green MD PhD, Tiberio Swartz MD MPH, Elana Mayshar JD, Boaz Lev MD, Alex Leventhal MD MPH, Paul E. Slater MD MPH and Joshua Shemer MD

Background: The large number of cases of West Nile fever diagnosed in Israel in 2000 once again brought into focus the confusion that frequently accompanies the use of the term “epidemic”.

Objective: To examine the different definitions of the term “epidemic” and to propose ways in which it can be used to both improve communication among professionals and provide the public with a better sense of the associated risks.

Methods: The literature wes reviewed for the various definitions of the terms “epidemic” and “outbreak”. Sources included popular and medical dictionaries, ancient documents, epidemiology texts, legal texts, and the medical literature.

Result: The term epidemic is variously defined. The broad definition given by epidemiologists - namely, more disease the is anticipated by previous experience - is less meaningful to the general public. In some ways it conflicts with the definitions found in the popular literature, which generally imply danger to the public and a very large number of victims.

Conclusions: The interpretation of the term epidemic may vary according to the context in which it is used. For risk communication, we suggest that every effort be made to add descriptive terms that characterize the epidemic.

Suzan Abedat MSc, Simcha Urieli-Shoval PhD, Eli Shapira PhD, Sima Calko, Eldad Ben-Chetrit MD and Yaacov Matzner MD

Background: Familial Mediterranean fever is an autosomal recessive disease characterized by sporadic attacks of inflammation affecting the serosal spaces. The gene associated with FMF[1] (MEFV), mainly expressed in neutrophils, was recently found to be expressed also in primary cultures of serosal origin (peritoneal and synovial fibroblasts). A C5a inhibitor, previously detected in normal serosal fluids, was recently identified in serosal cultures as well, and was found to be deficient in serosal fluids and cultures obtained from FMF patients.

Objective: To investigate the effect of colchicine (the main therapeutic agent for FMF patients) and certain inflammatory cytokines (IL-1b, TNF-a, IFN-a, IFN-g) on MEFV expression and C5a inhibitor activity in neutrophils and primary peritoneal fibroblast cultures.

Methods: Human primary peritoneal fibroblast cultures and neutrophils were studied for MEFV expression and C5a inhibitor activity, using reverse transcription-polymerase chain reaction and C5a-induced myeloperoxidase assay, respectively, in the presence and absence of colchicine and cytokines.

Results: MEFV expression in neutrophils was high and could not be induced further. Its expression in the peritoneal fibroblasts was lower than in neutrophils and could be induced using colchicine and cytokines parallel with induction of C5a inhibitor activity. Semi-quantitative RT-PCR[2] assays enabled estimation of MEFV induction by the cytokines at 10–100-fold and could not be further increased by concomitant addition of colchicine.

Conclusion: Serosal tissues, which are afflicted in FMF, express colchicine and cytokine-inducible MEFV and contain inducible C5a inhibitor activity. The relation between colchicine ability to induce MEFV and C5a inhibitor activity, and its efficacy in FMF treatment, require further investigation.

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[1] RT-PCR = reverse transcription-polymerase chain reaction

[2] FMF = familial Mediterranean fever

Kosta Y. Mumcuoglu, PhD, Avi Keysary, PhD and Leon Gilead, MD
November 2001
Daniel Cattan, MD, Michael Dervichian, MD, Michael Thomas, Catarine Dode Dpharm and Isabelle Touitou, MD

Background: Familial Mediterranean fever is a genetic disease in which some characteristic gene mutation have been found.

Objective: To analyze the phenotype-genotype correlations in North African Jews and Armedians with FMF.

Methods: We studied MEFV gene mutations and phenotype-genotype correlations in North African Jews and Armedians with Familial Mediterranean Fever living in France.

Results: M694V mutation was the most common mutation in Jews and in Armenians. Patients with M6801 homozygosity or M6801/M694V compound heterozygosity had a phenotype as severe as patients with M694V homozygosity.

Conclusions: This study characterizes the phenotype-genotype in specific ethnic groups of patients with FMF.

Kostas Konstantopoulos, MD, Alexandra Kanta, MD, Michael Tzoulianos, MD, Sophia Dimou, MD, Flora Sotsiou, MD, Marianna Politou, MD and Dimitris Loukopoulos, MD
July 2001
by Rasmi Megadle, MD, Paltiel Weiner, MD, Alexander Sotzkover, MD, Miri Mizrahi-Reuveni, MD and Noa Berar Yanay, MD
January 2001
Pnina Langevitz MD, Avi Livneh MD, Lily Neumann PhD, Dan Buskila MD, Joshua Shemer MD, David Amolsky MD and Mordechi Pras MD

Background: Familial Mediterranean fever is a genetic disorder manifested by recurrent attacks of peritonitis, pleuritis and arthritis, and characterized by clinical, histological and laboratory evidence for localized and systemic inflammation. Colchicine treatment usually prevents the attacks and the associated inflammation. Inflammation of atherosclerosis and ischemic heart disease.

Objective: To study the effect of inflammation and its prevention on occurrence of IHD, using FMF as a model.

Methods and Patients: We studied the presence of IHD and its risk factors in 290 FMF patients aged 40 years or more, and in two control groups – 233 spouses of the FMF patients’ and 126 patients with inflammatory diseases obtained from other outpatient clinics. FMF patients were also compared with age and gender-matched individuals from the population reference data of the Israel Ministry of Health.

Results: The prevalence of IHD in FMF patients was significantly lower than in the group of controls from other outpatient clinics (15.5% vs. 30.2% P< 0.05) and comparable with their spouses (11.2%) and with the matched general population in Israel (16%).

Conclusion: These findings suggest that despite the evidence of recurrent inflammation, colchicines-treated FMF patients are not more predisposed to IHD than the normal population.

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