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עמוד בית
Thu, 18.07.24

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February 2002
Eilon Shany, MD, David Greenberg, MD and Eliezer Shahak, MD
Nir Cohen, MD, David Keret, MD, Eli Ezra, MD and Franklin Lokiec, MD
Netta Notzer, PhD and Ruth Abramovitz, MA

Background: The importance of health promotion and disease prevention in health policy and clinical practice is widely accepted in many countries. However, a large number of medical schools do not dedicate a significant part of their curriculum to these aspects. In Israel, there are no reports on the training of the future physician towards his or her role as health promoter in general, or in the areas of cardiovascular and cancer diseases specifically.

Objectives: To examine the preparation of Israel medical students for the role of health promoter in cancer and cardiovascular diseases.

Methods: The study was carried out over 2 years in two of the four medical schools in Israel: the Sackler Faculty of Medicine at Tel Aviv University and the Faculty of Health Sciences at Ben Gurion University in Beer Sheva. The students (n=172, 70% response rate) were surveyed during 1999-2000 by means of a questionnaire, which included assessment of their training towards the role of health promoter, their clinical experiences and exposure to patients at different stages of illnesses at various medical sites, and the specific skills and relevant knowledge they acquired.

Results: Most of the students’ learning experiences occurred in hospitals with patients at the treatment stage and little time was dedicated to prevention, especially in the community. They demonstrated better knowledge, skills and satisfaction with their learning experiences in CVD than in cancer; and reported having insufficient exposure to several common cancer diseases and lacking examining skills for early detection of cancer. The students in Beer Sheva had significantly more interaction with patients at different stages of CVD and acquired more examination skills than the Tel Aviv students.

Conclusions: A change in the curriculum is urgently needed: namely training medical students in community settings and preparing them to promote the well-being of their patients, including prevention. Attention should be given to launching new learning modes in the pre-clinical and clinical curriculum. We propose that: a) pre-clinical courses include prevention techniques in CVD and cancer, problems of cancer patients, and some examining skills; and b) the clinical phase should integrate oncology concepts and total cancer and CVD care into existing clerkships in the hospitals and in the community.
 

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

Haim Bibi MD, Daniel Weiler-Ravell MD, David Shoseyov MD, Ilana Feigin MD, Yael Arbelli RN and Daniel Chemtob MD MPH DEA

Background: One of the measures adopted in Israel since 1959 as part of the tuberculosis control program was screening children aged 12–13 years old. The screening comprised single-step tuberculin skin testing using the Mantoux method.

Objective: To assess the efficacy of tuberculin skin screening for TB[1] in schoolchildren in southwestern Israel as well as the compliance to treatment for latent tuberculosis infection.

Methods: We retrospectively reviewed the records of children in the Ashkelon region who underwent a tuberculin skin test during the period 1995–99.

Results: Of the 28,016 eligible children, 27,232 were tested. In 923 children, mostly from the former USSR and Ethiopia, an induration of 10 mm or more was found. Only 52 Israeli-born children tested positive. Tuberculosis was found in seven children with a positive test, five of whom were from Ethiopia. All children who tested positive were referred to the local TB clinic; only 266 children (28.8%) presented. Only 151 completed the recommended treatment of isoniazid for 6 months. Thus, although screening included most of the targeted children aged 13, only a third of them presented to a TB clinic, of whom only about half completed treatment of latent infection.

Conclusions: Our results indicate that the current policy of screening for latent TB in our region is ineffective in terms of implementation of the recommended treatment. We suggest that only high risk groups be screened, and that a concerted effort be made to implement treatment.

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[1] TB = tuberculosis

Sydney Benchetrit MD, Jacques Bernheim MD and Eduardo Podjarny MD

Background: Primary aldosteronism is a common cause of non-renal secondary hypertension. A correct diagnosis results in curing the hypertension or targeting appropriate pharmacotherapy. In patients with low renin resistant hypertension (after treatment with three or more different anti-hypertensive drugs the blood pressure remains above 140/90 mmHg), screening for aldosteronism is mandatory.

Objectives: To demonstrate that normal blood levels of potassium in resistant hypertensive patients do not exclude the possible presence of hyperaldosteronism, and to suggest the use of the plasma aldosterone concentration (ng/dl)/plasma renin activity (ng/ml/hour) ratio in screening for hyperaldosteronism.

Methods: Blood tests, suppression and stimulation tests (2 L normal saline IV/4 hours and 20 mg furosemide IV for 60 minutes in a standing position) were systematically performed in 20 low renin normokalemic resistant hypertensive patients. None had renal disorders, known endocrine abnormalities or heart failure. They did not receive anti-hypertensive drugs affecting PAC[1] or PRA[2]. Basal PRA and PAC were measured twice: PAC after saline infusion and PAC/PRA after stimulation.

Results:. PAC/PRA above 50 was used to denote hyperaldosteronism. Serum K was 4 ± 0.07 mM/L, PAC 22.8 ± 1.8 ng/dl, PRA 0.13 ± 0.02 ng/ml/hour, PAC/PRA 190 ± 22 (above 100 in 17). After suppression PAC decreased from 25 ± 1.8 to 11 ± 1 ng/dl (normal <5 ng/dl). Stimulation did not affect PRA and PAC/PRA. Abdominal computed tomography scan revealed normal adrenal glands in 15 patients. Spironolactone (116 ± 60 mg/day) normalized blood pressure in all patients; it was used as a single therapy in 8, and in association with only one anti-hypertensive drug in the remaining 12 patients. In one patient the treatment was discontinued due to the presence of hyperkalemia.

Conclusions: Low renin resistant hypertension associated with normokalemia may be due to hyperaldosteronism. Normal aldosterone levels in the basal condition do not exclude the possibility of hyperaldosteronism. Using a PAC/PRA ratio above 50 as a screening test can aid the physician in deciding when to perform dynamic tests, thus increasing the sensitivity of the diagnosis of hyperaldosteronism. CT scan is frequently normal. Targeted pharmacotherapy leads to a normalization of blood values.






[1] PAC = plasma aldosterone concentration

[2]
 PRA = plasma renin activity


Haim Shirin MD, Yaron Davidovitz MD, Yona Avni MD, Paulina Petchenko MD, Zipora Krepel MSc, Rafael Bruck MD and Dina Meytes MD

Background: Epidemiological studies in different parts of the world have revealed controversial results on the association between hepatitis C virus infection and non-Hodgkin’s lymphoma. This discrepancy suggests that HCV[1] lymphotropism or its effect on host lymphocytes may be influenced by regional and racial factors, as well as by genomic variations.

Objective: To determine the prevalence of HCV infection in patients with lymphoproliferative disorders diagnosed and treated in our institute in Israel.

Methods: A total of 212 consecutive patients (95 males and 117 females) treated in our hematology outpatient clinic between August 1997 and September 1999 was screened for anti-HCV antibodies and hepatitis B surface antigen. HCV infection was confirmed by the presence of HCV RNA in the serum. The prevalence of HCV in patients with lymphoproliferative disorders was compared to a control group of patients with myeloproliferative disorders and myelodysplastic syndromes.

Results: HCV infection was more prevalent in the group of LPD[2] patients than in the control group, but this finding was not statistically significant. The prevalence of HCV among LPD patients was 7.8%, while that in the group with myeloproliferative and myelodysplastic disorders was 1.19% and in the general population 0.64%. Among the different classes of LPD, a significant association with HCV infection was established only in patients with diffuse large B cell lymphoma. Furthermore, HCV infection was significantly more prevalent than HBV infection in the LPD group, but not in the myeloproliferative and myelodysplastic disorders group.

Conclusions: Our finding of a significant association between HCV infection and diffuse large B cell lymphoma leads us to suggest that anti-HCV antibodies be performed routinely in such subjects.  

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 [1]LPD = lymphoproliferative disorders

[2] HCV = hepatitis C virus

Philip J. Hashkes, MD, MSc, Orit Friedland, MD and Yosef Uziel, MD, MSc
Alain Fischer, MD, Salima Hacein-Bey, MD, Franeoise Le Deist, MD, Geneviove De Saint Basile, MD and Marina Cavazzana-Calvo
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