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עמוד בית
Mon, 29.04.24

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October 2005
X. Giakoumi, M. Tsironi, C. Floudas, E. Polymeropoylos, E. Papalambros and A. Aessopos
April 2005
Y. Schlesinger, D. Reich, A.I. Eidelman, M.S. Schimmel, J. Hassanim and D. Miron
Background: The incidence of congenital cytomegalovirus in Israel has never been determined, either in general or in relation to various population subgroups. We recently proved the utility of newborn urine polymerase chain reaction as a screening tool for congenital CMV[1].

Objectives: To define the incidence of congenital CMV infection in two different subpopulations, as a model for the entire population of Israel.

Methods: Urine specimens were randomly collected from 2,000 newborns in Shaare Zedek Medical Center, Jerusalem, and HaEmek Medical Center, Afula (1,000 specimens each). These hospitals have many characteristic differences, presumably representing the diverse population of Israel. Urine specimens were subjected to a CMV PCR[2] reaction and positive specimens were validated by urine viral culture. Maternal seroprevalence was determined in a representative sample of the mothers in each hospital. Epidemiologic characteristics of the mothers were extracted from hospital records and compared.

Results: The population in Shaare Zedek Medical Center was mostly Jewish (95.8%) and urban (87.0%), as compared to that of HaEmek Medical Center (49.2% and 61.0%, respectively, P < 0.01). Nevertheless, CMV seroprevalence was similar: 81.5% and 85%, respectively. Ten (1.0%) and 4 (0.4%) newborns, respectively, were found to have congenital CMV infection (not significant).

Conclusions: The combined incidence of congenital CMV infection in the study population was 0.7% (95% confidence interval 0.3–1.0%). If this rate is extrapolated to the entire population of Israel, then a total of 945 cases of congenital CMV can be expected among the 135,000 annual deliveries. A nationwide screening program for congenital CMV should be considered.

________________

[1] CMV = cytomegalovirus

[2] PCR = polymerase chain reaction

February 2005
R. Yagev, E. Tsumi, J. Avigur, P. Polyakov, J. Levy and T. Lifshitz
 Background: Uveitis is an acute or chronic inflammatory process of the uvea caused by a number of etiologies. In many patients the etiology is unknown.

Objective: To investigate the effect of the Dead Sea environment (climatotherapy) on the signs, symptoms and clinical course of chronic uveitis.

Methods: Fifty-five patients with chronic uveitis were examined at the beginning and end of a 3–4 week stay at the Dead Sea region and on repeat visits to the region. Study data included demographic information, medical history, etiology, diagnosis, medication, and a complete ophthalmic examination.

Results: Statistically significant improvements were seen between the two examinations within each visit in four parameters (negative values indicate improvement): a) visual acuity for near and far: Jaeger (‑1.18 ± 0.28, P < 0.0001) and best corrected visual acuity (‑0.08 ± 0.02, P < 0.0001); b) anterior chamber flare (-0.18 ± 0.06, P < 0.01); c) anterior chamber cells (-0.16 ± 0.05), P < 0.001); and d) vitreous cells (-0.15 ± 0.09, P < 0.05). There was a significant mean improvement during visits to the Dead Sea area and a slight dissipation of the effect during the intervals between visits. Sixty-four percent of the patients reported that they required less medication and had fewer and milder attacks of uveitis following the visits.

Conclusions: The results of this study provide evidence of short- and possibly long-term improvement in the signs and symptoms of uveitis following exposure to the Dead Sea environment.

January 2004
C.E. Wrede, S. Hutzler, L.C. Bollheimer, R. Buettner, C. Hellerbrand, J. Schoelmerich and K-D. Palitzsch

Background: Genetic hemochromatosis leads to iron overload in many tissues and may lead to liver cirrhosis and hepatocellular carcinoma. Early diagnosis and therapy are crucial. Since 80–100% of hemochromatosis patients of European origin are homozygous for a cysteine to tyrosine exchange in the HFE gene at codon 282, genetic screening might be useful. Representative population studies are needed to evaluate the phenotype of people heterozygous and homozygous for the C282Y mutation.

Objective: To determine the correlation between parameters of iron metabolism and the hemochromatosis genotype in a large population-based study.

Methods: A representative population-based survey, the Diabetomobil study, analyzed 5,083 German probands. Serum transferrin saturation and ferritin levels were determined, and the C282Y mutation of the HFE gene was analyzed by restriction fragment length polymorphism- polymerase chain reaction analysis.

Results: Nine of 373 probands with a transferrin saturation > 55% (2.4%) and none of 264 randomly selected probands with a transferrin saturation £ 55% (0%) were homozygous for the C282Y mutation. Three of the nine homozygous probands had ferritin values less than 250 µg/L. The frequency of the heterozygous genotype was 8.8%, and the percentage of heterozygous probands increased with increasing levels of transferrin saturation.

Conclusion:We propose a population screening strategy with an initial transferrin saturation test, followed by genotyping for the C282Y mutation if the transferrin saturation is above 55%, regardless of the ferritin level. Heterozygous individuals with higher transferrin saturation values may be protected against iron loss but may also be more susceptible for certain liver diseases, depending on the simultaneous prevalence of other diseases.
 

May 2003
D.S Silverberg, D. Wexler, M. Blum, D.Schwartz, G. Keren, D. Sheps, and A. Iaina

Background: Congestive heart failure is extremely common in octogenarians and is associated with severe fatigue, shortness of breath, recurrent hospitalizations, and death. These patients, many of whom are anemic, are often resistant to standard CHF[1] therapy including angiotensin-converting enzyme inhibitors, beta-blockers and diuretics.

Objectives: To examine whether correction of the anemia (hemoglobin <12 g/dl) in CHF patients lowers their resistance to therapy.

Methods: Forty octogenarians with anemia and severe resistant CHF were administered a combination of subcutaneous erythropoietin and intravenous iron sucrose.

Results: This combination therapy led to a marked improvement in cardiac function, shortness of breath and fatigue, a marked reduction in the rate of hospitalization and a stabilizing of renal function.

Conclusion: Anemia appears to be an important but ignored contributor to the progression of CHF, and its correction may improve cardiac and renal status as well as the quality of life in elderly patients.






[1] CHF = congestive heart failure


November 2002
Tomas Ganz, PhD, MD

Systemic infection or inflammation causes a decrease in intestinal iron absorption and impairs the release of recycled iron from macrophages. Decreased availability of iron may deny this essential element to invading pathogens and may inhibit their multiplication and other metabolic processes but also results in anemia of chronic disease. This article reviews recent discoveries that shed light on the regulation of iron metabolism during infection and iron overload, and point to the central role of a newly discovered peptide, hepcidin. Evidence to date indicates that hepcidin is a negative regulator of intestinal iron absorption, placental iron transport, and the release of iron from macrophages that recycle iron from senescent red cells. It may also be the central mediator of iron sequestration during infections and inflammatory states and the mediator of anemia of chronic disease. Rapid progress in this area is a good example of the beneficial effects of improvements in peptide analysis and chemistry, advances in genomics, and the increasing use of transgenic mice to determine the function of newly discovered genes and proteins.

September 2002
Dan Miron, MD, Yoseph Merzel, MD, Amiram Lev, MD, Jean-Jack Meir, MD and Yoseph Horowitz, MD
March 2002
Zeev Rotstein, MD, MHA, Rachel Wilf-Miron, MD, MPH, Bruno Lavi BA, Daniel S. Seidman, MD, MMSc, Poriah Shahaf, MD, MBA, Amir Shahar, MD, MPH, Uri Gabay, MD, MPH and Shlomo Noy, MD, MBA

Background: The emergency department is one of the hospital’s busiest facilities and is frequently described as a bottleneck. Management by constraint is a managerial methodology that helps to focus on the most critical issues by identifying such bottlenecks. Based on this theory, the benefit of adding medical staff may depend on whether or not physician availability is the bottleneck in the system.

Objective: To formulate a dynamic statistical model to forecast the need for allocating additional medical staff to improve the efficacy of work in the emergency department, taking into account patient volume.

Methods: The daily number of non-trauma admissions to the general ED[1] was assessed for the period 1 January 1992 to 1 December 1995 using the hospital computerized database. The marginal benefit to shortening patient length of stay in the ED by adding a physician during the evening shift was examined for different patient volumes. Data were analyzed with the SAS software package using a Gross Linear Model.

Results: The addition of a physician to the ED staff from noon to midnight significantly shortened patient LOS[2]: an average decrease of 6.61 minutes for 80–119 admissions (P<0.001). However, for less than 80 or more than 120 admissions, adding a physician did not have a significant effect on LOS in the ED.

Conclusions: The dynamic model formulated in this study shows that patient volume determines the effectiveness of investing manpower in the ED. Identifying bottleneck critical factors, as suggested by the theory of constraints, may be useful for planning and coordinating emergency services that operate under stressful and unpredictable conditions. Consideration of patient volume may also provide ED managers with a logical basis for staffing and resource allocation.






[1] ED = emergency department



[2] LOS = length of stay


February 2002
December 2001
Rachel Dahan, MD, Shmuel Reis, MD, Doron Hermoni, MD and Jeffrey Borkan, MD
Yuri Viner, MD, Dan Miron, MD, Emanuel Gottfried, MD, Dora Segal and Anthony Luder, MBBS (UK)
August 2001
Rachel Wilf-Miron, MD, MPH , Kareen Nathan, MSc, Fabienne Sikron, MA and Vita Barell, BA
 Background: Investigation of causes of death can help inform intervention policy aimed at reducing preventable mortality.

Objectives: To assess mortality causes and trends over time and identify target groups with excessive mortality rates among Israeli youth aged 10-24, in order to formulate an intervention policy for prevention of adolescent mortality.

Methods: Mortality data for Israeli residents aged 10-24 were extracted from the Central Bureau of Statistics compu­terized death certificate file for the period 1984-95. Trends were evaluated by cause of death and demographic char­acteristics.

Results: The crude mortality rate among Israeli youth aged 10-24, during 1993-1995, was 39.6 per 100000. Rates were 2.7 times higher among males, increased with age, and reached a peak among 18-21 year olds. Rates were 1.4 times higher among Arabs than among Jews. The sharp increase in mortality among Jewish males of military service age (18-21 years) was due mainly to motor vehicle crashes and suicide. Although overall mortality decreased by 9.4% from 1984-86 to 1993-95, the gap between the subgroups increased. MVC­related mortality increased over time by 100% among Arab males. The rate of completed suicide among Jewish males increased by 110%. Although injury-related mortality is lower in Israel compared with the U.S., similar demographic differen­tials and trends were found in both countries.

Conclusions: Suicide among Jewish males of military service age, as well as MVC fatalities among Arab males, present a growing public health issue. Intervention strategies should therefore be targeted towards these subgroups in order to minimize the rates of preventable death.

July 2001
Michael D. Lockshin, MD
Autoimmune diseases are said to have high female/male (F/M) ratios, but these ratios are imprecise. Published definitions and classifications of autoimmune diseases differ substantially, as do the F/M ratios themselves. Imputed causality of auto-immune diseases requires better precision. Some thyroid, rheumatic and hepatic diseases consistently have high F/M ratios, but marked differences exist in the reported quantity of the ratios. Other autoimmune diseases have low F/M ratios. Because F/M ratios reflect incidence and not severity of disease, gonadal hormones, if they play a role, must do so through a threshold or permissive mechanism. Sex differences related to environmental exposure, X-inactivation, imprinting, X or Y chromosome genetic modulators, and intrauterine influences remain as alternate, theoretical, explanations for sex differences of incidence. The epidemiology of the sex­discrepant autoimmune diseases - young, female - suggests that an explanation for sex discrepancy lies in differential exposure, vulnerable periods, or thresholds, rather than in quantitative aspects of immunomodulation.

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