Israel Medical Association Journal

Background: Uncorrected refractive error is the leading cause of visual impairment in children. In 2002 a screening project was launched in Israel to provide data on the effectiveness of the illiterate E-chart in identifying Jewish and Arab schoolchildren in need of a comprehensive eye examination.

Objectives: To present the aims, design and initial results of the visual screening project and the prevalence of vision abnormality in the study population.

Methods: A cross-sectional population-based study was conducted during 2002–2003 among first- and eighth-graders in 70 schools in northern Israel. The nurse's test included use of the illiterate E-chart to measure visual acuity. The medical examination included vision history, clinical eye examination, VA[1] and retinoscopy. The ophthalmologist's evaluation as to whether a child needed a referral for diagnostic procedures, treatment and/or follow-up was recorded and compared with explicit referral criteria formulated after data collection.

Results: Of 1975 schoolchildren, 31% had abnormal VA, defined as VA worse than 6/6 in at least one eye, and a quarter had VA equal or worse than 6/12 in both eyes. The prevalence of vision abnormality among the children was 22.4% when based on the evaluation of the field ophthalmologist and 26.1% when based on two sets of explicit severity scores and referral criteria.

Conclusions: Vision abnormality is a significant health problem among northern Israeli schoolchildren. This project is unique in scope and importance, providing evidence to assist policy making with regard to vision screening for schoolchildren (including data on test reliability and validity) and optimal VA cutoff level, and confirming the need for clinical guidelines regarding referral criteria.

Background: The trefoils factor family is a relatively new family of peptides. Their abundant expression in the epithelial cells of the gastrointestinal tract in the normal physiological state and in various ulcerative conditions suggests an important role in mucosal defense and repair. Infection with Helicobacter pylori interferes with normal mucosal activity.

Objectives: To investigate whether H. pylori infection alters the expression of trefoils TFF1[1] and TFF2 in the gastric mucosa of patients with H. pylori-associated chronic active gastritis, positive or negative for the CagA strain.

Methods: During investigation for dyspepsia, gastric biopsies and blood samples were obtained from patients who underwent upper gastrointestinal endoscopy. Rapid urease testing, histology for determination of H. pylori-associated CAG[2] and Western analysis for TFF1 and TFF2 expression with antisera were performed. CagA state was determined using a commercial kit.

Results: TFF2 expression was significantly reduced in both groups of patients with H. pylori-associated CAG compared to healthy patients without H. pylori infection, particularly in CagA-positive patients. TFF1 expression showed a tendency of reduction (not significant) in this group only.

Conclusions: These results suggest that H. pylori-associated CAG has a deleterious effect on the expression of TFF2 in the gastric antrum. This reduced expression may contribute to the damage induced to the gastric mucosa by H. pylori.

Background: The Beer Sheva Psoriasis Severity Score is a novel instrument for the assessment of psoriasis severity, designed for use in routine clinical conditions.

Objective: To identify the main factors of the BPSS[1].

Methods: The sample used to study the BPSS comprised 70 patients with psoriasis vulgaris treated by climatotherapy at the Dead Sea. Psoriasis severity was assessed using BPSS and PASI (Psoriasis Area and Severity Index). Factor analysis was used to identify the main factors of BPSS. Internal consistency analysis was performed. Correlation matrices were generated to compare BPSS factors.

Results: Factor analysis demonstrated that BPSS included six factors that explained 74.0% of the variance as follows: patient assessment 26.0%; physician assessment 13.2%; palms and soles involvement 11.9%; genitals, nails, and pruritus 9.0%; face involvement 7.3%; and scalp involvement 6.6%. Total scale Cronbach’s alpha was 0.76; alpha for the factors ranged between 0.39 and 0.81.

Conclusion: The major factors of BPSS were identified. BPSS may be used as a comprehensive tool for measuring psoriasis severity.

[1] BPSS = Beer Sheva Psoriasis Severity Score

Background: Polymorphonuclear leukocyte priming and low grade inflammation are related to severity of kidney disease. Erythropoietin-receptor is present on PMNLs[1].

Objectives: To evaluate the effect of 20 weeks of EPO[2]-alpha treatment on PMNL characteristics in relation to the rate of kidney function deterioration in patients with chronic kidney disease.

Methods: Forty anemic chronic kidney disease patients, stage 4-5, were assigned to EPO and non-EPO treatment for 20 weeks. A group of 20 healthy controls was also studied. PMNL priming and PMNL-derived low grade inflammation were estimated, in vivo and ex vivo, before and after EPO treatment: The rate of superoxide release, white blood cells and PMNL counts, serum alkaline phosphatase and PMNL viability were measured. EPO-receptor on PMNLs was assayed by flow cytometry. The effect of 20 weeks of EPO treatment on kidney function was related to the estimated glomerular filtration rate.

Results: EPO treatment attenuated superoxide release ex vivo and in vivo and promoted PMNL survival ex vivo. Decreased low grade inflammation was reflected by reduced WBC[3] and PMNL counts and ALP[4] activity following treatment. EPO retarded the deterioration in GFR[5]. The percent of PMNLs expressing EPO-R[6] was higher before EPO treatment and correlated positively with the rate of superoxide release. After 20 weeks of EPO treatment the percent of PMNLs expressing EPO-R was down-regulated.

Conclusions: These non-erythropoietic properties of EPO are mediated by EPO-R on PMNLs, not related to the anemia correction. A new renal protection effect of EPO via attenuation of PMNL priming that decreases systemic low grade inflammation and oxidative stress is suggested.

Background: Diseases causing increased pulmonary pressure will subsequently cause a dilation of the pulmonary arteries and right heart chambers.

Objectives: To assess the capability of computed tomography angiography and high resolution CT to diagnose and estimate the severity of pulmonary arterial hypertension as compared with standard means of right heart catheterization, echocardiography and pulmonary function tests.

Methods: The study included 38 patients with PHT[1] who underwent CT angiography and HRCT[2] as part of their routine evaluation. Diagnose included: primary PHT (n=20), Eisenmenger syndrome (n=6), scleroderma (n=3), thromboembolic disease (n=3), and others (n=6). Mean pulmonary artery pressure was 58 mmHg (range 39–92 mmHg) by catheterization and peak systolic pressure 79 mmHg (range 40–135) by echocardiography. Findings for the diameters of the main pulmonary artery and its main branches, the ascending aorta, the right atria and ventricle as well as the position of the interventricular septum were compared with 22 chest CT scans as compared to patients with no known clinical history of pulmonary hypertension, performed for other reasons (trauma, oncology follow-up) during the study period. Correlations were also calculated with recent right heart catheterization, echocardiography and pulmonary function tests of the study group.

Results: Mean main pulmonary artery diameter in the study group was 3.55 ± 0.66 cm, pulmonary artery/ascending aorta ratio 1.2 ± 0.29, right pulmonary artery 2.63 ± 0.49 cm, left pulmonary artery 2.57 ± 0.5 cm. All diameters were significantly different from the control group (P < 0.0001). Main and right pulmonary artery diameters correlated to the pressure measurement by echocardiography (P = 0.001). Bronchial collaterals were found in 11 patients (30%). The position of the interventricular septum correlated well with the echocardiography study.

Conclusions: The size of the main pulmonary artery on CT angiography has a good predictive value regarding the severity of PHT.

Background: The prevalence of obesity among children and adolescents in the western world has increased dramatically.

Objective: To assess the efficiency of routine childhood obesity screening by primary physicians in the pediatric population in Israel and the utilization of health services by overweight children.

Methods: The electronic medical records of children aged 60–83 months registered in 39 pediatric primary care centers between January 2001 and October 2004 (n=21,799) were reviewed. Those in whom height and weight were documented during a clinic visit (index visit) were classified as overweight, at risk of overweight, and normal weight by body mass index percentiles. The number of visits to the pediatrician, laboratory tests and health care costs 12 months after the index visit were calculated.

Results: Anthropomorphic measurements were performed in 1556 of the 15,364 children (10.1%) who visited the clinic during the study period. Of these, 398 (25.6%) were overweight, 185 (11.9%) were at risk of overweight, and 973 (62.5%) were normal weight. Children in the first two groups visited the clinic slightly more often than the third group, but the differences was not statistically significant (P = 0.12), and had significantly more laboratory tests than the rest of the children visiting the clinics (P = 0.053). Health care costs were 6.6% higher for the overweight than the normal-weight children.

Conclusions: Electronic medical records are a useful tool for population-based health care assessments. Current screening for obesity in children during routine care in Israel is insufficient and additional education of community pediatricians in diagnosis and intervention is urgently needed.

Background: Rehabilitation camps can improve exercise tolerance and nutrition in cystic fibrosis patients.

Objectives: To assess weight gain, pulmonary function tests and daily symptoms in European CF[1] patients attending a rehabilitation camp at the Dead Sea, Israel.

Methods: We conducted a retrospective study assessing 94 CF patients who participated in winter camps held at the Dead Sea, Israel from 1997 to 2000. The camp program included daily physiotherapy, physical activities, and a high caloric diet. We assessed weight gain, pulmonary function tests, oxyhemoglobin saturation and daily symptoms before (pre), on departure (dep), and up to 3 months after the 3 week rehabilitation camp post). All data were analyzed by ANOVA for repetitive measurements. P < 0.05 was considered significant.

Results: Lung function tests and oxyhemoglobin saturation taken before, on departure and 3 months after camp were available for 35 patients. Forced expiratory volume in the first second (% predicted, average ± SD) improved by 8.2 ± 2.3% (pre, dep, post, P < 0.05). Oxyhemoglobin saturation mildly improved (1 ± 0.3%, pre, dep, post, P < 0.05). Forced vital capacity (% predicted) increased by 3.9 ± 1.2%, but was not significant (P = 0.19). Total body weight of 89 patients improved by 1.9 ± 0.9% during the camp time (P < 0.05, t-test), and in a group of 24 patients weight continuously increased up to 5.0 ± 1.7% at 3 months after the camp (P = 0.004, ANOVA).

Conclusions: In this attrition-limited retrospective study, European CF patients improved their pulmonary function and gained weight during and up to 3 months after a 3 week rehabilitation winter camp at the Dead Sea, Israel.

Background: Interleukin-8 is a prototypical inflammatory chemokine that induces leukocyte migration to inflammatory sites. Leukocyte recruitment in response to gradients of this chemokine is attenuated at advanced stages of inflammation to prevent damage to surrounding healthy tissues. Our published studies suggest that over-phosphorylation of focal adhesion kinase in migration-desensitizing conditions is involved in cessation of cell motility. This over-phosphorylation of FAK[1] was induced by IL-8[2] only when the receptor transmitting the chemokine signals was CXCR2, and not CXCR1, indicating that the two IL-8 receptors diverge in their signaling properties.

Objectives: To analyze the regulation of FAK in CXCR2-expressing hematopoietic cells under conditions of migratory desensitization, focusing on the roles played by adhesion-related components in this process.

Methods: Under conditions of migratory desensitization, we determined IL-8-induced cell spreading and FAK localization following disruption of actin filaments, and evaluated the role of integrins in FAK phosphorylation.

Results: The disturbance of intact activity of actin filaments resulted in inhibition of cell spreading and modification of FAK intracellular localization upon IL-8 stimulation. Also, adhesion-dependent pre-stimulation of integrins was required for IL-8-induced FAK phosphorylation.
Conclusions: Intact actin filaments and integrins are required for optimal IL-8-induced FAK phosphorylation in conditions of migratory desensitization. These observations suggest that lack of adequate activity/regulation of adhesion-related components may give rise to FAK activities that are not appropriately controlled, possibly leading to pathological conditions that are associated with perturbed leukocyte migration phenotypes