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עמוד בית
Thu, 26.12.24

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September 2000
Paul Froom, MD, Estela Kristal-Boneh, PhD, Samuel Melamed, PhD, Gil Harari, MSc, Jochanan Benbassat, MD and Joseph Ribak, MD, MPH

Background: The degree to which serum total cholesterol predicts cariovascular disease is uncertain. While most authors have placed TC among the most powerful risk indicators of CVD, some have claimed that it predicted CVD in women only, or even not at all.

Objective: To determine the predictive value of serum total cholesterol relative to diabetes, smoking, systolic blood pressure and body mass index (kg/m2), for cardiovascular disease mortality in 3,461 occupationally active Israeli males.

Methods: A prospective follow-up was carried out for the years 1987-1998 to determine the effect of age, smoking habits, a history of diabetes, SBP, BMI and TC, at entry, on CVD mortality.

Results: There were 84 CVD deaths during a total of 37,174 person-years follow up. The hazard ratios (95% confidence intervals) for CVD mortality with respect to variables at entry were: diabetes 5.2 (2.1-13.2), age 2.2 (1.7-2.9), smoking 1.3 (1.0-1.8), SBP 1.4 (1.1-2.0), TC 1.5 (1.0-2.1) and BMI 1.2 (0.7-2.2). Among non-obese, non-diabetic, normotensive subjects the hazard ratio of TC adjusted for age and smoking was 1.16 (1.09-1.22) per 10 mg/dl. In the remaining subjects it was 1.04 (0.98-1.12) only. There was a significant interaction between TC and diabetes, hypertension or obesity (P=0.003).

Conclusions: In this population of Israeli males we found an interaction between TC and other risk indicators for CVD. Confirmation is required for the unexpected finding that the predictive value of TC for CVD mortality among non-diabetic, non-obese and normotensive subjects exceeded that among subjects with either of these risk factors.
 

May 2000
Ziona Haklai MSc, Shimon Glick MD and Jochanan Benbassat MD

Background: The increasing utilization of general internal medicine hospital wards in Israel during the last decade is a source of concern for health policy makers.

Objectives: To report on the distribution of selected main and secondary diagnoses among GIM inpatients, and to estimate the proportion of disorders for which appropriate care in the community will reduce the need for hospital admissions and re-admissions.

Methods: Data from the Health Information and Computer Services of the Israel Ministry of Health (national hospitalization database) for a one year period were analyzed by distribution of diagnostic entities (ICD-9-CM) in GIM and in medical subspecialty wards.

Results: Of the 313,824 discharges from hospital divisions of medicine in 1995, 256,956 (81.9%) were from GIM and 56,868 (18.1%) from specialty wards. Main and secondary discharge diagnoses were available for 188,807 GIM and 35,992 specialty patients. Of all main diagnoses in GIM wards, 27% were coded as "general or systemic symptoms and signs" or as "abnormal laboratory or ill defined manifestations" (ICD-9-CM codes 780-799, 276,277), and heart diseases comprised another 27%. The remaining main diagnoses covered almost all medical conditions. The combined proportion of "ambulatory care sensitive hospital admissions" (bronchial asthma, hypertension, congestive heart failure, chronic obstructive pulmonary disease, diabetes) constituted 12% of all main diagnoses in GIM, and respiratory symptoms or signs comprised another 11%. A by-product of this analysis was an insight into the experience of undergraduate medical students in GIM.

Conclusions: Assuming that 12-75% of admissions for "ambulatory care sensitive disorders" are preventable, an improved review before hospital discharge and a closer outpatient follow-up may reduce the load on GIM wards by 1-17%. This wide range justifies controlled trials to determine the effect of improved community care on hospital utilization. GIM wards offer valuable learning opportunities, but they cannot be a substitute for primary care clinics. The unexplained high proportion of GIM inpatients who were discharged with an unspecified main diagnosis could be detrimental for the accuracy of hospitalization statistics, and justifies investigation by chart audits into physicians' habits of documentation.

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GIM= general internal medicine

April 2000
chondrocyte transplantation, joint cartilage, articular surface, bioengineering, cartilage repair, dror robinson, hana ash, david aviezer, gabriel agar, nahum halperin, zvi nevo, robinson, ash, aviezer, agar, halperin, nevo

Background: Articular cartilage is incapable of undergoing self-repair since chondrocytes lose their mitotic ability as early as the first year of life. Defects in articular cartilage, especially in weight-bearing joints, will predictably deteriorate toward osteoarthritis.  No method has been found to prevent this deterioration. Drilling of the subchondral bone can lead to fibrocartilage formation and temporary repair that slowly degrades. Animal experiments indicate that introducing proliferating chondrocytes such as cultured articular chondrocytes can reliably reconstruct joint defects.

Objectives: To describe our clinical experience in culturing and transplanting autologous chondrocytes. 

Methods: Biopsies were obtained from 10 patients, aged 18–45, undergoing a routine arthroscopy in which a cartilage defect was identified with indications for cartilage transplantation. The biopsies were further processed to establish chondrocyte cultures. ACT was performed in 8 of the 10 patients because of persistent symptoms for at least 2 months post-arthroscopy. All patients (6 men and 2 women) had a grade IV cartilage defect in the medial or lateral femoral condyle, and three had a defect in the trochlear region as well. Biopsies were removed from the lateral rim of the superior aspect of the femur, and cells were cultured in a clean room. Following a 2 order of magnitude expansion, cells were implanted under a periosteal flap.

Results: The eight patients implanted with autologous cells were followed for 6 months to 5 years (average 1 year). Complaints of giving-way, effusion and joint locking resolved in all patients, and pain as assessed by the visual analogue score was reduced by an average of 50%. Follow-up magnetic resonance imaging studies in all patients revealed that the defects were filled with tissue having similar signal characteristics to cartilage.

Conclusions: Chondrocyte implantation is a procedure capable of restoring normal articular cartilage in cases with isolated joint defects. Pain can be predictably reduced, while joint locking and effusion are eliminated. The effect on osteoarthritis progression in humans has not yet been elucidated.

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ACT = autologous chondrocyte transplantation

February 2000
Arie Levine MD, Yoram Bujanover MD, Shimon Reif MD, Svetlana Gass, Nurit Vardinon, Ram Reifen MD and Dan Lehmann PhD

Background: Anti-endomysial antibodies are sensitive and specific markers for celiac disease. This antibody has recently been identified as an antibody to tissue transglutaminase, an enzyme that cross-links and stabilizes extracellular matrix proteins.

Objectives: To evaluate the clinical usefulness of an enzyme-linked immunoassay for anti-transglutaminase antibodies, and to compare the results with those of AEA, the current gold standard serological test for celiac disease.

Methods: Serum samples were collected from 33 patients with biopsy-proven celiac disease and AEA tests were performed. Control samples for anti-transglutaminase were obtained from 155 patients. An ELISA test for immunoglobulin A anti-transglutaminase utilizing guinea pig liver transglutaminase was developed and performed on all sera.  Cutoff values for the test were performed using logistic regression and receiver operating curves analysis.

Results: An optical density cutoff value of 0.34 was established for the assay. The mean value was 0.18±0.19 optical density for controls, and 1.65±1.14 for patients with celiac disease (P<0.001). Sensitivity and specificity of the assay were both 90%, while AEA had a sensitivity and specificity of 100% and 94%, respectively.

Conclusions: A tissue transglutaminase-based ELISA test is both sensitive and specific for  detection of celiac disease.

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AEA = anti-endomysial antibody

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