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עמוד בית
Fri, 24.05.24

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June 2015
Idit F. Liberty MD, Naim Abu Freha MD, Yael Baumfeld MD, Shlomi Codish MD MPH, Fransisc Schlaeffer MD and Victor Novack MD PhD

Abstract

Background: The impact of admission glycated hemoglobin (HbA1c) on hospital outcome is controversial.

Objectives: To evaluate the association between admission glucose and HbA1c levels and mortality 1 year after hospitalization in the internal medicine ward.

Methods: HbA1c level of consecutive patients was measured during the first 24 hours of admission to the internal medicine ward and divided at the cutoff point of 6.5%. Three groups of patients were prospectively identified: patients with preexisting diabetes mellitus (DM), patients with glucose > 140 mg/dl (hyperglycemia) on admission and no known diabetes (H), and patients without diabetes or hyperglycemia (NDM). The primary end-point was 1 year all-cause mortality.

Results: A total of 1024 patients were enrolled, 592 (57.8%) belonged to the DM group, 119 (11.6%) to the H group and 313 (30.6%) to the NDM group. At 1 year, death occurred in 70 (11.9%) in the DM group, 12 (10.0%) in the H group and 15 (4.8%) in the NDM group (P = 0.002). Elevated admission glucose levels did not influence outcome in any of the groups. HbA1c levels were similar for survivors and non-survivors (P = 0.60). Within-group multivariate analysis adjusted for comorbidities and age showed that in the H group HbA1C levels of 6.5% or above were associated with increased mortality risk [hazard ratio (HR) 8.25, 95% confidence interval (CI) 1.93–35.21). In the DM group, HbA1c levels below 6.5% were associated with increased mortality risk (HR = 2.05, 95%CI 1.25–3.36).

Conclusions: Glucose levels upon admission did not affect mortality. However, HbA1c levels below 6.5% had opposite effects on 1 year mortality in diabetes patients and patients with hyperglycemia.

November 2013
I. Strauss, T. Jonas-Kimchi, Z. Lidar MD, D. Buchbut, N. Shtraus, B. W. Corn and A. A. Kanner, T. Wolak, E. Aliev, B. Rogachev, Y. Baumfeld, C. Cafri,, M. Abu-Shakra and Victor Novack.
 Background: Contrast-induced nephropathy (CIN) is one of the major causes of new-onset renal failure in hospitalized patients. Although renin-angiotensin-aldosterone system (RAAS) blocking agents are widely used among patients requiring contrast studies, data on the effect of these agents on the development of CIN are sparse and inconsistent.  

Objectives: To evaluate in a randomized control trial whether uninterrupted administration of angiotensin II (AngII) blockade medications influence estimated glomerular filtration rate (eGFR) in patients undergoing non-emergent coronary angiography.

Methods: Patients receiving treatment with angiotensin-converting enzyme inhibitors/angiotensin receptor blockers (ACE-I/ARB) were recruited consecutively. The enrolled subjects were randomized into three groups at a 1:1:1 ratio: group A (ACE/ARB stopped 24 hours prior to the procedure and restarted immediately after the procedure), group B (ACE/ARB stopped 24 hours prior to the procedure and restarted 24 hours after the procedure), and group C (ACE/ARB continued throughout the study period). Plasma creatinine was measured and eGFR was calculated according to the Cockroft-Gault equation before and 48 hours after the coronary angiography. The primary endpoint was a change in eGFR at 48 hours.

Results: Groups A, B and C comprised 30, 31 and 33 patients respectively. The mean age of the study population was 65 ± 12 years and 67% were males. Fifty percent of the subjects had diabetes mellitus. The primary endpoint analysis showed that at 48 hours after the procedure there was no difference in ΔeGFR between groups A and C (4.25 ± 12.19 vs. 4.65 ± 11.76, P = 0.90) and groups B and C (3.72 ± 17.42 vs. 4.65 ± 11.76, P = 0.82). In post-hoc analysis the patients were clustered according to the following groups: medical alternation (group A and B) versus control (group C) and to baseline eGFR ≥ 60 ml/min vs. eGFR < 60 ml/min. In patients with baseline eGFR < 60 ml/min the ΔeGFR (baseline eGFR-eGFR 48 hours post-angiography) was significantly different between the intervention vs. control group (median 5.61 vs. median -2.19, P = 0.03 respectively). While in patients with baseline eGFR ≥ 60 ml/min there was no significant difference in ΔeGFR between the intervention and control groups.

Conclusions: ACE-I and ARB can safely be used before and after coronary angiography in patients with eGFR ≥ 60 ml/min. 

April 2011
M. Harari, E. Dramsdahl, S. Shany, Y. Baumfeld, A. Ingber, V. Novack and S. Sukenik

Background: Ultraviolet B (UVB) rays are required by the skin for the production of vitamin D. The intensity of UVB at the Dead Sea area is the lowest in the world. Low vitamin D levels are often associated with musculoskeletal symptoms.

Objectives: To assess the effectiveness of climatotherapy at the Dead Sea on the production of vitamin D in Norwegian patients suffering from various rheumatic diseases and to investigate possible associations between increased vitamin D serum levels, musculoskeletal symptoms and disease severity.

Methods: Sixty Norwegian patients who came to the Dead Sea area for 21 days of medical rehabilitation were divided into three groups according to their diagnosis: chronic pain syndromes, i.e., low back pain or fibromyalgia (Group 1, n=33); rheumatoid arthritis (Group 2, n=16); and osteoarthritis (Group 3, n=11). Serum 25-hydroxyvitamin D (25-OH-D) levels were determined at arrival and prior to departure. The treatment protocol included daily sun exposure (climatotherapy), bathing in the Dead Sea and mineral spring water (balneotherapy), mud applications and fitness classes.

Results: 25-OH-D serum levels increased significantly from 71.3 ± 26.6 nM at arrival to 89.3 ± 23.2 nM prior to departure (P < 0.001). Adjusted for the initial levels of pain (assessed by a visual analog scale) and disease severity, a direct correlation was observed between increased 25-OH-D serum levels and pain reduction (P = 0.012) and reduction of disease severity (P = 0.02).

Conclusions: Climatotherapy at the Dead Sea induces significant changes in vitamin D. Increased 25-OH-D serum levels are associated with reduced musculoskeletal pain and disease severity.
 

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