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R. van Marum1, T.J.Cleophas1, T.F.Cleophas2, A.H.Zwinderman3 Schweitzer Hospital Dordrecht, 2Technical University Delft, 3Academic Medical Center Amsterdam Objective: To extend and update a recently published1 meta-analysis of the effects of second generation dihydropyridine calcium channel blockers and congestive heart failure. Search strategy: Search of the first meta-analysis included MEDLINE data base to June 2000 only, for the updated version were used the Cochrane Controlled Trial Register data base, the EMBASE data base, and MEDLINE data base extended to June 2001. Search was kindly performed by the British Cochrane Heart Group, Bristol, UK. Selection criteria: Double-blind, placebo-controlled, parallel-group studies of chronic 8 weeks ; treatment were included. Data collection and analysis: In addition to the 18 studies previously selected, 4 new studies could be included taking the patient count from 3, 128 to 5, 291 patients. We assessed the effects of treatment on cardiac index, left ventricular ejection fraction, exercise treadmill duration, plasma norepinephrine level, and mortality. For the absolute and percentage variables the increase on active treatment minus increase on placebo was used 95% confidence intervals, CIs ; . For mortality relative odds ratios were used as a measure of relationship between treatment and mortality 95% CIs ; . Data were pooled according to the standard guidelines of Oxmann and Guyatt. Results: The table gives an overview of the comparisons of dihydropyridine vs placebo. Both unupdated and updated meta-analysis shows a significant increase of cardiac index, left ventricular ejection fraction and exercise tolerance time on treatment vs placebo, while plasma norepinephrine and patient mortality were not increased. The unupdated effects were generally more substantial than the updated ones. Table: unupdated meta-analysis n 3128 p-value + 0.75 0.10 ; 0.0001 + 2.5 1.0 ; 0.001 + 43 42 ; 0.05 -45 56 ; ns -0.94 0.79-11.7 ; ns updated meta-analysis n 5291 p-value + 0.53 0.08 ; 0.0001 + 2.3 0.9 ; 0.01 + 27 24 ; 0.05 -45 56 ; ns 1.0 1.0-1.0 ; ns.
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BRUCE ETTINGER, MD Adjunct Research Scientist, Kaiser Permanente Northern California Clinical Professor of Medicine, University of CaliforniaSan Francisco hen deciding whether a patient should receive drug therapy to reduce the risk of osteoporotic fracture, the decision-making process should embrace more than bone mineral density BMD ; measurements alone. This article discusses the value of a comprehensive approach to fracture risk assessment to identify patients for whom drug therapy is warranted because their risk of fracture is high, as well as patients for whom drug therapy would be inappropriate because their risk of fracture is low. In this manner, scarce health care resources can be directed toward patients whose absolute risk of fracture is highest, regardless of their BMD measurements. Various models of the risk of osteoporotic fracture that have been developed by the National Osteoporosis Foundation and other organizations contain four independent risk factors: thinness, smoking, personal history of fracture, and family history of fracture mother or sister for a woman, father or brother for a man ; . Use of high-dose corticosteroids or excessive alcohol consumption also are recognized risk factors for osteoporotic fracture, but in the generally healthy population they do not play a contributing role. The clinical risk factors complement BMD measurement. BMD is reported in two ways: as a T score or Z score, in terms of standard deviations SD ; away from the mean. For women, the T score compares a woman's BMD to the mean BMD for healthy young women, while a Z score compares a woman's BMD to the mean for agematched women. Each decrease of 1 SD BMD approximates a loss of about 10 percent of total BMD and an increase in fracture risk of 50 to 100 percent Kulak 1999 ; . According to the World Health Organization, a woman whose T score is 2.5 or less is defined as osteoporotic, and a woman whose T score is between 2.5 and 1.0 is defined as osteopenic. The current gold standard for BMD measurement is dual-energy X-ray absorptiometry DXA ; of the lumbar spine or total hip. The American Association of Clinical Endocrinologists recommends using the lower measurement from either of the two sites Hodgson 2001 ; , because women in their 50s, or women using corticosteroids, tend to lose BMD to a greater extent at the spine than the hip, whereas in older patients, spinal, for example, zestril 10mg.
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Drug Name ZESTRIL 40MG TABLET ZESTRIL 2.5MG TABLET ZESTORETIC 10 12.5 TABLET ZESTORETIC 20 12.5 TABLET ZESTORETIC 20 25 TABLET ARIMIDEX 1MG TABLET ZOMIG 5MG NASAL SPRAY ZOMIG ZMT 2.5MG TABLET ZOMIG 2.5MG TABLET ZOMIG 5MG TABLET ZOMIG ZMT 5MG TABLET SEROQUEL 100MG TABLET SEROQUEL 100MG TABLET SEROQUEL 200MG TABLET SEROQUEL 200MG TABLET SEROQUEL 300MG TABLET SEROQUEL 300MG TABLET SEROQUEL 25MG TABLET ACCOLATE 10MG TABLET ACCOLATE 20MG TABLET IRESSA 250MG TABLET HIBICLENS 4% LIQUID HIBICLENS 4% LIQUID CASODEX 50MG TABLET TAMOXIFEN 10MG TABLET CRESTOR 10MG TABLET CRESTOR 10MG TABLET CRESTOR 20MG TABLET CRESTOR 40MG TABLET CRESTOR 5MG TABLET SULAR 10MG TABLET SA SULAR 20MG TABLET SA SULAR 30MG TABLET SA ZOLADEX 3.6MG IMPLANT SYRN ZOLADEX 10.8MG IMPLANT SYRN CLORPACTIN WCS-90 POWDER.
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Table 4. Effect of treatment length on the binding of insulin by liver membranepreparations The animals were submitted to their treatments for the times indicated. Membranes were prepared from the pooled livers of three animals. The techniques were as described in the Materials and Methods section and in the legends to Table 3 and Fig. 5. The insulin concentration was 40pmol I and the specific radioactivity was 54 Ci g. The results are expressed as fmol of insulin bound mg of membrane protein. Each number is the mean of three observations. The numbers in parentheses represent percentages of the values obtained for the lean control animals. Days of treatment and zocor.
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