Respiratory Insufficiency Correlated Strongly with Mortality of Rodents Infected with West Nile Virus

West Nile virus (WNV) disease can be fatal for high-risk patients. Since WNV or its antigens have been identified in multiple anatomical locations of the central nervous system of persons or rodent models, one cannot know where to investigate the actual mechanism of mortality without careful studies in animal models. In this study, depressed respiratory functions measured by plethysmography correlated strongly with mortality. This respiratory distress, as well as reduced oxygen saturation, occurred beginning as early as 4 days before mortality. Affected medullary respiratory control cells may have contributed to the animals' respiratory insufficiency, because WNV antigen staining was present in neurons located in the ventrolateral medulla. Starvation or dehydration would be irrelevant in people, but could cause death in rodents due to lethargy or loss of appetite. Animal experiments were performed to exclude this possibility. Plasma ketones were increased in moribund infected hamsters, but late-stage starvation markers were not apparent. Moreover, daily subcutaneous administration of 5% dextrose in physiological saline solution did not improve survival or other disease signs. Therefore, infected hamsters did not die from starvation or dehydration. No cerebral edema was apparent in WNV- or sham-infected hamsters as determined by comparing wet-to-total weight ratios of brains, or by evaluating blood-brain-barrier permeability using Evans blue dye penetration into brains. Limited vasculitis was present in the right atrium of the heart of infected hamsters, but abnormal electrocardiograms for several days leading up to mortality did not occur. Since respiratory insufficiency was strongly correlated with mortality more than any other pathological parameter, it is the likely cause of death in rodents. These animal data and a poor prognosis for persons with respiratory insufficiency support the hypothesis that neurological lesions affecting respiratory function may be the primary cause of human WNV-induced death

Prevalence of vitamin D inadequacy in European postmenopausal women

Objective: Inadequate vitamin D level is associated with secondary hyperparathyroidism and increased bone turnover and bone loss, which in turn increases fracture risk. The objective of this study is to assess the prevalence of inadequate serum vitamin D levels in postmenopausal European women. There are no clear international agreements on what constitutes a level of vitamin D inadequacy, but recent publications suggest that the circulating level of vitamin D should be over 80 nmol/L or at least between 50 and 80 nmol/L. Material and methods: Assessment of 25-hydroxyvitamin D [25(OH)D] was performed in 8532 European postmenopausal women with osteoporosis or osteopenia. European countries included France, Belgium, Denmark, Italy, Poland, Hungary, United Kingdom, Spain and Germany. Two cut-offs of 25(OH)D inadequacy were fixed < 80 nmol/L and < 50 nmol/L. Results: Mean (SD) age of the patients was 74.2 (7.1) years, body mass index was 25.7 (4.1)kg/m(2). Level of 25(OH)D was 61.0 (27.2) nmol/L. There was a highly significant difference of 25(OH)D level across European countries (p < 0.0001). The lowest level of 25(OH)D was found in France [51.5 (26.1) nmol/L] and the highest in Spain [85.2 (33.3) nmol/L]. In the whole study population, the prevalence of 25(OH)D inadequacy was 79.6% and 32.1 % when considering cut-offs of 80 and 50 nmol/L, respectively and when considering patients aged less than 65 years, the prevalence reached 86% (cut-off of 80 nmol/L) and 45% (cutoff of 50 nmol/L). Conclusion: This study indicates a high prevalence of vitamin D [25(OH)D] inadequacy in European postmenopausal women. The prevalence could be even higher in some particular countries. A greater awareness of the importance of vitamin D inadequacy is needed to address this public health problem

Improving diagnosis and treatment of osteoporosis: evaluation of a clinical pathway for low trauma fractures

The original publication is available at www.springerlink.comSummary: Diagnosis and treatment of osteoporosis in hospitals is poor. We compared patient outcomes before and after implementation of a clinical protocol for low-trauma fractures. Patients in the pathway were more likely to receive information about osteoporosis or osteoporosis medications. Therefore our clinical pathway is effective in improving osteoporosis information and treatment. Introduction: Effective therapies for reducing fracture risk are available, yet under-utilised in hospital settings. We aimed to increase rates of initiation of osteoporosis investigations, pharmacological treatment, treatment continuation, and follow-up general practitioner (GP) visits. Methods: Comparison of patient outcomes before and after implementation of a clinical pathway in patients admitted for low-trauma fractures to the Department of Orthopaedics and Trauma at The Queen Elizabeth Hospital, Adelaide. Results Patients enrolled in the osteoporosis clinical pathway (n = 28) were more likely than patients receiving usual care (n = 28) to have received information about (54% vs. 29%; p < 0.05), or a prescription for osteoporosis medication (53% vs. 25%, p < 0.05). Differences in proportions of patients visiting their GP post fracture and in osteoporosis investigations suggested or undertaken were not significant. At the later audit, the high proportion of patients receiving information about osteoporosis medication had been maintained (51%). Prescription of osteoporosis medications increased to 83% (p < 0.01), and more patients saw their GP post fracture (87%; p < 0.01). High rates of medication adherence were reported in patients in all groups receiving prescriptions. Conclusion: A clinical pathway for improving hospital management of osteoporosis is effective in improving education about, prescription for, and uptake of osteoporosis medications.L. L. Laslett, J. N. Whitham, C. Gibb, T. K. Gill, J. A. Pink, J. D. McNeil and on behalf of the Osteoporosis SA Refracture Prevention Pathway Steering Committe