RESUMEN
Patients are often referred to osteoporosis clinics with a radiological diagnosis of osteoporosis. Previous studies attempting to ascertain risk of osteoporosis from radiographs have been conflicting. The aim of our study was to determine how reliable spinal radiographs were at detecting low bone density compared with Dual Energy X ray Absorptiometry (DXA). We retrospectively measured the Bone Mineral Density (BMD) at the spine in 130 patients with a radiological diagnosis of osteopenia or osteoporosis in the absence of vertebral fractures. They were compared with a group of 119 age and sex matched patients with one or more low trauma vertebral fractures. There was a statistically significant difference in the mean BMD between these two groups. 12.7%, of the x-ray group with osteopenia reported, had a normal bone density, 49.2% had osteopenia (T-score -1 to -2.5) and 38.1% had osteoporosis (T-score <-2.5). Of those with a radiological report of osteoporosis, 12.8% had a normal bone density, 44.7% had osteopenia and 42.6% had osteoporosis. We conclude that a radiological report of low bone density is a strong predictor of osteopenia or osteoporosis by BMD measurement.
Asunto(s)
Densidad Ósea , Osteoporosis/diagnóstico por imagen , Enfermedades de la Columna Vertebral/diagnóstico por imagen , Absorciometría de Fotón , Adulto , Anciano , Anciano de 80 o más Años , Enfermedades Óseas Metabólicas/diagnóstico por imagen , Estudios de Casos y Controles , Femenino , Humanos , Masculino , Persona de Mediana Edad , Valor Predictivo de las Pruebas , Estudios RetrospectivosRESUMEN
BACKGROUND: Deposition of beta-amyloid in the brains of patients with Alzheimer's disease is thought to precede a chain of events that leads to an inflammatory response by the brain. We postulated that genetic variation in the regulatory region of the gene for the proinflammatory cytokine tumour necrosis factor alpha (TNF-alpha) leads to increased risk of Alzheimer's disease and vascular dementia. METHODS: A polymorphism in the regulatory region of the TNF-alpha gene was analysed in a case-control study. The polymorphism (C-850T) was typed in 242 patients with sporadic Alzheimer's disease, 81 patients with vascular dementia, 61 stroke patients without dementia, and 235 normal controls. These groups of individuals were also genotyped for the apolipoprotein E polymorphism, and the vascular dementia and stroke groups were typed at the HLA-DR locus. FINDINGS: The distribution of TNF-alpha genotypes in the vascular dementia group differed significantly from that in the stroke and normal control groups, giving an odds ratio of 2.51 (95% CI 1.49-4.21) for the development of vascular dementia for individuals with a CT or TT genotype. Logistic regression analysis indicated that the possession of the T allele significantly increased the risk of Alzheimer's disease associated with carriage of the apolipoprotein E epsilon4 allele (odds ratio 2.73 [1.68-4.44] for those with apolipoprotein E epsilon4 but no TNF-alpha T, vs 4.62 [2.38-8.96] for those with apolipoprotein E epsilon4 and TNF-alpha T; p=0.03). INTERPRETATION: Possession of the TNF-alpha T allele significantly increases the risk of vascular dementia, and increases the risk of Alzheimer's disease associated with apolipoprotein E. Although further research is needed, these findings suggest a potential role for anti-inflammatory therapy in vascular dementia and Alzheimer's disease, and perhaps especially in patients who have had a stroke.