Characteristics and outcomes of hospitalised patients with vertebral fragility fractures: a systematic review

Background: The complex management for patients presenting to hospital with vertebral fragility fractures provides justification for the development of specific services for them. A systematic review was undertaken to determine the incidence of hospital admission, patient characteristics, and health outcomes of vertebral fragility fracture patients to inform the development of such a service. Methods: Non-randomised studies of vertebral fragility fracture in hospital were included. Searches were conducted using electronic databases and citation searching of the included papers. Results: 19 studies were included. The incidence of hospital admission varied from 2.8-19.3 per 10,000/year. The average patient age was 81 years, the majority having presented with a fall. A diagnosis of osteoporosis or previous fragility fracture was reported in around one third of patients. Most patients (75% men and 78% women) had five or more co-pathologies. Most patients were managed non-operatively with a median hospital length of stay of 10 days. One third of patients were started on osteoporosis treatment. Inpatient and one year mortality was between 0.9-3.5%, and 20–25% respectively: between 34-50% were discharged from hospital to a care facility. Many patients were more dependent with activities of daily living on discharge compared to their pre-admission level. Older age and increasing comorbidities was associated with longer hospital stay and higher mortality. Conclusion: These findings indicate that specific hospital services for patients with vertebral fragility fractures should take into consideration local hospitalisation rates for the condition, and should be multifaceted - providing access to diagnostic, therapeutic, surgical and rehabilitation interventions

T-cell receptor gene rearrangements as markers of lineage and clonality in T-cell neoplasms.

Ig gene rearrangements represent markers of lineage, clonality, and differentiation of B cells, allowing a molecular diagnosis and immunogenotypic classification of B-cell neoplasms. We sought to apply a similar approach to the study of T-cell populations by analyzing rearrangements of the T-cell receptor beta-chain (T beta) gene. Our analysis, by Southern blotting hybridization using T beta-specific probes of DNAs from polyclonal T cells and from 12 T-cell tumors, indicates that T beta gene rearrangement patterns can be used as markers of (i) lineage, allowing the identification of polyclonal T-cell populations, and (ii) clonality, allowing the detection of monoclonal T-cell tumors. In addition, our data indicate that T beta gene rearrangements represent early and general markers of T-cell differentiation since they are detectable in histologically different tumors at all stages of T-cell development. The ability to determine lineage, clonality, and stage of differentiation has significant implications for future experimental and clinical studies on normal and neoplastic T cells

Analysis of T-cell receptor beta chain (T beta) gene rearrangements demonstrates the monoclonal nature of T-cell chronic lymphoproliferative disorders

We investigated the rearrangement patterns of the gene coding for the beta chain of the T cell receptor (T beta) in 11 patients with T-cell derived chronic lymphoproliferative disorders, including T-cell prolymphocytic leukemia (T-PLL) and T-cell chronic lymphocytic leukemia (T-CLL). We found that all five cases of T-PLL, and five of six cases of T-CLL, displayed T beta-gene rearrangements, clearly establishing their monoclonal nature. Clonality could not be determined in one case of T-CLL where the T beta gene was found unrearranged. Our results demonstrate that the majority of cases of both clinically aggressive T-PLL and clinically indolent T-CLL are monoclonal. These results suggest that the analysis of T beta gene rearrangements represents a valid tool for the differential diagnosis and clinical monitoring of T-cell derived chronic lymphoproliferative diseases

Analysis of T-cell receptor beta chain (T beta) gene rearrangements demonstrates the monoclonal nature of T-cell chronic lymphoproliferative disorders

We investigated the rearrangement patterns of the gene coding for the beta chain of the T cell receptor (T beta) in 11 patients with T-cell derived chronic lymphoproliferative disorders, including T-cell prolymphocytic leukemia (T-PLL) and T-cell chronic lymphocytic leukemia (T-CLL). We found that all five cases of T-PLL, and five of six cases of T-CLL, displayed T beta-gene rearrangements, clearly establishing their monoclonal nature. Clonality could not be determined in one case of T-CLL where the T beta gene was found unrearranged. Our results demonstrate that the majority of cases of both clinically aggressive T-PLL and clinically indolent T-CLL are monoclonal. These results suggest that the analysis of T beta gene rearrangements represents a valid tool for the differential diagnosis and clinical monitoring of T-cell derived chronic lymphoproliferative diseases