Epidemiology of distal radius fractures: a detailed survey on a large sample of patients in a suburban area.

BACKGROUND: Literature lacks data on correlations between epidemiology and clinical data of patients with distal radius fractures (DRFs). AIM: The aim of this study was to present a detailed epidemiologic survey of a large consecutive series of patient with DRFs. MATERIALS AND METHODS: This retrospective study included 827 consecutive patients (579 females, 248 men) who sustained a DRFs in the last 5 years. All fractures were radiographically evaluated. DRFs were classified according to Association of Osteosynthesis classification. Data on age, gender, side, period in which fracture occurred, and fracture mechanism were collected. Statistical analysis was performed. RESULTS: The patients' mean age was 60.23 [standard deviation (SD) 16.65] years, with the left side being most frequently involved (56.1%). The mean age of females at the time of fracture was significantly higher than that of males. The most frequent pattern of fracture was the complete articular fracture (64.3%), while the most represented fracture type was 2R3A2.2 (21.5%). Regarding the period in which the fracture occurred, 305 DRFs (37.5%) were observed in the warmer months and 272 (33.4%) in the colder months. Low-energy trauma occurring outside home was found to be the major cause of DRF throughout the year. In both genders, trauma mechanism 2 was more frequent (59.4% F; 31.9% M; p < 0.01). A bimodal distribution of fracture mechanisms was found in males when considering the patient's age with a high-energy mechanism of fracture (3 and 4), identified in 21% (n = 52) of males aged 18-45 years, and a low-energy mechanism (1 and 2) was observed in 39.9% (n = 99) of males aged > 45 years. A significant correlation between all trauma mechanisms (from 1 to 6) and different fracture patterns (complete, partial, and extraarticular) was found (p value < 0.001). The mean age of patients with extraarticular fractures (mean age 61.75 years; SD 18.18 years) was higher than that of those with complete (mean age 59.84 years; SD 15.67 years) and partial fractures (mean age 55.26 years; SD 18.31 years). Furthermore, considering different fracture patterns and patient age groups, a statistically significant difference was found (p < 0.001). CONCLUSIONS: DRFs have a higher prevalence in females, an increase in incidence with older age, and no seasonal predisposition. Low-energy trauma occurring at home is the main cause of fracture among younger males sustaining fractures after sports trauma; Complete articular is the most frequent fracture pattern, while 2R3A2.2 is most frequent fracture type. LEVEL OF EVIDENCE: Level IV; case series; descriptive epidemiology study.

The C-C chemokine receptors CCR4 and CCR8 identify airway T cells of allergen-challenged atopic asthmatics.

In vitro polarized human Th2 cells preferentially express the chemokine receptors CCR3, CCR4, and CCR8 and migrate to their ligands: eotaxin, monocyte-derived chemokine (MDC), thymus- and activation-regulated chemokine (TARC), and I-309. We have studied the expression of chemokines and chemokine receptors in the airway mucosa of atopic asthmatics. Immunofluorescent analysis of endobronchial biopsies from six asthmatics, taken 24 hours after allergen challenge, demonstrates that virtually all T cells express IL-4 and CCR4. CCR8 is coexpressed with CCR4 on 28% of the T cells, while CCR3 is expressed on eosinophils but not on T cells. Expression of the CCR4-specific ligands MDC and TARC is strongly upregulated on airway epithelial cells upon allergen challenge, suggesting an involvement of this receptor/ligand axis in the regulation of lymphocyte recruitment into the asthmatic bronchi. In contrast to asthma, T cells infiltrating the airways of patients with chronic obstructive pulmonary disease and pulmonary sarcoidosis produce IFN-gamma and express high levels of CXCR3, while lacking CCR4 and CCR8 expression. These data support the role of CCR4, of its ligands MDC and TARC, and of CCR8 in the pathogenesis of allergen-induced late asthmatic responses and suggest that these molecules could be considered as targets for therapeutic intervention.

Inhibition of Th1 development and treatment of chronic-relapsing experimental allergic encephalomyelitis by a non-hypercalcemic analogue of 1,25-dihydroxyvitamin D(3).

1alpha,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] inhibits production of IL-12, a cytokine involved in the development of Th1 cells and in the pathogenesis of Th1-mediated autoimmune diseases. Here, we show that 1,25(OH)(2)D(3) and a non-hypercalcemic analogue are selective and potent inhibitors of Th1 development in vitro and in vivo without inducing a deviation to the Th2 phenotype. Administration of 1,25(OH)(2)D(3) or its analogue prevents chronic-relapsing experimental allergic encephalomyelitis (CR-EAE) induced by the myelin oligodendrocyte glycoprotein (MOG) peptide 35 - 55 (MOG(35 - 55)) in Biozzi AB / H mice. The inhibition of EAE induction is associated with a profound reduction of MOG(35 - 55)-specific proliferation and Th1 cell development. Importantly, the non-hypercalcemic analogue also provides long-term protection from EAE relapses induced by immunization with spinal cord homogenate when administered for a short time at symptom onset or even after the first peak of disease. Neuropathological analysis shows a reduction of inflammatory infiltrates, demyelinated areas and axonal loss in brains and spinal cords of treated mice. These resuls indicate that inhibition of IL-12-dependent Th1 cell development is associated with effective treatment of CR-EAE and suggest the feasibility of an approach based on low molecular weight inhibitors of IL-12 production in the treatment of multiple sclerosis.

Inhibition of IL-12 production by 1,25-dihydroxyvitamin D3. Involvement of NF-kappaB downregulation in transcriptional repression of the p40 gene.

Interleukin 12 (IL-12), produced by myelomonocytic cells, plays a pivotal role in the development of T helper 1 (Th1) cells, which are involved in the pathogenesis of chronic inflammatory autoimmune disorders. 1,25-Dihydroxyvitamin D3 [1,25(OH)2D3] inhibits IL-12 production by activated macrophages and dendritic cells, thus providing a novel interpretation to its immunosuppressive properties. 1,25(OH)2D3 significantly inhibits mRNA expression for both IL-12 p35 and p40 subunits acting at the transcriptional level. The effect of 1,25(OH)2D3 on p40 promoter activation was analyzed by cotransfecting monocytic RAW264.7 cells with p40 promoter/reporter constructs and expression vectors for vitamin D3 receptor (VDR) and/or retinoid X receptor (RXRalpha). We observed transcriptional repression of the p40 gene by 1,25(OH)2D3, which required coexpression of VDR with RXR and an intact VDR DNA-binding domain. The repressive effect maps to a region in the p40 promoter containing a binding site for NF-kappaB (p40-kappaB). Deletion of the p40-kappaB site abrogates part of the inhibitory effect on the p40 promoter, confirming the functional relevance of this site. Activation of monocytic THP-1 cells in the presence of 1,25(OH)2D3 results in reduced binding to the p40-kappaB site. Thus, 1,25(OH)2D3 may negatively regulate IL-12 production by downregulation of NF-kappaB activation and binding to the p40-kappaB sequence.