Prognostic severity scores for patients with COPD exacerbations attending emergency departments.

SETTING: Reported predictors of the adverse evolution of patients with chronic obstructive pulmonary disease exacerbations (eCOPD) are various and inconsistent in the bibliography. OBJECTIVE: To develop clinical prediction rules for short-term outcomes in eCOPD patients attending an emergency department (ED). DESIGN: Prospective cohort study of patients with an eCOPD. Short-term outcomes were admission to an intensive care unit (ICU), admission to an intermediate respiratory care unit (IRCU) and death in these groups. Multivariate logistic regression models were developed for each of the outcomes. RESULTS: Predictors of ICU or IRCU admission were use of long-term home oxygen therapy (LT-HOT) or non-invasive mechanical ventilation (NIMV), elevated PCO2 and decreased pH upon ED arrival (area under the curve [AUC] 0.87 in the derivation sample; 0.89 in the validation sample). Among those admitted to an ICU or IRCU, predictors of death were increased age, use at home of LT-HOT or NIMV, use of inspiratory accessory muscles upon ED arrival and altered Glasgow Coma Scale (<15 points) (AUC 0.78). CONCLUSIONS: Three clinical predictors available in the ED can be used to create a simple score to predict the need for intensive treatment among eCOPD patients. Such a score can be a tool for clinical practice.

Validity of criteria for hospital admission in exacerbations of COPD.

AIMS: To validate a previously developed set of explicit criteria for the appropriateness of hospital admission among these patients using the RAND/UCLA Appropriateness Methodology (RAM). METHODS: We conducted a prospective cohort study of patients experiencing symptoms of COPD exacerbation seen in the emergency departments (ED) of 16 hospitals belonging to the Spanish National Health Service. Sociodemographic and clinical variables needed to assess appropriateness were recorded. Main outcomes were mortality, severe COPD evolution, complications at follow up, and three patient-reported measures: dyspnoea level, capacity for physical activity and perceived health status. RESULTS: Appropriately admitted patients were more likely to die (6.70% vs. 2.68%, p = 0.0102) than inappropriately admitted patients, and were more likely to develop severe evolution (27.09% vs. 6.08%, p < 0.0001) and complications (18.72% vs. 11.92%, p = 0.0244). Among discharged patients, no significant differences were observed in clinical outcomes. All patients exhibited worse dyspnoea and capacity for physical activity after exacerbation, but changes among appropriately admitted patients were less than among appropriately discharged patients. CONCLUSION: Our appropriateness criteria identified patients in worse condition at ED arrival who were more likely to benefit from admission in terms of mortality and COPD evolution.

Identification of the PTPN22 functional variant R620W as susceptibility genetic factor for giant cell arteritis.

OBJECTIVE: To analyse the role of the PTPN22 and CSK genes, previously associated with autoimmunity, in the predisposition and clinical phenotypes of giant cell arteritis (GCA). METHODS: Our study population was composed of 911 patients diagnosed with biopsy-proven GCA and 8136 unaffected controls from a Spanish discovery cohort and three additional independent replication cohorts from Germany, Norway and the UK. Two functional PTPN22 polymorphisms (rs2476601/R620W and rs33996649/R263Q) and two variants of the CSK gene (rs1378942 and rs34933034) were genotyped using predesigned TaqMan assays. RESULTS: The analysis of the discovery cohort provided evidence of association of PTPN22 rs2476601/R620W with GCA (PFDR=1.06E-04, OR=1.62, CI 95% 1.29 to 2.04). The association did not appear to follow a specific GCA subphenotype. No statistically significant differences between allele frequencies for the other PTPN22 and CSK genetic variants were evident either in the case/control or in stratified case analysis. To confirm the detected PTPN22 association, three replication cohorts were genotyped, and a consistent association between the PTPN22 rs2476601/R620W variant and GCA was evident in the overall meta-analysis (PMH=2.00E-06, OR=1.51, CI 95% 1.28 to 1.79). CONCLUSIONS: Our results suggest that the PTPN22 polymorphism rs2476601/R620W plays an important role in the genetic risk to GCA.

A case-control study suggests that the CCR6 locus is not involved in the susceptibility to giant cell arteritis.

OBJECTIVES: Polymorphisms of the CC chemokine receptor 6 (CCR6) gene have been recently reported to be associated with a number of autoimmune diseases. We aimed to investigate the possible influence of CCR6 rs3093024 gene variant in the susceptibility to and clinical expression of GCA. METHODS: The CCR6 polymorphism rs3093024 was genotyped in a total of 463 Spanish patients diagnosed with biopsy-proven GCA and 920 healthy controls using a TaqMan® allelic discrimination assay. PLINK software was used for the statistical analyses. RESULTS: No significant association between this CCR6 variant and GCA was observed (p=0.42, OR=0.94, CI95% 0.79-1.10). Similarly, when patients were stratified according to the specific clinical features of GCA such as polymyalgia rheumatica, visual ischaemic manifestations or irreversible occlusive disease, no statistical significant difference was detected either between the case subgroups and the control set or between GCA patients with and without the specific features of the disease. CONCLUSIONS: Our results suggest that the CCR6 rs3093024 polymorphism may not play a relevant role in the GCA pathophysiology.