BackgroundThe elderly are predisposed to septic arthritis (SA) because of the aging nature and increasing comorbidities. SA may in turn increase the long-term mortality in the geriatric patients; however, it remains unclear. We conducted this prospective nationwide population-based cohort study to clarify this issue.MethodsUsing Taiwan National Health Insurance Research Database (NHIRD), we identified 1667 geriatric participants (≥ 65 years) with SA and 16,670 geriatric participants without SA matched at a ratio of 1:10 by age, sex, and index date between 1999 and 2010. A comparison of the long-term mortality between the two cohorts through follow-up until 2011 was performed.ResultsGeriatric participants with SA had a significantly increased mortality than those without SA [Adjusted hazard ratio (AHR): 1.49, 95% confidence interval (CI): 1.34–1.66], particularly the old elderly (≥ 85 years, AHR: 2.12, 95% CI: 1.58–2.84) and males (AHR: 1.54, 95% CI: 1.33–1.79). These results were stated after adjustment for osteoarthritis, diabetes, gout, renal disease, liver disease, cancer, rheumatoid arthritis, systemic lupus erythematosus, alcoholism, and human immunodeficiency virus infection. The increased mortality risk was highest in the first month (AHR: 3.93, 95% CI: 2.94–5.25) and remained increased even after following up for 2–4 years (AHR: 1.30, 95% CI: 1.03–1.65). After Cox proportional hazard regression analysis, SA (AHR: 1.37, 95% CI: 1.20–1.56), older age (≥ 85 years, AHR: 1.79, 95% CI: 1.59–2.02, 75–84 years, AHR: 1.65, 95% CI: 1.53–1.78), male sex, diabetes, renal disease, liver disease, cancer, and gout were independent mortality predictors. There was no significant difference in the mortality for SA between upper limb affected and lower limb affected.ConclusionsThis study delineated that SA significantly increased the long-term mortality in geriatric participants. For the increasing aging population worldwide, strategies for the prevention and treatment of SA and concomitant control of comorbidities are very important.

Prior studies of upper gastrointestinal bleeding (UGIB) and acute myocardial infarction (AMI) are small, and long-term effects of UGIB on AMI have not been delineated. We investigated whether UGIB in patients diagnosed with coronary artery disease (CAD) increased their risk of subsequent AMI. This was a population-based, nested case-control study using Taiwan’s National Health Insurance Research Database. After propensity-score matching for age, gender, comorbidities, CAD date, and follow-up duration, we identified 1,677 new-onset CAD patients with AMI (AMI[+]) between 2001 and 2006 as the case group and 10,062 new-onset CAD patients without (AMI[−]) as the control group. Conditional logistic regression was used to examine the association between UGIB and AMI. Compared with UGIB[−] patients, UGIB[+] patients had twice the risk for subsequent AMI (adjusted odds ratio [AOR] = 2.08; 95% confidence interval [CI], 1.72–2.50). In the subgroup analysis for gender and age, UGIB[+] women (AOR = 2.70; 95% CI, 2.03–3.57) and patients < 65 years old (AOR = 2.23; 95% CI, 1.56–3.18) had higher odds of an AMI. UGIB[+] AMI[+] patients used nonsignificantly less aspirin than did UGIB[−] AMI[+] patients (27.69% vs. 35.61%, respectively). UGIB increased the risk of subsequent AMI in CAD patients, especially in women and patients < 65. This suggests that physicians need to use earlier and more aggressive intervention to detect UGIB and prevent AMI in CAD patients.

A 77-year-old man with hypertension presented with left flank pain for 1 day. He was initially treated as renal colic. Due to worsening of the clinical symptoms and deteriorated renal function, a computed tomography (CT) scan was obtained which demonstrated a huge infrarenal atherosclerotic abdominal aortic aneurysm (AAA) (about 8.3 cm in diameter) with lateral displacement and direct extrinsic compression of the left ureter (Picture 1), causing left hydronephrosis and hydroureter (Picture 2). After endovascular aneurysm repair, he had an uneventful recovery. Follow-up studies at 16 months showed a gradual decrease of the aneurysm sac, and complete resolution of the left obstructive uropathy.An AAA should be considered among the causes of obstructive uropathy. Most case reports are secondary to dense peri-aneurysmal fibrosis complicating inflammatory AAA, causing entrapment of the ureter within the aortic wall (1, 2). Atherosclerotic AAA rarely cause ureteral obstruction and lateral displacement of the ureter is a characteristic urographic finding (2).