Clinical Briefs
NSAID-associated Recurrent Gastrointestinal Bleeding
SOURCE: Chan FKL, Ching JYL, Tse YK, et al. Lancet 2017;389:2375-2382.
Gastrointestinal bleeding (upper and/or lower) is a well-recognized adverse effect of aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs). The COX-2 inhibitors (e.g., celecoxib) were offered to clinicians as an alternative to “non-selective” COX inhibitors (NSAIDs such as ibuprofen, diclofenac, naproxen, and many others). The putative advantage of celecoxib was an anticipated reduced risk of gastrointestinal bleeding, since relatively less COX-1 (the enzyme necessary to maintain gastric mucosal protection integrity) inhibition was occurring than with “traditional” non-selective NSAIDs. While the CLASS trial corroborated that during a six-month period, celecoxib incurred fewer serious bleeding events than non-selective NSAID therapy. This trial drew criticism later after an analysis of the study data at one year showed no meaningful differences between treatment arms.
Patients who have experienced a gastrointestinal bleed on NSAIDs are at particularly high risk to bleed again. Additionally, concern about cardiovascular risks associated with NSAIDs becomes problematic for our vasculopathic patients (post-stroke, myocardial infarction, stenting, etc.) who require antiplatelet treatment (e.g., clopidogrel, aspirin). Nonetheless, many such patients require both antiplatelet and NSAID treatment concomitantly. Chan et al reported on their double-blind study of Helicobacter-negative subjects (n = 514) randomized to celecoxib or naproxen, all of whom had experienced and resolved an episode of upper gastrointestinal bleeding. Because of prior cardiovascular events, all subjects also were taking 80 mg of aspirin per day. At 18 months, there was a clear advantage to the celecoxib/aspirin group vs. naproxen/aspirin: 5.6% cumulative bleeding events for the former vs. 12.3% for the latter. Persons who have experienced an NSAID-related upper gastrointestinal bleed would be better served by taking celecoxib than naproxen if continuation of NSAID treatment is required.
Rheumatoid Arthritis Disease Activity and Calprotectin Levels
SOURCE: Bae SC, Lee YH. Postgrad Med 2017;129:531-537.
Clinicians who see patients with inflammatory bowel disease (IBD), such as Crohn’s disease or ulcerative colitis, likely will be familiar with using fecal calprotectin levels as a diagnostic tool. Indeed, some experience suggests that because of “skip areas” observed in IBD, fecal calprotectin may be as or even more sensitive to diagnose IBD than endoscopy. Calprotectin also is measurable in plasma and synovial fluid, and has been recognized recently as a good marker of disease activity in rheumatoid arthritis (RA).
There are several validated metrics for assessment of disease activity in RA, including C-reactive protein (CRP) and Disease Activity in 28 Joints (DAS28). Bae and Lee performed a meta-analysis of RA patients (n = 849) to evaluate the correlation of calprotectin with CRP and DAS28. Significant positive correlations were demonstrated. Common treatment for RA patients includes biologic agents such as TNF-inhibitors. Calprotectin levels have been demonstrated to be good indicators of disease activity in patients on TNF treatment. Hence, calprotectin may provide a metric for confirmation of optimized control of RA, providing additional insight into disease activity beyond clinical symptoms alone.
Identification of Pneumococcal Pneumonia
SOURCE: Ceccato A, Torres A, Cilloniz C, et al. Chest 2017;151:1311-1319.
In approximately half of the cases of community-acquired pneumonia (CAP), an etiologic agent is not identified. CAP caused by Streptococcus pneumoniae (pneumococcal pneumonia) often is categorized as “invasive” (the bacteria was cultured from body fluids such as blood or pleural fluid) vs. “noninvasive” (body fluid cultures were negative, but urine antigen testing for S. pneumoniae was positive). Curiously, only pneumonia confirmed by invasive methodology has been incorporated into epidemiologic reporting of CAP traditionally. Cecatto et al noted that clinicians probably are significantly underestimating the burden of CAP by limiting the “gold standard” definition to cases identified “invasively.”
The authors studied all cases of CAP (n = 5,132) in non-immunocompromised adults treated at their Barcelona, Spain, emergency department over a 14-year interval. Of these, only 15% were confirmed to be pneumococcal. Slightly more patients were confirmed to be infected by S. pneumoniae through urinary antigen testing (54%) than by body fluid cultures (46%). Additionally, the 30-day mortality was the same regardless of which tool confirmed the diagnosis, dispelling the notion that CAP diagnosed though the “invasive” path is more lethal. Both methods of diagnosis are valid indicators of the pathogen, but there is no reason to consider urine antigen positivity as indicative of less pneumonia lethality.
In this section: nonsteroidal anti-inflammatory drugs and gastrointestinal bleeding; rheumatoid arthritis; and community-acquired pneumonia.
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