Abstract
Several case reports suggest that non-steroidal anti-inflammatory drug (NSAID) use is associated with development of thrombotic microangiopathy (TMA). We conducted a matched population-based case-control study using linked administrative healthcare data in Ontario, Canada to assess the relationship between TMA hospitalization and recent exposure to prescription NSAIDs versus acetaminophen (acetaminophen was chosen as the referent drug because it has no known association with TMA). Cases and controls were drawn from a source population of adults who filled a prescription for either NSAIDs or acetaminophen between 1991 and 2015 (restricted to adults with prescription drug benefits [n = 3.6 million]). We identified 44 eligible cases with a hospital admission for incident TMA and a recent prescription for NSAIDs or acetaminophen. We successfully matched 38 cases (1:4) to 152 controls without TMA on demographics, risk factors for TMA, and indications for NSAID use. Cases and controls were similar with respect to age (71 years) and sex (63% women); however, on average, cases had more comorbidities than controls (12 vs. 14; p<0.05) and more primary care visits in the year before the index date (19 vs. 12; p<0.05). Cases were significantly less likely than controls to have received a recent prescription for NSAIDs (19/38 [50%] vs. 115/152 [76%], respectively; adjusted odds ratio 0.37, 95% confidence interval: 0.16 to 0.84). Results were similar in several sensitivity analyses. Overall, the results of this study do not support a harmful association between NSAID use and the development of TMA.
Highlights
Patients treated with plasma exchange in Ontario for Thrombotic microangiopathy (TMA) with a recent history of non-steroidal anti-inflammatory drug (NSAID) use had medical chart data abstracted for another study; in this analysis, the diagnostic codes for TMA identified a group of patients (n = 22) with the following median, (25th, 75th percentile) blood results as nadir or peak values during hospital stay: hemoglobin 98 (71, 108) g/L, platelets 49 (22, 87) x 109/L, creatinine 180 (87–393) μmol/L and lactate dehydrogenase 1219 (439, 1981) U/L
There are over 30 million daily users of NSAIDs worldwide; many patients who present with TMA will have a prior history of NSAID use.[20,21]
Previous case reports suggest NSAIDs could be associated with TMA.[4,5,6,7,8]
Summary
We first searched the bibliographic databases Pubmed, EMBASE, Google Scholar, and Web of Science, and identified 8 case reports suggesting a possible link between TMA and NSAID usage.[4,5,6,7,8,9,10,11] The case reports were critically appraised based on an existing framework adapted from Al-Nouri et al in order to scrutinize the likelihood of association.[3] A summary of our review is provided in supporting information S1 Table, which includes an assessment of methodological quality and the likelihood that NSAIDs cause TMA.
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