The identification of a safe and reliable alternative for patients with non-steroidal anti-inflammatory drug (NSAID)-induced urticaria/angioedema is a frequent problem for dermatologists and other practitioners. Cyclooxygenase-2 (COX-2) inhibitors have been reported to be safe for NSAID-intolerant patients from the US and Europe but not all of them have yet been approved for use in Japan. It was our objective to investigate the clinical manifestations of oral NSAID challenges in Japanese patients with histories of urticaria and/or angioedema after the intake of NSAIDs and to find safe alternative drugs, including COX-2 inhibitors and a basic anti-inflammatory drug. Twenty subjects suspected NSAID-induced urticaria/angioedema from histories were included in a double-blind or single-blind, placebo-controlled oral challenge protocol using NSAIDs. Skin prick tests using NSAIDs, which were dissolved in saline, were conducted. The mean age of the patients was 37.3 years; 14 patients were female. The results of other challenge tests showed that the most frequently intolerated drugs was loxoprofen (100%), followed by acetyl salicylic (94.4%), etodolac (53.3%), dicrofenac (50%), acetaminophen (38.5%), meloxicam (33%), and tiaramide (21.4%). Urticaria and angioedema were induced after aspirin intake in 83.3% and 22.2% of patients, respectively, whereas an asthmatic response was seen in 5.6%. Skin prick tests with NSAIDs were 100% negative. This study showed that among the NSAIDs that are available in Japan and that were investigated in this study, tiaramide, which does not inhibit COX, is the relatively safe alternative drug for Japanese patients with NSAID-induced urtiacaria and/or angioedema. Furthermore, meloxicam seems to be better tolerated than etodolac between two selective COX-2 inhibitors.
Forty-five systemic lupus erythematosus (SLE) patients who had steroid at a prednisolone dose of 0.8 mg/kg/day or more were retrospectively studied for psychiatric events that developed after the therapy. Simple insomnia was excluded. Their age, sex, dose, and duration of steroid, autoantibodies, and prophylactic heparin use were examined. Seventeen patients (female/male: 16/1, 36.7 ± 10.7 years old) developed psychiatric events 18.2 ± 10.2 days after steroid start, whereas 28 patients (27/1, 37.9 ± 13.1) did not. Anti-SS-A (Ro) antibody was more prevalent in patients with the events (15/17 vs. 14/28, p = 0.009). When heparin was administered concurrently with steroid, psychiatric events developed less frequently either in all of the patients (2/17 vs. 11/28, p = 0.048) or in patients positive for the anti-SS-A antibody (2/15 vs. 7/14, p = 0.041). SLE patients positive for the anti-SS-A (Ro) antibody would much more likely develop psychiatric events after a substantial-dose steroid therapy, and a concurrent prophylactic heparin administration might reduce the risk.
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