Bullous Fixed Drug Eruption Following Ibuprofen Ingestion.

Fixed drug eruption (FDE) is a drug reaction involving skin and less commonly mucosal membranes. The common manifestation is localized well-demarcated patches or plaques appeared following receiving of a culprit drug. When re-exposure occurs, the rashes will appear at areas involved in previous episodes. Limited reports on bullous FDE due to ibuprofen have been documented before. Herein, we described an elderly man who experienced multifocal lesions in his oral mucosa, penis, and multiple sites of skin following ibuprofen ingestion confirmed as FDE by pathological studies. The culprit drug had been discontinued. Systemic and topical glucocorticoids as well as supportive care had been instituted. The patient's outcome was favorable and his lesions had been recovered within the next weeks. Patient's follow-up showed that he had received ibuprofen again sometime later resulting in anal mucosal lesion and similar penile involvement. In routine clinical practice, mucocutaneous adverse drug reactions should be considered. A high index of suspicion, the detailed medication history, the course of the symptoms, and distributing pattern of the lesions are essential clues for the diagnosis. However, judicious and prompt pathological studies can help to differentiate multifocal bullous FDE from major skin drug reactions such as Stevens-Johnson syndrome/toxic epidermal necrolysis.

Interactive involvement of hippocampal cAMP/PKA and cyclooxygenase-2 signaling pathways in spatial learning in the Morris water maze.

INTRODUCTION: Accumulated evidence shows that the cAMP-PKA signaling pathway plays a key role in memory functions. Cyclooxygenase-2, a critical player in neuroinflammation, has been confirmed in the pathogenesis of neurodegenerative diseases. This study is aimed to assess the effect of the interaction of cAMP-PKA and cyclooxygenase pathways on spatial memory acquisition in animal models. MATERIAL AND METHODS: In the present study, the effects of the four-day bilateral intra-hippocampal infusions of H-89 as a protein kinase AII inhibitor (10 µM/side), celecoxib (0.1 M/side) as a selective cyclooxygenase-2 inhibitor, cele-coxib/H-89 and bucladesine (10 µM/side)/celecoxib/H-89 on spatial memory acquisition in the Morris water maze were investigated. Control animals received bilateral intra-hippocampal infusions of dimethyl sulfoxide. Rats were trained for 4 days; each day included one block of four trials. Post-training probe trial tests were performed on day five. RESULTS: A bilateral intra-hippocampal infusion of H-89 and celecoxib led to a significant impairment in spatial learning compared to the controls through a notable decrease in escape latency and traveled distance. But, combination treatment of animals with celecoxib/H-89 and bucladesine/celecoxib/H-89 could considerably reverse celecoxib and H-89-induced spatial memory acquisition impairments in the Morris water maze. CONCLUSIONS: These results indicate the probable regulatory effects of cAMP/PKA and cyclooxygenase-2 signaling pathways on spatial memory acquisition in the Morris water maze.