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We aimed to compare the history of trauma and the profile and severity of dissociative symptoms of patients with obsessive-compulsive disorder (OCD) to those of patients with social anxiety disorder (SAD). Patients with OCD (n = 34) and patients with SAD (n = 30) were examined with the following instruments: Trauma History Questionnaire (THQ), Dissociative Experience Scale (DES), Obsessive-Compulsive Inventory (OCI), Liebowitz Social Anxiety Scale (LSAS), Beck Depression Inventory (BDI), and Beck Anxiety Inventory (BAI). Patients with OCD reported significantly lower rates of exposure to traumatic events. Nevertheless, the severity of dissociative symptoms was not significantly different between the groups. Regression analyses showed that, while the OCI scores better predicted the variance on DES scores in the OCD sample, the LSAS and the BAI better predicted the variance on the DES among patients with SAD. Patients with OCD are probably less vulnerable to some types of traumatic experiences. Dissociative symptoms may cut across different anxiety disorders.

To investigate whether selective COX 2 inhibitors (celecoxib, rofecoxib) would play a role in a model of leukocyte migration in rats. Bacterial endotoxin (Escherichia coli LPS) was intraperitoneally injected at time zero in rats that were previously treated with unspecific and selective cyclooxygenase inhibitors. LPS induced a dose and time-dependent increase in leukocyte number, which was predominantly related to the presence of PMN neutrophils. Only rats treated with selective COX 2 inhibitors and indomethacin showed a significant reduction in leukocyte numbers following LPS administration. Prostaglandins E(2) and F(2alpha) were injected into the peritoneum and the chemoatractant effect was studied. Only PGF(2alpha) was able to induce neutrophil increase following injection. Intraperitoneal reposition of PGF(2alpha) restored the abrogated leukocyte response to LPS, shown by rats pretreated with rofecoxib. It can be concluded that COX 2, through PGF(2alpha) release, is the isoform responsible for neutrophil recruitment in the rat model of LPS-induced inflammation.