Different ethnic background is associated with distinct clinical profiles in the spondyloarthritides in the North and South of Brazil.

The objective of this study was to analyze the clinical profile of the spondyloarthritides (SpA) in distinct Brazilian regions. A common protocol of investigation was prospectively applied to 202 SpA patients, including 138 patients from the South and 64 patients from the North. All the patients were classified as axial or peripheral SpA. Clinical and demographic variables and disease indexes were analyzed. Bonferroni correction was used to adjust the level of significance of each test; results with p value < 0.003 were considered statistically relevant. White ethnicity was associated with positive HLA-B27, while non-Whites presented higher frequency of peripheral arthritis, although not statistically significant. When comparing non-White patients from the North with those from the South, the Southerners presented significantly higher scores of Ankylosing Spondylitis Disease Activity Score using C-reactive protein (p = 0.001) and Health Assessment Questionnaire (p = 0.001). Although not statistically significant, Northern non-White patients were more frequently males, while Southerners had higher frequency of anterior uveitis and higher Bath Ankylosing Spondylitis Disease Activity Index and Ankylosing Spondylitis Quality of Life. Brazilian SpA patients present distinct patterns of disease according to the geographic region, especially regarding the non-White populations.

Piperine decreases pilocarpine-induced convulsions by GABAergic mechanisms.

Piperine, an alkaloid present in the Piper genus, was shown to have an anticonvulsant activity, evaluated by the pilocarpine-induced model, in mice. Pilocarpine (350mg/kg, i.p.) was administered 30min after piperine (2.5, 5, 10 and 20mg/kg, i.p.) which significantly increased latencies to 1st convulsion and to death, and percentage of survivals. These parameters were also increased in the pilocarpine groups pretreated with atropine plus piperine (10 and 2.5mg/kg, respectively), as related to the pilocarpine group. However, they were not altered in the pilocarpine groups pretreated with memantine (a NMDA-type glutamate receptors blocker, 2mg/kg, p.o.) or nimodipine (a calcium channel blocker, 10mg/kg, p.o.), both associated with piperine (1 or 2.5mg/kg), as compared to the piperine plus pilocarpine group. Moreover, the pilocarpine group pretreated with diazepam (which binds to the GABAA receptor, 0.2 and 0.5mg/kg, i.p.) plus piperine (1 and 2.5mg/kg) significantly increased latency to the 1st convulsion, as related to the pilocarpine group, suggesting that the GABAergic system is involved with the piperine action. Furthermore, the piperine effect was blocked by flumazenil (2mg/kg, i.p.), a benzodiazepine antagonist. Untreated P350 animals showed decreased striatal DA and increased DOPAC and HVA levels that were not affected in the piperine plus pilocarpine groups. Piperine increased striatal levels of GABA, glycine and taurine, and reversed pilocarpine-induced increases in nitrite contents in sera and brain. Hippocampi from the untreated pilocarpine group showed an increased number of TNF-α immunostained cells in all areas, as opposed to the pilocarpine group pretreated with piperine. Taken together, piperine anticonvulsant effects are the result of its anti-inflammatory and antioxidant actions, as well as TNF-α reduction. In addition, piperine effects on inhibitory amino acids and on the GABAergic system may certainly contribute to the drug anticonvulsant activity.