INTRODUCTION: Visceral leishmaniasis (VL; kala-azar) is a serious zoonosis that can be lethal, especially in untreated patients. Due to the fact that the State of Ceará is still an important area of transmission of VL, and based on the constant reports of the urbanization process of the disease in the country, it was necessary to monitor the occurrence of cases of leishmaniasis through epidemiological surveillance. OBJECTIVES: To describe the epidemiology of leishmaniasis cases in Ceará, Brazil. METHODS: We conducted an epidemiological survey of secondary data provided by SINAN/MS from January 2007 to December 2011. RESULTS: VL is an endemic disease in the State of Ceará, with cases notified in approximately 88% of the municipalities, with an average of 596.8 ± 29.6 cases, an incidence of 6.1 cases/100,000 inhabitants and prevalence of 7.1 cases/100,000 inhabitants. The Metropolitan Region of Fortaleza is the microregion with the largest number of cases reported in state (51.9% of cases), with the capital, Fortaleza, being the municipality with the highest number of cases in the country. Traditionally, the main age group affected by the disease are children; however, a reversal has been observed in the profile from 2008, when the population of adult patients exceeded the pediatric population. CONCLUSION: Ceará is still an endemic area for VL, and the city of Fortaleza reported the highest number of cases in the country. In the State, a change in the profile of patients with the disease has been observed, now affecting primarily adults.

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In the search for novel natural compounds effective against visceral nociception, the triterpenoid mixture alpha- and beta-amyrin, isolated from Protium heptaphyllum resin, was assessed in two established mouse models of visceral nociception. Mice were pretreated orally with alpha- and beta-amyrin (3, 10, 30, and 100 mg/kg) or vehicle, and the pain-related behavioral responses to intraperitoneal cyclophosphamide or to intracolonic mustard oil were analyzed. The triterpenoid mixture showed a dose-related significant antinociception against the cyclophosphamide-induced bladder pain, and at 100 mg/kg, the nociceptive behavioral expression was almost completely suppressed. Intracolonic mustard oil-induced nociceptive behaviors were maximally inhibited by 10 mg/kg alpha- and beta-amyrin mixture in a naloxone-reversible manner. While pretreatment with ruthenium red (3 mg/kg, s. c.), a non-specific transient receptor potential cation channel V1 (TRPV1) antagonist, also caused significant inhibition, the alpha (2)-adrenoceptor antagonist, yohimbine (2 mg/kg, s. c.), showed no significant effect. The triterpene mixture (10 mg/kg, p. o.) neither altered significantly the pentobarbital sleeping time, nor impaired the ambulation or motor coordination in open-field and rotarod tests, respectively, indicating the absence of sedative or motor abnormalities that could account for its antinociception. These results indicate that the antinociceptive potential of alpha- and beta-amyrin possibly involves the opioid and vanilloid (TRPV1) receptor mechanisms and further suggests that it could be useful to treat visceral pain of intestinal and pelvic origins.

The results indicate that this lectin is a potent anti-inflammatory molecule. Its effects engage diverse modulatory events.

The diterpene, 12-acetoxyhawtriwaic acid lactone (AHAL, tanabalin) isolated from the flower buds of Egletes viscosa Less. (Asteraceae) was evaluated on capsaicin-induced ear edema and hindpaw nociception in mice. AHAL (12.5, 25 and 50 mg/kg, P. O.) significantly attenuated the ear edema response to topically applied capsaicin (250 microg), in a dose-related manner. At similar doses, AHAL also suppressed the nocifensive paw-licking behavior induced by intraplantar injection of capsaicin (1.6 microg). These responses to capsaicin were also greatly inhibited by ruthenium red (3 mg/kg, S. C.), a non-competitive capsaicin receptor (TRPV1) antagonist. The anti-edema effect of AHAL (50 mg/kg) seems unrelated to either blockade of mast cell degranulation or to histamine and serotonin receptor antagonism since AHAL did not modify the paw edema response induced by intraplantar injections of compound 48/80, histamine or serotonin. However, the hindpaw edema induced by substance P and vascular permeability increase induced by intraperitoneal acetic acid were significantly suppressed by AHAL. The antinociceptive effect of AHAL (50 mg/kg) was unaffected by naloxone pretreatment but was significantly antagonized by theophylline and glibenclamide, the respective blockers of adenosine and K(ATP)-channels. AHAL (50 mg/kg, P. O.) did not impair the ambulation or motor coordination of mice in open-field and rota-rod tests. These data suggest that AHAL inhibits acute neurogenic inflammation possibly involving capsaicin-sensitive TRPV1-receptors, endogenous adenosine and ATP-sensitive potassium channels.