Quantitative analysis of fibrosis and mast cells in the tongue of chronic chagasic patients: autopsy study.

OBJECTIVE: Recently, an orally transmitted outbreak of Chagas disease was reported in Santa Catarina, Brazil, after ingestion of sugar cane juice (garapa). This disease is caused by Trypanosoma cruzi, a parasite that stimulates the development of chronic inflammatory response, characterized by fibrous connective tissue neoformation (fibrosis). As the density of tissue mast cells (MC) may be an index of fibroblast proliferation and development of local fibrosis, the purpose of this autopsy study was to quantify the fibrosis rate and the number of MC in the tongues of chronic chagasic (CC) patients, compared with a non-chagasic (NC) control group. METHODOLOGY: Twenty-four evaluations, with a quantitative assessment of fibrosis percentage and MC density were performed. RESULTS: The percentage of fibrosis in the tongue was higher among CC than in the control group. In the CC group, a positive and significant correlation was found when the fibrosis rate was compared with the MC density. CONCLUSIONS: These morphometric findings suggest that tongue biopsy may be useful to study specific changes associated with Chagas disease. They also suggest that the systematic analysis of oral cavity, including tongue histopathology changes, could be useful in forensic pathology of the orally acquired chronic Chagas disease.

The role of immunosuppressive drugs in aggravating renal ischemia and reperfusion injury.

UNLABELLED: Renal ischemia followed by reperfusion leads to acute renal failure in both native kidneys and renal allografts. Cyclosporine has known nephrotoxic effects. Thus, cyclosporine therapy subsequent to ischemia/reperfusion (I/R) injury may further exacerbate graft dysfunction. Rapamycin is a newer agent that suppresses the immune system by a different mechanism. In the present study, the effects of Cyclosporine and rapamycin at low and higher concentrations were investigated in an I/R-induced injury model. METHODS: Cyclosporine (100 mg/kg or 50 mg/kg), rapamycin (3 mg/kg per day or 1.5 mg/kg), or both were administered to mice before being subjected to 45 minutes of ischemia. Blood and kidney samples were collected at 24, 48, and 120 hours after surgery. We quantified acute tubular necrosis and tubular regeneration. RESULTS: Animals subjected to I/R showed impaired renal function that peaked at 24 hours (2.05 +/- 0.23 mg/dL), decreasing thereafter. Treatment with higher concentrations of cyclosporine or rapamycin caused even more renal dysfunction at 48 hours, which was sustained up to 120 hours after reperfusion (1.53 +/- 0.6 mg/dL), when compared to the low concentrations of cyclosporine or rapamycin (1.08 +/- 0.19 mg/dL; 0.99 +/- 0.14 mg/dL, P < .05, respectively). Cyclosporine delayed tubular regeneration, which was higher in controls at day 5 (67.0% vs 37.6%, P < .05). CONCLUSIONS: These results demonstrated that cyclosporine or rapamycin might further aggravate ischemically injured organs, negatively affecting posttransplantation recovery in a concentration-dependent fashion.