RESUMEN
Acute pancreatitis caused by eosinophilic gastroenteritis is a rare disease, and little has been reported so far. Diagnosing eosinophilic gastroenteritis is difficult because the symptoms and laboratory findings are not specific. We report a rare case of eosinophilic gastroenteritis related to acute pancreatitis as a possible cause of idiopathic acute pancreatitis. A 61-year-old man visited the hospital complaining of epigastric pain. Although no pancreatic abnormalities were confirmed on imaging studies, the patient showed hyperamylasemia and hyperlipasemia. Serum eosinophil fractions were initially normal. However, they were elevated on follow-up examinations, and a large number of eosinophils were observed in the biopsies of the stomach and duodenum, which led to the diagnosis of eosinophilic gastroduodenitis related to acute pancreatitis.
RESUMEN
OBJECTIVES: Apoptosis is a process of active cell death, distinct from necrosis and characterized by specific morphological and biochemical features. Apoptosis induced by metals and metal-related deleterious conditions has only recently been studied. Although the toxic effects of heavy metals are well described, little is known about the mechanism of apoptosis via cadmium toxicity. Therefore, this study is designed to define the induction mechanism of apoptosis by which cadmium exerts its cytotoxic effect on human promyelocytic leukemic HL-60 cells. The cytotoxic effects of cadmium on HL-60 cells are studied in regards to apoptotic signal transduction pathways. METHODS: The mode of cadmium-induced apoptosis was investigated in HL-60 cells. HL-60 cells were treated with various concentrations of cadmium and antioxidants after which the viability of the cells were measured by MTT assay. The morphological features of cadmium- induced apoptosis were evaluated by fluoromicroscopy and the DNA fragmentation was analyzed using 1.5% agarose gel electrophorosis. Kinase activity was assayed by autoradiography and activity of NF-kappaB and nuclear proteins were measured by EMSA. RESULTS: Cadmium (125 microM) induces the characteristic morphological features of apoptosis, which are characterized by a shrinkage of the cytoplasm and a condensation of chromatin. In addition, cadmium induced the ladder pattern of DNA fragmentation. Antioxidants(Sodium nitroprusside, glutathione and N-acethylcysteine), which were not toxic to the cells, did not suppress apoptosis induced by cadmium. Cadmium enhances the expression of several classes of genes at elevated cytotoxic concentrations. Poly(ADP-ribose) polymerase(PARP) was predominantly in the fragmented form when doses of 125 microM were used. Since PARP is cleaved by CPP32 (caspase-3), we next determined if cadmium was capable of effecting changes in CPP32 activity. The results of these experiments showed that cadmium increased caspase-3 activity in a time dependent manner, corresponding to the time of appearance of fragmented PARP. Cadmium also increased the phosphotransferase activities of c-JUN N-terminal kinase (JNK). Furthermore, cadmium increased the activation of transcriptional factors including the activation of protein-1 (AP-1) and NF-kappaB . CONCLUSIONS: These results suggest that cadmium induces the apoptotic death of HL-60 cells via the activation of a DEVD-specific caspase, JNK and transcriptional factors such as AP-1 and NF-kappaB .