Eosinophilic cholecystitis: a retrospective study spanning a fourteen-year period. / Colecistitis eosinofílica: estudio retrospectivo de 14 años.

INTRODUCTION AND AIMS: Eosinophilic cholecystitis is a rare entity that was first described in 1949 and is clinically indistinguishable from calculous cholecystitis. Histologically, there is transmural inflammatory infiltration of the gallbladder wall, more than 90% of which is composed of eosinophils. The aim of the present article was to review the prevalence of eosinophilic cholecystitis and analyze the clinical and surgical characteristics of patients diagnosed with the disease that were operated on at our hospital. MATERIALS AND METHODS: A retrospective study was conducted on patients that underwent cholecystectomy and whose postoperative histopathologic diagnosis was eosinophilic cholecystitis, within the time frame of January 2000 and August 2014. The demographic, clinical, paraclinical, surgical, and histopathologic variables were described. RESULTS: Over a period of 14 years, a total of 7,494 patients underwent cholecystectomy. Of those patients, 12 had a postoperative histologic diagnosis of eosinophilic cholecystitis. Mean patient age for disease presentation was 39 years (±11 years), and female sex was predominant, with 7 cases. All the patients had concomitant gallstones and 10 patients presented with acute cholecystitis that required urgent cholecystectomy. All the cases were considered idiopathic. We found a prevalence of 0.16%, corresponding to 1 case for every 625 cholecystectomies performed at our hospital. CONCLUSION: We found a low prevalence of eosinophilic cholecystitis (0.16%) in our study population. The clinical manifestations were similar to those of calculous cholecystitis. Cholecystectomy is adequate treatment in patients with idiopathic disease.

Hyperglycemia promotes p53-Mdm2 interaction but reduces p53 ubiquitination in RINm5F cells.

The apoptosis of ß cells induced by hyperglycemia has been associated with p53 mobilization to mitochondria and p53 phosphorylation. Murine double minute 2 (Mdm2) induces the degradation of p53 and thereby protects cells from apoptosis. We studied the effect of glucose at high concentration on the ability of Mdm2 to ubiquitinate p53 and promote its degradation. RINm5F cells were grown in RPMI-1640 medium with 5 or 30 mM glucose for varying periods of time. After this treatment, the expression of Mdm2 was measured using real-time PCR. The phosphorylation of Mdm2 at Ser166, p53 at Ser15, and the kinases Akt and ATM were measured by Western blotting. The formation of the p53-Mdm2 complex and p53 ubiquitination was assessed by p53 immunoprecipitation and immunofluorescence. Our results showed that high glucose reduced Mdm2 mRNA expression and protein concentration and increased Mdm2 and Akt phosphorylation, albeit with slower kinetics for Akt. It also promoted p53-Mdm2 complex formation, whereas p53 ubiquitination was suppressed. Furthermore, phosphorylation of both p53 Ser15 and ATM was increased in the presence of 30 mM glucose. These data indicate that high concentration glucose decrease the mRNA expression and cytosolic concentration of Mdm2. However, although the increase in glucose promoted the phosphorylation of Mdm2, it also decreased p53 ubiquitination, thus avoiding p53 degradation. In hyperglycemic conditions, such as diabetes mellitus, the reduction of pancreatic ß cells mass is favored by stabilization of p53 in association with low p53 ubiquitination and reduced expression of Mdm2.