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.

Ion channels, ion channel receptors, and visceral hypersensitivity in irritable bowel syndrome.

Ion channels are expressed throughout the gastrointestinal system and regulate nearly every aspect of digestion, including fluid secretion and absorption, motility, and visceral sensitivity. It is therefore not surprising that in the setting of functional bowel disorders, such as irritable bowel syndrome (IBS), ion channels are often altered in terms of expression level and function and are a target of pharmacological intervention. This is particularly true of their role in driving abdominal pain through visceral hypersensitivity (VH), which is the main reason IBS patients seek medical care. In the study by Scanzi et al., in the current issue of this journal, they provide evidence that the T-type voltage-gated calcium channel (Cav ) Cav 3.2 is upregulated in human IBS patients, and is necessary for the induction of an IBS-like disease state in mice. In this mini-review, we will discuss the contribution of specific ion channels to VH in IBS, both in human patients and rodent models. We will also discuss how Cav 3.2 may play a role as an integrator of multiple environmental stimuli contributing toward VH.