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High resolution esophageal manometry (HRM) is currently under development as can be seen in the various Chicago classifications. In order to standardize criteria in certain practical aspects with limited scientific evidence, the First National Meeting for Consensus in High Resolution Manometry of the Spanish Digestive Motility Group took place, bringing together a wide group of experts. The proposals were based on a prior survey composed of 47 questions, an exhaustive review of the available literature and the experience of the participants. Methodological aspects relating to the poorly defined analysis criteria of certain new high resolution parameters were discussed, as well as other issues previously overlooked such as spontaneous activity or secondary waves. Final conclusions were drawn with practical applications.

Objective: Our aim was to prospectively compare the behavior of interleukin 18 (IL-18) levels and other immunological parameters during the first week of hospitalization between acute pancreatitis patients with and without severity criteria, as well as between patients with and without late pseudocyst development., Patients and Methods: In 36 patients with acute pancreatis we compared sTNF-RI, IL-1Ra, IL-6, and IL-18 levels at days 1, 2, 3 and 7 after hospitalization between mild pancreatitis, severe pancreatitis, and a "control" group (13 patients) with uncomplicated biliary colic, as well as between patients with and without pseudocyst., Results: On comparing mild to severe pancreatitis, IL-18 was significantly higher only the first day in severe pancreatitis, while the other parameters were steadily higher after the second day. In patients developing pseudocyst, IL-18 was also noticeably higher the first day., Conclusions: IL-18 appears to be the earliest marker of complications and severity in acute pancreatitis at both the systemic and local level (pseudocyst).

Acute acalculous cholecystitis (AAC) is defined as an acute inflammation of the gallbladder in the absence of stones. We herein report a case of a young man who developed AAC after a Salmonella enteritidis gastrointestinal infection.

Acute esophageal necrosis is a rare disorder, and its etiology is unknown, the mechanism of damage being usually multifactorial and secondary to ischemic compromise, acute gastric outlet obstruction, and malnutrition. Endoscopic findings show circumferential black discoloration of the distal esophagus with proximal extension ending sharply at the gastroesophageal junction, which is the most common presentation. Prognosis depends on comorbid illnesses. In this study we analyze all cases reported in a retrospective analysis over a 2-year period to define risk factors, clinical presentation, endoscopic features, histological appearance, treatment and outcome. Our department has recorded 7 cases from 6,003 endoscopies performed in the last 2 years. The finding of a "black esophagus" represented 0.11% of cases.

Eosinophilic enteritis is an uncommon disorder of unknown etiology in which the digestive symptoms are associated with eosinophilic infiltration of the different layers of the intestinal wall. Clinical symptoms depend on the layers involved and are usually characterized by peripheral eosinophilia. Radiological findings depend on the layers involved. Definitive diagnosis is based on clinical and histopathological findings. Treatment of choice is currently with corticoids and prognosis is benign with relapses. The pathogenesis remains unclear. We report a patient who presented with intestinal obstruction and describe the follow-up.

Twenty-one asymptomatic patients presenting isolated elevations of gamma-glutamyltranspeptidase (GGT) were studied over the previous 10 years with all the findings being accidental. No other analytical alterations were demonstrated. Ingestion of alcohol, drugs or another type of toxic substance, diabetes, neurologic disease or neoplasm were discarded. Echography of the liver and the biliary tract was normal. In the first nine patients studied, liver biopsy was performed being normal or with minimum unspecific alterations. In two patients endoscopic retrograde cholangiography was carried out with no alterations being observed. Lipid study was performed in all the patients with alpha hypolipoproteinemia being found in 15 patients, compensated type II lipid profile in 5 and a normal lipid profile in one. To the author's knowledge there have been no reports of this lipid disorder causing elevations in GGT. However, on being the only abnormality found in these patients the authors believe that this may be the cause although the mechanism is unknown.

The case of a 59-years old patient with typical clinical manifestations of primary biliary cirrhosis (PBC): pruritus, asthenia, arthralgias and dry syndrome, with skin pigmentation and AMA positivity, hypergammaglobulinemia and an elevation of IgM is presented. Liver biopsy was compatible with stage II PBC. No analytical data of cholestasis, has been seen over 26 months of follow up with normal transaminases, alkaline phosphatase, gamma-glutamyltranspeptidase and cholesterol. The absence of cholestasis in the presence of symptoms is of interest.

An attempt is made to synthesize the fundamental information concerning the pathogenesis of chronic functional digestive disorders, which should be designated as "chronic functional dyspepsia". At present the term "irritable colon" does not seem justified since the disorder affects the entire gastrointestinal tract. In the development of this disorder three types of fundamental pathogenic factors apparently participate: 1. Deficient protein nutrition leading to hypotrophy of the intestinal mucosa. 2. Alterations of intestinal motility related fundamentally to neurotic dysfunction. These are hyperreactive phenomena by the smooth muscle in response to normal stimuli on a background of generalized gastrointestinal hypotonia. They seem to be due to an excess of certain neurotransmitters, principally dopamine, at the level of the myenteric plexus. 3. Infectious factors of the infectious Crohn type provoked by intestinal bacterial overgrowth. These derive from motility alterations, with stasis or delayed transit, and hypotrophy due to deficient nutrition that alters the intraluminal ecological medium. This alteration impairs the development of the normal saprophytic flora and facilitates the proliferation of anaerobic colonic germs, leading to intestinal bacterial overgrowth.