Diagnostic value of endoscopic markers for celiac disease in adults: a multicentre prospective Italian study.

AIM: Some endoscopic features of duodenal mucosa are marker of mucosal injury, the most common cause being celiac disease (CD). The aim of this study was to prospectively assess the diagnostic value of the endoscopic markers for the diagnosis of CD in the adult population undergoing routine upper endoscopy. METHODS: This was a prospective multicenter study conducted at 37 Italian endoscopic centers. A total of 509 consecutive patients submitted to routine upper endoscopy who presented one or more of following endoscopic markers were included: 1) mucosal mosaic pattern in the bulb and/or descending duodenum (DD); 2) nodularity in the bulb and/or DD; 3) scalloping of Kerkring's folds; 4) reduction in the number or absence of folds in the DD. 4 biopsies samples were taken from descending duodenum. In patients with histological findings consistent with CD, according to Oberhuber classification, sierologic test (EMA, tTGA) were performed for confirm the diagnosis. RESULTS: At endoscopy, 249 patients showed an isolated marker; 260 subjects showed a coexistence of more than one marker; 369 patients (72.5%) presented mucosal lesions at histological examination and in 347 of these patients the diagnosis of CD was confirmed by serologic markers (94.0%). For 10 patients the diagnosis remained uncertain because of negative sierology and exclusion of other other cause of mucosal lesions. The diagnosis of CD was made in 61.3% patients who showed the mosaic pattern, in 65.7% of patients with nodular mucosa, in 64.4% of patients with scalloping of folds, in 40.2% of patients with reduction of folds, and in 61.5% of patients with loss of folds and in 83.6% of patients who showed the coexistence of more than one marker. The endoscopic markers overall had a PPV of 68% for the diagnosis of CD; the markers that singularly have demonstrated a higher correlation with CD are: mosaic mucosa of DD (PPV 65.0%), nodular mucosa of the bulb and DD (PPV 75.5%), and scalloping of folds (PPV 64.4%). CONCLUSION: The study confirms the important role of endoscopy in the diagnostic process of CD not only for the bioptic sampling in patients with clinical suspicion of CD, but especially for the opportunity to evaluate alterations of the duodenal mucosa suggestive of CD in the general population and, consequently, to identify those patients who should undergo a duodenal biopsy.

Extracorporeal shock wave lithotripsy for clearance of refractory bile duct stones.

BACKGROUND AND STUDY AIMS: Following endoscopic sphincterotomy, 90% of bile duct stones can be removed with a Dormia basket or balloon catheter. The removal can fail in patients with large stones, intrahepatic stones, bile duct strictures or a difficult anatomy. The aim of this retrospective study is to investigate the efficacy and safety of extracorporeal shock wave lithotripsy in fragmenting and allowing the extraction of bile duct stones that could not be cleared by routine endoscopic means including mechanical lithotripsy. PATIENTS AND METHODS: From 1989 to January 2005, we treated with extracorporeal shock wave lithotripsy 376 patients (133 males and 243 females, median age 71.4 years) with bile duct stones that were not removable following endoscopic sphincterotomy, using the extracorporeal shock wave lithotripsy Lithostar Plus machine built by Siemens Co. of Erlangen, Germany. Stone targeting was performed fluoroscopically following injection of contrast via nasobiliary drain or T-tube in 362 patients and by ultrasonography in eight patients. Residual fragments were cleared at endoscopic retrograde cholangiopancreatograhy. Two hundred and ten of the 370 patients treated (56.7%) showed only 1 stone, 57 (15.4%) showed 2, 45 (12.1%) showed 3, 58 (15.6%) showed more than 3 stones. The median diameter of the stones was 21mm (range 7-80mm). RESULTS: Complete stone clearance was achieved in 334 of the 376 patients who underwent the extracorporeal shock wave lithotripsy procedure (90.2%). Six patients (1.5%) dropped out of treatment during their first sessions, mainly because of intolerance. Each patient averaged 3.7 treatments (1-12), at an average rate of 3470 shocks per session (1500-5400), at an average energy level of 3.4mJ (1-7). Complications were recorded in 34 patients (9.1%); 22 patients experienced symptomatic cardiac arrhythmia, 4 haemobilia, 2 cholangitis, 3 haematuria, 3 dyspnoea; no deaths were associated with the procedure. CONCLUSIONS: Extracorporeal shock wave lithotripsy is a safe and effective therapy in those patients in whom endoscopic techniques have failed with a clearing rate of 90.2% of refractory bile duct stones with a low rate of complications.

Gastrectomy, lack of gastric first pass metabolism of ethanol and alcoholic liver disease. Results of a multicentre study.

BACKGROUND: Some conditions characterized by a loss (anatomical or functional) of parietal cells of the gastric antrum, containing an alcohol-dehydrogenase, may reduce the first pass metabolism of ethanol at that level and, simultaneously, raise its bioavailability. The observation that the first pass metabolism was drastically suppressed after gastrectomy would appear to suggest that the latter condition represents a risk for the development of liver damage in patients who continue to consume alcohol even in a non relevant amount. METHODS: Consecutively enrolled in the study were 304 individuals of both sexes aged between 45 and 70 years of whom 114 gastrectomized and 190 pair-matched control subjects all submitted to an Upper Gastrointestinal Endoscopy for whatever disturbance. All the patients were diagnosed as having liver disease with routine clinical and instrumental means. Information was collected concerning the mean daily alcohol intake, both before and after the operation. RESULTS: The overall prevalence of hepatic lesions was shown to be higher in the gastrectomized than in the control group (42.1% vs 25.8%, p = 0.005). Moreover, referring only to alcohol-related hepatic lesions (steatosis, steato-fibrosis and cirrhosis), the prevalence was higher in the gastrectomized patients than in the controls (29.8% vs 17.9%, p = 0.02). As far as concerns alcohol consumption, the gastrectomized group had consumed 71 g/day and the control group 39 g/day alcohol per person (p < 0.05) in a similar period of time (35 and 33 years, respectively). Also the non alcohol-related liver damage (especially the viral type) was slightly higher in the gastrectomized patients (gastrectomized 12.3% vs control 7.9%, p = ns). Accordingly, the percentage of serum markers of viral infection was higher in this group (HBs Ag: gastrectomized 3.9% vs control 2.2%, p = ns; anti-HCV: gastrectomized 13.5% vs control 5.0%, p = 0.03). Finally, to test the eventual damaging effects of gastrectomy alone (excluding ethanol and/or viral infection), two groups of patients with a medium to low alcoholic negative assumption (30-60 g ethanol/day) and no signs of viral infection (HBsAg and anti-HCV negative) were extrapolated. In these two selected groups, the prevalence of alcoholic-related hepatic lesions were not statistically different (28 gastrectomized 20.3% vs 44 control 18.4%). CONCLUSIONS: In conclusion, data emerging from investigations on the population under study indicate that the alcohol and viral infection appear to play a more important role in determining hepatic lesions than gastroresection.

Chronic gastritis, intestinal metaplasia, dysplasia and Helicobacter pylori in gastric cancer: putting the pieces together.

Chronic gastritis may favour the development of gastric cancer more as a condition than as precancerous lesion. Since, in most cases, it is pathologically correlated with Helicobacter pylori infection, it is reasonable to postulate at least an indirect role for this organism in the pathogenesis of gastric cancer. H. pylori, however, is only one of the risk factors involved, in that additional factors (excess salt, cigarette smoking, deficiency of foodstuffs with an antioxidizing effect) may facilitate the malignant transformation of chronic atrophic gastritis into intestinal-type gastric cancer. Gastric carcinogenesis therefore presents itself as a multifactorial, multistage process, furthered by the occurrence of precancerous lesions which are usually interrelated (type-III intestinal metaplasia, severe dysplasia) and by functional alterations such as achlorhydria, which, though it is not enough in itself to cause gastric cancer, promotes abnormal intragastric bacterial development, a condition which may be followed by abnormal intragastric formation of cancerogenous nitroso compounds. The existence of a close correlation between both gastric cancer and H. pylori infection and low socio-economic and hygienic status of the population lends further strength to the hypothesis that an "H. pylori factor" is involved in gastric carcinogenesis. Consequently, to reduce the risk of gastric cancer, various strategies have been devised to prevent H. pylori infection (improvement in socio-environmental conditions, anti-H. pylori vaccine) and/or to eradicate the organism (by means of therapeutic regimens including antimicrobial agents, which, however, can be implemented only in patients who have not developed diffuse atrophy and/or dysplasia, in whom H. pylori may no longer be detectable). Definitive proof of the real extent of the relationship between H. pylori and gastric cancer and of the efficacy of therapeutic and preventive measures can be provided only by controlled trials in populations with a high prevalence of chronic non-atrophic gastritis which are difficult to organize.

The need for long-term treatment of peptic ulcer.

Some 10% of the population in Western countries will suffer a duodenal ulcer or gastric ulcer at some time in their lives. Although there has been an improvement in the survival rate of patients with peptic ulcer haemorrhage, the mortality is still approximately 10%. There is evidence to suggest that peptic ulcer disease is a life-long condition and that ulcers remain active with an unchanged potential for complications such as haemorrhage and perforation. Over the past 15 years anti-ulcer drugs with different mechanisms of action have been developed, and their use results in complete healing of an ulcer in four to eight weeks. However, most patients experience recurrence of their peptic ulcer after discontinuation of the healing therapy. Studies of continuous H2-receptor antagonist therapy have shown that recurrence occurs less frequently than in untreated patients, is largely asymptomatic, and is rarely characterized by haemorrhagic complications. Limited data on therapy for the eradication of Helicobacter pylori suggest that this may be an alternative approach for selected patients. As protection afforded by H2-receptor antagonists remains undiminished over the course of several years and is also observed in ulcers which have bled in the past, the implementation of long-term management with these agents constitutes a rational policy.