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.

[Diet and drugs in the therapy of nonorganic dyspepsia: the hypothesis and factual data].

Non-organic dyspepsia, although not frequently reported, is still a disorder which is difficult to classify in nosographic and physiopathological terms, a fact which inevitably influences the indications for its treatment. Non-pharmacological treatment of non-organic dyspepsia includes changes in dietary and behavioural habits which, even if established on empirical grounds, play a far from ancillary role. When considered appropriate, pharmacological treatment must be formulated solely on the basis of controlled clinical trials vs placebo given the well-known significance of the placebo effect in this and other so-called "functional" diseases.

Extracorporeal shock wave lithotripsy (ESWL) of gallbladder stones: experience in Bolzano.

During a period of 24 months, 115 patients with symptomatic gallbladder stones (77 females, 38 males; median age 46 years, range 22-87) were treated by extracorporeal shock wave lithotripsy with a Lithostar Plus. Concomitant bile acid dissolution therapy (ursodeoxycholic acid + chenodeoxycholic acid 7.5 mg/kg/day each or tauroursodesoxycholic acid 5-10mg/kg/day) was administered until 3 months after total fragment clearance.

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.

[Helicobacter pylori and the treatment of gastric ulcer. Reflections and uncertainties].

The authors examine the relationship between Helicobacter pylori and gastric ulcer therapy, analyzing both the data suggesting that eradication of the organism renders the gastric mucosa less susceptible to development of gastric ulcer and the substantial body of evidence to the contrary. They review the results reported in clinical trials with colloidal bismuth subcitrate, antimicrobial agents (furazolidone), and combinations of antiulcer and antimicrobial agents (H2-antagonist + cefixime, H2-antagonist + metronidazole). Also analyzed is the relationship between Helicobacter pylori eradication and ulcer recurrence; only one study is available on this aspect, and the limited evidence it provides in favour of a prophylactic effect of eradication therapy is not entirely convincing.

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.

Helicobacter pylori and gastric ulcer therapy: reflections and uncertainties.

The relationship between Helicobacter pylori (HP) and gastric ulcer therapy is examined by analyzing both the data that suggest that eradication of HP renders the gastric mucosa less susceptible to development of gastric ulcer as well as the substantial body of evidence that does not support this contention. The results reported in clinical trials with colloidal bismuth citrate, antimicrobial agents (furazolidone), and combinations of anti-ulcer and antimicrobial agents (H2-antagonist+cefixime, H2-antagonist+metronidazole) are reviewed. Also analyzed is the relationship between HP eradication and ulcer recurrence.

[No acid, no ulcer: such a simple axiom?].

According to the traditional view gastric acid and pepsin are a sine qua non for ulcer development. Acid suppression, however, is far from being the only successful therapeutic approach, and similar healing rates are achieved by drugs with substantially different mechanisms of action--antacids, H2-antagonists, antimuscarinics, cytoprotective and site-protective agents--thus denoting a multifactorial pathogenesis. Even with the antisecretory compounds, the relationship between gastric acid and ulcer healing gives rise to perplexity: antacids prove effective at widely varying doses; pirenzipine and H2-blockers, which are clinically equieffective, differ considerably in antisecretory efficacy; H2-antagonist studies on early vs late postprandial dosing yield contradictory clinical results; morning and bedtime single administrations of H2-antagonists prove equiactive on ulcer healing, leading to a reappraisal of the alleged importance of nocturnal acidity.

Antisecretory agents, peptic secretion and serum pepsinogen in man.

Less attention has been devoted to the effects of antisecretory agents on pepsin secretion than to those on gastric acid secretion, particularly in human subjects. Moreover, comparison of the various trials is far from being simple and straightforward owing to the fact that the studies available present substantial variability in terms of types of subjects (controls, DU patients), gastric secretion (basal, stimulated), type of stimulation (pentagastrin, histamine, insulin, meals, sham feeding) antisecretory drug administration route (oral, i.v.

The gastric acid conundrum in peptic ulcer.

According to the traditional view, gastric acid and pepsin are a sine qua non for ulcer development. Acid suppression, however, is far from being the only successful therapeutic approach, and similar healing rates are achieved by drugs with substantially different mechanism of action antacids, H2-antagonists, antimuscarinics, cytoprotective and site-protective agents-thus denoting a multifactorial pathogenesis. Even with the antisecretory compounds, the relationship between gastric acid and ulcer healing gives rise to perplexity: antacids prove effective at widely varying doses; pirenzipine and H2-blockers, which are clinically equieffective, differ considerably in antisecretory efficacy; H2-antagonist studies on early vs late postprandial dosing, yield contradictory clinical results; morning and bedtime single administration of H2-antagonists prove equiactive on ulcer healing, leading to a appraisal of the alleged importance of nocturnal acidity.

Powerful gastric acid inhibition: when is it justified?

Peptic ulcers fail to heal in up to 10% of patients after 8 weeks of therapy with H2-receptor antagonists largely owing to the multifactorial pathogenesis of the disease. Site-protective agents may heal the ulcers in many, but not all, of these non-responders. In ulcers which prove particularly refractory to therapy, only powerful gastric acid inhibition of the type best achieved with omeprazole is capable of healing most, and sometimes even 100% of patients in the short term.

Influence of ulcer healing agents on ulcer relapse after discontinuation of acute treatment: a pooled estimate of controlled clinical trials.

Whether or not the incidence of ulcer relapse varies according to the drug used to produce initial healing is a controversial matter. We tackled this problem using data from 15 eligible trials from 25 published controlled trials in patients followed up for six to 12 months. Pooled estimates of differences in ulcer relapse incidence between patients initially healed with H2-antagonists and patients initially healed with non-H2-antagonist drugs were calculated.