MR cholangiopancreatography: value of axial and coronal fast Spin-Echo fat-suppressed T2-weighted sequences.

OBJECTIVE: To compare axial and coronal fast Spin-Echo fat-suppressed T2-weighted sequences with three-dimensional (3D) maximum intensity projection (MIP) images in patients with suspected pancreaticobiliary obstruction. MATERIAL AND METHODS: MR cholangiopancreatography (MRCP) was performed in 108 consecutive patients with a non-breath-hold, fat-suppressed, 2D, heavily T2-weighted fast spin-echo sequence in coronal plane. Axial T1- and T2-weighted images were previously obtained. In addition, 3D reconstructions of the coronal images were analysed separately by using a MIP algorithm. Both two-dimensional (2D) (axial and coronal) and 3D MIP images were separately evaluated by two readers in conference and their results were compared with that of endoscopic retrograde cholangiopancreatography, percutaneous trans-hepatic cholangiography, surgery and/or imaging follow-up. Statistical analysis of 2D and 3D MRCP images in diagnosing the level and probable cause of pancreaticobiliary obstruction were separately calculated. RESULTS: 106/108 of MRCP examinations were judged diagnostic by the two reviewers for adequacy of visualisation of the biliary and pancreatic ducts. Sensitivity, specificity, positive predictive value, negative predictive value and global diagnostic accuracy of 2D (axial and coronal) and 3D MRCP images in diagnosing the pancreaticobiliary obstruction were 94 and 57%,, 95 and 93%, 97 and 92%, 91 and 60%, 94 and 72% respectively. CONCLUSION: Our results do indicate a higher global accuracy for axial and coronal fast Spin-Echo fat-suppressed T2-weighted sequences versus 3D MIP images in diagnosis of the level and probable cause of pancreaticobiliary obstruction and stress the limitations of 3D images in depiction of small intraductal pathology such as calculi and biliary neoplastic.

Operation of Randle's cycle in patients with NIDDM.

It has been suggested that the insulin resistance of non-insulin-dependent diabetes mellitus (NIDDM) may be caused by substrate competition between glucose and free fatty acids (FFAs) (Randle's cycle). We measured substrate oxidation and energy metabolism in 10 nonobese untreated NIDDM patients with fasting glucose levels of 7-8 mM with indirect calorimetry in the basal state and during an isoglycemic-hyperinsulinemic (approximately 100 mU/L) clamp without (control) and with a concomitant infusion (approximately 0.35 mmol/min) of Intralipid, a triglyceride emulsion. In the control study, fasting rates of total glucose turnover [( 3-3H]glucose) and glucose and lipid oxidation (9.4 +/- 1.4, 7.3 +/- 1.3, and 3.0 +/- 0.4 mumol.kg-1.min-1, respectively) were comparable with those of nondiabetic individuals. After insulin administration, lipid oxidation was normally suppressed (to 1.3 +/- 0.3 mumol.kg-1.min-1, P less than 0.01), as were the circulating levels of FFA, glycerol, and beta-hydroxybutyrate, whereas glucose oxidation doubled (14.1 +/- 1.8 mumol.kg-1.min-1, P less than 0.01). Because glycemia was clamped at 7.5 mM, endogenous glucose production (EGP) was completely suppressed, and total glucose disposal was stimulated (to 25.7 +/- 5.2 mumol.kg-1.min-1, P less than 0.01 vs. baseline), but glucose clearance (3.6 +/- 0.8 ml.kg-1.min-1) was 30% reduced compared with normal. With concomitant lipid infusion, FFA, glycerol, and beta-hydroxybutyrate all rose during the clamp; correspondingly, lipid oxidation was maintained at fasting rates (3.6 +/- 0.2 mumol.kg-1.min-1, P less than 0.01 vs. control).(ABSTRACT TRUNCATED AT 250 WORDS)

The long-term treatment of peptic ulcer after a bleeding episode.

We have studied 51 consecutive patients bleeding from peptic ulcer which was duodenal (D.U.) in 30, gastric in 17 (G.U.), anastomotic in 3 (Billroth 2), and oesophageal in 1 of them. One patient with G.U. was sent for surgery and 2 patients with D.U. died early; the others recovered through medical treatment and the ulcer healed after 6-8 weeks of treatment with ranitidine in 46 out of 48 patients. Subsequently, all the healed patients have been treated with ranitidine (150 mg at bedtime) for 6 months; by this time a new endoscopy showed an erosive antral gastritis in 2 patients with G.U. and 2 recurrences of D.U. Then the patients and their family doctors were invited to choose between the interruption of the treatment and its prolongation. 8 patients with previous G.U. preferred to stop treatment, and up to 1-2 years they did not show any recurrence; the remaining 5 patients carried on the maintenance treatment, and up to one year one of them showed an erosive antral gastritis. 15 patients with previous D.U. stopped the treatment and 5 of them after 1-24 months presented a recurrence with a new haemorrhage; 8 patients chose to continue the treatment and none of them for 6-24 months had recurrence. The limited number of the patients obviously does not allow a sound conclusion, but a trend is clearly seen which favours a prolonged maintenance treatment in patients with D.U. which has bled.

Prevention of relapse with various antiulcer drugs.

The relative value of maintenance therapy with cimetidine, ranitidine, pirenzepine, and antacids only (when used for symptomatic relief) has been evaluated in 205 patients with a subsequent follow-up period of 2 years. The patients had a completely healed duodenal ulcer after 8 weeks of treatment and were then randomly allocated to four groups, which were as follows: group 1: 60 patients treated with 400 mg cimetidine at night; group 2: 55 patients treated with 150 mg ranitidine at night; group 3: 50 patients treated with 50 mg pirenzepine at night; and group 4: 40 patients treated only with antacids as needed for symptomatic relief. Endoscopy was repeated after 6, 12, 18, and 24 months of treatment, and whenever symptoms suggested recurrence. Although the number of dropouts was high (27 in group 1, 20 in group 2, 18 in group 3 and 12 in group 4), statistical analysis by the life-table method showed that cimetidine, ranitidine, and pirenzepine had similar therapeutic value. After 1 and 2 years the relapse rate of duodenal ulcer was 17.5% and 43.6% respectively, for cimetidine, 21% and 69.3% for ranitidine, 21.7 and 50.2% for pirenzepine, and 49.8% and 77.7% for antacids. The incidence of erosions was lower in those groups with the higher ulcer relapse rate, a point discussed in the present study.

Comparison between ranitidine and cimetidine in the short-term treatment of duodenal ulcer.

Two groups of 46 and 49 patients each with endoscopically proved duodenal ulcer and not previously treated, received ranitidine (150 mg X 2 daily) and cimetidine (1 g/day) respectively for eight weeks. The disappearance of the ulcer was observed endoscopically in 78% of both the first and second groups of patients. Of the ten patients non-responders to ranitidine, six were treated again for eight weeks with ranitidine and four with cimetidine for eight weeks; all of them recovered completely apart from one of the cimetidine treated patients. Of the 11 patients non-responders to cimetidine, seven were retreated with cimetidine and 4 with ranitidine for a further eight weeks and all of them obtained a complete recovery except for one of the cimetidine treated patients. No relevant side-effects were observed with either drug. In conclusion cimetidine and ranitidine showed a comparable therapeutic value.

Sucralfate and carbenoxolone in the treatment of functional disturbances following partial gastrectomy.

30 patients submitted to partial gastrectomy (Billroth II) who later suffered digestive complaints (pain, "heartburn", bilious vomiting) showed gastric hyperemia, oedema and some erosions of the gastric stump when examined by endoscopy, the presence of cancer having been excluded by biopsy. These patients were randomly allocated into 2 groups of 15, one of which was treated with sucralfate (1 g 4 times), and the other with carbenoxolone (50 mg 4 times), daily for 8 weeks. After sucralfate the endoscopic finding showed a clear improvement in the gastric wall, accompanied by the almost complete disappearance of the complaint symptoms, in 13 cases (86.6%). After carbenoxolone the same improvement was observed at the endoscopy in 12 cases (80%), with similar recovery from symptoms. Nevertheless, no histological changes that could be attributed to the treatments were observed. In those patients whose endoscopic pattern remained unchanged by either drug, the complaints did not show any relief. No side-effects were detected during either of these drug treatments, each of which showed a similar therapeutic efficacy.

Pirenzepine in long-term therapy for duodenal ulcer.

A total of 60 patients with endoscopically diagnosed duodenal ulcer were treated with pirenzepine or cimetidine for 8-10 weeks until endoscopic healing of the ulcer. After ulcer healing 20 random patients received 50 mg pirenzepine per os daily for 6 months, 20 received 400 mg cimetidine per os daily for 6 months, and the remaining 20 received topic antacids for 6 months whenever they complained of pyrosis and/or epigastric pain. Endoscopic checks were repeated after 6 months (or earlier, if clinical picture was consistent with relapsing ulcer). Relapsing duodenal ulcer or erosive duodenitis was observed in 5 patients treated with pirenzepine (25%), in 4 patients treated with cimetidine (20%), and in 13 patients treated with occasional antacids (65%). Differences were significant between the antacid-treated patients and each of the other two groups, but not significant between pirenzepine-treated and cimetidine-treated groups.

Ranitidine, cimetidine and antacids in the prevention of recurrence after healed duodenal ulcer: one-year experience.

A total of 110 subjects with duodenal ulcer healed with cimetidine (C) (50 patients), ranitidine (R) (40 patients) or pirenzepine (20 patients) was randomly divided in 3 groups. The first group (40 patients) was treated with R (150 mg nightly); the second group (40 patients) with C (400 mg nightly) and the third group with antacids as needed for symptomatic relief. The presence of the ulcer and its healing were established by endoscopy, which was repeated after 6 and 12 months of treatment, or previously if symptoms suggested recurrence. At the end of the year's follow-up, no recurrence of ulcers was observed in 75% of the R group, in 77.5% of the C group and in 40% of the antacids group. Some erosive duodenitis developed in the first and second groups (17.5% and 20% respectively), but none in the antacids group. Most of the ulcers that recurred did so in the first 6 months of treatment. No relevant side-effects were observed with the treatments described. Although no significant difference was detected between C and R treatments, both appeared to be clearly more effective than antacids. The usefulness of adequate prophylactic treatment against the tendency of duodenal ulcer to recur is stressed.