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Background: Experience with proton pump inhibitor-based triple therapy is predominantly with omeprazole-containing regimens., Aim: To investigate the efficacy of a pantoprazole-based regimen, with either a 1 or 2-week course of antibiotic co-therapy, in eradicating H. pylori, healing duodenal ulcers and to assess the antibiotic sensitivity profiles of isolated H. pylori strains., Methods: A single-blind, multicentre, parallel group comparison of patients with endoscopically proven, H. pylori associated, active duodenal ulceration. All patients received pantoprazole, 40 mg b.d. for 2 weeks. Patients were randomized to receive either 1 or 2 weeks of therapy with amoxycillin, 1 g b.d. and clarithromycin 500 mg b.d. Patients were endoscoped at entry, at 14 days and a minimum of 4 weeks after cessation of all therapy. H. pylori status was determined by urease reaction, histological assessment and culture from antral and body biopsies. Antibiotic sensitivity was determined using the agar dilution technique., Results: Sixty-seven patients were randomized. One week co-therapy (n=33): eradication efficacy, ITT= 79% (95% CI: 61-91%); ulcer healing efficacy (at 6-week visit)=88% (95% CI: 72-97%). Two-week co-therapy (n=34): eradication efficacy, ITT=91% (95% CI: 76-98%: ulcer healing efficacy= 88% (95% CI: 73-97%). Both regimens were well tolerated and no primary antibiotic resistance was noted., Conclusion: Pantoprazole-based triple therapy, with either 1 or 2 weeks of co-therapy with amoxycillin and clarithromycin, is effective in eradicating H. pylori and healing duodenal ulceration.

We report a rare case of obstructive jaundice caused by an intrapancreatic hydatid cyst in a 17-year-old black girl. Ultrasonography and computed tomography demonstrated the obstructing cyst in the head of the pancreas. Cyst aspiration produced clear fluid with a low amylase content and no hydatid hooklets or protoscolices. Pancreaticoduodenectomy was performed for a presumed cystic neoplasm of the pancreas, but histology showed the true diagnosis. Pancreatic hydatidosis should be considered in the differential diagnosis of obstructing pancreatic cysts in the appropriate epidemiological setting.

Helicobacter pylori is an important cause of gastritis and a number of therapeutic trials suggest that it may be important in the genesis of duodenal ulcer recurrence. The reported prevalence of gastric colonisation by the organism varies considerably. The aim of this cross-sectional survey was to determine its prevalence in non-ulcer dyspeptics and to determine whether this is influenced by age, race, sex, socio-economic status, educational level and the number of persons sharing accommodation. One hundred and sixty-nine patients underwent endoscopy; biopsy specimens were taken from the antrum and H. pylori status was determined histologically. Gastric colonisation was found in 106 patients (63%). The prevalence showed a marked ethnic difference: 40% in whites and 71% in coloureds (P < 0.001). The ethnic groups were characterised by significant differences in socio-economic status (P < 10(-6)), educational level (P < 10(-6)), number of persons sharing accommodation (P < 10(-6)) and age (P < 0.001). These same differences were found when comparing the H. pylori-positive and negative groups, but were less marked and could be attributed to the marked differences between ethnic groups. We conclude that H. pylori prevalence differs between the ethnic groups studied. This may be because of varying degrees of exposure risk.

We describe a patient with severe common variable hypogammaglobulinemia (CVH) whose clinical course was dominated by resistant giardiasis requiring prolonged hospitalization. The giardiasis was eventually controlled by initial metronidazole and subsequent mepacrine therapy, but side effects necessitated the withdrawal of both of these drugs. Replacement immunoglobulin treatment failed to restore normal serum immunoglobulin levels, but despite this, they appeared to be of value in reducing the liability to recurrent giardiasis. We discuss the use of immunoglobulin supplementation in this condition and the frequent association between CVH and pentagastrinfast achlorhydria.

Two cases of intramural rupture of the oesophagus are described. In both cases the diagnosis was made endoscopically and confirmed radiologically. Both patients were successfully managed conservatively but were later found to have disordered oesophageal motility. The clinical presentation of severe retrosternal chest pain followed by haematemesis and then dysphagia is stressed, and the diagnostic features on barium swallow examination and endoscopy are described. It is suggested that the diagnosis should be made on clinical presentation and barium swallow, and that the possible hazards of endoscopy in the acute stage should be avoided.

We report two patients with periampullary cysts associated with recurrent attacks of acute pancreatitis. In both patients the diagnosis was made preoperatively by upper gastrointestinal endoscopy and ERCP, which was also useful in determining the relationship of the cysts to the biliary and pancreatic ductal systems. Simple marsupialisation of the cysts resulted in long term relief of symptoms. Congenital cystic anomalies in the second part of the duodenum should be diligently sought in patients with pancreatitis of unexplained cause, as surgical therapy is safe and effective.

Seventy-two patients with endoscopically proven gastric ulcers were entered into a prospective controlled trial to assess the efficacy of ranitidine and cimetidine in ulcer healing. All patients were biopsied on entry and at subsequent endoscopies. After exclusion of 7 patients during the first month of treatment, the remaining 65 patients, 47 males and 18 females, mean age 48.2 +/-1.5 years, at 1 month had a healing rate of 47% and 52% respectively. The non-healers continued their treatment for a further 4 weeks. This increased the healing rate to 77% and 76% respectively. If the defaulters and poor compliers are withdrawn the healing rate rises to 58% and 57% at 4 weeks and to 91% and 79% at 8 weeks respectively. There was no significant difference between the two groups as regarded initial ulcer size and severity of dyspepsia. Antacid tablet consumption during the study was comparable. The initial size of the ulcers which failed to heal after 4 weeks of treatment tended to be larger than those which healed (P less than 0.05), but smoking did not appear to influence ulcer healing. No obvious side-effects or evidence of dysplasia were found. The study shows that ranitidine is at least as effective as cimetidine in gastric ulcer healing.

Earlier studies have suggested that the rate of incorporation of labeled amino acids into duodenal juice proteins during pancreatic stimulation may be used to calculate pancreatic enzyme synthesis and function. In the present study, a pulse/4 h continuous intravenous infusion of 14C labeled leucine was used to compare synthesis rates in 6 patients with chronic calcific pancreatis(CP) to 4 controls. Analysis of duodenal juice protein demonstrated a delay of approximately 1 h in the appearance of labeled proteins, followed by a linear increase in specific activity, allowing calculation of synthesis that varied between 2.6-2.8 h in controls and 6-48 h in CP. The protein in controls was representative of enzyme protein, but that of CP was not, since it was heavily contaminated with albumin (up to 50%). The results indicate that enzyme secreted during the first hour of stimulation is derived from pancreatic stores and that the synthesis rate of enzymes secreted thereafter is approximately 2.7 h in normal humans. The method was, however, unable to determine rates in patients with CP owing to heavy contamination of enzymes with exudative proteins.

Patients with inflammatory bowel disease diagnosed in the greater Cape Town area between the years 1980 and 1984 inclusive were studied to establish the incidence and presenting features of these diseases. Case details were obtained from the records of the Groote Schuur Hospital group and Tygerberg Hospital as well as from questionnaires completed by 97% of 731 medical practitioners in the area. There were 134 patients with Crohn's disease, 197 with ulcerative colitis and 16 with indeterminate colitis. The incidences of Crohn's disease in the coloured, white and black population groups were calculated to be 1.8, 2.6 and 0.3/100 000 per year respectively and those for ulcerative colitis 1.9, 5.0 and 0.6/100 000 respectively. Among Jews the incidence was higher for both Crohn's disease (10.4/100 000) and ulcerative colitis (17.0/100 000). Of patients with ulcerative colitis 35% had limited proctitis, 26% proctosigmoiditis, 12% left-sided disease and 27% total colitis. Of patients with Crohn's disease 27% had colonic involvement alone, 37% ileocolitis and 36% small-bowel involvement alone. The incidence of inflammatory bowel disease has increased in the greater Cape Town area over the last 10 years, while the pattern of disease has remained similar to that previously reported for this geographical area.

Sixty patients with chronic alcohol-induced pancreatitis with endoscopic retrograde cholangiopancreatography evidence of common bile duct stenosis were studied to determine the clinical spectrum and natural history of this complication, as well as the indications for biliary bypass. In 17% of patients, common bile duct stenosis (CBDS) was an incidental finding at ERCP, while in the remaining cases pain and jaundice were the predominant symptoms in 35% and 48%, respectively. Biliary drainage was performed in 38% of patients for persistent or recurrent jaundice, cholangitis, and while undergoing pancreatic duct or cyst drainage procedures for pain. The benign nature of CBDS in chronic alcohol-induced pancreatitis (CAIP) in patients without persistent jaundice is emphasized. In particular, no histologically proved cases of secondary biliary cirrhosis were noted. The majority of patients with CBDS due to CAIP may be safely managed without biliary bypass but require close follow-up.

Fifty-seven patients with recently healed duodenal ulcers were entered into a 1-year trial of maintenance therapy with ranitidine ( Zantac ; Glaxo) 150 mg at night to assess the safety and efficacy of the drug. Twenty-two of the patients were withdrawn because they violated the trial protocol. No serious side-effects were noted, but only 19 of the 35 patients who met the requirements of the study were free of endoscopic evidence of ulcer recurrence at the end of the trial period. The relapse rate of 46% in the present study was of the same order as those found in two previous South African studies of maintenance therapy with cimetidine given in a dose of 400 mg at night. These findings leave the question whether routine maintenance therapy is warranted in our patients unanswered.

Seventy-two patients with recently healed gastric ulcers were entered into a double-blind, placebo-controlled, six-month maintenance trial to assess whether sucralfate, 1 g in the morning and 2 g at night, reduces the propensity for recurrent ulceration. Patients were assessed clinically at 0, 6, 12, 18, and 24 weeks. Endoscopy was performed at the time of entry into the study and at 24 weeks, or earlier if clinical relapse occurred during this period. Eleven patients were excluded from the study because they defaulted or for other protocol violations. The other 61 patients were followed for six months or until evidence of ulcer relapse. Endoscopic recurrence was found in five of 31 patients (16 percent) randomly assigned to receive sucralfate and in 21 of 30 patients (70 percent) assigned to receive placebo. Most recurrences occurred during the first 12 weeks, with relapse rates of 10 percent and 53 percent, respectively for the sucralfate- and the placebo-treated groups. Three of the recurrences noted at 24 weeks were asymptomatic; two of these were in the sucralfate-treated group. The results indicate that a 3 g per day maintenance dose of sucralfate offers meaningful protection against recurrent gastric ulceration.

Forty-seven patients with calcific pancreatitis were submitted to ERCP, 24 of whom were designated 'painless' and 23 'painful', according to whether or not pain had occurred during the previous year. The pancreatic duct was cannulated in 39 of these patients. The incidence of pancreatic duct obstruction or stricture was of the same order in the painless (13/20, 65 per cent) and painful (15/19, 79 per cent) groups. Alcohol was the aetiological factor in 46 patients. Twenty-four (52 per cent) continued to drink, and were equally divided between the painless (12) and painful (12) groups. Four out of 13 in the painless and 7 out of 14 in the painful groups, with a stricture or obstruction, continued to drink. The difference was statistically not significant. These results suggest that ERCP findings of pancreatic duct obstruction or stricture need not necessarily be pertinent to the pain in patients with chronic pancreatitis.

A consecutive personal series of 314 patients with alcohol-induced calcific pancreatitis were admitted to a long-term follow-up study between 1959 and 1979. The patients were subdivided into four arbitrary groups according to the date of entry into study, and the mortality rate and survivor status were determined for each of these groups. Adjusted mortality rates increased progressively with the duration of follow-up, from 11% in the 1976-1979 to 73% in the 1959-1969 group. Pancreatic insufficiency dominated in patients followed up for 10 - 20 years, and pain was more prominent in the more recent follow-up groups. The survivor status in Whites was better than in Blacks, but the mortality rates were comparable. The occurrence of pain in patients who continued to drink was significantly less in the 10 - 20 year follow-up group than in those followed up for a shorter period of time.

The conventional dosage schedule for sucralfate is 1 g 4 i.d., but a dose of 2 g 2 i.d. may be equally effective in duodenal ulcer healing. We compared the efficacy of these two regimens in duodenal ulcer healing. Seventy-seven patients with endoscopically proven duodenal ulceration were entered into a double-blind, controlled study and randomized to treatment with sucralfate 2 g 2 i.d. (on waking and at bedtime) or 1 g 4 i.d. (1/2 h before meals and at bedtime). The patients were endoscoped before entry into the study, after 4 weeks, and after 8 weeks if unhealed at 4 weeks. Of the patients considered suitable for analysis at 4 weeks, 79% (26/33) of those taking 2 g 2 i.d. had healed ulcers in comparison to 72% (23/32) of those taking 1 g 4 i.d. After 8 weeks, cumulative healing rates were 85% (28/33) and 80% (24/30), respectively. The results suggest that the more convenient dosage schedule of 2 g 2 i.d. is as effective as the 1 g 4 i.d. regimen in the short-term treatment of duodenal ulcer.

A double-blind placebo-controlled study of ranitidine 150 mg given twice daily for 4 weeks was carried out in 80 ambulant patients with endoscopically proven duodenal ulceration. Fifteen patients were withdrawn because of poor compliance or default. Of the remaining 65 patients, endoscopic healing (with or without residual erosion) was noted in 28 of the 34 ranitidine-treated patients (82%) and in 14 of the 31 placebo-treated patients (45%) (P less than 0.005). Twenty-three patients whose ulcers were unhealed after 4 weeks of ranitidine therapy or placebo were then given ranitidine for a further 4-week period. Four of these patients were withdrawn, but ulcer healing was achieved in 16 of the remaining 19 patients (4 out of 5 (80%) initially treated with ranitidine and 12 of 14 (86%) initially treated with placebo). No significant clinical, biochemical or haematological adverse reactions were noted in either treatment group. It is concluded that ranitidine is a safe and effective therapy in patients with duodenal ulceration and that initial unsuccessful treatment with placebo does not appear to influence the subsequent response to ranitidine.

The relapse rate following successful short-term therapy with sucralfate or cimetidine was studied in a group of 86 patients with recently healed duodenal or gastric ulcer. The patients were endoscoped on clinical relapse or, routinely, at 6 weeks, 6 months and one year. Patients whose ulcers had healed on cimetidine relapsed earlier than did those whose ulcers had healed on sucralfate (p less than 0.05 at 12 weeks), but the cumulative relapse rate by the end of one year was of the order of 70% in both treatment groups. The mean duration of remission in patients who developed a recurrence was significantly greater in patients treated initially with sucralfate than in those treated initially with cimetidine - 7.3 and 4.6 months, respectively (p less than 0.01).

A case of simultaneous infection with Yersinia enterocolitica and Crohn's disease is described. Only 1 similar case has been reported. The similarities between the two conditions and the differentiating features are described.

Sixty-seven patients with endoscopically proven duodenal ulceration were entered into a double-blind study and randomized to treatment with pirenzepine (PZ) (Gastrozepin; Boehringer Ingelheim) 50 mg twice daily or cimetidine (CM) (Tagamet; Smith Kline & French Laboratories) 400 mg twice daily, given 30 minutes before breakfast and supper. Patients underwent endoscopic examination before entry, at 4 weeks, and at 8 weeks if unhealed at 4 weeks. Once healing was achieved, 43 patients were entered into a single-blind maintenance study with either PZ 50 mg at night or CM 400 mg at night according to their original randomization. CM had a slight, but not significant, advantage over PZ after 4 weeks, but the 8-week data showed identical healing rates. The relapse rate appeared to be higher in the PZ-treated group, but this difference was also not significant. It is suggested that the evening dose of PZ be amended to 50 or perhaps 100 mg before bed in the short-term treatment of duodenal ulcer, and that a dose of 100 mg at night be considered for maintenance therapy in certain high-risk populations.

A single-blind, 1-year follow-up study of 70 patients with recently healed duodenal ulcers was undertaken to assess the value of sucralfate (Ulsanic; Continental Ethicals) in preventing recurrence and to establish the lowest dose required to achieve this. Endoscopy was repeated on clinical relapse and routinely at 6 and 12 months. Fifty of the 70 patients were followed up for 12 months or to recurrence proved on endoscopy; the remaining 20 patients were excluded from analysis because of default or protocol violation. Endoscopic evidence of recurrence was found in 6 of 19 patients (32%) given sucralfate 1 g twice a day (group B), in 7 of 15 (47%) on sucralfate 1 g at night (group A), and in 13 of 16 controls (81%). The recurrence rates in groups A and B were significantly lower than in the control group (P less than 0,05 and P less than 0,005 respectively), and there was a significant gradient between the number of patients in remission at 12 months and the amount of medication (P less than 0,05).

The pancreatograms, as assessed by endoscopic retrograde cholangiopancreatography, of 51 patients with alcohol-induced calcific pancreatitis (AICP), were compared after division of the patients into three groups according to their insufficiency patterns. The first group, consisting of 18 patients, was labelled as having 'disproportionate steatorrhoea' characterized either by overt steatorrhoea and mild or no diabetes or by mild steatorrhoea and a normal glucose tolerance test result. The second group of 15 patients had severe diabetes associated with overt, mild or no steatorrhoea and constituted the 'insufficiency' group. The third group consisted of 18 patients with little or no pancreatic insufficiency. Twelve of the 18 patients with disproportionate steatorrhoea had a proximal complete or incomplete obstruction of their main pancreatic ducts, compared with 3 out of 15 in the insufficiency group and 4 out of 18 in the group with little or no pancreatic insufficiency. In this study an increased incidence of complete or incomplete obstruction (P less than 0,002) was found in the patients with disproportionate steatorrhoea compared with the other two groups. This suggests that obstruction to pancreatic flow may account for the dominant clinical presentation of steatorrhoea in some patients with AICP.

A group of 47 carefully assessed patients with noncalcific pancreatitis was studied with ERCP and the secretin pancreozymin pancreatic function test (PFT). A simple scoring system was constructed for each of the PFT indices to create a PFT score for each patient and four grades of ERCP abnormality were documented, from minimal to gross. A simple pancreatic pain score was constructed to allow for the inclusion of patients with classical pancreatic pain in the absence of acute attacks associated with an elevated serum amylase. In general there was a correlation between the degree of structural change and functional impairment, with patients with the worst pancreatic function having the grossest ERCP changes. ERCP was abnormal in 45 of the 47 patients (96%) and the PFT in 34 of the 47 (72%). However, there were some marked discrepancies between the two methods, in particular two patients with normal function in the presence of gross structural changes. ERCP proved to be the more sensitive diagnostic technique than the PFT in this group of patients.

Fifty-four patients with recently healed duodenal ulcers were entered into a single-blind 1 year follow-up study to assess the value of sucralfate in preventing relapse and to establish the lowest dose required to achieve this. To date, 35 patients have completed a 6-month follow-up period. Endoscopic recurrences were found in 1 of 9 patients randomised to sucralfate 1 g bd, in 3 of 14 on sucralfate 1 g nocte, and in 7 of 12 of the controls. The relapse rates in the sucralfate treated groups were significantly lower than in the control group, but the small number of patients at this stage of the study precludes firm conclusion as to whether a maintenance dose of 1 g nocte is as effective as a dose of 1 g bd.

Results of pancreatic function tests, using simple aspiration, simple aspiration with marker correction and marker perfusion methods were compared. With simple aspiration alone, approximately one-third of the marker was not recovered. Yet with the marker correction method the volume (and consequently other measurements), appeared to be greatly overcorrected, probably owing to poor mixing of marker and endogenous secretions. In contrast, the marker perfusion method yielded data which were 8-24% higher than those for simple aspiration for the various outputs; this difference was not statistically significant. It is concluded, firstly, that marker correction of a simple aspiration technique is inaccurate because of poor mixing; secondly, that because marker perfusion methods yield arithmetically but not statistically greater outputs than simple aspirations tests, the latter are probably adequate for diagnostic tests of pancreatic function.

Ulcer healing and relapse rates after treatment with cimetidine and sucralfate in 112 subjects with endoscopically proven gastric and duodenal ulcers were compared in a randomized trial. Four grams of sucralfate were administered in four divided doses each day; 200 mg cimetidine was administered three times during the day with the fourth dose of 400 mg given at night. The subjects were divided into four treatment groups: (1) subjects with duodenal ulcers treated with sucralfate; (2) subjects with duodenal ulcers treated with cimetidine; (3) subjects with gastric ulcers treated with sucralfate; and (4) subjects with gastric ulcers treated with cimetidine. Endoscopy was repeated at 6 weeks after treatment was initiated; subjects with unhealed ulcers at 6 weeks were reendoscoped at 12 weeks. Eighty-three percent of duodenal ulcers in subjects treated with sucralfate healed at 6 weeks, the rest by week 12. Cimetidine-treated subjects with duodenal ulcer had healing rates of 71 and 86% at 6 and 12 weeks. Cimetidine-treated subjects with gastric ulcers showed healing rates of 75 and 89% at 6 and 12 weeks, respectively. In the gastric ulcer group, 63% of sucralfate-treated subjects were healed at 6 weeks, and 78% were healed by 12 weeks, respectively. Eighty-six of the subjects were followed for 1 year or until endoscopy showed relapse. Subjects treated with cimetidine on a short-term basis relapsed earlier than those were treated with sucralfate at 12 weeks, but at 1 year, the relapse rates were about 70% for both groups.

The results of 117 consecutive endoscopic retrograde cholangiopancreatographic (ERCP) examinations in patients with adenocarcinoma carcinoma of the pancreas, performed over a six year period, are reported. The diagnostic accuracy of this procedure (80.3 per cent) was higher than that of computed tomography (63.6 per cent) and ultrasonography (54.0 per cent). Fewer false negative diagnoses were made by retrograde cholangiopancreatography (7.7 per cent) than with the other procedures (28 per cent each). Analysis of the total ERCP experience during the study period revealed a false positive rate for malignancy of 5.6 per cent. In situations where investigations are performed by individuals with a broad spectrum of expertise, ERCP is superior to other methods in diagnosing pancreatic carcinoma, even in areas with a high prevalence of chronic pancreatitis.

We studied the pancreatic function, alcohol history, and ERCP findings in 26 patients with painless and 34 patients with painful alcohol-induced calcific pancreatitis (AICP). About 50% of patients in both the painless and painful groups continued to take alcohol, the incidence of duct stricture or obstruction was of the order of 62% in both groups, and the proportion of patients with duct stricture or obstruction and continued alcohol intake was comparable. In all instances the patients in the painless category had significantly greater pancreatic insufficiency, or more impaired function, than patients with pain. This applied to those patients who continued to take alcohol, to those with an obstruction or stricture on ERCP, and to the subgroup with both duct narrowing and continued alcohol intake. We conclude that grossly impaired pancreatic function confers a degree of freedom from painful attacks in AICP in those patients who continue to drink even in the presence of duct obstruction or stricture on ERCP; and that patients with AICP become free of pancreatic pain once gross pancreatic insufficiency supervenes.

A 31-year-old woman who had been investigated for almost lifelong iron deficiency anaemia caused by chronic gastro-intestinal blood loss was found to have a large cavernous haemangioma of the jejunum. The literature relating to the latter is reviewed and a diagnostic approach to obscure gastro-intestinal bleeding considered.