Effects of bolus somatostatin in preventing pancreatitis after endoscopic pancreatography: results of a randomized study.

BACKGROUND: Pancreatitis is a potential problem in patients undergoing endoscopic retrograde cholangiopancreatography (ERCP). Natural somatostatin reduces pancreatic secretion and has been administered in acute pancreatitis. To establish whether an injection of a single "bolus" of natural somatostatin is useful in preventing pancreatic reactions after endoscopic pancreatography, a randomized study was carried out in 160 patients undergoing pancreatography, associated or not, with endoscopic sphincterotomy. METHODS: Pancreatitis was considered to be present when there was the simultaneous appearance of serum amylase above 600 IU/mL and serum lipase above 200 IU, upper abdominal pain with tenderness, nausea and/or vomiting, and associated ileus, not completely resolved within 18 hours after the procedure and prolonging hospital stay. RESULTS: The incidence of pancreatitis (10% vs. 2.5%, p < 0.05) was higher in the placebo group than in the somatostatin-treated group. The difference in frequency of pancreatitis was statistically significant (18% vs 0%, p < 0.05) in the ERCP plus sphincterotomy subgroup but not significant (6% versus 4%) in the ERCP subgroup. CONCLUSIONS: These results suggest that the administration of a single bolus injection of natural somatostatin just before cannulation of the papilla may be useful in preventing pancreatitis. This procedure is useful in patients undergoing sphincterotomy. Further studies should be performed to determine whether this drug is useful in cases in which cannulation of the papilla is difficult or when therapeutic procedures require prolonged and/or aggressive manipulation of the papilla.

Chest pain at rest in patients with coronary artery disease. Myocardial ischemia, esophageal dysfunction, or panic disorder?

Severe nonexertional (resting) chest pain may be due to myocardial ischemia, esophageal dysfunction, psychiatric disorder, or any combination thereof and frequently poses a difficult diagnostic challenge. Our aim was to investigate causes of chest pain in patients with coronary artery disease. Forty-five patients with angiographically proven obstructive coronary lesions and recurrent chest pain at rest were studied; 18 had refractory pain despite cardiac therapy (problem group), and 27 had documented myocardial ischemia (control group). Esophageal manometry, edrophonium provocation, 24-hr pH studies, and psychiatric interview were performed in all patients. The clinical evolution and the outcome of specific treatment during follow-up was used to establish the etiology of chest pain. Esophageal dysfunction was identified in all problem patients and in 52% of controls, and the esophagus was incriminated as the source of pain in 8 (44%) and 5 (18.5%), respectively. After a mean follow-up of 49 months (range 24-76 months), the cause of chest pain in the problem group was identified as panic disorder in 9 patients (50%), gastroesophageal reflux in 6 (33%), esophageal dysmotility in 2 (11%), and gallstone disease in 1 (6%). Of the control patients, 18 (67%) had ischemic pain alone, while 9 had concurrent causes: panic disorder in 5 (19%) and esophageal dysfunction in 4 (15%). Esophageal dysfunction and psychiatric disturbances are common in patients with coronary artery disease presenting with resting chest pain, and may contribute to patients' symptoms.

High amplitude contractions in the middle third of the oesophagus: a manometric marker of chronic alcoholism?

BACKGROUND: Oesophageal motor abnormalities have been reported in alcoholism. AIM: To investigate the effects of chronic alcoholism and its withdrawal on oesophageal disease. PATIENTS: 23 chronic alcoholic patients (20 men and three women; mean age 43, range 23 to 54). METHODS: Endoscopy, manometry, and 24 hour pH monitoring 7-10 days and six months after ethanol withdrawal. Tests for autonomic and peripheral neuropathy were also performed. Motility and pH tracings were compared with those of age and sex matched control groups: healthy volunteers, nutcracker oesophagus, and gastro-oesophageal reflux disease. RESULTS: 14 (61%) alcoholic patients had reflux symptoms, and endoscopy with biopsy showed oesophageal inflammation in 10 patients. One patient had an asymptomatic squamous cell carcinoma. Oesophageal motility studies in the alcoholic patients showed that peristaltic amplitude in the middle third was > 150 mm Hg (95th percentile (P95) of healthy controls) in 13 (57%), the ratio lower/ middle amplitude was < 0.9 in 15 (65%) (> 0.9 in all control groups), and the lower oesophageal sphincter was hypertensive (> 23.4 mm Hg, P95 of healthy controls) in 13 (57%). All three abnormalities were present in five (22%). Abnormal reflux (per cent reflux time > 2.9, P95 of healthy controls) was shown in 12 (52%) alcoholic patients, and was unrelated to peristaltic dysfunction. Subclinical neuropathy in 10 patients did not effect oesophageal abnormalities. Oesophageal motility abnormalities persisted at six months in six patients with ongoing alcoholism, whereas they reverted towards normal in 13 who remained abstinent; reflux, however, was unaffected. CONCLUSIONS: Oesophageal peristaltic dysfunction and reflux are frequent in alcoholism. High amplitude contractions in the middle third of the oesophagus seem to be a marker of excessive alcohol consumption, and tend to improve with abstinence.

[Thoracic pain of esophageal origin. Assessment of 125 consecutive patients with resting angina and angiographically normal coronary arteries]. / Dolor torácico de origen esofágico. Evaluación de 125 pacientes consecutivos con angina de reposo y arterias coronarias angiográficamente normales.

BACKGROUND: The esophagus may be the origin of chest pain clinically indistinguishable from that of myocardial ischemia. Gastroesophageal reflux (GER) and esophageal motility disorders (EMDs) are the main causes of esophageal chest pain, and esophageal motility tests are important for an appropriate diagnosis. We studied 125 unselected patients with angiographically normal coronary arteries presenting with atypical (resting) angina which was shown not to be of cardiac origin. METHODS: Stationary esophageal manometry and 24-hour pH studies were performed in all patients, and 116 of them were submitted to edrophonium provocation test (Tensilon, 10 mg as IV bolus). RESULTS: Spastic EMDs were identified as an isolated abnormality in 23 patients (18%), whereas GER was documented in 70 patients (56%). Esophageal dysmotility at baseline manometry (n = 40), a positive edrophonium test (n = 19), abnormal acid reflux indices by 24-hour pH recording (n = 62), and association of chest pain with acid reflux during pH testing (n = 24) variably overlapped in many patients. The esophagus was directly blamed as the source of atypical angina in 33 patients (26%) who had induction of their usual chest pain by cholinergic stimulation and/or association of spontaneous pain events with acid reflux. CONCLUSIONS: Esophageal dysfunction in common in patients with atypical angina considered not to be of cardiac origin and contributes to patients' symptoms. Because they may detect treatable causes of chest pain such as GER or contribute to management by assessing the diagnosis of EMD, esophageal motility tests are indicated in many patients with noncardiac chest pain.

Value of Nissen fundoplication in patients with gastro-oesophageal reflux judged by long-term symptom control.

A total of 160 patients treated by Nissen fundoplication for uncomplicated gastro-oesophageal reflux disease were studied over a 20-year period. Recurrent reflux and side-effects were assessed yearly after surgery. No objective tests for reflux were performed during follow-up if patients were asymptomatic. Perioperative mortality and technique-related morbidity rates were both 2 per cent. At the latest evaluation, 79 per cent of patients were completely relieved of reflux symptoms, 85 per cent had symptoms of Visick grade 1 or 2 and 89 per cent would be willing to undergo surgery again under the same conditions. Actuarial analysis showed that the success rate of fundoplication was 92 per cent at 20 years. Fourteen patients (9 per cent) developed side-effects after fundoplication and had continuing disability. Nissen fundoplication achieves permanent control of reflux symptoms in most patients with few complications and has a high degree of patient satisfaction.

Predictive factors of the long term outcome in gastro-oesophageal reflux disease: six year follow up of 107 patients.

There is little information concerning the long term outcome of patients with gastro-oesophageal reflux disease (GORD). Thus 109 patients with reflux symptoms (33 with erosive oesophagitis) with a diagnosis of GORD after clinical evaluation and oesophageal testing were studied. All patients were treated with a stepwise approach: (a) lifestyle changes were suggested aimed at reducing reflux and antacids and the prokinetic agent domperidone were prescribed; (b) H2 blockers were added after two months when symptoms persisted; (c) anti-reflux surgery was indicated when there was no response to (b). Treatment was adjusted to maintain clinical remission during follow up. Long term treatment need was defined as minor when conservative measures sufficed for proper control, and as major if daily H2 blockers or surgery were required. The results showed that one third of the patients each had initial therapeutic need (a), (b), and (c). Of 103 patients available for follow up at three years and 89 at six years, respective therapeutic needs were minor in 52% and 55% and major in 48% and 45%. Eighty per cent of patients in (a), 67% in (b), and 17% in (c) required only conservative measures at six years. A decreasing lower oesophageal sphincter pressure (p < 0.001), radiological reflux (p = 0.028), and erosive oesophagitis (p = 0.031), but not initial clinical scores, were independent predictors of major therapeutic need as shown by multivariate analysis. The long term outcome of GORD is better than previously perceived.

Healing of erosive esophagitis with sucralfate and cimetidine: influence of pretreatment lower esophageal sphincter pressure and serum pepsinogen I levels.

Forty-eight patients with erosive reflux esophagitis were allocated to either sucralfate tablets, 4 g/day, or cimetidine, 1.6 g/day, for 8 weeks in a randomized, prospective, single-blind, cross-over therapeutic trial. Pretreatment lower esophageal sphincter (LES) pressure and serum pepsinogen I (PG-I) levels were investigated as possible predictors of healing with either drug. The trial was completed by 41 patients (21 in the sucralfate group and 20 in the cimetidine group); one patient in each group was removed because of side effects. Symptom improvement occurred to a similar extent in both groups. Endoscopic results after 8 weeks of treatment with sucralfate revealed complete healing of esophageal erosions in 48% (cimetidine, 55%) and improvement in an additional 19% (cimetidine, 20%). Neither of these differences was statistically significant. Some patients refractory to one drug had endoscopic healing of esophagitis when treated with the other drug after crossover. LES pressure did not influence outcome in patients treated with sucralfate, whereas significantly (p = 0.024) more patients refractory to cimetidine had an LES pressure less than 7 mm Hg than did those with a good response to the histamine-2 (H2)-receptor blockade. Patients whose esophagitis healed or improved after sucralfate tended to have lower serum PG-I levels than those with treatment failure (104 +/- 35 ng/mL vs 125 +/- 45 ng/mL), whereas the opposite occurred in patients treated with cimetidine (132 +/- 58 ng/mL in responders vs 78 +/- 27 ng/mL in nonresponders, p = 0.048). The results confirm that sucralfate is a valuable alternative to H2-receptor inhibitors for the treatment of reflux esophagitis. They also provide preliminary evidence that LES pressures and serum PG-I levels may have predictive value of the response to one or the other of these two drugs.