No abstract

SUMMARY Suppositories containing 300 mg 5‐aminosalicylic acid (1.96 mmol) or 425 mg acety1‐5‐aminosalicylic acid (1.96 mmol) were used in 40 patients with idiopathic proctitis to determine the efficacy of acetyl‐5‐aminosalicylic acid in treating this bowel inflammation. Each patient was treated with 5‐aminosalicylic acid or acetyl‐5‐aminosalicylic acid suppositories twice daily for 4 weeks in a double‐blind trial. Four patients were included twice in the trial. The second time they were treated with the alternative regimen. Six patients in the acetyl‐5‐aminoscylic acid group did not complete the trial, four of them because of diarrhoea. Complete clinical remission with normal rectal mucosa on sigmoidoscopy was achieved in 10 out of 18 patients on 5‐aminosalicylic acid and in only two out of 15 in the acetyl‐5‐aminosalicylic acid group (P= 0.03). A favourable histological improvement was demonstrated with 5‐aminosalicylic acid suppositories, but the difference with acetyl‐5‐aminosalicylic acid was not significant (P= 0.059). Three of the four patients who received both drugs recovered with 5‐aminosalicylic acid; in none of them was acetyl‐5‐aminosalicylic acid effective. The results from this study and from previous investigations show that acetyl‐5‐aminosalicylic acid is not superior to placebo.

After oral administration of 5-aminosalicylic acid a substantial proportion of the acetylated form is excreted in the faeces. We have studied the role of the faecal microflora in acetylating 5-aminosalicylic acid. In faeces incubated under both aerobic and anaerobic conditions there was acetylation of 5-aminosalicylic acid. Of the anaerobic bacteria isolated from a 10(8) faecal dilution 44% were able to acetylate 5-aminosalicylic acid. We conclude that the normal faecal microflora contribute to the acetylation of 5-aminosalicylic acid.

Granular cell tumors (GCT) of the esophagus are rare. The tumor is generally beleived to be of neurogenic origin and shows a malignant course in 2-4% of cases. No unanimity has been reached regarding the management of this tumor. A national survey was conducted on the incidence of GCT of the esophagus, related symptoms, management, and follow-up. A national survey was performed on all newly registered esophageal GCTs in the PALGA system (Dutch register of all pathology diagnoses) for seven consecutive years (1988-1994). Fifty-two new cases (17 men, 35 women; median age 46 years, range 22-77 years) were registered. In 44 cases clinical data could be obtained (survey response 85%). The majority of the GCTs were solitary (42/44) and localized in the distal esophagus (33/44). At endoscopy the size of the tumor was estimated at <5 mm in 50%, 5-10 mm in 25%, and 10-30 mm in 18%. Most patients (40/44) presented with nonspecific gastrointestinal symptoms, only four had dysphagia (tumor size >1 cm). No malignancies were reported. Management of the tumor included excisional biopsy (1/44), endoscopic polypectomy (3/44), and surgical excision (1/44). Endoscopic follow up (1-60 months) in 16 out of 17 patients left untreated showed either a stable tumor size or regression of the tumor. In one case with multiple GCT's a slight tumor growth was seen after a follow-up period of 48 months. Esophageal GCTs in the Netherlands are rare, and mostly diagnosed incidentally. Most patients suffer from nonspecific symptoms; dysphagia occurs only with tumors >1 cm. The usual clinical course of esophageal GCTs is benign. Patients without dysphagia probably do not require routine endoscopic follow-up, provided they are instructed to contact their physician, once dysphagia develops.

SUMMARY During a normal and an accelerated intestinal transit, in seven healthy volunteers, the recoveries of salicylazosulphapyridine (SASP) and its split products sulphapyridine (SP) and 5-aminosalicylic acid (5-ASA) were determined in urine and faeces. The azo-reduction of SASP and consequently the recovery of 5-ASA in the faeces was found to be substantially decreased during an accelerated intestinal transit. In addition, in 18 patients with inflammatory disease of the colon during maintenance therapy of SASP it could be demonstrated that the serum SP levels were related to the diarrhoeal state and did not correlate with disease activity. As recent studies have reported that 5-ASA is possibly the active therapeutic moiety of SASP, the ineffectiveness of SASP therapy in patients with active colitis may be ascribed to the reduced azo reduction of SASP as the result of profuse diarrhoea.Salicylazosulphapyridine (Salazopyrin, Sulphasalazine, SASP) has been widely used in the treatment of ulcerative colitis and Crohn's disease. However, its mode of action is still unknown. SASP is composed of sulphapyridine (SP) in azo-linkage with 5-aminosalicylic acid (5-ASA). After an oral dose of SASP in man, only a small fraction has been found to be absorbed in the small bowel and excreted in the urine. The greater part of the drug reaches the colon and is almost completely split at the diazo bond by bacterial azo-reductases into SP and 5-ASA (Schroder and Campbell, 1972;Peppercorn and Goldman, 1973). SP is then mostly absorbed and subsequently partially metabolised in the liver (acetylation and glucuronidation) before excretion in the urine. The 5-ASA moiety is largely recovered in the faeces and only a small portion is found in the urine as acetylated form.As SASP is particularly effective in the treatment of inflammatory disease of the large bowel, it has been suggested that one of the metabolites, rather than SASP itself, is responsible for the drug's activity at the site of breakdown. Although controlled trials have established the value of SASP in