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Biomedical subjects

D S Rampton

Publications and source records attributed to D S Rampton.

At least 109 records · Page 6Linked to original sources
PubMed1983

Nonspecific ulcerative colitis as a sequel to amebic dysentery.

In two patients, treatment of amebic dysentery was followed (despite the disappearance of the infecting organism) by an illness with the clinical, pathological, and radiological characteristics of nonspecific ulcerative colitis. Their case histories indicate that in addition to persistent or recurrent amebic infection, the irritable colon syndrome, and ulcerative postdysenteric colitis, nonspecific ulcerative colitis should be kept in mind in the evaluation and therapy of continuing symptoms in patients with treated amebic dysentery.

Adult↗
PubMed1983

Analgesic ingestion and other factors preceding relapse in ulcerative colitis.

To investigate factors which predispose to relapse in patients with ulcerative colitis, we conducted a survey to compare the events occurring in the four weeks preceding the clinic attendance of 62 outpatients in remission with those taking place in the same period before the onset of relapse in 21 patients attending with active disease. The only event which occurred significantly more often in patients who subsequently relapsed was ingestion of paracetamol and other inhibitors of prostaglandin synthesis (76% (16/21) relapse vs 39% (24/62) remission, p less than 0 . 01). Recent upper respiratory tract infection (38% vs 26%) was not significantly more common in patients in relapse than in remission, and emotional stress, atopic events, antibiotic treatment, dietary indiscretions, foreign travel, and gastroenteritis were relatively rare in both groups. The surprisingly high prevalence of analgesic ingestion before relapse itself requires confirmation but does lend indirect support to the theory that colonic mucosal prostaglandin deficiency induces relapse in some patients with ulcerative colitis.

Acetaminophen↗
PubMed1983

Effect of colonic perfusion with sulfated and nonsulfated bile acids on mucosal structure and function in the rat.

A single-pass perfusion system was used in conscious restrained rats to measure changes in water and electrolyte transport and in protein and deoxyribonucleic acid output after perfusing 5-15-mM solutions of sulfated or nonsulfated bile acids through the colon. Perfusion with 5 mM nonsulfated deoxycholic acid or chenodeoxycholic acid changed net water and sodium absorption to net secretion, provoked marked increases in protein and DNA output into the perfusion effluent, and caused microscopic mucosal damage. In contrast, perfusion with 5 and 15 mM sulfated deoxycholic acid or with 5 mM sulfated chenodeoxycholic acid had no effect on water and electrolyte transport and caused only modest changes in protein and DNA output. To see whether or not sulfated bile acid could prevent the effect of its nonsulfated parent compound on colonic structure and function, perfusion with a mixture of 5 mM nonsulfated and 10 mM sulfated deoxycholic acid was performed. This produced net secretion of water and sodium together with less marked increases of protein and deoxyribonucleic acid output and less pronounced microscopic mucosal damage than was seen after 5 mM nonsulfated deoxycholic acid alone. Finally, 5 mM nonsulfated cholic acid had no effect on water or sodium transport, but 5 mM sulfated cholic acid, with one alpha-hydroxyl group masked and two alpha-hydroxyl groups "exposed," reduced water transport. These results suggest that sulfation prevents the cathartic effect of alpha-dihydroxyl bile acids in the colon.

Animals↗
PubMed1982

The effect of disodium cromoglycate on rectal mucosal histamine release, eosinophil exudation and disease activity in active ulcerative colitis.

Disodium cromoglycate has been reported to benefit some patients with active ulcerative colitis. We have investigated the effect of cromoglycate in high dose on rectal mucosal mast cell degranulation (assessed indirectly by measurement of mucosal histamine release, using in vivo rectal dialysis, and the eosinophil content of the rectal inflammatory exudate) and on disease activity in eight patients in relapse. Although cromoglycate (1600 mg by mouth daily for 2 weeks) did not affect histamine release, it reduced (P less than 0.05) the eosinophil content of the exudate towards normal. Stool frequency also fell (P less than 0.05) but other aspects of bowel habit, sigmoidoscopic appearance, rectal mucosal potential difference and electrolyte transport were unaltered. Pre-treatment values of histamine release and eosinophil exudation could not be used to predict the response to cromoglycate. The reduction in eosinophil exudation produced by the drug could be due to inhibition of mast cell release of chemotactic factors other than histamine; the therapeutic effect of cromoglycate was unimpressive.

Adult↗
PubMed1981

Prostaglandin synthesis inhibitors in ulcerative colitis: flurbiprofen compared with conventional treatment.

It has been suggested that prostaglandins (PGs) play a pathogenetic role in ulcerative colitis (UC) and that treatment with inhibitors of PG synthesis might be of therapeutic benefit. We therefore performed a one-week open trial to compare the effects of oral flurbiprofen with those of conventional therapy with corticosteroids and sulphasalazine, in two groups of patients with active UC. Mean rectal mucosal release of PGE2, measured by in vivo rectal dialysis, fell by 44% (P less than 0.05) after one week's conventional treatment, and the effect of flurbiprofen was not significantly different. However, the patients given flurbiprofen fared significantly worse than those given conventional therapy in respect of rectal mucosal appearance at sigmoidoscopy (P = 0.01), rectal electrical potential difference (p less than 0.01), rectal mucosal sodium absorption (P = 0.01) and rectal bleeding (P less than 0.05). Furthermore, flurbiprofen-treated patients showed significant deteriorations in rectal potential difference (P less than 0.05) and sodium absorption (P less than 0.05). These results do not support the hypothesis that increased mucosal PG production is of major pathogenetic importance in active UC, and suggest that flurbiprofen is unlikely to prove a useful alternative to conventional therapy.

Colitis, Ulcerative↗
PubMed1981

Relapse of ulcerative proctocolitis during treatment with non-steroidal anti-inflammatory drugs.

In four patients with inactive ulcerative proctocolitis, oral administration of non-steroidal anti-inflammatory drugs appeared to precipitate relapse. These observations suggest that inhibitors of prostaglandin synthesis should be used with care in patients with this disease, and are consistent with the hypothesis that prostaglandins may have a protective role in the lower as well as the upper gastrointestinal tract.

Adult↗
PubMed1981

The effect of sulphasalazine withdrawal on rectal mucosal function and prostaglandin E2 release in inactive ulcerative colitis.

We have used in vivo rectal dialysis to assess mucosal prostaglandin E2 (PGE2) release and water and electrolyte transport before and 2 weeks after withdrawal of oral sulphasalazine in eight patients with inactive ulcerative colitis. Although rectal mucosal PGE2 release was unaffected by withdrawal of sulphasalazine, significant reductions in mucosal potential difference (P less than 0.01) and net absorption of water (P less than 0.05), sodium (P less than 0.05), and chloride occurred (P less than 0.05). Clinical assessment showed no change in disease activity. Sulphasalazine withdrawal thus has a detrimental effect on large-intestinal salt and water transport, which does not appear to be mediated through changes in net mucosal prostaglandin production.

Body Water↗
PubMed1980

Rectal mucosal histamine release in ulcerative colitis.

1. Rectal dialysis in vivo was used to assess rectal mucosal release of histamine in patients with ulcerative colitis and in control subjects. 2. Rectal mucosal histamine release was significantly increased in ulcerative colitis, whether the patients were in remission or relapse. The highest values were found in active colitis, but in several such patients histamine release was within the control range. Measurement of rectal mucosal electrical potential difference suggested that increased mucosal histamine release in this group of patients was not due to enhanced epithelial permeability. 3. Rectal dialysis appears to be a useful method for assessing mucosal histamine production and the results obtained are consistent with the hypothesis that immediate hypersensitivity reactions could be of importance in some patients with ulcerative colitis.

Colitis, Ulcerative↗
PubMed1980

Rectal mucosal prostaglandin E2 release and its relation to disease activity, electrical potential difference, and treatment in ulcerative colitis.

In vivo rectal dialysis was used to study rectal mucosal release of immunoreactive prostaglandin E2-like material and its relation to disease activity, rectal electrical potential difference (PD), and treatment in 24 patients with ulcerative colitis. In untreated colitics in remission and in relapse, median values for apparent mucosal prostaglandin E2 (PGE2) release were increased three-fold (P < 0.05) and 13-fold (P < 0.002) respectively over that found in control subjects. In patients in remission during treatment with sulphasalazine and/or corticosteroids, median apparent PGE2 release was similar to that of controls, but in colitics in relapse, despite treatment, it was greatly increased (P< 0.002). Ulcerative colitis in relapse was associated with a significant reduction in rectal PD(P < 0.002); in patients with quiescent ulcerative colitis, a smaller reduction was found (P < 0.05). In nine patients studied serially before and during treatment, there were associations between changes in disease activity assessed sigmoidoscopically, in PD and in apparent mucosal PGE2 release. Furthermore, rectal mucosal PGE2 release and PD were linearly correlated (P < 0.01). These findings indicate that mucosal PGE2 release is markedly enhanced in active ulcerative colitis, and they confirm the value of rectal PD as a guide to disease activity. In addition, they suggest that rectal dialysis may be a useful way of studying rectal prostaglandin metabolism in man.

Colitis, Ulcerative↗
PubMed1979

Oxalate loading test: a screening test for steatorrhoea.

To investigate the possibility of measuring urinary oxalate output instead of faecal fat excretion as an outpatient screening test for steatorrhoea, we determined 24 hour urinary oxalate and five day faecal fat excretion before and during an oral load of sodium oxalate 600 mg daily (oxalate 4.44 mmol), in 32 patients with suspected malabsorption on a diet containing oxalate 30 mg (0.33 mmol), fat 50 g (180 mmol), and calcium 1 g (25 mmol). Nineteen patients proved to have steatorrhoea (mean faecal fat 62 mmol/24 h, range 19--186 mmol) of varying aetiologies. On the diet alone, urinary oxalate was raised in only nine of these patients (mean 0.25 mmol/24 h, range 0.08--0.59 mmol) (normal less than 0.20). By contrast, when the diet was supplemented with oral sodium oxalate, all 19 patients with steatorrhoea had hyperoxaluria (mean 0.91 mmol/24 h, range 0.46--1.44 mmol) (normal less than 0.44). There was a significant positive linear relationship between urinary oxalate and faecal fat when the 32 patients were on the high oxalate intake (r = 0.73, P less than 0.001), but not when they were on the low oxalate intake. Mean percentage absorption of orally administered oxalate was 5.8 +/- 0.99% (+/- 1 SD) in normal subjects and 14.7 +/- 6.0% (P less than 0.002) in patients with steatorrhoea. Measurement of urinary oxalate output during oral sodium oxalate loading appears to be a reliable and convenient screening test for steatorrhoea.

Adult↗