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Biomedical subjects

R I Russell

Publications and source records attributed to R I Russell.

At least 91 records · Page 5Linked to original sources
PubMed1991

Nonsteroidal peptic damage in rheumatoid patients receiving second-line drugs.

Using endoscopy, we assessed the prevalence of peptic ulceration in 281 rheumatoid patients receiving nonsteroidal antiinflammatory drugs alone, or in combination with second-line agents. Ulcers were found in 33 of 96 patients who took nonsteroidals only (33/96, 34%), compared with 8/33 (24%) on hydroxychloroquine, 10/30 (33%) on penicillamine, 13/46 (28%) on sulphasalazine, but only 11/76 (14%) on intramuscular gold plus nonsteroidals (chi 2 = 7.95, 0.001 less than p less than 0.01, p less than 0.05 using Bonferroni correction). Second-line drugs do not seem to increase the prevalence of ulcers related to nonsteroidal antiinflammatory drugs; on the contrary, fewer ulcers were found in patients receiving gold therapy, and this might have therapeutic implications.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1991

Comparison of different measurements of intestinal permeability in inflammatory bowel disease.

We have compared different measurements of small intestinal permeability in 28 patients with Crohn's disease affecting the small intestine, 14 with ulcerative colitis and 17 controls. Patients and controls were given a drink containing 100 microCi (3.7 MBq) of 51Cr-ethylene diamine tetraacetic acid (51Cr-EDTA), 5 g lactulose, 5 g cellobiose, 1 g rhamnose, and 2 g mannitol. Urine was collected to 6 h after dosing, and then from 6 until 24 h. Recoveries of 51Cr-EDTA, lactulose, rhamnose, and mannitol were expressed as percentages of the amount administered. The only measurement that distinguished patients with Crohn's disease from both controls and patients with ulcerative colitis was the recovery of 51Cr-EDTA in the first 6 h after dosing. The mean recovery in patients with Crohn's disease was 1.07%; in controls, it was 0.35% (p = 0.013); in ulcerative colitis it was 0.39% (p = 0.032 compared to Crohn's; p = 0.492 compared to controls). No other measurement of permeability differentiated the three groups. Recoveries of 51Cr-EDTa and lactulose were highly correlated in each of the three groups. Recovery of rhamnose was significantly correlated with that of mannitol. In the patients with Crohn's disease, recovery of 51Cr-EDTA to 6 h was significantly correlated with some nonspecific laboratory indicators of inflammatory activity, namely, erythrocyte sedimentation rate, platelet count, white blood cell count, serum albumin, and C-reactive protein, but not with hemoglobin.

Adolescent↗
PubMed1991

Bedside assessment of phrenic nerve function in infants and children.

Phrenic nerve damage is widely recognized after cardiac operations and is associated with an increased morbidity and mortality. Retrospective studies in children have estimated a prevalence of phrenic damage of between 0.5% and 2.2%, but all these studies have limited their investigations to patients who have clinical problems postoperatively, and they have all used clinical or radiologic methods to diagnose the damage. These methods are indirect and hard to evaluate, making the accurate early diagnosis of phrenic nerve damage very difficult. Measurement of phrenic nerve conduction time (phrenic latency) allows direct evaluation of phrenic function and integrity, making it potentially much more specific than indirect methods. Using a simplified method of direct phrenic nerve stimulation, we have developed a method of measuring phrenic latency at the bedside in infants and children. A 1 Hz electrical stimulus is applied over the phrenic nerve in the neck and a diaphragmatic electromyogram from the seventh and eighth intercostal spaces is displayed on a storage oscilloscope. Phrenic latency can be measured directly from the screen. Using these methods we have now studied 37 children (aged 2 days to 15 years) before and after cardiac operations. Mean phrenic latency was 5.4 +/- 1.0 msec on the right and 5.4 +/- 1.0 msec on the left. Prolongation of phrenic latency by more than 2 msec was found in seven of 66 postoperative measurements (10.6%). These patients had a substantially worse postoperative course. We believe this technique to be an important contribution to the diagnosis of postoperative phrenic nerve damage, and one that can help in clinical practice to elucidate an important cause of postoperative morbidity and mortality.

Adolescent↗
PubMed1990

Endoscopic evaluation of etodolac and naproxen, and their relative effects on gastric and duodenal prostaglandins.

Etodolac has been shown to have a favorable safety profile in short-term and long-term studies in both osteoarthritis (OA) and rheumatoid arthritis (RA). Two studies were conducted to further assess the gastrointestinal (GI) safety profile of this drug. These studies were designed to compare the therapeutic efficacy and upper GI effects of etodolac (600 mg/day) and naproxen (1000 mg/day) administered over 4 weeks in patients with active rheumatoid arthritis. In addition, the relative effects of the drugs on prostaglandin levels in the stomach and duodenum were assayed in one study. Fifteen patients were included in each study and received either 300 mg b.i.d. of etodolac or 500 mg b.i.d. of naproxen. In both studies, endoscopic examinations were performed on day 1 of the study and again 4 weeks later. In the second study, at the time of each endoscopy, samples of gastric and duodenal mucosa were taken for histologic study and prostaglandin assay. Endoscopy results from the first study showed significant differences in favor of etodolac between the two treatment groups. In the second study more naproxen-treated patients had abnormal endoscopy results than did etodolac-treated patients. Results from prostaglandin assays in gastric and duodenal mucosa showed no overall suppression of gastric or duodenal prostaglandin levels for etodolac-treated patients in contrast to naproxen-treated patients, who showed suppression of PGE2 and PGI2. The results of these studies show that etodolac therapy caused less gastric and duodenal injury than naproxen and also support the theory that the GI safety of etodolac may be due to selective sparing of cytoprotective prostaglandins.

Adolescent↗
PubMed1990

Magnesium deficiency in patients on home enteral nutrition.

Home enteral nutrition (HEN) is an established method of long term nutritional support. Many patients receiving HEN have Crohn's disease complicated by intestinal failure and malnutrition, including magnesium deficiency. It is unknown if HEN can correct magnesium deficiency or if patients on HEN can become magnesium deficient. We measured total magnesium intake in nine patients receiving HEN, and assessed their magnesium status. Two patients had magnesium intakes below the recommended dietary allowance of 15 mmol/day. Four patients (44%) had biochemical evidence of magnesium deficiency, although no patient had clinical signs of magnesium deficiency. Several magnesium deficient patients used a liquid feed which had a low magnesium content. Patients on HEN should have their magnesium status checked regularly and may require magnesium supplements.

Journal Article↗
PubMed1990

The interaction between Helicobacter pylori culture filtrate and indomethacin: effects on the integrity of human gastric antral mucosa and its prostaglandin E2 production in vitro.

Histopathological methods and radioimmunoassay were used to assess the microstructure and prostaglandin E2 production by paired specimens of human gastric antral mucosa; the specimens were studied after 48 h of incubation in base-line tissue culture medium, Helicobacter pylori culture filtrate, H. pylori culture control fluid, indomethacin, and H. pylori culture filtrate plus indomethacin. When applied alone, the filtrate did not affect the structure of the mucosal tissue or its prostaglandin E2 synthesis. In the overall group (n = 21), specimens incubated with the mixture of H. pylori filtrate and indomethacin had a median histological grade of 1 and prostaglandin E2 of 29 pg/mg tissue, compared to 2 pg/mg (P = 0.04) and 60 pg/mg (P = 0.0007) respectively, in specimens incubated with indomethacin alone. These results indicate that an interaction may exist between indomethacin and a factor contained in H. pylori culture filtrate. Such interaction is damaging to the human gastric antral mucosa, and its understanding might have therapeutic implications.

Adult↗
PubMed1990

Effect on gastric and duodenal mucosal prostaglandins of repeated intake of therapeutic doses of naproxen and etodolac in rheumatoid arthritis.

The synthesis of gastric and duodenal mucosal prostaglandin E2, prostaglandin I2, and thromboxane B2 during a 60 minute incubation of biopsy specimens, the degree of endoscopic and histological damage, and the anti-inflammatory response were all studied after a four week, double blind study of therapeutic doses of two non-steroidal anti-inflammatory drugs, naproxen and etodolac, received by 27 patients with active rheumatoid arthritis (13 receiving naproxen, 14 etodolac). Prostaglandin values after treatment did not differ from the baseline levels when all the patients were analysed as one group. Subgroup analysis showed that naproxen suppressed gastric prostaglandin E2 from a median of 29 to 9 ng/mg protein, duodenal prostaglandin E2 from 34 to 11 ng/mg, and duodenal prostaglandin I2 from 62 to 15 ng/mg protein. No overall suppression occurred with etodolac. Also, on the second assessment patients receiving naproxen had lower gastric and duodenal prostaglandin E2 and prostaglandin I2, but higher values of duodenal thromboxane B2, than patients receiving etodolac. Both drugs had comparable anti-arthritic activity and caused microscopic gastritis in similar proportions of patients. No correlation was detected between prostaglandin values and the mucosal damage which developed in seven patients receiving naproxen (54%) and three receiving etodolac (21%). These findings indicate that, unlike naproxen, etodolac does not seem to affect gastric or duodenal prostaglandin synthesis; other mechanisms of injury need to be considered.

Adolescent↗
PubMed1990

Iron deficiency anaemia in patients with rheumatic disease receiving non-steroidal anti-inflammatory drugs: the role of upper gastrointestinal lesions.

Upper gastrointestinal lesions associated with non-steroidal anti-inflammatory drug (NSAID) treatment are commonly implicated as the cause for iron deficiency anaemia in patients with rheumatic diseases. Such patients, however, may also have other causes for iron deficiency, including blood loss from the intestine. One hundred and four patients (mean age 58 years; male 21, female 83; smokers 14) with rheumatic disease (rheumatoid 91, others 13) and absent bone marrow iron stores (mean haemoglobin 83 g/l) were examined. At endoscopy 47 of 104 (45%) had upper gastrointestinal lesions (oesophageal ulcer 4, gastric ulcer 25, gastric erosion 13, duodenal ulcer 4, gastric ulcer and duodenal ulcer 1). Endoscopic healing was assessed in 23 patients with upper gastrointestinal lesions. Eighteen of 23 (78%) lesions healed with treatment. An improvement of anaemia occurred in 10 of 18 (56%) patients with healed lesions. Twenty three of 104 (22%) patients had dyspeptic symptoms. Ten of 23 (43%) patients with dyspepsia had an upper gastrointestinal lesion as compared with 30 of 81 (37%) patients without dyspepsia. A faecal occult blood test result was available in 53 patients. Of these, 13 were positive while 40 were negative. An upper gastrointestinal lesion was present in seven of 13 (54%) patients positive for the faecal occult blood test as compared with 14 of 40 (35%) negative for the test. Thus upper gastrointestinal lesions have previously been overestimated as the cause of iron deficiency anaemia in patients receiving NSAIDs. A positive faecal occult blood test or the presence of dyspepsia is not associated with upper gastrointestinal lesions in such patients.

Adult↗
PubMed1990

Helicobacter pylori: bridging the credibility gap.

In summary, therefore, there are interesting associations between H pylori, duodenal ulcer, and non-ulcer dyspepsia. In type B gastritis there may be enough evidence to suggest a causal role. The relation between gastritis and upper gastrointestinal symptomatology, however, remains contentious. The relation between H pylori and acid secretion may be more intimate than was previously thought. 'Pylorites' must temper their enthusiasm and provide hard data; 'Schwartzians' must broaden their horizons.

Campylobacter Infections↗
PubMed1990

Gastric antral vascular ectasia (watermelon stomach)--therapeutic options.

We have encountered five cases of chronic iron deficiency anaemia due to bleeding from gastric antral vascular ectasia (watermelon stomach). Two cases were associated with a lymphoma and in three cases there was evidence of portal hypertension. Two patients were treated conservatively by blood transfusions. The other patients required either surgery or tranexamic acid or endoscopic laser therapy to control the chronic haemorrhage.

Aged↗
PubMed1990

Wilson's disease presenting as acute fulminant hepatic failure.

A fatal case of fulminant hepatic failure in an adolescent is described. Post-mortem examination revealed the cause to be Wilson's Disease. This rare presentation is characterised by apparently atypical changes in copper metabolism. Wilson's Disease should be a differential diagnosis of any adolescent presenting in liver failure.

Adolescent↗
PubMed1990

Hypolactasia and Crohn's disease: a myth.

A retrospective analysis was made of jejunal biopsies performed on 62 patients with Crohn's disease for disaccharidase levels and routine histology. Thirteen patients with irritable bowel syndrome acted as a control group. Two patients with Crohn's disease had hypolactasia. Two patients had marginally low sucrase levels, but all patients had normal maltase levels. Only one patient with irritable bowel syndrome had hypolactasia with normal histology. There were no significant differences between the two groups. Four patients with Crohn's disease had abnormal jejunal histology. The prevalence of hypolactasia in patients with Crohn's disease is not increased. Ideally lactase deficiency in patients with Crohn's disease should be confirmed before starting a lactose-free diet which can produce further restrictions on dietary intake.

Adult↗
PubMed1990

Gastric mucosal prostaglandin synthesis in the presence of Campylobacter pylori in patients with gastric ulcers and non-ulcer dyspepsia.

It is unclear how Campylobacter pylori (CP) interacts with gastric mucosal prostaglandins (PG). In a double-blind study we measured gastric PG synthesis in 22 patients with benign gastric antral ulcers (GU) and 26 with non-ulcer dyspepsis (NUD). CP status was determined by histology and bacteriology: 26 (16 GU plus 10 NUD) were CP positive, and 22 (6 GU plus 16 NUD) were CP negative. Patients with severe gastritis regardless of CP status) had significantly higher PGE2 and PGI2 values than those with mild gastritis. Severe gastritis was found in 36% of CP-negative subjects and 77% of the CP-positive patients (chi 2 = 8.64, p less than 0.01), but no significant differences in PG values were found between CP-positive or -negative patients.

Adult↗
PubMed1989

Campylobacter pylori and gastroduodenal disease. Is there a relationship?

Much has been discovered about Campylobacter pylori in the past 6 years. Yet, many questions remain: Is the organism commensal or is it a pathogen? What is its environmental source? How is it transmitted? What is its role in gastroduodenal disease? The authors of this article discuss these and other issues relating to this common organism.

Breath Tests↗
PubMed1989

Pulmonary abnormalities in Crohn's disease.

Abnormalities of pulmonary function in Crohn's disease have been described, although the results are conflicting and anecdotal accounts of lung involvement are few. In this study we assessed the prevalence of lung function abnormalities in Crohn's disease, and the relative contributions of age, sex, smoking and past medical history, and Crohn's disease activity to the pulmonary abnormalities found. Twenty-nine patients with Crohn's disease and 29 age-, sex- and smoking-matched volunteer controls underwent detailed respiratory assessment. Airways obstruction due to chronic bronchitis and asthma was present in 13 patients with Crohn's disease, but was not more prevalent than in the control group. FEV1 was similar in both Crohn's disease and control subjects (84.2 +/- 21.2% predicted, mean +/- SD; 93.7 +/- 16.3%, respectively: n.s.). The vital capacity was significantly lower in the Crohn's disease patients than in controls (86.7 +/- 16.6%; 95.9 +/- 12.7%; P less than 0.01), but this may have been influenced by the higher prevalence of past or intercurrent medical illnesses affecting the chest in Crohn's disease patients. No patient had evidence of fibrosing alveolitis or bronchiectasis. The haemoglobin corrected transfer factor was significantly lower in the Crohn's disease patients than in controls (100.4 +/- 17.4%; 113.2 +/- 25.1: P less than 0.05) but the diffusing coefficient was not significantly different. There was a significant correlation (r = 0.44, P less than 0.05) between the residual volume and the Crohn's disease activity index but otherwise no close relationship was observed between Crohn's disease activity, extent or duration and the indices of lung function. These findings suggest that the lungs are relatively unaffected by Crohn's disease.

Adult↗