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Biomedical subjects

M Ström

Publications and source records attributed to M Ström.

72 records · Page 4Linked to original sources
PubMed1988

Histologic changes in the gastroduodenal mucosa after long-term medical treatment with cimetidine or parietal cell vagotomy in patients with juxtapyloric ulcer disease.

Biopsy specimens were collected during endoscopy from pre-established sites in the corpus (n = 60), antrum (n = 53), and the duodenal bulb (n = 54) from the same patient before and 2-3 years after parietal cell vagotomy (PVC) or after a similar period of treatment with cimetidine. There was a significant increase in scores of chronic body gastritis after PCV (p less than 0.001) even in comparison with the cimetidine group (p less than 0.01), for which the scores of chronic body gastritis remained essentially unchanged. The scores of chronic antral gastritis and the incidence of intestinal metaplasia of the antrum increased significantly (p less than 0.05) in both the PCV and the cimetidine groups when the two treatment groups were analyzed together. The degree of polymorphonuclear infiltration in the body and antral mucosa, the incidence and severity of duodenitis, and the incidence of gastric metaplasia in the duodenal cap were unaffected by the treatment. In contrast to maintenance treatment with cimetidine PCV seems to accelerate the development of chronic body gastritis. The kappa statistics, as indicator of the reproducibility of histopathologic scoring, were acceptable.

Adult↗
PubMed1988

Comparison between medical and elective surgical treatment of peptic ulcers.

During the last decades we have learnt how to treat chronic peptic ulcer disease both with surgery (mainly vagotomy) and with long term medical treatment (mainly H2-receptor antagonists) with great success and safety. Although much attention has lately been given to 'cytoprotective' agents, it is still too early to regard them as alternatives to acid reducing treatment in the long term management of severe peptic ulcer disease. The importance of campylobacter pylori for long term outcome is today only speculative. Only a few randomized studies have been performed comparing surgical and medical treatment. The hitherto published studies involve small numbers of patients or do not use an optimal dosage of the drug given. Nevertheless for most patients with severe peptic ulcer disease one can conclude that we have both medical and surgical alternatives of comparable efficacy and safety to choose among. The final decision if an elective operation or not should be performed must be based on the preference of the individual patient.

Clinical Trials as Topic↗
PubMed1987

Modified sham feeding test after parietal cell vagotomy for juxtapyloric ulcer disease in patients with and without recurrent ulcers.

The mean of individual coefficients of variation of acid output after modified sham feeding was 39% in 22 patients operated on with parietal cell vagotomy. The reproducibility of the interpretation of the sham feeding test as 'positive' or 'negative' was good. An intragastric infusion of a marker to correct for pyloric loss did not increase the accuracy of the test. The prognostic value of the qualitative estimation of the sham feeding test 2 months after operation to predict recurrent ulcer after parietal cell vagotomy was poor in 39 patients studied prospectively over 3 years. With the criterion sham feeding minus basal acid output over 1.0 mmol/30 min as a positive test, 63% of patients with a positive and 24% with a negative test later had recurrent ulcers. The consistency of the interpretation as either positive or negative was low in annual tests during the 3 years of follow-up study. After parietal cell vagotomy the sham-feeding-stimulated acid output was higher in patients with duodenal than in those with prepyloric recurrent ulcers and also in those without recurrences. This indicates that the amount of vagal innervation left after parietal cell vagotomy is of special importance in the occurrence of duodenal ulcer relapse.

Duodenal Ulcer↗
PubMed1986

Duodenal, prepyloric, and combined duodenal/prepyloric ulcer disease: three distinct entities of juxtapyloric ulcer disease?

One hundred and seven patients with long-standing and severe chronic juxtapyloric ulcer disease were classified in accordance with the location of the present ulcer and previous ulcers into 1) pure duodenal (DU), 2) pure prepyloric (PU), and 3) combined duodenal/prepyloric (DU/PU) or prepyloric/duodenal (PU/DU) ulcer disease. In a prospective follow-up study over a 3-year period after parietal cell vagotomy (n = 39) or during continuous treatment with cimetidine (n = 62) patients with DU had recurrent ulcers located exclusively to the duodenal bulb and patients with PU, exclusively to the prepyloric region. In patients with DU/PU and PU/DU recurrent ulcers occurred on either side of the pylorus. Basal acid and basal pepsin outputs were higher and bile acid in gastric juice was lower in patients with DU than in those with PU. There are a considerable number of patients who possess features of both duodenal and prepyloric ulcer disease. The clinical outcome of both continuous cimetidine treatment and vagotomy in these patients (DU/PU and PU/DU) was less satisfactory than in pure DU. All patients presenting with active DU should therefore be investigated for evidence of previous prepyloric ulceration.

Bile Acids and Salts↗
PubMed1986

Results of short- and long-term cimetidine treatment in patients with juxtapyloric ulcers, with special reference to gastric acid and pepsin secretion.

One hundred and seven patients with active juxtapyloric ulcers and a history of chronic ulcer disease were treated with cimetidine. After ulcer healing 67 patients were selected for medical management, testing the value of cimetidine maintenance treatment. Time to healing was shorter for patients with duodenal ulcers when compared with those with active prepyloric ulcers. Recurrences were fewer for patients with pure duodenal ulcer disease (DUD) when compared with those with active or previous prepyloric ulcer disease (PUD). Patients whose ulcers were slow to heal and those with active or previous prepyloric ulcers (PUD) required a higher dose of cimetidine for effective control of their disease. All patients with slowly healing ulcers (more than 6 weeks) relapsed with 400 mg cimetidine at night. Among patients with relapse 46% with DUD and 31% with PUD were controlled by increasing cimetidine to 400 mg twice daily. Tests of acid secretion were of no value in predicting the rate of ulcer healing or relapse rate. Pepsin secretion studies, however, were of predictive value for patients with DUD but of indeterminate value for patients with PUD. Long-term cimetidine produced a significant decrease in pentagastrin-stimulated pepsin secretion (without treatment) in both patients with and without relapse. No significant changes in acid secretion were observed. As a result of these studies we recommend a cimetidine maintenance dosage of 400 mg twice a day for all patients whose ulcers are slow to heal on 1 g cimetidine a day and in patients with prepyloric ulcer disease regardless of rate of healing.

Cimetidine↗
PubMed1986

24-H study of gastric acidity and bile acid concentration after parietal cell vagotomy.

Intragastric pH and bile acid concentration (BAC) were measured over 24 h in 15 sham-feeding-negative patients, 7 with and 8 without recurrence after parietal cell vagotomy (PCV). Nocturnal acidity was significantly higher (p less than 0.02), and BAC at night significantly lower (p less than 0.02), in the group with recurrent ulcers after PCV. There were no significant differences postoperatively in acidity or BAC between seven patients who had duodenal ulcers preoperatively and eight patients with prepyloric ulcers. High nocturnal acidity may be a predisposing factor for the recurrence of ulcers after PCV.

Adult↗
PubMed1985

Metabolic consequences of reduced gastric acidity.

A review of the effect on metabolism of antacids, anticholinergics and histamine H2-antagonists is given. It is stated that long-term treatment with antacids by a variety of mechanisms can cause severe metabolic complications such as the milk-alkali syndrome and phosphorus depletion. The interaction with other drugs can also be marked. There is very little known of the effect of anticholinergics on metabolism. Clinical experience has not indicated that any serious consequences will occur. The authors have investigated the effect continuous treatment with cimetidine 400 mg at night or twice daily for three years on weight, haemoglobin, plasma iron, plasma folate, plasma vitamin B12, albumin and plasma calcium. The only significant difference that occurred was a slight decrease of plasma calcium within the reference values. In conclusion it is stated that there is very little indication that the moderate and inconstant reduction of acidity over 24 hours which can be achieved by anticholinergics or twice daily administration of presently available H2-antagonists will result in metabolic consequences arising from reduced acidity. Higher doses given more frequently might give a risk for bacterial overgrowth with metabolic consequences.

Antacids↗
PubMed1985

Prevention of ulcer recurrence--medical vs surgical treatment. The physician's view.

What factors should be considered in the choice between medical and surgical treatment of peptic ulcer disease? We would suggest the factors included in Table I. It is our opinion that we have concentrated too much on the recurrence rate, that is on how many of the patients who have a recurrence and not so much on the severity of recurrences in terms of symptoms, duration and influence on ability to work. It is also our firm belief that with regard to costs too much attention has been paid to one small part of the total cost, namely the cost for drugs. The strategy in the choice of the treatment for patients with a peptic ulcer depends on many factors as shown in Table II. At our department, the pharmacological part of the treatment of the first episode of an active duodenal ulcer as well as the first recurrences will usually consist of cimetidine 800 mg as a single nocturnal dose or in divided doses, for 4-6 weeks. Antacids are often given for relief of pain. The treatment will be continued for another 2 weeks if the patient is not symptomless after 4 weeks. The patient is then instructed to make further contact in the event of new symptoms suggesting a recurrence. Personally, we usually perform another endoscopy at that time as a guidance for the decision whether to give maintenance treatment or not. If we find an ulcer or signs of duodenitis, we give another 4-6 weeks course of cimetidine.(ABSTRACT TRUNCATED AT 250 WORDS)

Cimetidine↗
PubMed1984

Cimetidine or parietal-cell vagotomy in patients with juxtapyloric ulcers.

83 patients with severe juxtapyloric ulcers were randomly allocated to either long-term cimetidine treatment (400-800 mg/day) or to parietal-cell vagotomy (PCV). All were followed up for more than 3 years. The endoscopically proven relapse-rate with a dose of 400 mg at bed time was 54%; it fell to 32% when the dose was increased to 400 mg twice a day. In the PCV group the relapse-rate was 33%. Patients with prepyloric ulcers alone or in combination with duodenal ulcers relapsed at a higher rate (57% and 82%, respectively) than did patients with "pure" duodenal ulcer disease (17% and 14%, respectively). No patient, not even those with a history of bleeding or perforated ulcers, experienced any bleeding or perforation during relapses, either when on long-term cimetidine treatment or after operation. Previous haemorrhage or perforation per se is thus not an indication for surgery in favour of maintenance treatment with cimetidine.

Adult↗
PubMed1981

Antacid/anticholinergic, cimetidine, and placebo in treatment of active peptic ulcers.

Seventy-two patients with duodenal (54) or prepyloric (18) ulcers have taken part in a 12-week double-blind trial. Twenty-four patients received cimetidine, 1 g/day; 24 patients received 10 ml of an antacid suspension (buffering 85 mmol acid) 1 and 3 h after every meal and at bedtime and 0.6 mg L-hyoscyamine in sustained-release tablets twice a day; and 24 patients received placebo. The healing rate after 3 weeks' treatment was 67% (p less than 0.005 compared with placebo) with cimetidine, 50% (p less than 0.01) with antacid/anticholinergic, and 13% with placebo. After 6 weeks' treatment 83% were healed with cimetidine (p less than 0.005 compared with placebo), 96% with antacid/anticholinergic (p less than 0.005), and 33% with placebo. A further 6 weeks' treatment gave healing rates of 96% for cimetidine, of 100% for antacid/anticholinergic, and of 50% for placebo. Compared with placebo, cimetidine but not antacid/anticholinergic caused a faster relief of night-time ulcer pain (p less than 0.05). There was a significant correlation between healed ulcers and complete relief of ulcer symptoms (p less than 0.05). In the placebo group the ulcers of nonsmokers healed to a higher extent than those of smokers (p less than 0.05). During 1 year of follow-up there was no difference between the two actively treated groups in number or severity of symptomatic relapses. Time to relapse was, however, significantly shorter after treatment with cimetidine than after antacid/anticholinergic (p less than 0.05). Recurrences occurred more often (p less than 0.05) after slow healing (6-12 weeks) than after fast healing (3 weeks).

Aluminum Hydroxide↗
PubMedDate not supplied

Laboratory evaluation of the TDx assay for detection of cannabinoids in urine from prison inmates.

The TDx (Abbott Laboratories) and the EMIT-Cobas (Syva Corp. & Roche) techniques for cannabinoid assay were evaluated. Authentic urine samples submitted for narcotics screening were analyzed for cannabinoids. All positive findings were confirmed by an HPLC procedure. The results indicated that the EMIT assay detects a few more positive samples, but also yields a higher rate of unconfirmed positive results compared to the TDx. Those additional "true" positives by EMIT had concentrations of the delta 9-THC-11-carboxylic acid below 10 ng/mL.

Cannabinoids↗