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Biomedical subjects

B Kollberg

Publications and source records attributed to B Kollberg.

At least 19 recordsLinked to original sources
PubMed1996

Oral budesonide versus prednisolone in patients with active extensive and left-sided ulcerative colitis.

BACKGROUND & AIMS: Systemic glucocorticosteroids (GCSs) have proven efficacy in active ulcerative colitis but cause undesired systemic side effects. Therefore, new GCSs with high topical activity and a high rate of metabolism may be of clinical value in this condition. The aim of this study was to explore the efficacy and safety of the topically acting GCS budesonide in an oral controlled-release formulation in extensive or left-sided, mild to moderately active ulcerative colitis. METHODS: A 9-week, randomized, double-blind, controlled trial was performed, and treatments with 10 mg budesonide or 40 mg prednisolone daily, both gradually tapered, were compared. Endoscopic improvement and effect on endogenous plasma cortisol were assessed. RESULTS: Thirty-four patients were administered budesonide, and 38 patients were administered prednisolone. Mean endoscopic scores improved significantly in both groups but without difference between the groups. Five patients in the budesonide group and 7 patients in the prednisolone group deteriorated and were withdrawn from the study. Morning plasma cortisol levels were suppressed in the prednisolone group (entry, 449 nmol/L; 2 weeks, 116 nmol/L; 4 weeks, 195 nmol/L) but were unchanged in the budesonide group. CONCLUSIONS: The GCS budesonide administered in an oral controlled-release formulation seems to give an overall treatment result in active ulcerative colitis approaching that of prednisolone but without suppression of plasma cortisol levels. This concept merits further evaluation.

Administration, Oral↗
PubMed1995

Circulating granulocyte antibodies in first attacks of colitis.

BACKGROUND: Antineutrophil cytoplasmic antibodies (ANCA) have recently been demonstrated in the sera of patients with inflammatory bowel disease (IBD). METHODS: The presence of ANCA was studied in 107 sera obtained during 1 year from 48 patients with a first attack of IBD and in 33 such sera from 19 patients with infectious or infectious-type colitis (non-relapsing colitis (NRC)). RESULTS: In 65% (31 of 48) of the IBD patients positive immunofluorescence reactivity against granulocytes was observed, compared with in 5% of the NRC patients. No significant difference in granulocyte reactivity was found either between patients with colonic Crohn's disease and those with ulcerative colitis or between active and inactive phases of the disease. Most of the sera showed a perinuclear immunofluorescence staining pattern (68%), in contrast to the classical cytoplasmic staining pattern seen in Wegener's granulomatosis. In sera obtained at the first visit from the 31 IBD patients with positive granulocyte reactivity a hitherto unknown antibody against beta-glucuronidase was found in 42%, whereas in 45% the specificity was not identified. Other antibodies, rarely seen, were directed against myeloperoxidase, lactoferrin, elastase, and cathepsin G. No antibody directed against lysozyme was detected. CONCLUSIONS: Positive granulocyte reactivity practically excluded NRC and was seen in more than half of IBD patients. Antibodies against beta-glucuronidase were common, but still almost half of the antibodies remained unknown.

Adult↗
PubMed1995

Olsalazine versus sulphasalazine for relapse prevention in ulcerative colitis: a multicenter study.

OBJECTIVE: To compare the relapse-preventing effect and the frequency of adverse events of olsalazine and sulphasalazine in sulphasalazine-tolerant patients with ulcerative colitis. METHODS: Patients in remission, with at least two episodes of active disease during the last 5 yr, were randomized to 2 g of sulphasalazine or 1 g of olsalazine daily and were followed for 6-18 months. Relapse rates in the two groups were compared using frequency and life-table analysis. Sixty-nine patients with proctitis, 140 with left-sided colitis, and 113 with subtotal or total colitis were evaluated. RESULTS: In the intention-to-treat analysis, the failure rate (relapses plus withdrawals) was 54.7% in the olsalazine and 47.2% in the sulphasalazine group. In the per-protocol analysis excluding withdrawals, 44.7% relapsed in the olsalazine and 39.3% in the sulphasalazine group. Remission curves did not differ significantly, although at all time intervals the frequency of remission was slightly higher in the sulphasalazine group (p = 0.19 in the intention-to-treat analysis and p = 0.42 in the per-protocol analysis estimated by the log-rank test). Twelve patients (of whom five had diarrhea) in the olsalazine group versus eight patients in the sulphasalazine group discontinued the study because of side effects. CONCLUSION: The relapse-preventing effect of olsalazine and sulphasalazine in sulphasalazine-tolerant patients did not differ. Furthermore, the tolerability of olsalazine, particularly concerning diarrhea, appears to be better than previously reported.

Adult↗
PubMed1994

A prospective study of first attacks of inflammatory bowel disease and infectious colitis. Clinical findings and early diagnosis.

In 105 patients with a first attack of colitis, clinical, microbiologic, laboratory, and histologic features were studied prospectively with the aim of differentiating inflammatory bowel disease (IBD) from infectious colitis as early as possible. Of the patients who proved to have IBD the mode of onset of diarrhoeal symptoms was insidious in 56% and non-insidious in 44%, whereas in 81% of those who proved to have infectious colitis the onset was acute. Most patients with infectious colitis presented within 1 week, had early fever, and did not show histologic features characteristic of IBD. Most IBD patients with a more acute onset had clinical warning signs of IBD such as slight previous bowel symptoms, a late presentation time (> 1 week), and absence of early fever or had histologic features characteristic of IBD. These features were basal plasmacytosis, crypt distortion, more than two vertical crypt branches, villous mucosa, mucosal atrophy, epithelioid granuloma, and Paneth cell metaplasia. Moreover, 61% of the IBD patients with a non-insidious onset fell ill in connection with travelling abroad, gastrointestinal infection, or treatment with antibiotics. Knowledge of the above clinical and histologic factors will facilitate differentiation of IBD from infectious-type colitis.

Adolescent↗
PubMed1994

A prospective study of first attacks of inflammatory bowel disease and infectious colitis. Histologic course during the 1st year after presentation.

To investigate the possibilities of differentiating between inflammatory bowel disease (IBD) and infectious colitis on histologic grounds, a prospective histologic study of 105 patients with a first attack of colitis was undertaken. Rectal biopsies were performed on four occasions during 1 year. The strongest predictor of IBD was basal plasmacytosis, followed by more than two vertical crypt branches per medium-power field, crypt distortion, villous mucosa, and mucosal atrophy. These signs were rarely found among patients with infectious colitis. Their frequency increased with the interval between initial symptoms and the first biopsy. To study the development of histologic features in the absence of treatment, the IBD patients were divided into groups depending on this interval. Focal or diffuse basal plasmacytosis increased from 38% in the group with an interval of 1-15 days to 89% in those who presented in 121-300 days, and crypt distortion from 0% to 78%, whereas absence of signs indicating IBD decreased from 62% to 11%. The presence of focal basal plasmacytosis seems to be the earliest sign of IBD. The frequency of histologic signs indicating IBD was maximal (88%) at the 1-week biopsy. After recovery, the basal plasmacytosis and villous mucosa decreased, whereas crypt distortion and mucosal atrophy remained unchanged. Early treatment did not prevent the appearance of any feature.

Adult↗
PubMed1993

A prospective study of first attacks of inflammatory bowel disease and non-relapsing colitis. Microbiologic findings.

In 105 patients with a first attack of colitis, thorough microbiologic investigations of rectal biopsy, faecal, and serum samples were performed with the aims of identifying the colitis-causing agents and shedding light on factors that may precipitate or aggravate the onset of inflammatory bowel disease. Sixty-one patients were found to have inflammatory bowel disease. In 13 (21%) of these patients microbial findings were positive. Eight of the 61 patients fell ill during or immediately after antibiotic treatment, and 10 while travelling abroad. Forty-one of the 105 patients had non-relapsing colitis. In 32 (78%) of these the microbial findings were positive. Six of these 41 patients fell ill during or immediately after antibiotic treatment, and 14 while travelling abroad. Alteration of the intestinal microflora on travelling, gastrointestinal infection, or treatment with antibiotics seems to precipitate or aggravate the symptoms in latent inflammatory bowel disease. In such patients the mode of onset is often changed from insidious to more acute, which may cause difficulty in differentiation from non-relapsing colitis.

Acute Disease↗
PubMed1991

Clinical and histologic features differentiating non-relapsing colitis from first attacks of inflammatory bowel disease.

This is a study of first attacks of colitis, evaluating prospectively the overall course with repeated histologic, clinical, laboratory, and initial microbiologic examinations. Forty-two attacks of colitis could after a follow-up period of 5.5 years be separated into relapsing and non-relapsing types. Relapse was chosen as a prerequisite for a final diagnosis of inflammatory bowel disease. In the non-relapsing group 72% of the patients harboured enteropathogenic bacteria. An insidious onset of diarrhoeal symptoms was highly discriminant of inflammatory bowel disease, whereas an acute onset mostly occurred in patients with non-relapsing colitis. Macroscopic differentiation at sigmoidoscopy was not possible. Distorted crypt architecture (92%) and/or basal plasmacytosis (77%) at initial biopsies strongly indicated inflammatory bowel disease but was also found transiently in patients with infectious colitis (19%). Thus, careful microbiologic and clinical investigation and repeated histologic examinations are necessary to distinguish infectious colitis from inflammatory bowel disease.

Adult↗
PubMed1991

The effect of omeprazole and ranitidine on ulcer healing, relief of symptoms, and incidence of adverse events in the treatment of duodenal ulcer patients.

In a Swedish double-blind multicenter study involving 143 patients, the new proton pump inhibitor omeprazole (30 mg taken as a single morning dose) was compared with ranitidine (400 mg b.i.d.). Clinical assessment and laboratory investigations were carried out at 2 and 4 weeks, and again at 6 weeks if patients had not healed earlier. Endoscopy was repeated at two-weekly intervals until the ulcer was healed. The patients in the two treatment groups were well matched prior to treatment. There was a higher ulcer healing rate in the omeprazole group (70%) than in the ranitidine group (55%) after two weeks of treatment. This difference reached statistical significance in 128 patients adhering to the protocol as shown by a logit model analysis with drug, ulcer size and smoking as the prognostic factors (p = 0.04). There were no major differences between the two treatment groups in terms of symptomatic relief. Both drugs were generally well tolerated, and the number of adverse events in the two treatment groups were similar. After healing, 127 patients entered a follow-up study, with endoscopy either after 6 months or on recurrence of symptoms. There was no significant difference between the two treatment groups, with the relapse frequency within 6 months being 39% in the omeprazole group and 47% in the ranitidine group. These results, with a 15 percentage points higher ulcer healing rate for omeprazole as compared with H2-receptor antagonists after two weeks, are in accordance with results reported in other studies.

Duodenal Ulcer↗
PubMed1987

Hepatotoxicity associated with low-dose, long-term methotrexate treatment of rheumatoid arthritis.

Liver biopsies were performed in 17 patients with therapy-refractory rheumatoid arthritis who were treated successfully with 5-15 mg/week methotrexate (mtx). The average duration of exposure to mtx therapy for each patient was 2.8 years (range 1.5-5 years). Total cumulative mtx doses ranged between 633 and 1,655 mg (mean 1,060 mg). The biopsies revealed 16 cases of normal histology, of which 3 showed nuclear variability in the hepatocytes; 4 with mild fatty infiltration, 2 with mild fatty infiltration and portal round cell infiltration. Portal fibrosis was found in one patient who had psoriasis in addition to clinical RA.

Adult↗
PubMed1982

The effect of prostaglandin E2 on duodenal ulcer healing.

Oral prostaglandin E2 (PGE2) has specific protective effects so called cytoprotection on the gastrointestinal mucosa that are independent of the acid secretion. This has recently been documented in man. A clinical study was performed to test whether this mucosal reinforcing property also could be used to accelerate duodenal ulcer healing. Twenty-eight patients with endoscopically confirmed duodenal ulcers were randomized to treatment with PGE2 0.5 mg three times daily and 1 mg at night or to placebo under double-blind conditions during a four week period. To reduce antacid consumption a fluid placebo antacid was given regularly. An active antacid could be used for pain relief. Healing rate was assessed with repeated endoscopies after 2 and 4 weeks. The treatment groups were comparable with respect to age, duration of ulcer history and present ulcer symptoms, smoking habits, family history, gastric acid secretory rate and number of patients with blood group 0. There was a slight difference in sex distribution. 2 mg PGE2 did not reduce pentagastrin-stimulated acid secretion in five of the patients. After the treatment significantly more in the PGE2-group (12/14, 86%) had healed than in the placebo-group (6/14, 43% P less than 0.05). There was no difference in pain relief between PGE2 and placebo-treated. The antacid consumption was very low in both PGE2 and placebo-treated. No significant side effects or changes in laboratory test-results were recorded. It is suggested that the cytoprotective effect of PGE2 can be used to accelerate healing of duodenal ulcer.

Administration, Oral↗
PubMed1981

Protection of the rat gastric mucosa by prostaglandin E2: possible relation to stimulation of the alkaline secretion.

Exogenous prostaglandins have specific protective effects on the gastric mucosa called cytoprotection which is proposed to be connected to the stimulatory effects of prostaglandins on the gastric nonparietal secretions. The protection by oral prostaglandin E2 (PGE2) against indomethacin-induced gastric erosions was studied in the rat, as was the effect on the protection of blocking the gastric alkaline secretion by acetazolamide. PGE2 reduced dose-dependently the indomethacin gastric erosion formation, confirming previous results from others. Acetazolamide caused very little damage when given alone but potentiated the indomethacin erosion formation in a dose-related way. PGE2 was less protective or without effect against lesions caused by indomethacin when given together with acetazolamide, but protection could be obtained by increasing the doses of PGE2. Indomethacin and acetazolamide are both blockers of the gastric bicarbonate secretion, which is stimulated by PGE2. The potentiation of indomethacin induced lesions by acetazolamide and the antagonistic actions between acetazolamide and PGE2 on mucosal protection are compatible with the hypothesis that stimulation of the alkaline secretion is one mechanism of cytoprotection of the gastric mucosa by PGE2.

Acetazolamide↗
PubMed1981

Effects of graded doses of somatostatin on gallbladder emptying and pancreatic enzyme output after oral glucose in man.

Effects of intravenous somatostatin on the secretion, motility and absorption in the upper gastrointestinal tract after 75 g oral glucose were examined in healthy subjects with a quantitative multiple indicator dilution method. This report deals with the effects on the gallbladder emptying and the pancreatic enzyme output. Intake of a hypertonic glucose solution induces rapid gallbladder emptying. After early peaks, both biliary and pancreatic enzyme outputs remain at a steady lower level to the end. Somatostatin, started 20 min before the oral load, inhibited dose-dependently the gallbladder emptying and pancreatic enzyme secretion. A maximal inhibition was attained by 1.5 microgram . min-1, and 0.05 microgram . min-1 somatostatin gave a significant 40% reduction. The inhibition persisted in the postinfusion period and was followed by delayed rebound outputs. The gallbladder emptying was completely arrested for variable periods of time, but the pancreatic enzyme secretion was never totally blocked. The promptly established arrest of the gallbladder differed from the slowly initiated inhibition of the gastric and intestinal propulsion. It is proposed that the multiple ways of action of somatostatin and different stimulatory levels contribute to the discrepancies. The study shows that somatostatin induces dose-dependent, long-lasting inhibitions of the biliary and pancreatic responses to oral glucose. The minimal effective dose was a hundred times lower than the dose tested in previous studies in man.

Administration, Oral↗