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Biomedical subjects

K Seppälä

Publications and source records attributed to K Seppälä.

At least 19 recordsLinked to original sources

The efficacy of bovine lactoferrin in the treatment of cows with experimentally induced Escherichia coli mastitis.

The effect of bovine lactoferrin (Lf) was studied in experimental Escherichia coli mastitis, using enrofloxacin as a comparator. Mastitis was induced in six clinically healthy primiparous dairy cows by infusing 1500 colony-forming units of E. coli into a single udder quarter. The challenge was repeated into a contralateral quarter of the same cows 3 weeks later. At the first challenge, three cows were treated with 1.5 g of bovine lactoferrin intramammarily three times (12, 20 and 36 h postchallenge, PC), and the other three cows received 5 mg/kg of enrofloxacin (Baytril) parenterally (12, 36 and 60 h PC). Flunixin meglumine (2.2 mg/kg) was administered to all cows twice at 24-h intervals. During the second challenge, the treatments for the two groups were reversed. Intramammary challenge with E. coli produced clinical mastitis in all cows, but the severity of the disease varied markedly. No statistically significant differences between treatment groups were observed in clinical signs such as rectal temperature, rumen motility and general attitude. Milk somatic cell count, daily milk yield and bacterial counts in cows treated with Lf and those receiving enrofloxacin also did not differ significantly. However, a trend for a more rapid elimination of bacteria was seen in the cows treated with enrofloxacin. Milk NAGase activity also decreased significantly faster in the group treated with enrofloxacin. The concentration of lipopolysaccharide in milk compared with the number of bacteria was significantly lower in Lf than in enrofloxacin-treated cows (20 h PC).

Administration, Oral↗

Active treatment of chronic neck pain: a prospective randomized intervention.

STUDY DESIGN: A randomized comparative study with single-blind outcome assessments. OBJECTIVES: To compare the efficacy of a multimodal treatment emphasizing proprioceptive training (ACTIVE) with activated home exercises (HOME) and recommendation of exercise (CONTROL) in patients with nonspecific chronic neck pain. SUMMARY OF BACKGROUND DATA: The efficacy of active exercises and passive physiotherapy for neck trouble has been somewhat disappointing in the previous few studies. METHODS: Seventy-six patients (22 men, 54 women) with chronic, nonspecific neck pain participated. Sixty-two participated the 1-year follow-up. Subjective pain and disability, cervical ranges of motion, and pressure pain threshold in the shoulder region were measured at baseline, at 3 months, and at 12 months. The ACTIVE treatment consisted of 24 sessions of proprioceptive exercises, relaxation, and behavioral support. The HOME regimen included a neck lecture and two sessions of practical training for home exercises and instructions for maintaining a diary of progress. The CONTROL treatment included a lecture regarding care of the neck with a recommendation to exercise. RESULTS: The average self-experienced total benefit was highest in the ACTIVE group, and the HOME group rated over the CONTROL group (P < 0.001). Differences between the groups in favor of the ACTIVE treatment were recorded in reduction of neck symptoms and improvements in general health and self-experienced working ability (P < 0.01-0.03). Changes in measures of mobility and pressure pain threshold were minor. CONCLUSIONS: Regarding self-experienced benefit, the multimodal treatment was more efficacious than activated home exercises that were clearly more efficacious than just advising. No major differences were noted in objective measurements of cervical function between the groups, but the content validity of these assessments in chronic neck trouble can be questioned.

Adult↗

Cure of Helicobacter pylori infection after failed primary treatment: one-center results from 120 patients.

BACKGROUND: Treatment with a proton pump inhibitor (PPI) and antimicrobials cures Helicobacter pylori infection in about 90% of patients. This is a retrospective overview of our studies aiming to cure the infection in all compliant patients with failed initial therapy. METHODS: We retreated 120 (19% of 644) H. pylori-infected patients whose initial therapy had failed. The retreatments included (i) triple therapy (TT): colloidal bismuth subcitrate, metronidazole, amoxicillin (or tetracycline); (ii) quadruple therapy (QT): TT and a PPI; or (iii) high doses of both a PPI and clarithromycin combined with a further 1-3 individually selected antimicrobials. The eradication results were determined after 6-12 months. RESULTS: The 1st retreatment was successful in 70 of 120 patients. The 2nd retreatment cured 25 of the remaining 42 patients, the 3rd 13 of 17, and the 4th the last 4 patients. The cumulative eradication rate (ITT) was 93% (95% CI: 88.9%-97.9%; 8 patients withdrew after a failed 1st retreatment) and the rate was 100% in the remaining 112 patients who accepted several retreatments. The 1st retreatment with TT cured 23% (95% CI: 12%-34%) of 57 patients and QT 85% (95% CI: 74%-96%) of 41 patients who had initially undergone a failed metronidazole-based treatment. All retreatments were well tolerated. CONCLUSIONS: In this study, high doses of a PPI and clarithromycin combined with 1-3 antimicrobials according to susceptibility data proved to be the best drug combination in the cure of H. pylori infection after failed primary treatment. Giving imidazole- and bismuth-based QT (without clarithromycin) as the first-line treatment of H. pylori infection ensures that the number of failures remains low.

Anti-Bacterial Agents↗

Duodenal secretion of phospholipase A2, amylase, and bicarbonate in chronic pancreatitis.

Phospholipase A2 has been suggested to be involved in the pathogenesis and pathophysiology of acute pancreatitis. We determined phospholipase A2 and amylase activities in duodenal juice collected during a secretin test from 30 consecutive patients who were suspected to have chronic pancreatitis or biliary disease. The patients underwent endoscopic retrograde cholangiopancreatography (ERCP) the following day. In the 8 patients with ERCP findings of advanced chronic pancreatitis, the mean outputs of phospholipase A2, amylase, and bicarbonate were reduced by 74%, 72%, and 60% compared to the respective values in the 13 (control) patients without a diagnosis of any pancreatic disorder or jaundice. In the 3 patients with recurrent pancreatitis but normal ERCP findings and in the 6 patients with jaundice the output values were not significantly reduced compared to those in the patients without any pancreatic disorder or jaundice. The outputs of amylase and phospholipase A2 were not significantly interrelated, whereas the outputs of phospholipase A2 and bicarbonate correlated well. Receiver characteristic (ROC) curves confirmed the high specificity and sensitivity of phospholipase A2 or bicarbonate output in patients with ERCP findings of advanced chronic pancreatitis compared to those with no changes in pancreatic ducts, with similar probability values of 0.880 +/- 0.111 (SEM), compared to the respective lower value of amylase, 0.676 +/- 0.118. Phospholipase A2 and bicarbonate output proved of equal value as markers of chronic pancreatitis and were superior to amylase output in the secretin test.

Acute Disease↗

Long-term treatment of ulcerative colitis with ciprofloxacin: a prospective, double-blind, placebo-controlled study.

BACKGROUND & AIMS: Although bacterial bowel flora may be one of the contributing factors in the pathogenesis of chronic mucosal inflammation, antibiotic treatment has no established role in ulcerative colitis. The aim of the study was to evaluate the role of ciprofloxacin in the induction and maintenance of remission in ulcerative colitis in patients responding poorly to conventional therapy with steroids and mesalamine. METHODS: Ciprofloxacin (n = 38; 500-750 mg twice a day) or placebo (n = 45) was administered for 6 months in a double-blind, randomized study with a high but decreasing dose of prednisone and maintenance treatment with mesalamine including follow-up for the next 6 months. Clinical assessment and colonoscopic evaluation were performed at 0, 3, 6, and 12 months. Treatment failure, the primary end point, was defined as both symptomatic and endoscopic failure to respond. RESULTS: During the first 6 months, the treatment-failure rate was 21% in the ciprofloxacin-treated group and 44% in the placebo group (P = 0.02). Endoscopic and histological findings were used as secondary end points and showed better results in the ciprofloxacin group at 3 months but not at 6 months. CONCLUSIONS: Addition of a 6-month ciprofloxacin treatment for ulcerative colitis improved the results of conventional therapy with mesalamine and prednisone.

Adult↗

Review article: Pathogenesis of the transformation from gastritis to malignancy.

Helicobacter pylori acquisition is the main cause of chronic gastritis in humans. In up to half of the infected subjects, chronic gastritis progresses to atrophic gastritis and intestinal metaplasia. During this course, various mechanisms are triggered that may contribute to the pathogenesis of gastric cancer. Such mechanisms include the inflammation-related cascades of cytokine and free radical reactions, up- and downregulation of growth factors and their receptors, and the atrophy-related impairment of acid output and intraluminal acidity. An array of other factors may also have become significant including overgrowth of bacteria other than H. pylori in the hypochlorhydric or achlorhydric stomach, a high dietary consumption of salt, nitrate, or nitrite, smoking, deficiency of vitamins or micronutrients, influence of sex hormones, or an inherited liability of the dividing epithelial cells to gene errors. These factors may vary in effect between populations and individuals but, if active, may affect the cell genome which may further influence the course and progression of chronic gastritis, and can finally result in overt gastric neoplasia. The molecular biology of gastric cancer has revealed a spectrum of gene errors which vary in type and extent between different histological types of cancer, and between individual cases. There now is evidence that the intestinal metaplasia or the gastric epithelium in atrophic gastritis reveal signs of abnormal expression of various regulatory genes well before the appearance of gastric neoplasia. It is possible that the mechanisms leading to mutation of the genes in epithelial cells are triggered very early in the H. pylori gastritis cascade, and that atrophic gastritis and intestinal metaplasia result from these processes.

Animals↗

Culture of Helicobacter pylori from gastric biopsies transported in biopsy urease test tubes.

Gastric biopsy specimens of 57 consecutively observed dyspeptic patients were studied for the presence of Helicobacter pylori by histological examination, biopsy urease test (BUT) and culture. For culture, biopsy samples were transported in both Stuart media and BUT tubes. All 15 isolates could be cultured from both Stuart and BUT tubes. Thus, if the main reason for culture of Helicobacter pylori is for antimicrobial susceptibility testing, only positive BUT tubes need to be submitted. This would reduce both the expense and the number of biopsies needed.

Adult↗

The relationships between chronic gastritis and gastric acid secretion.

Helicobacter pylori is the main cause of chronic gastritis in humans. Autoimmune mechanisms and Helicobacter heilmannii infection are other causes, both of which are of minor significance in a worldwide perspective. Atrophic gastritis is a quite common late consequence of H. pylori gastritis and will develop on a multifactorial basis, but not in all infected persons. The evolution of atrophic gastritis is a slow and gradually worsening process leading to subtypes, in which the antrum and corpus are affected to dissimilar extent and degree. The distal part of the stomach is the site where the atrophic sequelae (atrophic gastritis and intestinal metaplasia) of H. pylori infection occur most often. A minority of cases develop corpus-limited, or corpus-predominant atrophic gastritis. Along with the worsening of atrophic gastritis, inflammation and density of colonization of the mucosa by H. pylori tend to decrease in grade. In general, the degree of gastric mucosal inflammation, acute and chronic, is positively related to the degree of colonization of the mucosa by H. pylori. Acid secretion and local acidity are factors which modulate the ecology and density of colonization of H. pylori in the stomach, and may thus also modulate the evolution of chronic gastritis into topographically dissimilar subtypes. Acid secretion varies among individuals, this variation being perhaps caused by hereditary differences in parietal cell mass, or by differences in the sensitivity of parietal cells to hormonal or neural stimuli. It is hypothesized that in genuine hypersecretors, H. pylori colonization and subsequent gastritis with atrophic and metaplastic sequelae may be limited to the antrum, while in hyposecretors gastritis predominates in the corpus. In the latter, atrophic gastritis in the corpus then leads to further impairment of acid output. In these cases, H. pylori infection and gastritis may, finally, heal in the antrum, resulting in hypochlorhydria and atrophic gastritis that is limited to, or predominant in the corpus.

Adolescent↗

Gastric inflammation and neutrophil-activating and cytotoxin-producing Helicobacter pylori strains.

BACKGROUND: Some Helicobacter pylori strains activate human neutrophils without opsonins and/or produce vacuolating cytotoxin. METHODS: Human gastric isolates of H. pylori were studied for their ability to nonopsonized induce an oxidative burst in human neutrophils as measured by chemiluminescence and for the production of vacuolating cytotoxin. In all, 80 strains were examined, and the type and grade of inflammation in the gastric biopsy specimens from the antrum and corpus of these patients were assessed in accordance with the Sydney system. RESULTS: CL+ (rapid, strong response in chemiluminescence) strains (p < 0.0001) and Tox+ (cytotoxin-producing) strains (p < 0.0001) were associated with higher acute inflammation scores in gastric ulcer patients. CL+ (p = 0.0002) and Tox+ (p < 0.0001) strains were also associated with higher chronic inflammation scores in gastric ulcer patients. CONCLUSIONS: CL+ and Tox+ strains seem to cause more severe inflammation in the gastric mucosa during H. pylori infection.

Cytotoxins↗

A placebo-controlled trial of primary biliary cirrhosis treatment with colchicine and ursodeoxycholic acid.

BACKGROUND/AIMS: Ursodeoxycholic acid (UDCA) and colchicine have beneficial effects in primary biliary cirrhosis (PBC). The efficacy of colchicine and UDCA in PBC was compared in a 2-year placebo-controlled study (n = 90). METHODS: Clinical events, laboratory test results, and liver histology were recorded at the beginning and end of the trial. RESULTS: There were significantly fewer dropouts for hepatic reasons with UDCA than with placebo. Pruritus was reduced by both active drugs. Colchicine improved liver function test results only modestly, whereas UDCA significantly decreased the serum activities of aminotransferases, alkaline phosphatase, and gamma-glutamyltransferase compared with colchicine and placebo. Serum total bilirubin levels were decreased only by UDCA. Both colchicine and UDCA reduced serum cholesterol levels, and UDCA also reduced high-density lipoprotein cholesterol levels. Furthermore, UDCA reduced the serum levels of immunoglobulin (Ig) M and IgG, and colchicine reduced IgG levels compared with placebo. The elevated serum level of aminoterminal propeptide of type III procollagen remained unchanged by colchicine or UDCA, whereas the serum level of carboxyterminal propeptide of type I procollagen was significantly decreased by UDCA. UDCA significantly decreased ductular proliferation compared with colchicine or placebo. CONCLUSIONS: These data suggest that UDCA frequently is superior to colchicine and especially to placebo in the treatment of PBC.

Alanine Transaminase↗

Cure of peptic gastric ulcer associated with eradication of Helicobacter pylori. Finnish Gastric Ulcer Study Group.

The effect of Helicobacter pylori eradication on ulcer healing and the relapse rate were investigated in a multicentre trial of 239 gastric ulcer patients. Patients with H pylori positive gastric ulcer were randomly assigned to one of three groups: (A) 10 days' treatment with metronidazole and eight weeks' treatment with colloidal bismuth subcitrate (CBS) (84 patients); (B) 10 days' treatment with metronidazole placebo and eight weeks with CBS (73 patients); or (C) ranitidine (82 patients). At 12 weeks in 210 patients, gastric ulcer was present in three (9%) of 35 H pylori negative patients, and in 45 (26%) of 175 H pylori positive patients (p < 0.05). Results after one year of follow up were available for 205 patients. Between 12 and 52 weeks, two (7%) ulcer relapses occurred in 29 H pylori negative patients and in 60 (47%) of 128 H pylori positive patients (p < 0.001). After two weeks of open triple therapy (CBS 120 mg four times daily, amoxicillin 500 mg four times daily, and metronidazole 400 mg three times daily), given to the patients with ulcer relapse, only one (an NSAID user) of 55 successfully treated patients had an ulcer relapse during the one year follow up. Healing of gastric ulcer is rapid and recurrence is infrequent after successful H pylori eradication. H pylori eradication changes the natural history of the gastric ulcer disease.

Adult↗

New options in eradication of Helicobacter pylori.

Better treatment options to eradicate Helicobacter pylori are needed, while we await a possible effective vaccine against the world's most common infection. The goals of therapy for H. pylori infection should be an effective and low-cost therapy with a low frequency of side-effects. The currently available eradication regimens are cumbersome, which can lead to a reduction of compliance and a lower efficacy. More recent studies have shown, however, that the duration of antimicrobial treatment may be shortened, which also makes the treatment more cost-effective and more tolerable. At this point it seems relevant to treat H. pylori infection first with some antisecretory modification of triple therapy, while the therapeutic failures can be treated with other more relevant and suitable alternatives. Metronidazole is still a cornerstone of triple therapy and the more expensive clarithromycin is an alternative second-line treatment. Time will show the effectiveness and suitability of the latest topical 1-day treatments.

Helicobacter Infections↗

Serum cholestanol, cholesterol precursors, and plant sterols during placebo-controlled treatment of primary biliary cirrhosis with ursodeoxycholic acid or colchicine.

A randomized placebo-controlled 2-year study was performed in 69 patients with primary biliary cirrhosis (PBC) on serum lipids during ursodeoxycholic acid (URSO) and colchicine treatments. In addition to serum bilirubin and alkaline phosphatase (AFOS), two variables considered to reflect liver function, serum lipoproteins, cholesterol precursors (squalene, delta 8-cholestenol, lathosterol and desmosterol), markers of cholesterol synthesis, cholestanol and plant sterols (campesterol and sitosterol), markers of liver function and cholesterol absorption, were studied before and during the treatments. Serum bilirubin was inconsistently improved by URSO, whereas improvement of AFOS values was better by URSO than colchicine, especially in patients with initially more advanced PBC. Serum total cholesterol was reduced by both drugs, very low-density lipoprotein (VLDL) and high-density lipoprotein (HDL) cholesterol by URSO. Cholesterol precursor sterols were increased by both URSO and colchicine mainly in patients with initially less severe PBC. On the other hand, the cholestanol values were markedly increased initially, and the values were related to bilirubin during the 2-year period, were further increased in the placebo group, and reduced in the URSO and colchicine groups, so that the improvement was highest in the URSO-treated patients with the severe form of PBC. The increase of the serum plant sterols, particularly that of sitosterol, was retarded by the two drugs so that the campesterol/sitosterol ratio, which was related to serum bilirubin, was increased especially in the cases with initially more advanced PBC.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗

High frequency of silent inflammatory bowel disease in spondylarthropathy.

OBJECTIVE: To search for an association between gut infection, gut inflammation, and spondylarthropathies. METHODS: Ileocolonoscopy was performed in 118 patients with various inflammatory and noninflammatory joint diseases and in 24 patients with uncomplicated acute bacterial gastroenteritis. RESULTS: Endoscopic lesions were more frequent in patients with spondylarthropathy (44%) compared with those with other inflammatory arthritides (6%; P = 0.001). Ileal changes were observed only in patients with spondylarthropathy (20% versus 0%; P = 0.01). Inflammatory bowel disease was the endoscopic diagnosis in 19% of the arthritis patients. Possible or definite Crohn's disease was diagnosed in 26% of patients with chronic spondylarthropathy, and ulcerative colitis in 1 patient with rheumatoid arthritis and in 1 with chronic uroarthritis. Histologic evidence of inflammation differed less distinctly than endoscopy findings between patients groups. There was no association of gut lesions with the use of nonsteroidal antiinflammatory drugs or with the presence of HLA-B27. CONCLUSION: Gut inflammation is frequent in patients with spondylarthropathy, and one-fourth of the patients who have chronic disease have early features of Crohn's disease.

Adolescent↗

Budesonide enema in active haemorrhagic proctitis--a controlled trial against hydrocortisone foam enema.

BACKGROUND: The aim was to compare budesonide enema, 2 mg/100 mL (Entocort) and hydrocortisone acetate foam enema, 125 mg (Colifoam) in patients with active haemorrhagic proctitis. METHODS: The trial was a controlled, randomized, investigator-blind study with two parallel groups. Endoscopy, histology and diary cards were used to assess the response to therapy. Safety was assessed by laboratory tests and adverse event recording. RESULTS: Seventy-two patients were included. Investigations were made before treatment and after 2 and 4 weeks. Both treatment groups showed statistically significant improvement in endoscopic scores but significant differences between the groups were not found. In the hydrocortisone group, plasma cortisol was significantly lowered after 4 weeks compared with budesonide. Bowel habits and quality of life variables did not differ between the treatments. The recorded adverse events were mild or moderate and may have been due to the proctitis. CONCLUSIONS: These results suggest that budesonide enema is as effective as hydrocortisone foam enema, but without the potential for side-effects associated with suppression of plasma cortisol.

Adult↗

Ribotyping patterns and emergence of metronidazole resistance in paired clinical samples of Helicobacter pylori.

Metronidazole-susceptible pretreatment isolates and metronidazole-resistant posttreatment isolates of Helicobacter pylori from 11 patients before and after unsuccessful triple therapy consisting of metronidazole, amoxicillin, and colloidal bismuth subcitrate were studied. Ribotyping (rRNA gene restriction pattern analysis) of the isolates demonstrated that all patients except one had identical digest patterns for pre- and posttreatment isolates.

Amoxicillin↗

Fall in the prevalence of chronic gastritis over 15 years: analysis of outpatient series in Finland from 1977, 1985, and 1992.

To investigate whether the occurrence of chronic gastritis (and Helicobacter pylori acquisition) has changed in Finland in the past 15 years, the prevalence rates of chronic gastritis in biopsy specimens in consecutive series of outpatients (aged 20 or more) who had undergone diagnostic upper gastrointestinal endoscopy in 1977 (702 patients), 1985 (1309 patients), or 1992 (1447 patients) were compared. The prevalences of gastritis in these series were also compared with that in a random sample (438 subjects) of people who underwent endoscopy in 1974-76. It seemed that the prevalence of gastritis was significantly lower in the outpatients in 1992 than in the random endoscopy sample in 1974-76. The reduction was most noticeable in young age groups (20-49 years) in which the decline was 38% (drop from 66% to 41%). In addition, it seemed that the prevalence of gastritis was very dissimilar in different birth cohorts. The prevalence was high (70-80%) in 1977, 1985, and 1992 in the cohorts born at the beginning of the century and lower (40-50%) in those born during later decades. The prevalence rates had remained unchanged in the same cohorts over the 15 years (from 1977 to 1992) suggesting that the people had mainly been infected with H pylori and contracted gastritis before the age of 20. In conclusion, gastritis is a cohort phenomenon and its prevalence has fallen in Finland in the last 15 years. This decrease is caused by a decline of the rate of H pylori acquisition in birth cohorts, particularly in childhood and adolescence (below age of 20).

Age Factors↗

Chronic nonatropic ('superficial') gastritis increases the risk of gastric carcinoma. A case-control study.

Atrophic gastritis is a well-known risk condition for gastric carcinoma (GCA). Less is known about the risk of GCA in subjects with nonatrophic ('superficial') gastritis. To investigate this, we estimated the risk of GCA in patients with nonatrophic gastritis as compared with that in subjects with normal, nongastritic mucosa. Two hundred and forty-three consecutive GCA patients and 1408 non-GCA outpatients (controls), for whom histologic data (endoscopic biopsy) of gastric mucosa was available, were included in the study. To estimate the relative risk (RR) of GCA, the odds ratio of gastritis was calculated in patients and controls by adjusting for age and sex. The RR (95% confidence interval) of GCA in patients with nonatrophic antral gastritis and with nonatrophic pangastritis was 1.8 (1.2-2.7) and 2.5 (1.4-4.3), respectively. Correspondingly, the risks of GCA were 9.1 (5.4-15.5) in patients with atrophic antral gastritis or pangastritis (atrophy of any degree) and 4.4 (1.9-10) in those with severe atrophic corpus gastritis (severe corpus limited atrophy of 'A type'). In nonatrophic gastritis the risk of diffuse-type GCA was emphasized, whereas the risk of intestinal-type GCA was emphasized in patients with atrophic gastritis. These results indicate that an increased risk of GCA is not confined to subjects with atrophic gastritis but is also slightly but significantly increased in patients with chronic nonatrophic gastritis.

Adult↗