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Biomedical subjects

P Fric

Publications and source records attributed to P Fric.

At least 19 recordsLinked to original sources
PubMed2006

[Effect of administration of Escherichia coli Nissle (Mutaflor) on intestinal colonisation, endo-toxemia, liver function and minimal hepatic encephalopathy in patients with liver cirrhosis].

The purpose of the study was to verify effects of Escherichia coli Nissle (Mutaflor) on intestinal colonisation, endotoxin levels, hepatic encephalopathy and liver function in patients with liver cirrhosis. The study involved 39 patients (22 taking Mutaflor and 17 taking placebo). Even though the number combination test showed extended reaction time in patients with described minimal hepatic encephalopathy the drop was not significant in the trend evaluation. However, the treated group displayed significant improvement of intestinal colonisation (p < 0.001) and a trend towards significant reduction of endotoxin levels on day 42 (p = 0.07) and improvement of liver function assessed with the Child-Pugh classification on days 42 and 84 (p = 0.06). Probiotic preparations can therefore represent a significant contribution to this group therapy.

Adult↗
PubMed2004

Maintaining remission of ulcerative colitis with the probiotic Escherichia coli Nissle 1917 is as effective as with standard mesalazine.

BACKGROUND AND AIMS: Evidence exists for the pathogenic role of the enteric flora in inflammatory bowel disease. Probiotics contain living microorganisms which exert health effects on the host. We compared the efficacy in maintaining remission of the probiotic preparation Escherichia coli Nissle 1917 and established therapy with mesalazine in patients with ulcerative colitis. PATIENTS AND METHODS: In total, 327 patients were recruited and assigned to a double blind, double dummy trial to receive either the probiotic drug 200 mg once daily (n = 162) or mesalazine 500 mg three times daily (n = 165). The study lasted for 12 months and patients were assessed by clinical and endoscopic activity indices (Rachmilewitz) as well as by histology. The primary aim of the study was to confirm equivalent efficacy of the two drugs in the prevention of relapses. RESULTS: The per protocol analysis revealed relapses in 40/110 (36.4%) patients in the E coli Nissle 1917 group and 38/112 (33.9%) in the mesalazine group (significant equivalence p = 0.003). Subgroup analyses showed no differences between the treatment groups in terms of duration and localisation of disease or pretrial treatment. Safety profile and tolerability were very good for both groups and were not different. CONCLUSIONS: The probiotic drug E coli Nissle 1917 shows efficacy and safety in maintaining remission equivalent to the gold standard mesalazine in patients with ulcerative colitis. The effectiveness of probiotic treatment further underlines the pathogenetic significance of the enteric flora.

Adult↗
PubMed2003

[Celiac sprue (review)].

Celiac sprue may be defined as a model autoimmune disease with known trigger (gluten), a tight genetic linkage (with HLA-DQ2 and HLA-DQ8) and a specific humoral autoimmune response (autoantibodies to tissue transglutaminase, tTG). Gliadin peptides are repeatedly presented to HLA-DQ2 and HLA-DQ8 positive cells and induce an immune response in small-intestinal mucosa. tTG is a specific endomysial autoantigen released during cellular stress and by deamidation of gliadin peptides as well as by binding with them facilitates their interaction with HLA-DQ2 and HLA-DQ8 cells. CS is the consequence of an inappropriate by T-cells mediated immune reaction to gluten. The diagnosis is based on criteria of the European Society of Paediatric Gastroenterology, Hepatology and Nutrition revised in 1990. The availability of sensitive and specific detection methods of serum antibodies to endomysium (AEA) and tTG (AtTGA) was followed by recognition of a broad spectrum of both the clinical presentation and histologic changes of intestinal mucosa in CS. The majority of patients have atypical clinical symptoms. The present prevalence of CS amounts to approximately 1:250. The following forms of CS are distinguished: classic (typical), latent, potential, subclinical, and silent. CS is frequently associated with other diseases and many of them are also of autoimmune origin. Serologic testing is indicated in subjects with atypical symptoms and autoimmune diseases. In cases with distinct suspicion biopsy should be always performed irrespective of the serologic tests. In refractory sprue the cryptic form of enteritis associated T-cell lymphoma should be excluded. Gluten-free diet is the cornerstone of CS therapy. The Alimentary Codex in individual countries admits different amounts of residual gluten in gluten-free products. In future years new basic knowledge as well as practical diagnostic and therapeutic recommendations may be expected.

Celiac Disease↗
PubMed2002

[Probiotics in gastroenterology].

Probiotics are defined as live microorganisms of human origin. Their use may favorably influence human health and ameliorate or prevent certain diseases. Prebiotics are non-digestible foodstuffs (fiber, oligofructans - "colonic foods"), which enter the colon and are metabolized by the probiotics. Probiotics should fulfill the following criteria: Phenotypic and genotypic classification, no pathogenic properties, human origin, application in the living state, resistance to gastric acid and bile, ability to adhere to colonocytes, ability to colonize the gut, clinically proved favorable health-effect, and safety. Experimental and clinical studies supplied evidence of the possible use of probiotics in the following diseases: Traveler's diarrhea, antibiotic-associated diarrhea, relapsing Clostridium difficile colitis, infantile diarrhea, rotavirus enteritis, inflammatory bowel disease, irritable bowel syndrome, colon cancer, peritonitis, acute pancreatitis, and diarrhea associated with HIV infection. Probiotics displayed the following effects in these studies: Involvement in production of essential nutrients of the colonic mucosa, beneficial effect on intestinal immunity, recovery of the disturbed gut mucosal barrier and prevention of microbial translocation, elimination of toxins and eradication of microbial pathogens, production of steroids from cholesterol and reduction of its pool in circulation, participation in regulation of intestinal functions, reduced incidence of chemically induced colon tumors in rodents. Probiotics open new therapeutic modalities in a number of diseases and it may be expected that their importance will increase with growing knowledge and experience.

Colitis↗
PubMed2002

[Screening programs for sporadic colorectal carcinoma].

In developed countries colorectal cancer (CRC) is the second most frequent organ malignancy of both genders. According to the world statistics Czech Republic occupies the top position in incidence of this disease. Approximately 75% of all CRC are the sporadic CRC in subjects with negative family or personal history of the disease. The low (average) risk factor in these subjects is age over 50 years, from which the incidence of CRC nearly doubles in each decade. The following options of screening are available for these subjects: 1. faecal occult blood test (FOBT), 2. flexible sigmoidoscopy, 3. combination of both previous procedures, 4. colonoscopy, 5. virtual colonography. FOBT is the mostly used programme in asymptomatic subjects over age 50 at one-year or at least two-years intervals. In FOBT-positive persons colonoscopy is considered the optimal diagnostic and in the case of polyps also therapeutic method. Prospective randomized studies proving a decrease of CRC-mortality in the range of 15-33% are available only for this type of programme. Screening of sporadic CRC was introduced on national basis in Federal Republic Germany in 1977 and in Czech Republic since the second half of the year 2000. With so many people dying of the disease, we cannot afford not to do its screening.

Colonoscopy↗
PubMed2002

[Conservative therapy of chronic pancreatitis].

Conservative therapy is applied to various extent in all subjects with chronic pancreatitis. It includes removal of the provoking agent (most frequently alcohol abuse and biliary disease), dietary regimen, treatment of pain, maldigestion, and diabetes. Removal of the provoking agent prevents progression of the disease and relieves intensity of the main symptoms, particularly of pain. Diet in remission should include approximately 1g of protein/kg body mass. Fat intake should be encouraged within limits of individual tolerance. With low caloric intake carbohydrates should be enriched up to 65 - 70% of total energy intake. Abdominal pain may be due to a complication or to the underlying disease itself. For this reason one approach cannot be effective in all subjects. Conservative methods represent the first line of pain therapy. They include alcohol withdrawal, analgesics, narcotics and negative trypsin-induced feedback control of pancreatic secretion. Pancreatin medication is the cornerstone of maldigestion therapy. This is indicated with weight loss and/or symptoms associated with steatorrhea or with 15 - 20 g stool fat/day without additional symptoms. The effect may be evaluated by increase of body mass, decrease of loose stools and by markers of the nutritional status. Adequate replacement therapy with pancreatic enzymes influences also elaboration and secretion of some gastrointestinal hormones. The appearance of secondary diabetes makes abstinence from alcohol again mandatory. Food intake should be divided into 5 - 6 daily doses and adequate enzyme replacement should be applied. Peroral antidiabetics may be considered at the early stage, but many of these patients ultimately require insulin therapy. Its dosage should be adjusted to glucose urinary losses rather than to adhere to tight normoglycemia because of the increased risk of hypoglycemia. The therapeutic options in chronic pancreatitis may stabilize the disease and prevent its progression. The patients may be at the best asymptomatic, but not cured.

Humans↗
PubMed2001

Changes of E-cadherin and beta-catenin in human and mouse intestinal tumours.

An immunohistochemical analysis of E-cadherin and beta-catenin was performed in human colorectal cancer as well as in surrounding normal intestinal tissue. We also analysed the expression of these two cell adhesion proteins in transgenic Apc1638N mice as a model of human familial adenometous polyposis syndrome. In the normal intestinal mucosa of both species, E-cadherin and beta-catenin were localized along the lateral plasma membranes of epithelial cells. In intestinal tumour cells, however, they were also present in the cytoplasm. The expression of both proteins was reduced in human and mouse tumours. The pattern of their distribution was frequently heterogenous with strongly positive cells in a mosaic of negative ones. Further, E-cadherin and beta-catenin expression did not correlate to the Duke's staging of tumours and therefore neither can be used as prognostic criteria.

Adenocarcinoma↗
PubMed2000

Different expression of some molecular markers in sporadic cancer of the left and right colon.

The expression of cytoplasmic c-erbB2, epidermal growth factor receptor (EGFR), proliferating cell nuclear antigen (PCNA) and dipeptidylpeptidase IV (DPP IV) was significantly higher in sporadic cancer of the right than of the left colon. In addition, cytoplasmic c-erbB2 displayed the same difference in the adjacent (less than 2 cm) and distant (more than 5 cm from the tumour margin) mucosa. The findings cannot be related to Dukes staging. It is suggested that different ontogenic development of the right (from the midgut) and the left (from the hindgut) colon may be a possible explanation. Therefore, data on the expression of different molecular markers in colorectal cancer and surrounding mucosa should always be supplemented by data on tumour location.

Adult↗
PubMed1999

Are intestinal tumours in Apc+/-mice a suitable model of colorectal carcinoma in man?

In snap frozen sections of the duodenum, jejunum, ileum, the right and left colon of APC+/-mice mucosubstances, activities of brush border glycosidases and proteases, immunoreactivity of sucrase and activities of some enzymes of pericellular proteolysis were studied. Multiple adenomas (tubular or tubulovillous) the numbers of which decreased in the aboral direction occurred in the small intestine. Two tubulovillous adenomas with dysplastic nuclei but with no invasion were found in the right colon. The morphological and histochemical findings resembled those of human colorectal tumours. Activities of brush border enzymes and sucrase immunoreactivity were decreased to various extent or were not present at all. The findings fluctuated even within the same section. Activities of enzymes of pericellular proteolysis were slightly increased in comparison with non affected mucosa. This model is suitable and deserves further studies.

Adenoma↗
PubMed1997

Double-blind comparison of an oral Escherichia coli preparation and mesalazine in maintaining remission of ulcerative colitis.

BACKGROUND: Aminosalicylates are used as standard treatment for maintaining remission in ulcerative colitis. As yet, there is no other existing alternative with proven efficacy. In light of the hypothesis that the intestinal environment may contribute to the pathophysiology of ulcerative colitis, a trial was conducted to test the effects of probiotic treatment with an oral preparation of non-pathogenic E. coli. METHODS: A total of 120 patients with inactive ulcerative colitis were included in a double-blind, double-dummy study comparing mesalazine 500 mg t.d.s. to an oral preparation of viable E. coli strain Nissle (Serotype 06: K5: H1) for 12 weeks with regard to their efficacy in preventing a relapse of the disease. Study objectives were to assess the equivalence of the clinical activity index (CAI) under the two treatment modalities and to compare relapse rates, relapse-free times and global assessment. RESULTS: The start and end scores of the CAI demonstrated no significant difference (P = 0.12) between the two treatment groups. Relapse rates were 11.3% under mesalazine and 16.0% under E. coli Nissle 1917 (N.S.). Life table analysis showed a relapse-free time of 103 +/- 4 days for mesalazine and 106 +/- 5 days for E. coli Nissle 1917 (N.S.). Global assessment was similar for both groups. Tolerability to the treatment was excellent and did not differ. No serious adverse events were reported. CONCLUSIONS: From the results of this preliminary study, probiotic treatment appears to offer another option for maintenance therapy of ulcerative colitis. Additional support is provided for the hypothesis of a pathophysiological role for the intestinal environment in ulcerative colitis.

Adult↗
PubMed1997

Differences of alkaline phosphatase and arginase activities in human colorectal carcinoma cell lines.

Remarkable differences in the levels of alkaline phosphatase and arginase were found in colorectal cell lines tested. In HT-29 cells, which are extremely sensitive to the induction of cell differentiation, very low levels of arginase were detected. On the other hand, high levels of arginase were present in cell lines derived from highly malignant tumours. Both findings support a prognostic significance of arginase activity in colorectal carcinomas.

Alkaline Phosphatase↗
PubMed1996

[Treatment of duodenal ulcer with pantoprazole. A multicenter study].

BACKGROUND: The inhibition of H+/K(+)-ATPase (proton pump) of gastric parietal cells by substituted benzimidazoles represents a new therapeutic approach in conditions connected with hypersecretion of hydrochloric acid. Pantoprazol is the newest member of this group of drugs. Monotherapy of duodenal ulcer with pantoprazole or ranitidine was evaluated in terms of healing rate, tolerance and compliance. METHODS AND RESULTS: A double-blind, parallel-group comparing study (double dummy technique) of treatment florid duodenal ulcer (diameter 5-20 mm) was performed in 95 subjects (age 18-74 years). The active substances were either pantoprazole (40 mg before breakfast-47 subjects) or ranitidine (300 mg before bedtime-48 subjects). The average diameter of the ulcer and subjective complaints before treatment were comparable in both groups. After 2 weeks of pantoprazole therapy 88.5% of ulcers (a) and 87.2% patients (b) were cured, whereas the corresponding values in the ranitidine series amounted to 66% (a) and 62.5% (b) only (p = 0.006 for both (a) and (b)). The rate of healing in relative values of reducing the ulcer size was significantly higher after 2 weeks of pantoprazole therapy (p = 0.026 (a) and 0.0027 (b)). All ulcers healed after 4 weeks of this regimen. The difference between the pantoprazole and ranitidine series after 4 weeks was closely above the 5% level of significance (p = 0.589 for (a) and 0.0588 for (b) respectively). This was due to the low number of patients in both groups at this time interval, particularly in the pantoprazole group. Pain during day-time and regurgitation were observed significantly more frequently after ranitidine therapy. The compliance was very good and practically no adverse effects of pantoprazole therapy were observed. CONCLUSIONS: The healing rate of duodenal ulcer with pantoprazole monotherapy (40 mg before breakfast) was significantly higher than with ranitidine (300 mg before bedtime). The compliance of patients and the tolerance of pantoprazole were very good and its administration was not associated with any side-effects.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1996

Sucrase-isomaltase and other brush border glycosidases in colorectal tumors.

Sucrase-isomaltase (SI), trehalase (T) and lactase-beta-glucosidase (LG) activities were assessed histochemically in samples of colorectal adenomas (11 tubular, 12 tubulovillous, 10 villous) and 30 adenocarcinomas obtained by biopsy during colonoscopy or from specimens removed by surgical intervention. Small samples of tumor tissue, tissue of the transitional zone and of macroscopically normal mucosa were quenched in heptan cooled in an acetone-dry ice mixture. Cryostat sections, transferred to non-precooled slides and in some cases to semipermeable membranes, were dried and subjected to the histochemical reactions for SI, T and LG. Sucrose, 2-naphthyl, 6-Br-2-naphthyl, and 5-Br-4-Cl-3-indoxyl alpha-D-glucosides, trehalose, and 5-Br-4-Cl-3-indoxyl-beta-D-fucoside were used as substrates. Sections of jejunal biopsies with normal activities of brush border glycosidases were used as controls. From samples of 5 adenomas, 5 adenocarcinomas and collected rests of jejunal biopsies with a normal finding 10% (w/vol) homogenates in 2% Triton X-100 were prepared. Homogenates were frozen and thawed 3 times and their supernatants subjected to isoelectric focusing on polyacrylamide gel plates. Zymograms were developed with the same methods as for the detection of alpha-glucosidases in sections. In no colorectal tumor LG was present. SI was found in 70% adenocarcinomas, 50% villous, 25% tubulovillous and 19% tubular adenomas when the method with sucrose, glucose oxidase-peroxidase and 3,3'-diaminobenzidine was used. Hardly discernible traces of activity were found in tumors with azo-coupling reactions applied at pH 5, 6 and 6.5. No reaction was detected with the indigogenic method applied at pH above 6.0. However, jejunal biopsies displayed very strong reactions confined to the brush border of enterocytes under the same conditions. A strongly positive reaction was seen in 7 of 12 tumors investigated recently when the indigogenic reaction was applied at pH below 6.0 (particularly at pH 5.0). In this case the deposition of indigo was due to membrane and lysosomal alpha-glucosidases of the tumor cells and lysosomal alpha-glucosidase of macrophages and leukocytes. These findings were corroborated by zymograms. T was detected in the same tumors as SI; its activity was lower, however. SI activity in colorectal tumors is a useful, but not general marker of these tumors.

Colorectal Neoplasms↗
PubMed1996

Arginase activity determination. A marker of large bowel mucosa proliferation.

Arginase activity of the intestinal mucosa was tested as a proliferative marker in the adenoma-carcinoma sequence. The enzyme activity was determined by an end-point colorimetric method with L-arginine as substrate. Arginase activity was evaluated in 430 biopsy samples of large bowel mucosa, polyps and cancer tissue. The activities (U/g protein, mean +/- SE; n) were: normal mucosa 83.2 +/- 7.3; 25, adenomas 199.4 +/- 19.1; 40, carcinomas 1269.7 +/- 174.9; 40, inflammatory bowel disease 1210.7 +/- 247.1; 34. The arginase activity differs significantly in the adenoma-carcinoma sequence according to the Duncan's test (p < 0.05).

Arginase↗
PubMed1996

Changes in jejunal mucosa after long-term feeding of germfree rats with gluten.

BACKGROUND: Coeliac disease (CD) or gluten-sensitive enteropathy is a chronic gastrointestinal disease of children and adults. An experimental model using inbred germfree rats has been developed to study the effects of intragastric gliadin application on intestinal mucosa. METHODS: AVN strain Wistar rats (inbred F 87)-germfree were used. Gliadin was applied by intragastric probe from birth until day 63 (0.5-5 mg of gliadin per immunization). Intraepithelial lymphocytes (IEL) were separated from the jejunum, and surface marker characterization was performed using flow cytometry. Isolated IEL were labelled with fluorescein isothiocyanate and injected into control jejunal loops. After 1 h and 6 h the abdominal cavity was reopened. The samples of jejunum were fixed. RESULTS: Prolonged application of gliadin led to the shortening of jejunal villi, crypt hyperplasia, increased number of mitoses in the crypt epithelium, and increased number of IEL-characteristic CD8+, RGL-1+, and TcR alpha/beta +. Transfer of IEL separated from rats fed with gliadin into the intestinal loops of untreated rats led to tight junctions in the enterocytes of the intestinal loops. The IEL isolated from controls (albumin-treated) induced no mucosal changes in intestinal loops. CONCLUSION: These data suggest that IEL isolated from gliadin-treated rats transfer mucosal damage and that gluten-induced enteropathy has an autoimmune component.

Animals↗
PubMed1995

Natural killer cell activity in coeliac disease: effect of in vitro treatment on effector lymphocytes and/or target lymphoblastoid, myeloid and epithelial cell lines with gliadin.

To analyze the possible involvement of natural killer (NK) cell activity in the pathogenetic mechanism of coeliac disease (CD) we measured the spontaneous cytotoxic cell activity of peripheral blood mononuclear cells (PMNC) from patients with CD and from healthy donors. No significant differences were found between the NK cell activity of PMNC from healthy donors and from patients with CD using a standard 51 Cr release assay. However, a 30-min treatment of PMNC with gliadin inhibited NK cell activity in patients with CD. On the other hand, a 1-d incubation with gliadin induced cytotoxic cell activity of PMNC against the NK-resistant target cells such as the epithelial HT-29 and the lymphoblastoid RAJI cell lines, suggesting that activation of PMNC by cultivation with gliadin can occur.

Adult↗
PubMed1995

Characterization of human, mouse and rabbit anti-gliadin antibodies by ELISA and western blotting.

Monoclonal, hyperimmune rabbit and human serum anti-gliadin antibodies were analyzed by ELISA and immunoblotting techniques. In Western blotting the difference in reactivity between monoclonal and human antibodies was quantitative rather than qualitative. Rabbit antisera differed in reactivity according to the protein used for immunization. The rabbits immunized by the peptic-tryptic pancreatic digest of gliadin reacted similarly to the patients. In ELISA, significantly higher reactivity with crude, A-, glyc-gli, alpha-, beta- and omega-gliadins was found in the patients' sera than in controls.

Animals↗