Biomedical subjects

A M Hirschl

Publications and source records attributed to A M Hirschl.

At least 37 records · Page 2Linked to original sources

PubMed2000

Two enzyme immunoassays and PCR for detection of Helicobacter pylori in stool specimens from pediatric patients before and after eradication therapy.

This study of pediatric patients was intended to determine the suitability of stool PCR and two antigen enzyme immunoassays (EIAs; Premier Platinum HpSA and the novel FemtoLab H. pylori), which detect Helicobacter pylori antigens in feces, as pretreatment diagnostic tools and especially as posttreatment control. Forty-nine H. pylori-infected children with dyspepsia received eradication therapy. Successful treatment was determined by a negative [(13)C]urea breath test 4 and 12 weeks after discontinuation of therapy. Fecal specimens were collected prior to eradication therapy as well as 4 weeks after the end of treatment. Successfully treated children delivered stool samples at 6, 8, and 12 weeks posttreatment also. Specimens were examined by seminested PCR and Premier Platinum HpSA and were reexamined by both EIAs as soon as FemtoLab H. pylori was available. In the first test series, the overall sensitivities of PCR and Premier Platinum HpSA were 93.0 and 91.1%, respectively. With specimens collected at 4 weeks after treatment, the respective specificities were 68.8 and 79.3%. After longer follow-up periods, however, they gradually increased to 100 and 96.9%, respectively. In the new test series, Premier Platinum HpSA delivered a considerably lower number of false-positive results (4 versus 18), indicating intertest variations. The overall test sensitivity was 94.6%, and the overall specificity was 97.5%. FemtoLab H. pylori showed an excellent performance with an overall sensitivity and specificity of 98.2 and 98.1%, respectively. Thus, in contrast to PCR, both EIAs were shown to be suitable for early posttreatment control.

Adolescent↗

PubMed1999

Diagnosis of Helicobacter pylori infection with a new non-invasive antigen-based assay. HpSA European study group.

BACKGROUND: Helicobacter pylori is a common human pathogen implicated in certain gastrointestinal diseases. In the search for new non-invasive techniques to diagnose H. pylori infection, we evaluated an EIA for H. pylori antigen in stool (HpSA). METHODS: In a prospective multicentre study, stool specimens from 501 patients (276 men, 225 women; age range 17-88 years, mean 52) undergoing gastroscopy in 11 centres throughout Europe were tested with HpSA and the carbon-13-urea breath test. At endoscopy, four biopsy samples were taken for histology (haematoxylin and eosin) and H. pylori detection (giemsa in both antrum and corpus, culture and rapid urease test). Patients were defined as positive for H. pylori if histology (antrum, corpus, or both) and urease test were positive, or if culture was positive. Patients classified as having H. pylori infection received an eradication regimen; 107 were reassessed 4 weeks after therapy. FINDINGS: Of 272 patients with H. pylori infection by the predefined criteria, 256 were positive by HpSA (sensitivity 94.1% [95% CI 90.6-96.6]). Of 219 patients without infection, 201 were negative by HpSA (specificity 91.8% [87.3-95.1]). INTERPRETATION: The stool assay was a reliable and easy-to-use tool for diagnosis of H. pylori infection. The test was accurate even shortly after treatment.

Adolescent↗

PubMed1999

Detection of Chlamydia pneumoniae DNA in atheromatous tissues by polymerase chain reaction.

Chlamydia pneumoniae is an important human respiratory pathogen. Recently, seroepidemiological data and the demonstration of chlamydial DNA or antigen within parts of atherosclerotic lesions have suggested a causal association between chlamydial infections and atherosclerosis. As the results obtained by different groups show considerable variations, we provide further data based on a highly specific and sensitive nested PCR method. Positivity was confirmed by nonradioactive hybridization with a specific probe, and sensitivity was determined by titration experiments. C. pneumoniae DNA was detected in 8/29 (28%) of carotid artery samples and 3/14 (21%) of aortic aneurysms.

Aged↗

PubMed1999

Enteroaggregative and enterotoxigenic Escherichia coli among isolates from patients with diarrhea in Austria.

In a 3-month prospective study among 203 Austrian outpatients with diarrhea, the role of pathogenic Escherichia coli and the use of the polymerase chain reaction in screening Escherichia coli isolates from clinical stool specimens were evaluated. Enteroaggregative Escherichia coli and enterotoxigenic Escherichia coli combined were identified as the second most frequent cause of diarrhea. Of a total of 85 bacterial pathogens isolated from 80 patients, 15 were pathogenic Escherichia coli, 13 enteroaggregative Escherichia coli and two enterotoxigenic Escherichia coli. Enteropathogenic, enteroinvasive, and enterohemorrhagic Escherichia coli isolates were not detected.

Adolescent↗

PubMed1999

Helicobacter pylori type I strains among Austrian and Portuguese patients with gastritis, peptic ulcer or gastric cancer.

The frequency of occurrence of Helicobacter pylori type I strains in isolates from Austria and Portugal and different polymerase chain reaction-based approaches to detect the cag pathogenicity island were assessed. Of the 41 Austrian strains, eight of 14 (57.2%) isolated from patients with gastritis, 14 of 19 (73.7%) from patients with peptic ulcer and eight of eight (100%) from patients with gastric cancer were type I strains. Among the Portuguese strains, eight of 14 (57.2%) isolated from patients with gastritis, ten of 12 (83.3%) from patients with peptic ulcer and five of 13 (38.5%) from patients with gastric cancer were classified as type I. Thus, Helicobacter pylori type I strains occur frequently in both populations but show no significant correlation with peptic ulcer disease. The prevalence of the type Igenotype in Austrian cancer patients, however, was significantly higher (P=0.007). The cagE-specific polymerase chain reaction was found to be a reliable and efficient method for detection of the cag pathogenicity island.

Adolescent↗

PubMed1999

Famotidine versus omeprazole in combination with clarithromycin and metronidazole for eradication of Helicobacter pylori--a randomized, controlled trial.

BACKGROUND: One-week low-dose triple therapy is currently considered the gold standard regimen for treatment of Helicobacter pylori infection. However, the mechanisms involved in the synergy between antibiotics and proton pump inhibitors are controversial. AIMS: To test the hypothesis that acid suppression represents the crucial mechanism by which the antibacterial activity of antibiotics can be enhanced, and to assess the impact of primary resistance on treatment outcome. METHODS: One hundred and twenty patients with H. pylori infection and duodenal ulcer, gastric ulcer or non-ulcer dyspepsia were randomly assigned to a 1 week course of either famotidine 80 mg b.d., clarithromycin 250 mg b.d. and metronidazole 500 mg b.d. (FCM group; n = 60) or omeprazole 20 mg o.d., clarithromycin 250 mg b.d. and metronidazole 500 mg b.d. (OCM group; n = 60). Gastroscopy was performed at baseline and 5 weeks after completion of treatment. H. pylori status was assessed by biopsy urease test, histology and culture. RESULTS: In the intention-to-treat analysis, eradication of H. pylori was achieved in 47 of 60 patients (78%; 95% CI: 66-88%) in the FCM group, compared to 44 of 60 patients (73%; 95% CI: 60-84%) in the OCM group (N.S.). Using per protocol analysis, eradication therapy was successful in 47 of 52 patients (90%; 95% CI: 79-97%) treated with FCM and 44 of 57 patients (77%; 95% CI: 64-87%) treated with OCM (N.S.). Primary metronidazole resistance was present in 27% and primary clarithromycin resistance in 8% of strains. Overall per protocol eradication rates in strains susceptible to both antibiotics and strains with isolated metronidazole resistance were 93% and 84%, respectively. No patient with clarithromycin resistance responded to treatment. CONCLUSIONS: High-dose famotidine and omeprazole, combined with clarithromycin and metronidazole, are equally effective for eradication of H. pylori. In 1-week low-dose triple therapy, metronidazole resistance has no major impact on eradication rates whereas clarithromycin resistance is associated with a poor treatment outcome.

Adult↗

PubMed1999

IgG subclass reactivity to human cardiac myosin in cardiomyopathy patients is indicative of a Th1-like autoimmune disease.

Studies performed in mice together with the demonstration of increased levels of heart-specific autoantibodies, cytokines and cytokine receptors in sera from cardiomyopathy (CMP) patients argued for a pathogenic role of autoimmune mechanisms in CMP. This study was designed to analyse the presence of IgG anti-heart antibodies in sera from patients suffering from hypertrophic and dilatative forms of CMP as well as from patients with ischaemic heart disease and healthy individuals. Patients' sera were analysed for IgG reactivity to Western-blotted extracts prepared from human epithelial and endothelial cells, heart and skeletal muscle specimens as well as from Streptococcus pyogenes. The IgG subclass (IgG1-4) reactivity to purified human cardiac myosin was analysed by ELISA. While sera from CMP patients and healthy individuals displayed comparable IgG reactivity to a variety of human proteins, cardiac myosin represented the prominent antigen detected strongly and preferentially by sera from CMP patients. Pronounced IgG anti-cardiac myosin reactivity was frequently found in sera from patients with dilatative CMP and reduced ventricular function. ELISA analyses revealed a prominent IgG2/IgG3 anti-cardiac myosin reactivity in CMP sera, indicating a preferential Th1-like immune response. Elevated anti-cytomegalovirus, anti-enterovirus IgG titres as well as IgG reactivity to nitrocellulose-blotted S. pyogenes proteins were also frequently observed in the group of CMP patients. If further work can support the hypothesis that autoreactivity to cardiac myosin represents a pathogenic factor in CMP, specific immunomodulation of this Th1- towards a Th2-like immune response may represent a promising therapeutic strategy for CMP.

Adolescent↗

PubMed1999

Influence of Helicobacter pylori infection on the phenotype of Crohn's disease.

OBJECTIVE: Very little is known about the impact of Helicobacter pylori (H. pylori) infection on Crohn's disease. In this study we investigated a possible influence of H. pylori on the phenotype of Crohn's disease. METHODS: Patients with Crohn's disease who had gastric biopsy between 1990 and 1994 and a clinical follow-up in our outpatient clinic for at least 2 yr were included in the study. The mean number of flare-ups per year of follow-up, the mean numbers of intestinal resections per year of disease duration, and primary disease location were compared in H. pylori-positive and -negative patients. Various regression models were calculated to test the influence of H. pylori status on these parameters, correcting for smoking habits and disease duration. RESULTS: Of 131 patients, 50 (38.2%) were H. pylori positive and 62 (47.3%) were smokers. Due to a significant interaction between smoking habits and H. pylori infection, regression models were calculated separately for smokers and nonsmokers. Nonsmokers without H. pylori infection had more flare-ups than nonsmokers with H. pylori infection (0.77 [0.57-0.97] vs 0.29 [0.16-0.42]; p < 0.01; mean [95% confidence interval]). In contrast, nonsmokers without H. pylori infection had less intestinal resections than nonsmokers infected with H. pylori (0.08 [0.04-0.12] vs 0.11 [0.07-0.15]; p < 0.05). These differences were not significant for smokers (p < 0.41 and p < 0.07). There was a predominance of small bowel disease in H. pylori-positive patients, which did not reach statistical significance. CONCLUSIONS: Our data indicate that H. pylori influences the phenotype of Crohn's disease, especially in nonsmokers.

Adult↗

PubMed1998

Cytokine and prostaglandin production by amnion cells in response to the addition of different bacteria.

OBJECTIVE: Our goal was to evaluate the effect of Escherichia coli, Bacteroides fragilis, Mycoplasma hominis, and Staphylococcus aureus on cytokine and prostaglandin production by amnion cells in vitro. STUDY DESIGN: Amnion cells were obtained from women undergoing elective cesarean section before the onset of labor and cultured in a primary cell culture. Confluent amnion cells were incubated with heat-inactivated bacteria in different concentrations (10(1) to 10(6) colony-forming units/ml) for 48 hours. Samples for quantification of interleukin-1 beta, interleukin-6, interleukin-8, tumor necrosis factor-alpha, and prostaglandin E2 were collected at 6, 12, 24, and 48 hours. RESULTS: Under basal conditions, minor amounts of interleukin-6 and interleukin-8 were detectable. Incubation of amnion cells with E. coli enhanced the secretion of interleukin-8 and also induced an transient increase of prostaglandin E2 in a dose-dependent manner. B. fragilis produced an increase in the secretion of interleukin-6 and interleukin-8. M. hominis and S. aureus did not cause an increase in either interleukin-6, interleukin-8, or prostaglandin E2. CONCLUSION: The gram-negative bacteria E. coli and B. fragilis stimulated interleukin-6 and interleukin-8 to a greater degree than the other bacteria investigated in this study. This finding may be of clinical interest in the onset of preterm birth.

Amnion↗

PubMed1998

Hyperemesis gravidarum associated with Helicobacter pylori seropositivity.

OBJECTIVE: To test the hypothesis that infection with Helicobacter pylori is associated with hyperemesis gravidarum. METHODS: From January 1995 to November 1996 we enrolled 105 patients with hyperemesis gravidarum in a prospective study. The Helicobacter serum Immunoglobulin (Ig) G concentrations in these patients were compared with those in asymptomatic gravidas matched for week of gestation. RESULTS: Positive serum IgG concentrations were found in 95 of the 105 hyperemesis patients (90.5%) compared with 60 of 129 controls (46.5%). A chi2 test showed statistical significance (P < .001). The mean (+/-standard deviation) index percentages of the IgG titers were 74.2+/-23.6% in the hyperemesis group and 24.3+/-4.4% in the control group (P < .01, Student t test). CONCLUSION: Infection with H pylori may cause hyperemesis gravidarum.

Adolescent↗

PubMed1998

Helicobacter pylori urease significantly reduces opsonization by human complement.

The role of Helicobacter pylori urease in opsonization by human complement was investigated. H. pylori wild type strain N6 and isogenic mutants lacking either the large urease subunit (UreB) or an accessory urease protein (UreG) were incubated with different sera. C3b bound to the bacteria was measured by specific staining and flow cytometry. As compared with opsonization of N6 and the UreG-lacking mutant, opsonization of the UreB-lacking mutant was significantly increased after incubation with sera from both H. pylori uninfected (P<.001) or infected (P<.05) persons. However, when sera from uninfected persons were used, effective opsonization of this mutant proved to be dependent mainly on the classical pathway of complement activation. Irrespective of the serum used, opsonization values were very low after selective inactivation of the classical or the alternative pathway. Reduced opsonization of the urease-expressing strains could, to some extent, result from degradation of bound C3b.

Bacterial Proteins↗

PubMed1998

Highly significant role of Helicobacter pylori urease in phagocytosis and production of oxygen metabolites by human granulocytes.

The contribution of Helicobacter pylori urease, the vacuolating cytotoxin VacA, and the 128-kDa protein CagA to the stimulation of human granulocytes in terms of phagocytosis and oxidative burst was evaluated. Blood was incubated with H. pylori strains and corresponding isogenic mutants lacking either the large urease subunit (UreB) or an accessory urease protein (UreG) or VacA or CagA. Phagocytosis and oxidative burst were monitored by flow cytometry. The UreB-lacking mutant was phagocytosed more efficiently (P < .001) and induced significantly less oxidative burst (P < .001) than its parental strain or the UreG-lacking mutant, which produces an enzymatically inactive urease. Values of the other mutants did not differ greatly from those of their parental strain. These data indicate inflammatory effects of H. pylori urease causing inhibition of phagocytosis and stimulation of oxidative burst by a pathway being largely independent of ammonia production.

Antigens, Bacterial↗

PubMed1998

Isolation of cDNA clones coding for IgE autoantigens with serum IgE from atopic dermatitis patients.

Recently we demonstrated that a high percentage of atopic dermatitis (AD) patients displayed specific immunoglobulin E reactivity to human proteins. Here we show that IgE autoreactivity is found predominantly in AD patients with severe skin manifestations and reveal the molecular nature of four IgE autoantigens. An expression cDNA library constructed from a human epithelial cell line (A 431) was screened with serum IgE from two AD patients. DNA sequence analysis of three IgE-reactive clones identified the alpha-chain of the nascent polypeptide-associated complex, cytokeratin type II, and the BCL7B oncogen as atopy-related IgE autoantigens (ara). The fourth cDNA coded for an IgE autoantigen containing a typical calcium binding motif that occurred in histogenetically different cells and tissues (keratinocytes, muscle, brain). Recombinant Escherichia coli-expressed IgE autoantigens bound IgE from AD but not from patients with other immunologically mediated disorders (graft vs. host disease, systemic lupus erythematosus) and elicited immediate type skin reactions in AD patients. In serum samples collected from an AD patient over a period of 5 years, IgE anti-ara NAC antibody levels peaked during disease exacerbation. Our finding that ara BCL7B was detected in serum bound to IgE antibodies suggests that intracellular IgE autoantigens can become released after tissue damage and may occur as IgE immune complexes. Via binding to antigen presenting cells as well as to effector cells, IgE autoantigen immune complexes may contribute to exacerbation and/or perpetuation of severe atopic diseases even in the absence of exogenous allergens.

Amino Acid Sequence↗

PubMed1998

Detection of Helicobacter pylori in stool specimens by PCR and antigen enzyme immunoassay.

A highly sensitive seminested PCR assay to detect Helicobacter pylori DNA in feces was developed. PCR with stool specimens and a novel antigen enzyme immunoassay (EIA) for H. pylori detection in feces were evaluated as diagnostic tools and in follow-up with samples from 63 infected and 37 noninfected persons. Infected individuals received eradication therapy followed by endoscopic follow-up 35 days after the start of treatment. At that time, a second stool specimen was obtained from 55 of these patients. Before eradication, the sensitivity of PCR was 93.7% and that of EIA 88.9%. Specificities were 100 and 94.6%, respectively. Of the 55 follow-up specimens, 41 originated from patients from whom H. pylori had been eradicated. Of these, 21 were still positive by PCR and 13 were positive by EIA, indicating that 1 month may be too short a period for follow-up evaluation of stool specimens by these tests.

Adult↗

PubMed1997

[Vancomycin resistant enterococci in Austria].

This study reports pheno- and genotypical analysis of 9 isolates of vancomycin-resistant enterococci (VRE) and 5 vancomycin-sensitive enterococci (VSE) in Austria: 5 E, faecium isolates of 4 patients (the sole patients demonstrating VRE at the University Hospital of Innsbruck in 1994 and 1995), 3 glycopeptide-sensitive isolates collected in Innsbruck in February 1996 for epidemiological analysis, and 6 enterococcus isolates from the University Hospitals of Vienna and Graz. The pheno- and genotypical analyses of all glycopeptide highly resistant E. faecium and E. faecalis isolates indicated the presence of VanA type resistance. One E. casseliflavus strain with intrinsic VanC-1 resistance showed a characteristic constitutive low-level resistance to vancomycin and susceptibility to teicoplanin. Genotyping with macro-restriction analysis demonstrated that 3 VRE isolates of the 5 E. faecium specimens were identical; the same applied to 2 VSE isolates. The two patients with VRE had been cared for at the same time in a surgical ICU and likewise, the two patients with VSE were simultaneously treated at a neurological ICU. The genotyping of E. faecalis strains showed that two strains of the three VRE isolates exhibited identical patterns. Epidemiological investigation did not reveal a mode of transmission for this cluster. Two of the 8 patients with VRE died within 60 days after isolation of the bacteria; the doctors in charge did not consider that the enterococci had been the cause of death. The results of our study indicate that oral vancomycin administration to humans is a primary cause of VRE in Austrian hospitals. In Austria approximately 66 kg vancomycin, 20% of it given orally, are administered to patients per year. Approx. 18-20 tons Avotan (active ingredient Avoparcin-10%)/year were used in Austria; as of April 1, 1997 the use of this animal foodstuff supplement is prohibited by the European Commission.

Administration, Oral↗

PubMed1997

Molecular typing of Acinetobacter baumannii from ten different intensive care units of a university hospital.

Thirty-one isolates of Acinetobacter baumannii were collected from ten intensive care units of an Austrian university hospital. All isolates were typed by enterobacterial repetitive intergenic consensus polymerase chain reaction (ERIC-PCR). Two strains colonizing 13 infants in the neonatal intensive care unit were identified by ERIC-PCR. All other Acinetobacter baumannii isolates had highly divergent ERIC-PCR patterns, despite having the same antibiogram. Thus, a hospital-wide clonal distribution, as suggested by identical antibiogram patterns, was excluded by ERIC-PCR.

Acinetobacter↗

PubMed1996

Comparison of vancomycin, teicoplanin, metronidazole, and fusidic acid for the treatment of Clostridium difficile-associated diarrhea.

We conducted a prospective, randomized study to compare the efficacy of oral fusidic acid, oral metronidazole, oral vancomycin, and oral teicoplanin for the treatment of Clostridium difficile-associated diarrhea. Treatment resulted in clinical cure for 94% of the patients who were treated with vancomycin, 96% of those treated with teicoplanin, 93% of those treated with fusidic acid, and 94% of those treated with metronidazole. Clinical symptoms recurred in 16% of patients treated with vancomycin, 7% of those treated with teicoplanin, 28% of those treated with fusidic acid, and 16% of those treated with metronidazole. There was asymptomatic carriage of C. difficile toxin in 13% of patients treated with vancomycin, 4% of those treated with teicoplanin, 24% of those treated with fusidic acid, and 16% of those treated with metronidazole. No adverse effects related to therapy with vancomycin or teicoplanin were observed. Considering the costs of treatment, our findings suggest that metronidazole is the drug of choice for C. difficile-associated diarrhea and that glycopeptides should be reserved for patients who cannot tolerate metronidazole or who do not respond to treatment with this drug.

Administration, Oral↗

PubMed1996

Clarithromycin or amoxycillin plus high-dose ranitidine in the treatment of Helicobacter pylori-positive functional dyspepsia.

OBJECTIVE: This study was intended to investigate the effect of ranitidine in dual anti-Helicobacter pylori therapy. Simultaneously, it was to evaluate the potential effect of H. pylori eradication on the symptomatology of H. pylori-positive dyspepsia. PATIENTS AND METHODS: Fifty-four patients with H. pylori infection and symptoms of non-ulcer dyspepsia were randomly assigned to treatment with either amoxycillin 500 mg four times daily plus ranitidine 300 mg four times daily, clarithromycin 500 mg twice daily plus ranitidine 300 mg twice daily, clarithromycin 500 mg four times daily plus ranitidine 300 mg twice daily or clarithromycin 500 mg four times daily plus ranitidine 300 mg four times daily for a period of 12 days. In addition, ranitidine 150 mg twice daily was given for a further 16 days. RESULTS: Eradication of H. pylori using the assigned treatments was achieved in 47% (seven out of 15), 50% (five out of 10), 70% (seven out of 10) and 77% (10 out of 13) of patients, respectively. Failure of therapy with clarithromycin was associated with primary or acquired resistance after treatment in 91% (10 out of 11). Symptom improvement was significant (P = 0.0001) and similar in all of the four treatment groups up to week 8. As regards H. pylori status, no differences in the mean symptom score improvement could be found between patients with eradication and those with persistent infection (12.3-7.0, P = 0.0001, n = 29 compared with 13.0-6.5, P = 0.004, n = 19). After 1 year the symptom score had increased both in patients with persistent H. pylori (9.1) and in those remaining free of infection (10.0). No reinfection could be found. CONCLUSION: These results suggest that clarithromycin plus high-dose ranitidine is a combination which achieves reasonably high H. pylori eradication rates. However, treatment failure inevitably leads to clarithromycin resistance. The improvement of non-ulcer dyspepsia symptoms during acute therapy is independent of H. pylori eradication. Long-term benefit of H. pylori eradication with respect to the symptoms of functional dyspepsia was not observed.

Adult↗