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Biomedical subjects

D Vaira

Publications and source records attributed to D Vaira.

At least 37 records · Page 2Linked to original sources

Infection by CagA-positive Helicobacter pylori strains in patients with ischemic heart disease: prevalence and association with exercise-induced electrocardiographic abnormalities.

The role of H. pylori infection in increasing the risk of ischemic heart diseases (IHD) is still debated. We determined serologically the prevalence of overall H. pylori and CagA-positive H. pylori infection in 63 consecutive patients with IHD and 189 gender- and age-matched controls. We also determined in patients the influence of the infection and the CagA serological status on the results of an exercise ECG test and other parameters considered possible variables that may enhance the risk of IHD. The prevalence of H. pylori infection in patients and controls was 79.3% and 73.0%, respectively (P = 0.403) and that of CagA-positive H. pylori infection was 69.8% and 42.3%, respectively (P = 0.0002). The scores of the ECG S-T segment and T-wave abnormalities in the course of an exercise ECG in uninfected patients and in patients infected by CagA-negative and CagA-positive H. pylori strains were (mean +/- SD): 1.59 +/- 0.67, 1.92 +/- 0.64, and 2.19 +/- 0.70, respectively; (P = 0.011, 95% confidence limits of difference 0.15-1.07, CagA-positive infected vs uninfected patients). There was no intergroup difference in the levels of peripheral white blood cells, glucose, cholesterol, triglycerides, creatinine, and systolic and diastolic pressure. In conclusion, genetic heterogeneity of H. pylori could possibly explain some conflicting results concerning the association of H. pylori infection with IHD. Coronary vessels of IHD patients infected by CagA-positive H. pylori strains may be damaged more severely than those of uninfected patients.

Adult↗

Review article: Helicobacter pylori infection from pathogenesis to treatment--a critical reappraisal.

The main areas of this review are Helicobacter pylori and disease pathogenesis; the relationship of H. pylori to lower gastrointestinal diseases, liver disease and extra-gastrointestinal conditions; the relationship of H. pylori to gastro-oesophageal reflux disease; infection in the very young and very old; diagnostic techniques; and management of H. pylori infections with particular emphasis on eradication regimens and antibiotic resistance.

Adult↗

Specific identification of three low molecular weight membrane-associated antigens of Helicobacter pylori.

BACKGROUND: A large number of Helicobacter pylori proteins are antigenic, but antibodies to these proteins persist in spite of the eradication of the infection. METHODS AND RESULTS: The analysis of sera from H. pylori-infected and non-infected patients, before and 3 and 5 months after eradication, showed that the antibody response against unknown H. pylori antigens at 32, 30, 22 and 14 kDa in sodium dodecylsulphate polyacrylamide gel electrophoresis decreased by > or = 60% at 3 months and > or = 70% at 5 months after treatment. Two-dimensional gel electrophoresis and mass spectrometry allowed the identification of eight proteins at these positions: neuraminyl-lactose-binding haemagglutinin precursor, 3-oxoadipate CoA-transferase subunit A, elongation factor P, peptidoglycan-associated lipoprotein precursor, hypothetical protein HP0596, adhesin-thiol peroxidase, 50S ribosomal protein L7/L12 and subunit b' of the F(0) ATP synthase. Three of these eight, expressed as recombinant proteins (32 kDa neuraminyl-lactose-binding haemagglutinin precursor, 30 kDa peptidoglycan-associated lipoprotein precursor and 22 kDa hypothetical protein HP0596), reacted specifically with sera from infected patients, while the 14 kDa 50S ribosomal protein L7/L12 cross-reacted with one out of five sera from H. pylori-negative patients. The other recombinant proteins did not show significant immunoreactivity. CONCLUSIONS: Four low molecular weight antigens were identified by these methods, three of which were specific. Immunoreaction with these three proteins (neuraminyl-lactose-binding haemagglutinin precursor, peptidoglycan-associated lipoprotein precursor and hypothetical protein HP0596) could provide a serological assessment not only of H. pylori infection, but also of eradication.

Aged↗

Helicobacter pylori infection, anti-cagA antibodies and peptic ulcer: a case-control study in Italy.

AIM: To evaluate the association between infection with specific strains of Helicobacter pylori and peptic ulcer in patients referred for upper gastrointestinal endoscopy. METHODS: One thousand, six hundred and twenty-six consecutive dyspeptic patients, referred to one Endoscopy Unit in Bologna, Italy, were enrolled. For each participant, a blood sample was obtained for the measurement of distinct immunoglobulin G antibodies against H. pylori lysate and cytotoxin associated gene A (cagA). A case-control study included the whole series: patients diagnosed with duodenal (n=275) or gastric (n=71) ulcer were identified and independently compared with controls with non-ulcer dyspepsia (n=1280). RESULTS: H. pylori seroprevalence (at least one positive marker) was associated with increasing age, male sex and a diagnosis of peptic ulcer. This association was stronger with duodenal ulcer (multivariate odds ratio (OR), 5.2; 95% confidence interval (CI), 3.5-7.9) than with gastric ulcer (OR, 2.3; 95% CI, 1.2-4.4). Further analyses showed that H. pylori lysate+/cagA- subjects had a moderately increased risk of duodenal (OR, 3.2), but not gastric (OR, 1.1), ulcer. When cagA+ subjects were separately compared with seronegative patients, there was a six-fold increased risk for duodenal ulcer and a three-fold increased risk for gastric ulcer. CONCLUSIONS: A strong positive association between infection with a cagA+ H. pylori strain and the presence of peptic disease was found. The seroprevalence of anti-cagA antibodies among patients with non-ulcer dyspepsia is so high (41%) to preclude its use as a pre-endoscopic screening test.

Adult↗

Review article: diagnosis of Helicobacter pylori infection.

Helicobacter pylori (H. pylori) infection can be diagnosed by invasive techniques requiring endoscopy and biopsy (histological examination, culture, polymerase chain reaction) and by noninvasive techniques (serology, urea breath test, urine or blood, detection of H. pylori antigen in stool specimen). At present, no single test can be absolutely relied upon to detect colonization by H. pylori, and a combination of two tests is recommended if feasible. The tests used should depend on the clinical circumstances, the likelihood ratio of positive and negative tests, the cost-effectiveness of the testing strategy, and the availability of the tests. Some clinical circumstances warrant invasive studies, principally patients with alarm symptoms (bleeding, weight loss, etc.) as well as older patients with new-onset dyspepsia. Endoscopy may also be advisable in patients who have failed eradication therapy and need culture and antimicrobial sensitivity testing to determine an appropriate regimen. Recent studies have also demonstrated that a strategy to 'test and treat' for H. pylori in uninvestigated, young (< 50 years), dyspeptic patients in primary care is safe and reduces the need for endoscopy. Indeed, a number of clinical guidelines recommend noninvasive testing followed by treatment of H. pylori for dyspeptic patients in primary care based on clinical and economic analyses.

Biopsy↗

Helicobacter pylori infection and infertility.

OBJECTIVE: To determine (1) the prevalence of Helicobacter pylori infection in male and female patients with reproductive disorders and controls; (2) the presence of anti-H. pylori antibodies in samples of follicular fluid, vaginal secretions and sperm; and (3) the existence of a structural homology between a major spermatozoa protein, tubulin, and H. pylori proteins. PATIENTS AND METHODS: Serum samples from 167 patients with infertility and 837 age- and gender-matched controls (blood donors) were examined by enzyme-linked immunosorbent assay (ELISA) and Western blotting to determine the seropositivity for H. pylori infection. The presence of anti-H. pylori antibodies in samples of follicular fluid, vaginal secretions and sperm was determined using the same techniques. The possible cross-reactivity with spermatozoa of anti-H. pylori hyperimmune sera and human antibodies was studied by immunofluorescence. The N-acid homology of human tubulin with the principal H. pylori proteins was assayed by the WU-blastp program available on the Internet. RESULTS: The prevalence of infection was significantly higher in patients than controls (49.1% v. 33.5%, P < 0.001). Follicular fluids from infected patients contained specific antibodies in all cases, sperm samples in about 50% of cases, and vaginal secretions in a minority of cases. Sera to H. pylori whole antigens and VacA reacted with the tails and the pericentriolar area of human spermatozoa (which are rich in tubulin); sera to urease and heat-shock protein (Hsp) did not. Follicular fluids with anti-H. pylori antibodies immune reacted with spermatozoa. A linear homology was found between beta-tubulin and three H. pylori proteins, flagellin, VacA and CagA. CONCLUSIONS: H. pylori infection may increase the risk of developing reproductive disorders or worsen the clinical expression of this syndrome.

Adolescent↗

Prevalence of Helicobacter pylori in Sri Lanka as determined by PCR.

Fifty-seven Sinhalese patients were investigated for the presence of Helicobacter pylori by PCR. A prevalence of 70.1%, with 47.5% positive for cagA, was demonstrated. The most common vacA allele was s1am1. There was no significant association between either the s1 allele or the cagA allele and severe gastroduodenal disease. There was an association between the s1 allele and the cagA locus.

Adolescent↗

Accuracy of stool antigen test in posteradication assessment of Helicobacter pylori infection.

Our aim was to evaluate the accuracy of HpSA test in the diagnosis of Helicobacter pylori infection after the end of eradication therapy. In all 106 H. pylori-positive patients (55 men and 51 women, mean age 51 years, range 19-82) were treated with a course of eradicating regimen. [13C]Urea breath test (UBT) and HpSA were performed four weeks after stopping the treatment. The diagnostic accuracy of HpSA was evaluated in comparison with the results of [13C]UBT. In 90 patients (85%) H. pylori was eradicated according to [13C]urea breath test. After eradication, sensitivity of HpSA was 87.5%, specificity 95.5%, positive predictive value 77.8%, negative predictive value 97.7%, and diagnostic accuracy 94.3%. HpSA is a valuable test in the posteradication assessment of H. pylori infection.

Antigens, Bacterial↗

Review article: the transmission of Helicobacter pylori from stomach to stomach.

The mode of transmission of Helicobacter pylori is largely unknown and is a matter of circumstantial evidence and speculation rather than fact. However, the principle evidence is of two sorts: the epidemiological data, providing evidence of possible risk factors associated with transmission, and the identification of potential sources from which H. pylori could be acquired. Evidence exists for several potential sources of infection and several possible modes of transmission, and it is feasible that the transmission of H. pylori varies according to the cultural and demographic circumstances. However, the most likely recognized source for H. pylori is the human stomach, although it is not known by what route the organism is transmitted to the stomach. Evidence suggests close personal contact is important and that acquisition occurs mainly in childhood. This article reviews the evidence for the source of infection and the route of transmission of H. pylori.

Age Factors↗

Accuracy of the stool antigen test in the diagnosis of Helicobacter pylori infection before treatment and in patients on omeprazole therapy.

AIM: To evaluate the Helicobacter pylori stool antigen (HpSA) test in the assessment of H. pylori infection and the effect of omeprazole treatment on its accuracy. METHODS: Study 1: 140 dyspeptic patients were enrolled in the study and defined as H. pylori positive if histology and rapid urease test, or culture alone were positive. HpSA was performed on all patients and 13C-urea breath test (UBT) on 87. Study 2: 75 patients testing positive using both UBT and HpSA, were given omeprazole 20 mg for 2 weeks (Group A) or omeprazole 40 mg for 2 weeks (Group B), or OAC for 1 week (group C). A Helicobacter pylori stool antigen test was performed on all patients on days 3, 5, 7 and 14 during treatment, and also on days 7 and 14 post-treatment in groups A and B. UBT was performed in groups A and B on days 7 and 14 during treatment, and days 7 and 14 post-treatment. RESULTS: 80/140 patients were H. pylori positive. The sensitivity and specificity of HpSA were 93.8 and 90%, similar to UBT (93.9 and 92.1%). Omeprazole significantly reduced both HpSA and UBT values, resulting in a decreased accuracy. Of 25 patients receiving 20 mg omeprazole, HpSA gave 5 and 6 false negatives after 7 and 14 days treatment respectively, while UBT gave 4 and 7 false negatives after 7 and 14 days treatment. Of 25 patients receiving 40 mg omeprazole, HpSA gave 7 and 9 false negatives after 7 and 14 days of treatment, while UBT gave 8 and 9 false negatives after 7 and 14 days of treatment. Two weeks after stopping omeprazole treatment, the HpSA and UBT were positive in all cases. CONCLUSIONS: The Helicobacter pylori stool antigen test is valuable in the assessment of H. pylori infection. Short-term omeprazole treatment decreases the accuracy of both HpSA and UBT in a similar manner.

Adult↗

Helicobacter pylori in school children from the Western province of Sri Lanka.

BACKGROUND: Little is known about the prevalence of Helicobacter pylori in Sri Lanka and nothing is known about its prevalence in children. Therefore the prevalence of H. pylori in a group of school children in Sri Lanka was determined. MATERIALS AND METHODS: The presence of H. pylori colonisation was determined by detection of faecal antigen and salivary antibody (IgG) by enzyme immuno assay, in 184 children aged between 5 and 19 years, in the Western Province-Colombo district of Sri Lanka. RESULTS: Overall, only 12/184 (6.5%) had detectable H. pylori antigen in their stools and were considered infected with H. pylori, while 51/184 (27.7%) had H. pylori IgG in saliva. H. pylori salivary IgG declined with age while H. pylori antigen detection increased with age. H. pylori infection, as determined by salivary antibody (66%), was greater in children living in overcrowded conditions, although this was not statistically significant. CONCLUSION: The prevalence of H. pylori among school children in Sri Lanka was 6.5% by detection of faecal antigen and 27.7% by detection of salivary antibody, respectively. Initial infection with H. pylori appeared to occur in early childhood whilst active disease began in late childhood. Overcrowding appears to facilitate the transmission of the organism. Overall the prevalence of H. pylori was low in Sri Lanka compared with other countries in South-east Asia.

Adolescent↗

Helicobacter pylori infection in an urban African population.

We have studied 221 adults drawn from an impoverished urban population with high human immunodeficiency virus (HIV) seroprevalence (35%) to determine the prevalence of gastroduodenal pathology and its relationship to serological markers of Helicobacter pylori virulence proteins and other potential environmental and immunological determinants of disease including HIV infection. Eighty-one percent were H. pylori seropositive, and 35% were HIV seropositive. Urban upbringing and low CD4 count were associated with a reduced likelihood of H. pylori seropositivity, as was current Ascaris infection, in keeping with recent evidence from an animal model. One hundred ninety-one adults underwent gastroduodenoscopy, and 14 had gastroduodenal pathology. Mucosal lesions were a major cause of abdominal pain in this population. While the majority of patients with gastroduodenal pathology (12 of 14) were seropositive for H. pylori, none were seropositive for HIV. Smoking was associated with increased risk of macroscopic pathology, and a history of Mycobacterium bovis BCG immunization was associated with reduced risk. Antibodies to H. pylori lipopolysaccharide were associated with pathology. HIV infection was associated with protection against mucosal lesions, suggesting that fully functional CD4 lymphocytes may be required for the genesis of gastroduodenal pathology.

Adolescent↗

Detection of Aspergillus species DNA by PCR in bronchoalveolar lavage fluid.

The usefulness of a nested PCR assay for detection of Aspergillus sp. DNA was evaluated in 177 bronchoalveolar lavage (BAL) fluid specimens. This test was accurate both to diagnose culture-negative BAL fluid specimens from patients with invasive pulmonary aspergillosis and to confirm culture-positive samples. However, it did not differentiate between infection and colonization.

Aspergillosis↗

How valuable is the application on consensus guidelines in the management of functional gastrointestinal disorders?

When patients complain of problems, physicians are used to look for some physical or physiological abnormality ruling out infections, inflammatory or cancer. Unfortunately, when we talk about functional disorders we usually cannot observe any defects and it is only possible for us to know of them through the words of our patients. Developing criteria and guidelines is not an easy process, in particular for functional gastrointestinal diseases, when no disease-based biological markers exist. It is difficult to define a medical disorder in the absence of a biological "gold standard". The Rome II classification is based on the assumption that for each disorder there are symptom clusters. Symptoms have in common disturbances in sensory and/or motor gastrointestinal function, which sometimes may overlap across anatomic regions. Nevertheless, several studies provide evidence for site-specific syndromes.

Colonic Diseases, Functional↗

Prevalence of genotypic resistance among antiretroviral drug-naive HIV-1-infected patients in Belgium.

OBJECTIVES: To estimate the prevalence and the evolution over time (1995-1998) of genotypic resistance to antiviral drugs in antiretroviral drug-naive HIV-1-infected patients in Belgium. DESIGN: Belgian Aids Reference Laboratories provided retrospective samples and clinical data from antiretroviral drug-naive HIV-1-infected patients who visited the hospital for the first time in 1995 (n=45), 1997 (n=75) and 1998 (n=111). Genotypic resistance to the three available classes of drugs was monitored using the Line Probe Assay (Innogenetics, Gent, Belgium). Additionally, ARMS-151 was performed for scoring multinucleoside resistance. RESULTS: The prevalence of genotypic resistance at baseline to nucleoside analogue reverse transcriptase inhibitors (NRTIs) and non-nucleoside reverse transcriptase inhibitors (NNRTIs) were each between 10% and 20% for 1995, 1997 and 1998 without an increasing trend over time. For NRTIs, resistance mutations were mainly related to zidovudine in 1995, whereas in 1997 and 1998 baseline resistance was scored for zidovudine, lamivudine or for both drugs simultaneously. No patients displayed the multi-nucleoside resistance Q151M mutation. Baseline resistance mutations to protease inhibitors (PIs) did not rise significantly: 4.4% in 1995, 8% in 1997 and 9.9% in 1998. When scoring any resistance-related mutation, 26.6% displayed genotypic baseline resistance in 1995, 26.6% in 1997 and 31.5% in 1998. DISCUSSION: The prevalence of genotypic baseline resistance to any drug, as scored with LiPA, in naive HIV-1 patients in Belgium is 29%, with baseline resistance mutations to one or several drugs from all available classes of antiviral drugs. The ability of LiPA to pick up minor variants could be an explanation for the higher overall prevalence we observe, when compared to recent estimates in other countries of 16.3% and 22%, which were based on sequencing methods. According to the European guidelines for resistance testing, resistance testing in Belgium before starting antiviral therapy should be considered.

Acquired Immunodeficiency Syndrome↗