what is h pylori serology?

Answer 1

Very interesting question!

when I was a lad (in a galaxy far far away), I was taught that poor diet, irregular meals, spicy food and smoking caused ulcers.

In the 90s someone looking at biopsies from ulcers noticed a number of spiral organisms associated with the ulcer. The more they looked the more they found. There organisms were isolated, they are now called helicobacter pylorii, and one brave chap gave them to himself!

It was thus proved that this stomach infection is present in 85% of people with ulcers and is thought to be the cause.

The blood test for the bug- helicobacter serology is positive in 85 % of patients who have the organism. (If they are treated however it may remain positive!). It is a useful screen test but has this 15% false -ve rate, which also makes it a little unreliable. The definitive test for helicobacter is the 'Breath Test', its a bit fiddly but just about 100% accurate if carried out properly.

Answer 2

Helicobacter pylori (H.Pylori) serology is the most reliable method of testing in active GI tract hemorrhage. Serology means the study of antigen-antibody reactions in Vitro (in glass, as in a test tube).
Serology: Serological tests detect the presence of antibodies to H.pylori. Positive serology indicates current or past infection with H.pylori. A positive test does not confirm active disease. A negative serological test provides >95 % assurance that there is no H.pylori infection. Serology should not be used in the evaluation of treatment of H.pylori because the antibody titre takes many months (or even years) to decline.
Please see the web pages and Google search for more details on Helicobacter pylori serology.

Answer 3

As your question was solely referencing serology, and not a breakdown of the symptoms, causes and treatments for the gastric results of an infection by H.pylori, I will just discuss that matter. Serological tests detect the presence of antibodies to H.pylori. Positive serology indicates current or past infection with H.pylori. A positive test does not confirm active disease. A negative serological test provides up to 95 % assurance that there is no H.pylori infection. Serology should not be used in the evaluation of treatment of H.pylori because the antibody titre takes many months (or even years) to decline. There is more on this subject, the details are quite technical, and therefore probably not suitable for inclusion here.

I add a link which might be of interest.


http://www.jr2.ox.ac.uk/bandolier
/band35/b35-4.html

Hope this helps
Matador 89

Answer 4

Here is a natural remedy to cure your acid reflux/gerd and hearth burn http://acidreflux.toptips.org

Acid reflux disease, also known as gastro-esophageal reflux disease, or GERD, occurs due to the coexistence of two medical conditions. The first acid reflux disease contributing condition is a retrograde flow of stomach contents into the esophagus. However, the reflux itself does not necessarily lead to gastro-esophageal reflux disease symptoms or histologic changes, and can occur among healthy individuals as well. In this case, the process is referred to as "physiologic gastroesophageal reflux".

Answer 5

it is a bacteria that thrives in stomach acid .it can be difficult to eliminate and can have serious consequences.it can be detected on your breath or by endoscopy.a course of three drugs is given to try to eliminate it

Answer 6

Several methods can be used to diagnose Helicobacter pylori infection. Most of them require upper gastrointestinal endoscopy for retrieval of a gastric biopsy specimen. For serology, no upper gastrointestinal endoscopy is required, but blood must be obtained to detect H. pylori antibodies. H. pylori serology is attractive in comparison with other diagnostic methods because it is simple, inexpensive, and less of a burden for the patient. Several kits for the detection of H. pylori by serology have become commercially available since the discovery of H. pylori by Warren (87) in 1983. Most of these H. pylori serology kits are based on various antibody preparations and different techniques.

The introduction of commercially available H. pylori kits has led to an increase in the number of studies that have evaluated kit characteristics. Recently, a systematic review comparing the accuracies of commonly used commercial serology kits for the detection of H. pylori infection has been conducted (48). To account for the different reference standards and designs used by various investigators, only studies that evaluated pairs of serology kits and that compared the kits only within those studies were included. A more appropriate method of comparing different diagnostic tests and the performance of different interpreters of one test is to calculate the area under the receiver operating characteristics curve (AURC) for each test (83). To correct for dependence between AURCs within the same study population, we used a random-effect model. By reviewing the literature, we also tried to determine whether H. pylori serology can accurately diagnose H. pylori infection. However, in contrast to the study by Loy et al. (48), we reviewed all the studies that evaluated commercially available H. pylori serology kits.
DATA COLLECTION AND EXTRACTION

Identification and eligibility of publications. A computerized and manual literature search was performed in early 1998. Relevant publications were identified in MEDLINE (1983 to 1997) with the medical subject heading terms Helicobacter or pylori, Sero*, Sera*, Seru*, Sensitivity, and Human in checktags. Furthermore, additional publications were retrieved by reviewing references in publications found by MEDLINE. The criteria used to select publications were as follows: H. pylori infection was established before treatment; the H. pylori serology kit was commercially available; the number of patients, prevalence of infection, and the sensitivity and specificity of the H. pylori serology kit were described or could be calculated; and the studies were published in Dutch, English, French, or German.

Data analysis. New diagnostic tests are mainly evaluated by determining the sensitivity and specificity of the test. For evaluative purposes, the sensitivity and specificity are less useful (83). On the basis of the receiver operating characteristic (ROC) curve, we calculated the AURC, which is a measure for the diagnostic performance of a test (42). It is independent of cutoff points and reasonably immune to selection bias. Depending on the serology kit result, one should use different methods to calculate the AURC. We used a method to estimate the AURC for kits with a quantitative test result by using one combination of a true-positive rate and a false-positive rate on the basis of the assumption that the data for the H. pylori-infected and noninfected persons were logistically distributed and had equal variances (84). On the other hand, for serology kits with a qualitative test result, we used the trapezium method to calculate the AURC (36). However, comparison of the H. pylori serology kits revealed that the diagnostic performance differed substantially depending on how the AURC was calculated. Therefore, we decided to estimate the AURCs by the trapezium method, irrespective of the distribution of the test result. Use of the trapezium method to estimate the AURC of a serology kit with a quantitative test result possibly underestimates its diagnostic performance (36).
The AURC was used to explore possible differences between clinical features of study populations and methodological aspects of the serology kits. The tests were stratified into the following: report type (abstract, letter, or article), publication year (1991 to 1997), whether the study population was a consecutive series or a selection of a relevant study population, whether or not the patients had dyspeptic symptoms, the nationality of the study population, the reference standard used, the serology kit used, kit scale (quantitative, qualitative), the type of immunoglobulin (immunoglobulin A [IgA], IgG, and IgM simultaneously, IgA alone, or IgG alone) used to detect serum antibodies, the analysis technique of the serology kits (agglutination, enzyme immunoassay [EIA], enzyme-linked immunosorbent assay [ELISA], fixation, or immunochemical analysis), and whether whole blood or serum was used. We could not examine whether the generation of the test influenced performance because few studies mentioned this.

Statistical methods. We first tried to model the heterogeneity between the studies by means of an ordinary least-squares regression equation, in which all the clinical features and methodological aspects were simultanously included. Unfortunately, this was not possible because of convergence problems. A best subset analysis was also not possible for the same reasons. Therefore, we decided to perform a separate regression analysis for each clinical feature. It is very likely that the AURCs for different serology kits are correlated when they are used with the same study population. By introducing a random effect for study population, we could model dependency between kits within the same study population (24) (see the Appendix). Moreover, the imprecision of the AURCs varied per study. In order to correct for the heterogeneity in the precision of the AURCs caused by different study sizes, we also performed a weighted regression analysis with weights proportional to 1/SE2, where SE is the standard error (see the Appendix). Whenever AURC is equal to 1 or 0, SE will be 0. If this occurred, the study was excluded from the analysis.
For each regression model an overall F(NDF,DDF) test, where NDF is the degree of freedom in the numerator and DDF is the degree of freedom in the denominator of the F test, was used to examine whether the hypothesis beta 1 = 0, beta 2 = 0, . . ., beta k = 0 (no fixed effect) should be rejected. Akaike's information criterion (AIC) is given to choose between the ordinary least-squares model, the random-effects model, and the weighted-random-effects model for each feature. The higher the AIC, the better the model fit. We also performed a weighted-random-effect regression analysis, using the significant features from the previous model simultaneously, in order to correct for possible confounding. These analyses were performed with SAS software (70). For multiple comparisons the Bonferroni correction was used to keep the overall alpha level at 0.05.





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http://www.dhaarvi.blogspot.com

Answer 7

Helicobacter pylori is a spiral, Gram(-) bacterium that inhabits the stomach of more than half the people of the world. In developing countries, 50 to 90% of the population is infected, and children acquire infection at an early age. Lower socioeconomic status correlates with higher prevalence. In developed countries, the prevalence in the younger population is around 5 to30%. H. pylori likely is spread via the fecal-oral route, but also may be transmitted by the oral-oral route and the spread of contaminated secretions.

Most individuals infected with H. pylori are asymptomatic and unlikely to develop a serious medical problem from the infection. However, H. pylori is the single most common cause of peptic ulcer disease and has been implicated as a risk factor for gastric adenocarcinoma. The low-grade gastric lymphoma of mucosa-associated lymphoid tissue (MALT) is strongly associated with H. pylori infection. The causal relationship between H. pylori and nonulcer dyspepsia remains controversial. Controversy also persists regarding the role of H. pylori in gastroesophageal reflux disease (GERD).



In 1998, the American College of Gastroenterology developed clinical guidelines that suggest the approach to management of H. pylori in the American population. These guidelines were based on the interpretation of scientifically valid literature data. Since then, a number of published clinical trials have addressed the role of H. pylori in non-investigated and non-ulcer dyspepsia, GERD, and NSAID use. With a few exceptions, well-designed, randomized, controlled trials are still lacking in these areas, and existing information has not been able to sway the recommendations unanimously in one direction or another. The guidelines concluded that:

H. pylori infection is common in the general population.
Most infected individuals are asymptomatic and unlikely to develop serious medical problems from the infection.
Diagnostic tests for H. pylori should only be performed if treatment is intended.
Testing for H. pylori is indicated in patients with active peptic ulcer disease, a past history of documented peptic ulcer disease, or gastric MALT lymphoma.
H. pylori is classified as a group I (definite) carcinogen by the World Health Organization's International Agency for Research on Cancer. It, therefore, will be difficult to withhold treatment for this infection in any individual with a positive test.
Principles of testing for H. pylori infection.

Patients with non-bleeding gastric ulcer at endoscopy (strongly recommended*) The test of first choice is a urease test (Clotest, Pyloritek, Hp-fast). Absence of H. pylori on biopsies taken from different gastric sites should suggest the possibility of aspirin or NSAID use. Histology, unless indicated, is not generally necessary and is expensive. Biopsy urease tests have reduced sensitivity in patients taking proton-pump inhibitors (PPIs) (~41%), H2-receptor antagonists (~76%), antibiotics or bismuth-containing compounds, and in patients with recent or active bleeding. In such patients, obtaining biopsies from different gastric sites improves sensitivity of the urease test, though it remains significantly lower than results on antral biopsies taken from patients not on antisecretory therapy (~97%). If reduced sensitivity is suspected, serology testing for H. pylori antibodies is appropriate (86-94% sensitive, 79-95% specific). Documentation of eradication is unnecessary for uncomplicated ulcer disease, assuming an appropriate treatment regimen was used and the patient was compliant.

Patients with non-bleeding duodenal ulcer at endoscopy (strongly recommended*) Approximately one fourth of duodenal ulcers may be H. pylori-negative. Therefore, it is recommended that confirmatory testing for H. pylori be done when the diagnosis of duodenal ulcer is made endoscopically. A urease test on an antral biopsy is most cost-effective. Similar principles of management, as noted above, apply to duodenal ulcers.

Patients with recently bleeding ulcer at endoscopy (strongly recommended*) Urease testing or biopsy may be compromised if there is blood in the gastric lumen. If possible, biopsies should be taken from the antrum and corpus for histology. H. pylori serology is the most reliable method of testing in active GI tract hemorrhage. Eradication should be confirmed. The preferred method is urease breath test (UBT; ~96% sensitive; ~99% specific). The UBT should be delayed for up to four weeks after completing treatment. A newer test, the H. pylori stool antigen (HpSA; sensitivity ~90%, specificity ~95%) may have utility in the primary diagnosis and eradication evaluation of H. pylori. Given the limited number of studies that evaluated the performance of the HpSA, it is premature to reach a conclusion regarding its clinical utility. If serology is used to confirm eradication, it would be preferable to perform the identical ELISA at the same time on a six-month post-treatment serum sample and on a stored pretreatment sample. Serum antibody titers may take as long as two years to disappear.

Patients with past history of peptic ulcer (strongly recommended*) Previous radiologic or endoscopic studies should be reviewed to confirm the presence of peptic ulcer. A serologic test should be performed to determine H. pylori infection status. Eradication need not be confirmed.

Patients with gastric MALT lymphoma (strongly recommended*) Since endoscopy is routinely performed in the management of gastric MALT, H. pylori status is best determined by histology. It will be necessary to confirm successful eradication in all cases. Since patients will require follow-up biopsies to follow the neoplasm, histology should be used to confirm eradication.

Patients with early gastric adenocarcinoma (reasonable**) Limited data suggest that eradication of H. pylori may be beneficial in patients with early gastric cancer treated with local resection. In one study, after a mean of six years, cancer had recurred in 10 (14.9%) of 67 untreated patients, and in one (1.5%) patient treated for H. pylori. This study was nonrandomized and subject to bias. Randomized trials may provide valuable support for eradication of H. pylori in preventing recurrence of early gastric adenocarcinoma.

Patients with non-investigated dyspepsia (reasonable**) Dyspepsia is defined as "pain or discomfort centered in the upper abdomen." Before embarking on the diagnostic journey to determine the cause of dyspepsia, a patient may be said to have "non-investigated" dyspepsia. Some studies have suggested that the "test and treat" approach in patients with non-investigated dyspepsia may be cost-effective, but well-designed, randomized controlled trials to validate this approach are needed. Eradication in such patients is not a guarantee of long-term relief. Patients may be tested on a case-by-case basis and treatment offered to those with a positive result. Follow-up testing is not recommended in this scenario, or in any of the clinical situations noted below.

Patients with nonulcer dyspepsia (reasonable***) Approximately 40% of patients with dyspepsia have endoscopic evidence of peptic ulcer, reflux esophagitis, or malignancy. The remainder are classified under non-ulcer dyspepsia (NUD). Although about half the patients diagnosed with NUD have H. pylori infection, convincing evidence of a causal relationship with H. pylori is currently not available despite recent large clinical trials and subsequent meta-analyses. On the basis of existing data, it is conceivable that a subset (5-10%) of patients with NUD will be cured by H. pylori eradication. Predictors of treatment response remain obscure. Patients may be tested on a case-by-case basis and treatment offered to those with a positive result.

Patients with family history of gastric adenocarcinoma (reasonable***) Patients of Japanese, Korean, or Chinese descent with either a family history or perceived fear of gastric adenocarcinoma may be tested for H. pylori. Treatment should be offered to any individual who tests positive.

GERD patients on long-term treatment with PPI (not recommended***) The preponderance of data presently suggests that there is no need to test for H. pylori in GERD patients on long-term treatment with PPI or patients being considered for PPI treatment. The role of H. pylori infection in GERD remains controversial.

Patients treated long-term with NSAID or ASA (not recommended**) At present, the weight of evidence does not suggest that H. pylori infection increases the risk of ulcer formation or ulcer complications in NSAID users. Limited data raise the possibility that H. pylori infection may, however, potentiate the effect of low-dose aspirin on ulcer bleeding. Since an extremely large number of Americans are on low-dose aspirin, a strong recommendation to test and eradicate all positive cases cannot be made based on a few studies. Further studies are needed to provide definitive recommendations regarding H. pylori testing in long-term aspirin users.

Asymptomatic individuals (not recommended*) Asymptomatic individuals should not be tested for H. pylori infection. However, in any person testing positive for infection, treatment may be offered after a full discussion about the potential risks, including the possibility of Clostridium difficile infection from antibiotic use as well as minor adverse events.

Suggested regimens for the treatment of patients with H. pylori infection. The highest eradication rates are achieved with the following regimens:

PPI (lansoprazole 30 mg or omeprazole 20 mg) + amoxicillin 1000 mg OR metronidazole 500 mg + clarithromycin 500 mg (each drug given bid for 14 days).

Bismuth subsalicylate 525 mg qid + metronidazole 500 mg tid + tetracycline (each drug given bid for 14 days, not FDA approved).

Bismuth subsalicylate 525 mg qid + metronidazole 500 mg tid + tetracycline 500 mg qid + PPI qd. Given for 14 days.

Cure rates:
Approximate cost to patient:

PPI + A + C = 85-90%
$230

PPI + M + C = 80-90%
$225

B + M + T = 82-96%
$15

PPI + B + M + T = 94-98%
$130

H2RA + B + M + T=84-94%
$25



Treatment failures. Poor compliance on the part of patients and the development of antibiotic resistance are the most common causes of treatment failure. Patient compliance can be improved by choosing a simple and well-tolerated regimen. Metronidazole resistance is increasing in the U.S. and is found in about half the strains. This can vary from region to region. In contrast, clarithromycin resistance is low (7-11%). However, there may be a trend of rising resistance due to widespread use. Resistance to amoxicillin is rare.

First, compliance should be addressed. If the initial regimen contained metronidazole or clarithromycin, then second-line treatment should replace clarithromycin with metronidazole or vice versa. If the first-line therapy contained both clarithromycin and metronidazole, quadruple therapy consisting of a PPI, bismuth, tetracycline, and metronidazole should be selected. The antibiotic sensitivity pattern of the organism can be established before the second-line therapy is chosen. However, it is equally acceptable to manage a patient with failed eradication by re-treating with a different antibiotic regimen without recourse to culture and sensitivity.

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