Evidence Based Management of H-Pylori

Evidence-Based Management of H-Pylori

A Brief Description Of The Selected Complaint

Infection with Helicobacter pylori (H. pylori) occurs when H. pylori bacilli contaminate any area of the gastrointestinal tract. H. pylori infection is the most common cause of both duodenal and gastric ulcers. H. pylori is a gram-negative, spiral-shaped organism with sheathed flagella that has been found in at least 90% of duodenal ulcer patients (Cash et al., 2021). Furthermore, this pathogen has been found in 40% to 70% of people who have gastric ulcers (Cash et al., 2021). In H. pylori-infected individuals, the lifetime risk of developing PUD is estimated to be around 15%. (Wang et al., 2015). At the same time, gastric cancer remains the third leading cause of cancer-related death worldwide, with H. pylori infection accounting for 74.7% of total noncardiac gastric cancer occurrences (Wang et al., 2015). However, H. pylori infection has also been observed in people with asymptomatic gastritis and dyspepsia without ulceration; however, eradicating the organism does not appear to improve symptoms in these patients.

Evidence suggests that H. pylori disease affects a sizable and growing number of people worldwide. However, due to the lack of obvious signs or symptoms of active disease, the vast majority are unaware of this ailment. The annual prevalence of peptic ulcers is estimated to be between 0.1% and 1.8%. (Cash et al., 2021). The annual ulcer incidence in pylori-infected individuals is approximately 1%. (Cash et al., 2021). Ulcer formation is caused by two fundamental pathophysiological factors: decreased mucosal protection and increased acid production (Berkowitz, 2020). As previously stated, H-pylori infection is one of the most common causes of ulcers. H. pylori, in particular, causes ulcer formation through both mechanisms: the bacterium damages the mucosal lining and causes an inflammatory process that results in increased acid secretion.

Furthermore, H. pylori infection continues to be transmitted via the oral-faecal and oral-oral routes, with infection rates approaching 100% in developing countries with contaminated water supplies (Berkowitz, 2020). In developed countries with clean water, at least 75% of people over the age of 50 have been infected at some point (Berkowitz, 2020). The risk of relapse is drastically reduced when the organism is eradicated. Thus, social determinants such as living in an overcrowded household, living without a reliable supply of clean water, living in a developing country, and living with someone who has previously been diagnosed with Helicobacter pylori infection all predispose to acquiring the disease (Diaconu et al., 2017). There are, however, numerous antimicrobial combinations and evidence-based management strategies that are effective in treating H.pylori infections.

System Review Is Required

pylori infection continues to be the most common and persistent bacterial infection worldwide; thus, obtaining an accurate, detailed, and necessary review of the systems is critical. H. pylori infection, according to current evidence, jeopardizes not only gastrointestinal tract balance but also affects other systems such as cardiac, haematological, neurological, and metabolic syndromes.

According to Diaconu et al. (2017), the role of H. pylori in the development of idiopathic thrombocytopenic purpura, vitamin B12 deficiency, and iron deficiency anaemia is well understood. Furthermore, current evidence indicates that children with type 1 diabetes are more likely to contract H. pylori infection, especially in cases where diabetes has been present for a longer period of time (Bazmamoun et al., 2016). Another study analysis to consider is the link between Helicobacter pylori infection and preeclampsia. This clinical study data shows abnormal uterine artery Doppler velocimetry, suggesting a role for H. pylori infection in undermining placental development and increasing the risk of developing preeclampsia (Di Simone et al., 2017). Furthermore, evidence suggests that H. pylori infection is linked to metabolic syndrome disorders. According to Upala et al., Helicobacter pylori infection is strongly associated with higher triglycerides, BMI, homeostatic model assessment of insulin resistance (HOMA-IR), systolic blood pressure, and lower HDL (2016).

Thus, H. pylori infection occurs primarily in the gastrointestinal tract; however, relevant evidence-based research quickly urges the association of H. pylori with a variety of conditions other than the gastrointestinal tract. To be sure, this bacterium causes a low-grade inflammatory phase, induces molecular mimicry mechanisms, and interferes with nutrient and drug absorption, likely influencing the occurrence or progression of a variety of conditions (Roubaud Baudron et al., 2013). As a result, screening for H. pylori infection is beneficial by assessing multiple systems holistically rather than focusing solely on the gastrointestinal system. The above research evidence appraisal reveals an innovative perspective of assessing multiple body systems associated with H. pylori infections.

What Would Be Found During A Physical Exam For This Complaint?

The clinical manifestations of Helicobacter pylori infection are not always obvious, ranging from asymptomatic gastritis to gastrointestinal malignancy. The body’s reaction to H. pylori varies. Not everyone infected with H. Pylori goes on to develop ulcers. H. pylori, on the other hand, causes intestinal metaplasia in the stomach, resulting in chronic atrophic gastritis and, in some cases, stomach cancer (Diaconu et al., 2017). H. pylori, on the other hand, alters gastric secretion and causes tissue damage, resulting in Peptic Ulcer Disease (PUD) (Diaconu et al., 2017). In short, many factors influence the response to H. pylori and its clinical manifestations, including genetics, the location and type of PUD, the environment, and diet.

When it comes to specific clinical manifestations of H. pylori, multiple research studies show no significant differences in the appearance, including recurrence of manifestations such as nausea, vomiting, pain, heartburn, or diarrhoea, in patients who are infected with H. pylori and those who are not (Santacroce & Bhutani, 2021). There is no conclusive evidence of a link between H. pylori-related gastritis, abdominal pain, or dyspeptic symptoms and other diseases (Santacroce & Bhutani, 2021).

However, specific clinical manifestations can occur in health conditions where H. pylori infection is the primary contributing factor. For example, the presence of an ongoing H. pylori infection is the most common aetiology of duodenal ulcers. Thus, epigastric burning, gnawing pain about 2-3 hours after meals, relief with foods and antacids, tenderness at the epigastrium and left upper quadrant of the abdomen, and slightly hyperactive bowel sounds are the presenting signs and symptoms for this specific condition (Fitzgerald, 2017). A pylori infection is also the primary cause of non-erosive gastritis and chronic type B (antral) gastritis. The most common presenting signs and symptoms are nausea, burning, and pain in the upper abdomen without reflux symptoms (Fitzgerald, 2017). Primary-care clinicians frequently encounter patients with dyspepsia, which can result from a variety of causes. However, evidence suggests that between 20% and 60% of people with functional dyspepsia have Helicobacter pylori gastritis (Diaconu et al., 2017).

Differential Diagnoses for H. Pylori and the Reasons for Them Acute Gastritis:

This condition encompasses a wide range of events that aggravate inflammatory changes in the gastric mucosa. Many distinct disorders contribute to similar overall clinical manifestations; however, they differ in their distinct histologic characteristics. Furthermore, this disorder can be classified as erosive or non-erosive (caused by Helicobacter pylori) (El-Nakeep, 2020).

Peptic Ulcer Disease (PUD):

PUD is a circumscribed ulceration of the GI mucosa that occurs in areas vulnerable to acid and pepsin. The client’s previous ulcer records tend to predict expected behaviour and the pathological likelihood of future complications. Although the precise mechanisms of ulcer formation remain unknown, the process appears to involve the interaction of acid production, pepsin secretion, H. pylori bacterial infection, and mucosal defence mechanisms (Cash et al., 2021).

Lymphoma of the Gastric Mucosa-Associated Lymphoid Tissue (MALT):

The pathogenetic cascade of gastric lymphoma is being revealed by research data. H. pylori-related gastritis has been shown to be the primary cause of MALT in the gastric mucosa. Certainly, the presence of MALT in the gastric mucosa is a pathological sign of H. pylori infection (Zullo et al., 2014). In contrast, every infected person is at significant implied risk of developing gastric MALT lymphoma, particularly if the infection is prolonged (Zullo et al., 2014).

A Comparison and Contrast of Two H. Pylori Clinical Guidelines

Clinical Guidelines are intended to provide clinicians with up-to-date, evidence-based treatment recommendations for any disorder. The two clinical guidelines for the treatment of H. Pylori for this assignment incorporate recommendations from the American College of Gastroenterology and the American Family Physicians. All patients with active peptic ulcer disease (PUD), a history of PUD (MALT) lymphoma, or a history of endoscopic resection of early gastric cancer (EGC) should be tested for H. pylori infection, according to one implication of both guidelines (American College of Gastroenterology, 2017; American Family Physicians, 2015). Continuous non-endoscopic testing for H. pylori infection is a strategy for people under the age of 60 who have dyspepsia but no other warning signs (American College of Gastroenterology, 2017; American Family Physicians, 2015). Both guidelines also state that whenever H. pylori are identified and treated, retesting to ensure complete eradication of the infection is required. This complete eradication confirmation should be arranged by using a urea breath test, faecal antigen test, or biopsy-based testing at least four weeks after the end of antibiotic treatment and after a one-to-two-week absence from the use of PPIs (American College of Gastroenterology, 2017; American Family Physicians, 2015).

Although the majority of the evidence examined was comparable between the two guidelines, some inconsistencies were noted. On the one hand, the American College of Gastroenterology recommends that, despite an appropriate evaluation, all patients with unexplained iron deficiency (ID) anaemia be tested for H. pylori infection (2017). The American Academy of Physicians, on the other hand, recommends testing for H. Pylori in patients with ID only if dyspepsia is present (2015). Continuous quadruple bismuth therapy for 10-14 days consisting of a PPI, bismuth, tetracycline, and nitroimidazole is a recommended first-line treatment option (American College of Gastroenterology, 2017). Although the American Academy of Physicians acknowledges that other regimens may be used, they maintain that non-bismuth-based quadruple therapy has the highest success rate in eradicating H. pylori (2015). Furthermore, the American Academy of Physicians maintains that quadruple bismuth therapy should not be used as first-line therapy; however, it may be used as first-line therapy in areas of high resistance or when the cost is an important consideration (2015).

Evidence-Based Diagnostic Strategy

Stool antigen testing is the most well-known low-cost method of diagnosing H. pylori, especially when combined with a clinical presentation consistent with other disorders as determined by multiple relevant research appraisals. According to recent evidence-based literature, endoscopy with biopsy is the most accurate test, and the rapid urease test is the preferred diagnostic test for H. Pylori. For example, in a relevant Cochrane report analysis, data from 99 comparisons were used to examine the diagnostic accuracy of these non-invasive tests to detect any H. Pylori bacterium infection (Fischbach & Malfertheiner, 2018). The study findings support the fact that breath tests are more diagnostically accurate than serology tests but have similar accuracy to the stool antigen detection test (Fischbach & Malfertheiner, 2018).

The organism, as previously stated, produces urease, which breaks down urea into ammonia and CO2; this allows the organism to control pH in its local environment in the stomach by neutralizing H+ ions in gastric acid (Fitzgerald, 2017). As a result, urea breath testing is a valuable diagnostic method for determining the presence of H. pylori infection, albeit more expensive than the stool antigen test. Important data indicates that current PPI use may cause a false negative with faecal and urea breath testing. Ideally, the patient should refrain from taking PPI for two weeks prior to these tests (American College of Gastroenterology, 2017).

Serological testing for H. pylori is also available, with the caveat that titers can take years to fade even after successful treatment. However, 12 to 18 months after therapy, 50% of serologically tested individuals have undetectable titers (Fitzgerald, 2021). Endoscopy with biopsy tests should be used in adults over the age of 50 who have new-onset PUD signs and symptoms to rule out the presence of H. Pylori, gastric ulcers, or cancers (American College of Gastroenterology, 2017).

Pharmacological Management Plan

Pharmacological Regimen

The eradication of the H. Pylori bacteria in infected individuals is the empirical pharmacological treatment for H. Pylori. The current pharmacological strategy combines antimicrobial and antisecretory agents. Furthermore, although the mechanism of action is unknown, phytomedicines and probiotics are being used to improve H. pylori eradication (Yang et al., 2014). Guidelines for the management of H. pylori infection are still being developed, and recommendations for first-line therapy, second-third-line therapy, and subsequent therapy differ depending on geographic area. The standard triple therapy of a PPI and two antibiotics (clarithromycin and amoxicillin/metronidazole) is generally used as the first-line regimen for treating H. Pylori infection, according to current evidence-based guidelines. As a result, the standard triple therapy for H. Pylori will include clarithromycin (Biaxin) 500mg BID plus amoxicillin 1g BID or metronidazole (Flagyl) 500mg BID for 14 days plus a PPI for 4 to 8 weeks. Furthermore, because of its high efficiency, safety, and tolerance, bismuth-containing quadruple therapy (BQT) is approved as a first-line optional therapy for eradicating H. pylori in areas with high or low clarithromycin resistance (Hu et al., 2020). This quadruple therapy includes 12 days of treatment with bismuth subsalicylate tablet 525mg four times per day, metronidazole 250mg four times per day, tetracycline cap 500mg four times per day, and a PPI or ranitidine 150mg twice daily. Subsequent therapies and failure therapy regimens for H. Pylori are available for clinical use, but their efficacy and prognosis vary.

Patient Instruction

Individuals infected with H. Pylori must be educated on proper pharmacological treatment to avoid antimicrobial resistance or complications. Educate the client on the importance of taking the prescription as directed. Even if your signs and symptoms have improved, do not stop taking your medication. Medication-specific education should be considered as well. Inform the patient, for example, that metronidazole or clarithromycin may cause a metallic taste in the mouth.

Additionally, education on the use of probiotics and vitamins is required. According to evidence-based research, probiotics as an adjunct to triple therapy can improve triple therapy effectiveness and reduce the incidence of therapy-related diarrhoea, potentially preserving and restoring the intestinal microbiota in adults and children undergoing Pylori therapy (Hu et al., 2020). In addition, an RCT study looked at the effect of H. pylori therapy and vitamin supplementation (C&E) on the incidence and mortality of gastric cancer. This study discovered that vitamins C and E have an inhibitory effect on H. pylori intensity and neutrophilic activity, which aids in the eradication of H. pylori (Li et al., 2019)

Furthermore, education about lifestyle changes, such as avoiding alcohol and smoking, as may interact with current medications or worsen symptoms of the H. Pylori infection. Caffeine, spicy foods, chocolate, and peppermint should be avoided as they may increase acid production (Cash et al., 2021). Reduce your salt intake as well, as evidence suggests that a high salt diet aggravates H. pylori-induced inflammation (Haley & Gaddy, 2016).

Finally, knowing when to notify your primary care provider about worsening symptoms is critical.

Follow-Up

A combination of lifestyle changes and the appropriate pharmacological treatment should provide relief. Following the completion of the entire course of therapy, there must be follow-up visits. It is empirical to repeat the breath test to confirm H. Pylori eradication. Alternative therapies should be considered if the initial therapy is unsuccessful. The selection of the regimen, the patient’s adherence to a multi-drug regimen with various side effects, and the sensitivity of the H. pylori strain to the combination of antibiotics administered are the primary determinants of successful H. pylori eradication (Chey et al., 2017). To determine the erasure of an H. Pylori infection, the clinician must order a urea breath test, faecal antigen test, or biopsy-based testing at least four weeks after the completion of antibiotic therapy and 1-2 weeks after discontinuing PPI use (Chey et al., 2017).

Referrals

When symptoms of haemorrhage, penetration, perforation, or gastric outlet obstruction are present, a consultation with both a surgeon and a gastroenterologist is required, as is admission to a hospital. Clients with recurrences or refractory disease should be referred to a physician for an endoscopy or breath test to rule out H. Pylori.

Case Analysis

M.M., a 64-year-old Hispanic female, arrives at the clinic with a four-week history of intermittent, moderately intense burning/gnawing epigastric pain. The patient denied having melena, hematochezia, or hematemesis symptoms. Her medical history included peptic ulcer disease. M.M. claims to have travelled from a rural Colombian town to Camden City about two months ago. M.M. lives with her entire extended family. M.M. recalls her husband experiencing similar signs and symptoms. She also admitted to using an over-the-counter analgesic containing acetaminophen, aspirin, and caffeine in the past. Bowel sounds were heard in all four quadrants during the examination. However, there was mild tenderness over the epigastrium.

Conclusion

Based on current evidence-based research, Nurse Practitioners are critical clinicians in a variety of healthcare settings for assisting with H. Pylori diagnosis and treatment. This paper presented H. Pylori management based on current guidelines for successfully treating and eradicating the infection. In summary, this paper presented the available interventions as well as the regimen goals for the treatment of H. Pylori, with a focus on alleviating pain and discomfort, promoting healing, limiting complications, and preventing recurrences while minimizing treatment costs and side effects.

References

American College of Gastroenterology. (2017). ACG Clinical Guideline: Treatment of Helicobacter pylori Infection, American Journal of Gastroenterology. 112(2), 212-239. 10.1038/ajg.2016.563

American Family Physicians. (2015). Diagnosis and Treatment of Peptic Ulcer Disease and H. pylori Infection., National Center for Biotechnology Information. 91(4), 236–242.

Bazmamoun, H., Rafeey, M., Nikpouri, M., & Ghergherehchi, R. (2016). Helicobacter Pylori Infection in Children with Type 1 Diabetes Mellitus: A Case-Control Study. Journal of research in health sciences, 16(2), 68–71.

Berkowitz, A. (2020). Clinical Pathophysiology of Systems. MedMaster, Inc.

Cash, J. C., Glass, C. A., & Mullen, J. (2021). Family practice guidelines. Springer Publishing Company.

Chey, W., Leontiadis, G., Howden, C., Moss, S. (2017). ACG Clinical Guideline: Treatment of Helicobacter pylori Infection, American Journal of Gastroenterology: 112(2), 212-239 doi: 10.1038/ajg.2016.563

Diaconu, S., Predescu, A., Moldoveanu, A., Pop, C. S., & Fierbințeanu-Braticevici, C. (2017). Helicobacter pylori infection: old and new. Journal of medicine and life, 10(2), 112–117.

Di Simone, N., Tersigni, C., Cardaropoli, S., Franceschi, F., Di Nicuolo, F., Castellani, R., Bugli, F., de Waure, C., Cavaliere, A. F., Gasbarrini, A., Sanguinetti, M., Scambia, G., & Todros, (2017). Helicobacter pylori infection contributes to placental impairment in preeclampsia: basic and clinical evidence. Helicobacter, 22(2), 10.1111/hel.12347.

El-Nakeep, S. (2020). Acute Gastritis. Medscape Physician. https://emedicine.medscape.com/article/175909-overview.

Fischbach, W., & Malfertheiner, P. (2018). Helicobacter Pylori Infection. Deutsches Arzteblatt international, 115(25), 429–436. https://doiorg.felician.idm.oclc.org/10.3238/arztebl.2018.0429

Fitzgerald, M. A. (2017). Nurse practitioner certification examination and practice preparation. F.A. Davis Company.

Haley, K. P., & Gaddy, J. A. (2016). Nutrition and Helicobacter pylori: Host Diet and Nutritional Immunity Influence Bacterial Virulence and Disease Outcome. Gastroenterology research and practice, 2016, 3019362. https://doi.org/10.1155/2016/3019362

Hu, Y., Zhu, Y., & Lu, N. H. (2020). Recent progress in Helicobacter pylori treatment. Chinese medical journal, 133(3), 335–343. htts://doi-org.felician.idm.oclc.org/10.1097/CM9.0000000000000618

Li W.Q, Zhang Y, Ma JL, Li., Zhang L., Zhang Y., et al. (2019). Effects of Helicobacter pylori treatment and vitamin and garlic supplementation on gastric cancer incidence and mortality: follow-up of a randomized intervention trial. BMJ 2019; 366:l5016.doi: 10.1136/bmj.l5016

Roubaud Baudron, C., Franceschi, F., Salles, N., & Gasbarrini, A. (2013). Extragastric diseases and Helicobacter pylori. Helicobacter, 18 Suppl 1, 44–51. https://doi-org.felician.idm.oclc.org/10.1111/hel.12077

Santacrose, L., & Bhutani, M. S. (2021). Helicobacter Pylori Infection Clinical Presentation. Emedicine. https://emedicine.medscape.com/article/176938-clinical – :~:text=No definite evidence demonstrates a pylori eradication results in sustained.

Upala, S., Jaruvongvanich, V., Riangwiwat, T., Jaruvongvanich, S., & Sanguankeo, A. (2016). Association between Helicobacter pylori infection and metabolic syndrome: a systematic review and meta-analysis. Journal of digestive diseases, 17(7), 433–440. https://doi.org/10.1111/1751-2980.12367

Wang, Y. K., Kuo, F. C., Liu, C. J., Wu, M. C., Shih, H. Y., Wang, S. S., Wu, J. Y., Kuo, C. H., Huang, Y. K., & Wu, D. C. (2015). Diagnosis of Helicobacter pylori infection: Current options and developments. World journal of gastroenterology, 21(40), 11221–11235. https://doi-org.felician.idm.oclc.org/10.3748/wjg.v21.i40.11221

Yang JC, Lu CW, Lin CJ. (2014). Treatment of Helicobacter pylori infection: Current status and future concepts. World J Gastroenterology; 20(18): 5283-5293

Zullo, A., Hassan, C., Ridola, L., Repici, A., Manta, R., & Andriani, A. (2014). Gastric MALT lymphoma: old and new insights. Annals of gastroenterology, 27(1), 27–33.

ORDER A PLAGIARISM-FREE PAPER HERE

We’ll write everything from scratch

---

Discuss the drug therapy used in the treatment of H. pylori to alleviate symptoms, promote healing, prevent complications, and prevent a recurrence.

2 paragraphs

APA format

2 peer-reviewed references