<?xml version="1.0"?>
<xml><ArticleSet><Article><Journal><PublisherName>Radiance Research Academy</PublisherName><JournalTitle>International Journal of Current Research and Review</JournalTitle><PISSN>2231-2196</PISSN><EISSN>0975-5241</EISSN><Volume>12</Volume><Issue>4</Issue><IssueLanguage>English</IssueLanguage><SpecialIssue>N</SpecialIssue><PubDate><Year>2020</Year><Month>February</Month><Day>28</Day></PubDate></Journal><ArticleType>Healthcare</ArticleType><ArticleTitle>Blind Helicobacter pylori Treatment in Dyspeptics in a High Prevalence Area&#xD;
</ArticleTitle><ArticleLanguage>English</ArticleLanguage><FirstPage>01</FirstPage><LastPage>07</LastPage><AuthorList><Author>Wadzani Gashau</Author><AuthorLanguage>English</AuthorLanguage><Author> Aisha Shehu Adamu</Author><AuthorLanguage>English</AuthorLanguage></AuthorList><Abstract>Background: The initial management of dyspepsia is shifting away from the invasive endoscopic biopsy procedure to identify H. pylori before eradication treatment. A test-and-treat strategy is firmly in place, but choices can be limited in resource constrained environments.&#xD;
Objective: To investigate the short term effect of blind eradication therapy in management of dyspeptic patients prior to knowledge of H. pylori infection status by serology and histology.&#xD;
Patients: A cross sectional study of 125 consecutive patients presenting at a tertiary facility with dyspepsia were screened for other diseases and then offered blind triple H. pylori eradication therapy.&#xD;
Methods: Participants underwent clinical evaluation and completion of a structured questionnaire eliciting sociodemographic, smoking and drinking habits and drug history. Stored sera were tested for liver transaminases, total protein, albumin, creatinine, urea, Hepatitis B surface antigen, Hepatitis C virus antibody and H. pylori IgG antibody by ELISA at the end of recruitment, while stool microscopy, occult blood test and abdominal ultrasound scan were done before upper gastrointestinal endoscopy, where antral biopsy specimens obtained were processed for H. pylori identification and histological assessment. Patients received oral amoxicillin 1g and clarithromycin 500mg twice daily or metronidazole 400mg three times daily (in place of clarithromycin) and omeprazole 20mg twice daily for fourteen days andcame for follow-up at two and four weeks for assessment of treatment response. Data were entered into a computer and analysed using SPSS Version 16. Descriptive statistics, Chi- square test with Yates correction, t-test, ANOVA and the Cochran-Mantel Haenszel test to compare proportions of treatment success were used. Sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) were determined. P values &lt; 0.05 were considered significant.&#xD;
Results: All patients (125) completed the study, 76 (60.8%) were females and the mean age of subjects was 35.3 &#xB1; 12.70 years (range 18 &#x2013; 84); 74.4% of respondents were &lt; 42years of age and 90% &lt; 55 years. H. pylori were detected by histology in 100 (80.0%) patients, 99 of whom were among the 117 (93.6%) positive by serology (Sensitivity 99%, PPV 84.6%, efficiency 84.9%). Endoscopy was normal in 5% of patients and gastritis 39.5%, oesophagitis 27.7%, and duodenitis 22.7%. The relationship between chronic gastritis inflammatory activity and H. pylori infection status was highly significant. Chi square X2 = 24.33 p= 0.000001; Yates correction X2 = 20.04 p=0.000008. Symptom improvement was highly significant at both 2 and 4 weeks from baseline and between the two visits. (p=.000). Cochran-Mantel Haenszel test to compare proportions of treatment success by H. pylori status was highly significant (Q=112.067 p=.000)&#xD;
Conclusion: On a short term basis, blind empirical H. pylori eradication therapy is effective in the management of dyspeptic patients in a high prevalence area and can obviate the need for testing before treatment. Serology concurred very well with histology as a method of infection identification.&#xD;
</Abstract><AbstractLanguage>English</AbstractLanguage><Keywords>Dyspepsia, Helicobacter pylori, High prevalence, Empirical treatment, Outcome</Keywords><Fulltext>Introduction&#xD;
&#xD;
Dyspepsia is a common and often bothersome symptom complex related to the upper gastrointestinal tract and has an extensive differential diagnosis including gastroduodenal, oesophageal and biliary disorders among others. At presentation, patient symptoms tend to be multiple and do not reliably predict underlying causes or endoscopic findings. &#xD;
&#xD;
Pooled data from 99 studies put the global prevalence in the community at 20.8% with North European and American studies at 22% and Africa and South America, 35.7% and 37.7% respectively.1 In Nigeria, a prevalence of 26% in a community-based study in northeastern2 and 45% in the middle belt regions were noted over the same period.3 Chronic or recurrent dyspeptic symptoms have been reported in 20-30% of people in Britain4,5 and the incidence of the first time symptoms at 1% annually in the community.6 The wide variation in prevalence persists even when same diagnostic criteria are used.1 Dyspepsia increases with age2,3 and is commoner in smokers, NSAID users and in females.1&#xD;
&#xD;
In the past, the need to identify the underlying cause of dyspepsia led to wide spread use of endoscopy where in the United Kingdom for instance, more than 1% of the population underwent gastroscopy each year.7 However, despite its high degree of diagnostic accuracy, qualitative systematic review does not support its effectiveness in managing dyspeptics, thus making generalized usage unrealistic.8&#xD;
&#xD;
With the identification of Helicobacter pylori (H. pylori) as the most important aetiological agent of chronic active gastritis and peptic ulcer disease, and epidemiological causal relationship to gastric cancer and classification as a group 1 carcinogen9 a lot of progress has been made in detecting this organism in non-invasive ways in place of endoscopy in patients with upper gastrointestinal symptoms with the assurance that the subgroup with underlying ulcer disease could be cured and the risk of developing actual ulcer disease10,11gastric cancer and lymphoma12 removed in non-ulcer dyspepsia.&#xD;
&#xD;
H. pylori as the most common chronic bacterial infection in humans13 affects 4.4 billion people worldwide according to pooled data from 62 countries.14 In Northern Europe and America, approximately one third of the population is affected15 but prevalence varies amongst ethnic groups, while more than 50% are infected15 in Eastern Europe, South America and Asia, and in Africa, 70.1%.14&#xD;
&#xD;
Reported pooled prevalence of 87.7% is highest in Nigeria14 where rates in north are 58%, 69% and 91% in children  0.05). This differential age prevalence in our cohort supports the suggestion that serology can be used for screening young dyspeptics, as inaccurate test results are said to be more common in the elderly.33&#xD;
&#xD;
Epigastric pain and tenderness as previously documented in the same community34 as the commonest clinical features in the index population is in consonance with a report from Zaria35 unlike nocturnal pain in Kano subjects.18 Patients who were H. pylori positive had more symptoms than those without, but this did not achieve statistical significance. While data from multicenter studies have suggested that age should be discountenanced in favour of alarm symptoms due to its poor predictability of underlying pathology36 neither age nor alarm symptoms were predictive of underlying pathology in this study group which further supports the NICE recommendation that all dyspeptic patients without alarm symptoms irrespective of age should initially be managed without endoscopy.37&#xD;
&#xD;
As previously documented in this population, antral gastritis (37.6%) remains the most frequent finding38 as against gastritis with duodenitis in some series.17,35&#xA0; We found no endoscopic abnormalities in 5% of patients who belonged to the H. pylori negative group, which agrees with the 6% from Ife.39 Our findings support the report that systematic review of models using risk factors, history, and symptoms did not reliably distinguish between functional dyspepsia and organic disease40or severity of gastritis41 as all our cases could be categorized as non-ulcer dyspepsia, unlike a study in northwestern Nigeria which reported equal rates of non-ulcer dyspepsia and peptic ulcer disease (34.5% and 35% respectively), distantly followed by gastritis (9.9%).18&#xD;
&#xD;
As previously highlighted as the African enigma, peptic ulceration is still lower in this population compared to the rate of H. pylori infection.38 This is attributed to the strains of H. pylori42 and the lower basal acid and maximum acid outputs in asymptomatic African controls43 compared to westerners, possibly due to the less pathogenic effect of H. pylori infection acquired in childhood than in adulthood as suggested by Graham.44&#xD;
&#xD;
Histology to a significant extent corroborated the validity of serology in detecting H. pylori in our patients not minding the possibility that prior antibiotic treatment or inadequate biopsies could have reduced the detection rate.&#xD;
&#xD;
The degree of histological activity was more in those positive by either serology or histology or both attaining high statistical significance (p &lt; 0.000001), thus comparable with studies utilizing 13C levels where the degree of histological gastritis corresponded to the number of H. pylori organisms.45&#xD;
&#xD;
Giardiasis which can be chronic and may not produce diarrhoea, and responds to metronidazole46 has been suggested as an important differential in dyspepsia in Scottish children47 was not detected in any of our patients.&#xD;
&#xD;
Abdominal ultrasound scan is still important in evaluating dyspepsia as demonstrated in two patients positive for H. pylori, yet had gallbladder disease. &#xD;
&#xD;
The reported presence of both HBV (13%) and HCV (6.8%) and dual (1.6%) infections occurring exclusively in the H. pylori serology positive subjects may just be a reflection of the trend in the population48,49 as there was no significant statistical relationship to the status of infection.&#xD;
&#xD;
All the serologically positive patients at 2 weeks after H. pylori eradication therapy indicated improvement in symptoms with 5.1% showing much improvement. By 4 weeks, an even higher proportion (88.9%) had much improved (p=.000) which is the expected outcome of specific therapy.&#xD;
&#xD;
Conversely, in the H. pylori negative group, all patients who reported initial improvement at 2 weeks had a decline in outcome at 4 weeks. The 6 subjects (75%) who reported much improvement declined to &#x201C;improved&#x201D; and the other 2 (25%) reverted to the &#x201C;same&#x201D; (status quo ante). This is the anticipated response when eradication therapy is used in non-H. pylori dyspepsia.&#xD;
&#xD;
While this inferior response in the uninfected group supports the view that the empirical use of antibiotics without the confirmation of H. pylori is not recommended50 the overwhelming (98.4%) response in our patients, (83.2% much improved and 15.2% improved) at 4 weeks strongly supports the empirical use of antibiotics; more so, they all received eradication therapy before their infection status were known. Only 2 (1.6%) of 125 patients at 4 weeks that reverted to status quo ante can be assumed to have inappropriately received eradication therapy. &#xD;
&#xD;
Those who benefitted included patients with oesophagitis and reflux symptoms (gastric and biliary) though the beneficial effect of PPI related acid suppression in this group cannot be ruled out considering the short period of follow up. &#xD;
&#xD;
If we depended solely on the gold standard test, the relief reported by 23 patients (17 histological and 6 of 8 serological) would have been denied them, thus supporting the suggestion that a response to eradication of H. pylori in 5&#x2013;10% of all patients with non-ulcer dyspepsia would make screening and treatment for H. pylori a bene?cial option, irrespective of any other potential bene?ts.51&#xD;
&#xD;
Limitations of the study&#xD;
&#xD;
Our study showed that all our patients could initially be started on eradication therapy and other approaches used if some showed no improvement, however, concerns still remain because of the possibility of delayed diagnosis of gastric cancer, 87 cases of which were reported in our hospital52 a referral tertiary institution over a 16-year period. Reports from other parts of Nigeria also indicate that gastric malignancies have been seen in the third and fourth decades in patients though they presented with complicated dyspeptic symptoms some lasting 12 months.53 Even though endoscopy in all our patients removed intervention bias as may be seen in comparative studies of test-and-treat versus endoscopy and treatment54 the possibility of patient satisfaction after detailed explanation of the procedure may have positively impacted treatment outcome in the short term. &#xD;
&#xD;
In light of the reported resistance issues, it must be emphasized that the triple therapy we employed in our patients may no longer be appropriate as the antibiotic stewardship in Nigeria is suboptimal due to the high rate of over-the-counter availability of prescription-only medicines including antibiotics and antibiotic-containing triple therapy ulcer drugs.55,56&#xD;
&#xD;
The fear of empirical treatment increasing the problem of community-acquired antimicrobial resistance in view of the rather high inappropriate prescription rates in primary care practice in some countries57 can be minimized if appropriate antibiotic stewardship is embraced.57,58&#xD;
&#xD;
Conclusion&#xD;
&#xD;
H. pylori must be viewed as an infection which requires specific eradication therapy using appropriate regimen where susceptibility testing is available in dyspepsia management in view of the widespread resistance to clarithromycin and metronidazole reported in several regions of the world. Where it is not as is often the practice among gastroenterologists, empirical therapy must be based on usage of quadruple therapy, local bacterial resistance patterns and recommendations, and drug availability.&#xD;
&#xD;
While it has been advocated that even in high prevalence areas there should be testing before treatment for H. pylori our study has conclusively shown that in high prevalence resource limited areas, blind H. pylori eradication is effective and feasible and can obviate the need for specific methods of H. pylori detection and endoscopy in most of our patients. Therefore, the suggested cost-effective approach to dyspepsia management in our population is: treat to eradicate, and if no improvement; give empirical PPIs, and lastly administer endoscopy as appropriate. We recognize however, that the management of dyspepsia should vary in different countries depending on the incidence of H. pylori infection and gastric cancer rates as cancers are commoner in some regions than others.&#xD;
&#xD;
Conflict of Interest&#xD;
&#xD;
The authors have no conflict of interest to declare&#xD;
&#xD;
Funding&#xD;
&#xD;
The study was partly funded by the University of Maiduguri Teaching Hospital, Maiduguri as grant for Dr. Aisha S. Adamu&#x2019;s fellowship dissertation preparation.&#xD;
&#xD;
&#xD;
	&#xD;
	Northeastern Nigeria remains a high prevalence area for H. pylori infection&#xD;
	&#xD;
	&#xD;
	Serology concurred very well with histology as a method of infection identification.&#xD;
	&#xD;
	&#xD;
	Blind H. pylori eradication therapy was effective in the management of dyspeptic patients &#xD;
	&#xD;
	&#xD;
	The need for testing before treatment can be obviated in most of our patients&#xD;
	&#xD;
&#xD;
&#xD;
Glossary of Abbreviations&#xD;
&#xD;
ANOVA &#x2013; Analysis of variance&#xD;
&#xD;
HBV &#x2013; Hepatitis B virus&#xD;
&#xD;
HCV &#x2013; Hepatitis C virus&#xD;
&#xD;
IgG &#x2013; Immunoglobulin G&#xD;
&#xD;
MALT &#x2013; Mucosa associated lymphoid tissue&#xD;
&#xD;
NICE &#x2013; National Institute for Health and Care Excellence&#xD;
&#xD;
NPV &#x2013; Negative predictive value&#xD;
&#xD;
PPV &#x2013; Positive predictive value&#xD;
&#xD;
SPSS &#x2013; Statistical Package for Social Sciences&#xD;
&#xD;
UMTH &#x2013; University of Maiduguri Teaching Hospital&#xD;
</Fulltext><FulltextLanguage>English</FulltextLanguage><URLs><Abstract>http://ijcrr.com/abstract.php?article_id=2653</Abstract><Fulltext>http://ijcrr.com/article_html.php?did=2653</Fulltext></URLs><References>1. Ford AC, Marwaha A, Sood R, Moayyedi P. Global prevalence of, and risk factors for uninvestigated dyspepsia: a meta-analysis. Gut 2015; 64(7): 1049-1057&#xD;
&#xD;
2. Holcombe C, Omotara BA, Padonu MK et al. The prevalence of symptoms of dyspepsia in Nigeria. A random community based study.&#xA0; Trop Geogr Med 1991; 43; 209-214&#xD;
&#xD;
3. Ihezue CH, Oluwole FS, Onumiya JE et al. Dyspepsia among the highlanders of Nigeria; an epidemiological survey. Afr J Med Sci 1996; 25: 23-29.&#xD;
&#xD;
4. Talley NJ, Zinsmeister AR, Schleck CD et al. Dyspepsia and dyspepsia subgroups: a population-based study. Gastroenterology 1992; 102(4 Pt 1): 1259&#x2013;1268. &#xD;
&#xD;
5. Agreus L, Svardsudd K, Nyren O et al. Irritable bowel syndrome and dyspepsia in the general population: overlap and lack of stability over time. Gastroenterology 1995; 109: 671&#x2013;680.&#xD;
&#xD;
6. Talley NJ, Weaver AL, Zinsmeister AR et al. Onset and disappearance of gastrointestinal symptoms and functional gastrointestinal disorders. Am J Epidemiol 1992; 136: 165&#x2013;177&#xD;
&#xD;
7. Ryder SD, O&amp;#39;Reilly S, Miller RJ et al Long term acid suppressing treatment in general practice. BMJ1994; 308:827&#x2013;830.&#xD;
&#xD;
8. Ofman JJ, Rabeneck L. The effectiveness of endoscopy in the management of dyspepsia: a qualitative systematic review. Am J Med1999; 106:335&#x2013;346.&#xD;
&#xD;
9. Graham DY. Evolution of concepts regarding H. pylori from a cause of gastritis to a public health problem [Editorial] Am&#xA0;&#xA0; J Gastroenterol, 1994, 89: 469 - 472&#xD;
&#xD;
10. McColl KEL, Murray L, El-Omar E et al. Symptomatic benefit from eradicating Helicobacter pylori infection in patients with non-ulcer dyspepsia. N Engl J Med1998; 339:1869&#x2013;1874.&#xD;
&#xD;
11. Gilvarry J, Buckley MJM, Beattie S. et al Eradication of Helicobacter pylori affects symptoms in non-ulcer dyspepsia. Scand J Gastroenterol1997; 32:535&#x2013;540.&#xD;
&#xD;
12. Forman D, Newell DG, Fullerton F. et al. Association between infection with Helicobacter pylori and risk of gastric cancer: evidence from a prospective investigation. BMJ1991; 302:1302&#x2013;1305.&#xD;
&#xD;
13. Pounder RE, Ng D. The prevalence of H. pylori infection in different countries. Aliment Pharmacol Ther 1995; 33 -37&#xD;
&#xD;
14. Hooi JKY, Lai WY, Ng WK, Suen MMY, Underwood FE, Tanyingoh D et al. Global prevalence of Helicobacter pylori infection: Systematic review and meta-analysis. Gastroenterology 2017; 153(2): 420-429&#xD;
&#xD;
15. Eusebi LH, Zagari RM, Bazzoli F. Epidemiology of Helicobacter pylori infection. Helicobacter 2014 Sep; Suppl 1:1-5&#xD;
&#xD;
16.&#xA0;&#xA0; Holcombe C.&#xA0;&#xA0; Prevalence of antibody to H. pylori in children in northern Nigeria. Trans R Soc Trop. Med. Hyg 1993; 87: 79 &#x2013; 80.&#xD;
&#xD;
17. Otegbola SA, Oluwasola OA, Yakubu A, et al. H. pylori serology and evaluation of Gastroduodenal disease in Nigerians with dyspepsia. African J of Clin and Exp Microbiology. 2004; 5 (1):131-138&#xD;
&#xD;
18. Tijjani BM, Borodo MM, Samaila AA. Upper gastrointestinal endoscopic findings in dyspeptic patients at Kano, Nigeria.Nig. J of Basic and Clinical Sci 2005; (2): 1-2&#xD;
&#xD;
19. Ismaila AA. Epidemiology of non &#x2013; ulcer dyspepsia among patients with dyspepsia at the Jos University Teaching Hospital in a dissertation submitted to the West African College of Physicians 2002. &#xD;
&#xD;
&#xA0;20. Graham DY, Klein PD, Evans DJ. Campylobacter pylori detected non-invasively by the 13-C urea breathe test. Lancet 1987; 1: 1174&#x2014;1177&#xD;
&#xD;
21. Heaney A, Collins J S A, Watson R G P et al. A prospective randomised trial of a &#x201C;test and treat&#x201D; policy versus endoscopy based management in young Helicobacter pylori positive patients with ulcer-like dyspepsia, referred to a hospital clinic. Gut 1999; 45: 186&#x2013;190&#xD;
&#xD;
22. Bazzoli F, Zagari RH, Foss I. Short term low dose triple therapy for the eradication of H. pylori. Eur J. Gastroenterol Hepatology 1994; 6: 773 &#x2013; 777&#xD;
&#xD;
&#xA0;23. D. Y. Graham, &#x201C;History of Helicobacter pylori, duodenal ulcer, gastric ulcer and gastric cancer,&#x201D; World Journal of Gastroenterology 2014; (20)18:5191&#x2013;5204.&#xD;
&#xD;
24. Grossman MI. Closing remarks. Gastroenterology 1978; 74:487&#x2013;488.&#xD;
&#xD;
25. IARC Helicobacter pylori Working Group. Volume 8. Helicobacter pylori eradication as a strategy for preventing gastric cancer. Lyon, France: International Agency for Research on Cancer, 2014&#xD;
&#xD;
26. Ferlay J, Shin HR, Bray F, et al. Estimates of worldwide burden of cancer in 2008: GLOBOCAN 2008. Int J Cancer 2010; 127:2893&#x2013;2917.&#xD;
&#xD;
27. Malfertheiner P, Megraud F, O&#x2019;Morain CA et al. Management of Helicobacter pylori infection: The Maastricht IV/Florence Consensus Report. Gut 2012; 61: 646&#x2013;664&#xD;
&#xD;
28.&#xA0; Olokoba AB, Gashau W, Bwala S, Adamu A, Salawu FK. Helicobacter pylori infection in Nigerians with Dyspepsia. Ghana Med J 2013; 47 (2): 79-81&#xD;
&#xD;
29. Dixon MF, Genta RM, Yardley JH, Gorrea P. Classification and grading of gastritis. The updated Sydney System. Am J Surg Pathol 1996; 20:1161-1181&#xD;
&#xD;
30. Holcombe C, Umar H, Lucas SB, Kaluba J. Low incidence of clinically significant gastroduodenal pathology despite a high incidence of H. Pylori infection. Trans R Soc Trop Med Hyg. 1994; 88(5): 569-571.&#xD;
&#xD;
31. Bytzer P, Howell S, Lemon M et al. Low socioeconomic class is a risk factor for upper and lower gastrointestinal symptoms: A population based study in 15,000 Australian adults. Gut&#xD;
&#xD;
2001; 49: 66-72. doi:10.1136/ut.49.1.66&#xD;
&#xD;
32. Current European concept in the management of H. pylori. The Maastricht consensus report. Gut 1997; 41:8 &#x2013; 13&#xA0; &#xD;
&#xD;
33. Sobala GM, Crabtree JE, Pentith JA, et al. Screening dyspepsia by serology to H.pylori. Lancet 1991; 338: 94 &#x2013; 96.&#xD;
&#xD;
&#xA0;34. Holcombe C, Kaluba J, Lucas SB. Non-ulcer dyspepsia in Nigeria: A case control study. Trans R Soc Trop Med Hyg 1991; 4:553-555&#xD;
&#xD;
35. Danbauchi SS, Keshinro IB, Abdu-Gusau K. Afr J Med MedSci1999; 28(1-2):87-90&#xD;
&#xD;
36. Wallace MB, Durkalski VL, Vaughan J et al. Age and alarm symptoms do not predict endoscopic ?ndings among patients with dyspepsia: a multicentre database study. Gut 2001; 49: 29&#x2013;34.&#xD;
&#xD;
37. Dyspepsia: Managing dyspepsia in adults in primary care. NICE Guideline. Available at: www.nice.org.uk/guidance/cg17/documents/dyspepsia-second-consultation-nice-guideline2 &#xD;
&#xD;
38.Holcombe C. H pylori; the African enigma. Gut 1992; 33: 429-431.&#xD;
&#xD;
39. Agbakwuru EA, Fatusi AO, Ndububa DA, et al. Pattern and validity of clinical diagnosis of upper gastrointestinal diseases in southwest Nigeria. African Health Sciences 2006; 6: 98-103. &#xD;
&#xD;
40. Moayyedi P, Talley NJ, Fennerty MB, Vakil N. Can the clinical history distinguish between organic and functional dyspepsia? JAMA 2006; 295(13): 1566-1576.&#xD;
&#xD;
41. Dooley CP, Cohen H. The clinical significance of H. pylori. Ann Intern Med 1998; 108:70-790&#xD;
&#xD;
42. Crabtree JE, Taylor DD, Nyah JL. Mucosal IgA recognition of H. pylori 12 kilodalton proteins in Peptic ulceration and gastric pathology.Lancet 1991; 338: 332-335.&#xD;
&#xD;
43. DaRocha-Afodu JT, Adesola AO. Gastric acid secretion studies in Nigerians using pentagastrin stimulation. Niger Med J 1973; 3(1):19-24&#xD;
&#xD;
44. Graham DY, Rakel RE, Fendrick AM, et al. Scope and consequence of peptic ulcer disease: how important is asymptomatic H. pylori infection. Postgrad Med J 1999; 105:106-119&#xD;
&#xD;
45. Brown KE, Peura DA, Diagnosis of H. pylori infection. Gastroenterol Clin North Am 1993; 22: 105 &#x2013; 115.&#xD;
&#xD;
46. Goel KM, Shanks RA, McAllister TA, Follett EA. Prevalence of intestinal parasitic infestation, salmonellosis, brucellosis, tuberculosis, and hepatitis B among immigrant children in Glasgow. Br Med J 1977; 1:676-9.&#xD;
&#xD;
47. Letters www.annals.org. Annals of Internal Medicine 2 April 2002; 136 (7): 555&#xD;
&#xD;
48.Gashau W, Mohammed I. Hepatitis B viral markers in Nigerian patients with primary liver carcinoma. Tropical and Geographical Medicine 1991; 43 (1-2): 64-67.&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0;&#xA0; &#xD;
&#xD;
49. Mohammed MD, Gashau W, Yusuph H, Alkali MD. The Role of Traditional Skin piercing practices in the Transmission of Hepatitis C virus in Northeastern Nigeria. Borno Med J. 2004; 1: 7 &#x2013; 9&#xD;
&#xD;
50.&#xA0; Zar S, Mendall MA. Clinical practice&#x2013;strategies for management of dyspepsia.Br Med Bull 1998; 54: 217&#x2013;228.&#xD;
&#xD;
51. Sonnenberg A. Cost-bene?t analysis of testing for Helicobacter pylori in dyspeptic subjects. Am J Gastroenterol 1996; 91: 1773-1777.&#xD;
&#xD;
52. Bakari AA, Ibrahim AG, Gali BM et al. Pattern of gastric cancer in north-eastern Nigeria: A clinicopathologic study. J Chin Clin Med. 2010; 5: 211-5.&#xD;
&#xD;
53. Olokoba AB, Obateru OA, Bojuwoye MO et al.&#xA0; That dyspepsia in the young could be cancer. Nig. Med J. 2013;54(2):143-145.&#xD;
&#xD;
54. Moayyedi P. Helicobacter pylori test and treat strategy for young dyspeptic patients: new data. Gut 2002(50 Suppl 4): iv47&#x2013;iv50&#xD;
&#xD;
55. Akinyandenu O, Akinyandenu A. Irrational use and non-prescription sale of antibiotics in Nigeria: A need for change. J of Scientific and Innovative Research 2014; 3 (2): 251-257&#xD;
&#xD;
56.Badger-Emeka LI, Emeka PM, Okosi M. Evaluation of the extent and reasons for increased non-prescription antibiotics use in a University town, Nsukka Nigeria. Intern J of Health Sciences. 2018; 12(4):11-17&#xD;
&#xD;
57. Megraud F, Coenen S, Versporten A et al. Helicobacter pylori resistance to antibiotics in Europe and its relationship to antibiotic consumption. Gut 2012; 62:34&#x2013;42. &#xD;
&#xD;
58. Gonzales R, Steiner JF, Sande MA. Antibiotic prescribing for adults with colds, upper respiratory tract infections, and bronchitis by ambulatory care physicians. JAMA 1997; 278: 901&#x2013;904.&#xD;
</References></Article></ArticleSet><ArticleSet><Article><Journal><PublisherName>Radiance Research Academy</PublisherName><JournalTitle>International Journal of Current Research and Review</JournalTitle><PISSN>2231-2196</PISSN><EISSN>0975-5241</EISSN><Volume>12</Volume><Issue>4</Issue><IssueLanguage>English</IssueLanguage><SpecialIssue>N</SpecialIssue><PubDate><Year>2020</Year><Month>February</Month><Day>28</Day></PubDate></Journal><ArticleType>Healthcare</ArticleType><ArticleTitle>Study of Prevelance and Pattern of Senserineural Hearing Impairment in Stage 5 Chronic Kidney Disease Patients on Haemodialysis- at a Tertiary Health Care Setup in India&#xD;
</ArticleTitle><ArticleLanguage>English</ArticleLanguage><FirstPage>08</FirstPage><LastPage>13</LastPage><AuthorList><Author>Poulomi Saha</Author><AuthorLanguage>English</AuthorLanguage><Author> Kapil Mondal</Author><AuthorLanguage>English</AuthorLanguage></AuthorList><Abstract>Background: In patients with established CKD, multiple risk factors have been hypothesized to cause senserineural hearing loss. There is high rise in the prevalence of CKD in India due to rise in conditions such as diabetes and hypertension.&#xD;
Aim of the Study: To identify the pattern of sensorineural hearing loss (SNHL) in stage 5 CKD patients on haemodialysis and to study the association between haemodialysis and degree of hearing changes.&#xD;
Study Design: Case control, observational, analytical study.&#xD;
Method: In this case control study 500 stage-5 Chronic kidney disease adult patients on haemodialysis and 500 age and gender-matched healthy individuals were included over the period of 3 years. Upper age limit was restricted till 55 years to avoid presbyacusis. After base line investigations, they were subjected for all cases and controls were subjected otoscopic examination and hearing assessment using standard pure tone audiometry. Descriptive statistical analysis has been carried out in this study.&#xD;
Result: In CKD group, 96.5 % patients (5 patients had natural death) suffered from hearing loss and 3.5%(17) patients had normal hearing. In control group, 31.2% suffered from Sensorineural hearing loss and 68.2%(343) have no hearing loss . Among the Stage 5 CKD group, 11.9% had mild SN hearing loss, 14.2% had moderate sensorineural hearing loss,14.8% had moderately severe sensorineural hearing loss, 25.7% had severe SNHL, and 33.2% had profound SNHL. In the control group, 9% had mild SNHL, 7.6% had moderate SNHL, 7.1% had moderately severe SNHL,5.4% had severe SNHL and 2.2% had profound SNHL. Deterioration of hearing acuity occurred in 62% of the patients at the end of follow-up and 12.4% of the participants showed improvement in hearing acuity. 25.6% patients showed no improvement.&#xD;
Conclusion: Our finding in present study is that CKD patients with hearing loss received significantly lesser haemodialysis sessions is interesting as it suggests a possible beneficial association between increasing number of dialysis sessions and hearing loss.&#xD;
</Abstract><AbstractLanguage>English</AbstractLanguage><Keywords>Haemodialysis, Hearing loss, Sensori-neural hearing loss</Keywords><Fulltext>INTRODUCTION&#xD;
&#xD;
Chronic kidney disease (CKD) refers to a gradual and usually irreversible reduction of glomerular filtration rate (GFR) which can be caused by trauma, genetic disorders, infections and effect of drugs that are toxic to the kidneys.&#xD;
&#xD;
Other disease conditions such as diabetes and hypertension increase the risk of an individual developing kidney failure. About 10% of the world&#x2019;s population is&#xD;
&#xD;
affected by various forms of kidney disease making it a global public health challenge. The association between chronic kidney disease (CKD) and hearing impairment was first reported more than 80 years ago by Alport , who described a case of familial kidney disease related to hearing impairment. The etiopathogenetic mechanisms of Sensorineural hearing loss in CKD is due to osmotic alteration resulting in loss of hair cells, collapse of the endolymphatic space, edema and atrophy of specialized auditory cells and in some, complications of &#xA0;hemodialysis itself . Because of certain anatomic, physiological&#xA0; and ultrastructural similarities between the stria vascularis of the inner ear and basement membranes of glomeruli and evidence for similar antigenicity of the cochlea and kidney, may explain this association of CKD and SN loss can be explained &#xA0;to some extent. In patients with established CKD, multiple risk factors have been hypothesized to cause hearing loss such as use of hypertension ototoxic drugs, hypertension, nephrotoxic drugs, electrolyte disturbances, diabetes, particularly in association with hypertension and hemodialysis itself &#xA0;&#xA0;and age of patient have been implicated in various studies. Despite the multitude of studies regarding hearing loss in CKD, some dark domains still persists regarding the role of haemodialysis and duration of disease. There is high rise in the prevalence of CKD in India due to rise in conditions such as diabetes and hypertension. Comparatively, hearing loss has been found to be more prevalent among CKD patients than the general population in different parts of the world ranging from &#xA0;28% to 67% have been recorded in similar studies.&#xD;
&#xD;
OBJECTIVE&#xD;
&#xD;
&#xD;
	&#xD;
	To determine the &#xA0;pattern of sensorineural hearing loss (SNHL) &#xA0;&#xA0;in CKD patients on haemodialysis attending Medicine Department . &#xD;
	&#xD;
	&#xD;
	To study the association between haemodialysis&#xA0;&#xA0; and degree of hearing changes.&#xD;
	&#xD;
&#xD;
&#xD;
STUDY DESIGN&#xD;
&#xD;
Case control, observational, analytical study&#xD;
&#xD;
MATERIALS AND METHODS&#xD;
&#xD;
Study area: Department of MEDICINE, Heamodialysis unit, Mursidabad Medical College, Berhampore. West Bengal. &#xD;
&#xD;
Study period: November, 2016 &#x2013; November, 2019. &#xD;
&#xD;
Ethical clearance: Institutional ethics committee clearance was taken prior to the commencement of the study. &#xD;
&#xD;
Study sample&#xD;
&#xD;
&#xA0;&#xA0;Cases-500 CKD stage 5 (End Stage Renal Disease, ESRD) patients aged 18 to 50 years &#xA0;who have undergone at least one session of haemodialysis. Particularly, age was limited to 50 years for purposes of excluding presence of &#xA0;&#xA0;presbyacusis.&#xA0; CKD patients with conductive hearing loss and syndromic etiologies of CKD in&#xD;
&#xD;
which hearing loss is a known component, were excluded from this study. &#xD;
&#xD;
Controls: As control group of 500, age and gender-matched healthy individuals were included in this study. These are the individuals without any history of ototoxic medications within the last three months, as well as those with no chronic diseases such as diabetes, hypertension, renal impairment and rheumatoid diseases, without&#xA0; family history of hearing loss, no&#xA0; prolonged noise exposure, no history of otosclerosis, other ear diseases and ear surgery.&#xD;
&#xD;
METHODOLOGY&#xD;
&#xD;
From all cases and controls documented informed consent was obtained&#xD;
&#xD;
&#xD;
	&#xD;
	All patients were investigated using standard performa containing details of age, gender, chronic illness, hypertension, diabetic status and past or recent administration of ototoxic medications.&#xD;
	&#xD;
	&#xD;
	Duration of&#xA0; stage 5 chronic kidney disease and total number of haemoldialysis sessions obtained were documented. &#xD;
	&#xD;
	&#xD;
	Both case and control groups were subjected to have complete haemogram, coagulogram, fasting and post prandial blood sugar, serum LFT and RFT, electrolytes ,viral serology of HIV 1, HIV 2 and HBs Ag.&#xD;
	&#xD;
	&#xD;
	&#xA0;All CKD patients and controls were subjected otoscopic examination and hearing assessment using standard pure tone audiometry at 250, 500, 1000, 2000, 3000, 6000, 7000, and 8000 Hz. As bone conduction threshold is limited upto 4000Hz,so the audiometric recordings &#xA0;&#x2265;4000 Hz&#xA0; were done by air conduction&#xA0; testing&#xA0; only because &#xA0;High frequency sensorineural hearing&#xA0; recording by air conduction mode is unaffected by middle ear effusion. An average of the threshold levels of &gt;26 db was considered as abnormal. A hearing loss of 26&#x2013;40 db was classified as mild, 41&#x2013;55 db as moderate, 56&#x2013;70 as moderately severe, 71&#x2013;90 as severe, and &gt;90 db as profound hearing loss. Air and bone conduction thresholds were compared to identify the type and degree of hearing loss.&#xD;
	&#xD;
&#xD;
&#xD;
Descriptive statistical analysis has been carried out in this study. Results on continuous measurements are presented on mean standard deviation (minimum&#xA0; and maximum) and results on categorical measurements are presented in number (%). Chi square test is used to compare the difference in proportions. The significance is assessed at 5% level of significance. Differences were considered&#xD;
&#xD;
significant if the p value was less than 0.05.&#xD;
&#xD;
&#xD;
&#xD;
&#xA0;&#xD;
&#xD;
Total 500 stage 5 chronic kidney disease patients were studied to measure the burden of sensorineural hearing loss in them. This was a case-control study. Five CKD&#xA0;&#xA0; patients succumbed to death &#xA0;in the course of the disease. They were excluded from the study. In the control group too one patient expired due to cerebrovascular accident (CVA).&#xD;
&#xD;
&#xA0;&#xD;
&#xD;
After exclusion and inclusion criteria, among five hundred CRF control patients treated with hemodialysis, 357 were males and 143 females. Mean age in the case group was 51.9 for males and 42.5 for females. Duration of illness was 1&#x2013;5 years (mean 3.2). In control group 315 patients were &#xA0;male&#xA0; and 184 patients were female. Mean age in the control group was 50.3 for males and 41.2 for females.&#xD;
&#xD;
&#xD;
&#xD;
In CKD group, 96.5 % patients (478 out of 495) suffered from hearing loss and 3.5%(17) patients &#xA0;had normal hearing. In control group, 31.2% (156 out of 499 patients) suffered from SN hearing loss and 68.2%(343) have no hearing loss .&#xD;
&#xD;
&#xA0;Among the Stage 5 CKD group, 11.9%(57 patients) had mild SN hearing loss, 14.2% had (68 patients)had moderate SNHL(sensori-neural hearing loss),14.8%(71 patients) had moderately severe SNHL , 25.7%(123 patients) had severe SNHL, and 33.2%(159 patients) had profound SNHL.&#xD;
&#xD;
In the control group, 9% (45 people) had mild SNHL, 7.6%(38 people) had moderate SNHL,7.1% (35 people) had moderately severe SNHL,5.4% (27 people) had severe SNHL and 2.2%(11 people) had profound SNHL.&#xD;
&#xD;
&#xD;
&#xD;
65 % Stage 5 CKD patients had high frequency(8000Hz) SNHL(62 % bilateral &amp; 3% unilateral), 25% had mid frequency (4000Hz) SNHL (19% bilateral &amp; 6 % unilateral) and 10 % had low or at speech frequency (500&#x2013;2000 Hz) SNHL(8% bilateral &amp; 2% unilateral).&#xD;
&#xD;
&#xD;
&#xD;
104 patients( 20.84%)&#xA0; who were on haemodialysis for less than 1 year&#xA0; presented with hearing loss (hearing threshold above 20 dB). 215 patients(43.08%) presented hearing loss who were on haemodialysis for more than 1 year but less than 3 years. The patients who were on haemodialysis for more than 3 years but less than 5 years were 135(27.2 %) in number.&#xA0; 50 patients (10.1%) who were on haemodialysis for more than 5 years presented with hearing loss. The dominant hearing loss was obvious at high frequencies.&#xD;
&#xD;
&#xD;
&#xD;
Deterioration of hearing acuity occurred in 62% of the patients at the end of follow-up and 12.4% of the participants showed improvement in hearing acuity.25.6% patients showed no improvement.&#xD;
&#xD;
&#xD;
&#xD;
Among CKD patients with hearing loss, the majority of the patients, 215 patients&#xA0;received 151 to 450 sessions. 104 patients received less than 150 sessions.135 patients received 451-750 sessions. 50 patients received more than 750 sessions.&#xD;
&#xD;
DISCUSSION&#xD;
&#xD;
A number of studies conducted in India and abroad have documented and published higher incidence of hearing loss among children and adults with chronic renal disease. The prevalence of &#xA0;&#xA0;hearing loss in CRF &#xA0;&#xA0;greatly varies&#xA0; in different countries. In India, it was reported to be 63.5%, in Nigeria 67% , in Iran 46% , and in Croatia 63.6% . Earlier studies showed higher prevalence of hearing loss even upto 70%&#x2013;75%. This variation could be due to differences in the age of patients, methods of assessment of hearing loss, or duration of CRF and &#xA0;hemodialysis.&#xD;
&#xD;
The exact pathophysiology between hearing impairment and CKD is addressed in various ways. Over many years&#x2019;, research have&#xA0; linked &#xA0;CRF and hearing loss in patients with rare diseases like mitochondrial myopathy, lactic acidosis, stroke, Alport syndrome &#xA0;and Fabry&#x2019;s disease.&#xD;
&#xD;
Electrolyte disturbances, particularly sodium, water imbalance, hypertension, Vitamin D deficiency, and elevated serum urea levels are some proposed mechanisms for hearing impairment in patients with CRF. Defects in the cationic gradient of endolymphatic fluid can adversely affect hearing .&#xA0; Along with this alterations in the peripheral and central nervous system, &#x201C;uremic neuropathy,&#x201D; may lead to hearing impairment in CRF. Di Paolo et al reported a high incidence of nerve conduction dysfunction in patients with CRF. They found decreased conduction velocity in the sensory and motor units, with the sensory units being more compromised than the motor. &#xD;
&#xD;
Rossini et al &#xA0;were unable, to arrive at a definite conclusion regarding the effect of haemodialysis on hearing in CKD. In contrast, Peyvandi et al &#xA0;proposed in a recent study that prevalence and severity of &#xA0;hearing loss increases with duration of CKD and haemodialysis.&#xD;
&#xD;
Ozen et al reported audiometric improvement of 20 decibel of hearing perception of chronic kidney disease patients following haemodialysis. They hypothesized that haemodialysis causes change in serum osmolarity, BUN and fluid retention&#xA0; which may reverse the hearing impairment in post dialysis period. Though contradicting studies like are there questioning hearing improvement following haemodialysis.&#xD;
&#xD;
Contributory evident data to indicate beneficial role of&#xA0; haemodialysis on hearing threshold in CKD patients is present in this study. Possible beneficial association between increasing number of dialysis sessions and hearing threshold improvement is documented in 12.4% patients of&#xA0; chronic kidney disease because we found that chronic kidney disease&#xA0; patients with hearing loss received significantly lesser haemodialysis sessions in comparison to those having higher number of&#xA0; haemodialysis sessions. We concluded the hearing threshold improvement occurred due to improvement of serum osmolality following haemodialysis. Improved serum osmolality may have reverted the collapse of endolymphatic space and may have reduced the edema of &#xA0;some functionally active auditory cells. Thus causing improvement of &#xA0;&#xA0;hearing threshold to some extent.&#xD;
&#xD;
In our study deterioration of hearing &#xA0;&#xA0;occurred in 62% of the patients at the end of follow-up. 12.4% of the participants showed improvement in hearing acuity. 25.6% patients showed no improvement.&#xD;
&#xD;
We also observed that hearing loss at high frequencies might be the most common audiometric abnormality in CKD patients, but not the typical one. This audiometric difference , that is the presence of high frequency, mid frequency and even low frequency SN loss in CKD may be due to several reasons. But typical detection of high frequency in the above studies were mostly due to small sample sizes in both studies(49 and 63 CKD patients, respectively). Secondly, the questions &#xA0;were only used to access high-frequency SN loss in audiometry&#xA0; in patients, possibly&#xA0; not designing questionnaire for patients with &#xA0;mild and moderate frequency&#xA0; SN loss in conventional audiometry.&#xD;
&#xD;
So these number of studies clearly established&#xA0; prevalence of hearing loss among CKD patients, but&#xA0; well-designed studies with larger sample sizes were needed to adress relationships between hearing loss in CKD and haemodialysis. Also another important question that arises in this context is whether a blanket audiometric screening of all CKD patients would help identify mild hearing loss and prevent progression to severe degrees, especially if a beneficial role for haemodialysis can be definitely established in long-term prospective studies. This present study answers&#xA0;&#xA0; both of the questions to some extent. &#xD;
&#xD;
This study found &#xA0;96.5%(478 patients) of CKD patients on haemodialysis had hearing loss, considerably higher than the normal population who had 31.2% hearing loss[FIGURE: 1] . In other words, mostly all stage 5 CKD patient on haemodialysis experiences some degree of hearing impairment.&#xA0; 11.9%(57 patients) had mild SN hearing loss, 14.2% had (68 patients)had moderate SNHL(sensori-neural hearing loss),14.8%(71 patients) had moderately severe SNHL , 25.7%(123 patients) had severe SNHL, and 33.2%(159 patients) had profound SNHL. That is 40.5%, majority of the patients had moderately severe to severe SN loss. Hearing thresholds were abnormal in CKD patients on haemodialysis across all frequencies ranging from 250Hz to 8 kHz. SN loss was&#xA0; high frequency in 65% patients, mid frequency in 25% patients and&#xA0; low frequency in 10% patients [FIGURE: 2]&#xD;
&#xD;
The prevalence of hearing loss in CKD patients varies from&#xA0;28 per cent to&#xA0; 77 per cent according to different studies. Notably, many older studies have shown higher prevalence of hearing loss, possibly due to small sample sizes. The prevalence of this study is 48.9%.&#xD;
&#xD;
The high prevalence of hearing loss at enrollment in the study reflects the significant effect of CRF on hearing function. Yet, the impact of hemodialysis on&#xA0;the hearing threshold after 18 months was still substantial. The hearing threshold deteriorated from 30.5 &#xB1; 15.1 dB at the start of the study to 45.2 &#xB1; 11.3 dB after 18 months, which was a highly significant difference (P &lt; 0.001).This study also showed that CKD patients with hearing loss received [ FIGURE: 5 ]&#xA0;significantly fewer haemodialysis sessions compared to those without hearing loss. Our finding that CKD patients with hearing loss received significantly fewer haemodialysis sessions is interesting as it suggests a possible beneficial association between increasing number of dialysis sessions and hearing loss.&#xD;
&#xD;
Thus, it is evident that there are data to indicate contributory as well as beneficial roles for haemodialysis on hearing in CKD patients. The finding of Lasisi&#xA0;et al. supports this result. The role of hemodialysis in the occurrence of hearing loss among patients with CRF could be due either to changes in the fluid and electrolyte composition of endolymph or accumulation of amyloid materials in inner ear tissues. Aluminum toxicity associated with chronic dialysis&#xA0;may play a role in hearing loss. &#xD;
&#xD;
Nikolopoulos et al, Ozturan and Lam , Stavroulaki et al , and Pandey et al showed that auditory functions and thus hearing acuity were not affected by hemodialysis, particularly short term dialysis , or at least in the first 5 years of treatment. In contrast, other researchers reported that hearing is improved by hemodialysis. Aspris et al indicated that although there is improvement in neural auditory function following hemodialysis, it is not restored to a normal level. Gafter et al. concluded that although dialysis may have some temporary beneficial effect, the longterm effect is not assured. The acceptable &#xA0;explanation of hearing improvement particularly in low frequency hearing loss is that hemodialysis promotes normalization and stabilization of hydroelectric and metabolic changes in the endolymph that were induced by CRF, leading to enhancement of neural conduction and restore hair cell function.&#xD;
&#xD;
CONCLUSION&#xD;
&#xD;
Mild sensorineural hearing impairment in CKD patients on haemodialysis is well documented in number of studies. Though this hearing loss is mostly high frequency but other emerging studies marks significant&#xA0; presence of low frequency and mid frequency loss .These patients were likely to be older and had a significantly longer exposure to ototoxic drugs. Haemodialysis might have a promising effect on hearing loss in CKD patients, but further research by long-term prospective studies are required to&#xA0; link common pathophysiology between kidney dysfunction and cochlear impairment to potentially modify the normal care of CKD patients of higher stages. &#xA0;It should encourage clinicians to regularly question about hearing function in their preventive care protocols and &#xA0;to refer all CKD patients with hearing loss to otorhinolaryngologists for evaluation and rehabilitation .&#xD;
&#xD;
&#xA0;ABBREVIATION:&#xD;
&#xD;
&#xD;
	&#xD;
	CKD&#xA0;&#xA0; =Chronic kidney disease&#xD;
	&#xD;
	&#xD;
	CRF&#xA0;&#xA0; =Chronic renal failure.&#xD;
	&#xD;
	&#xD;
	SNHL = Senserineural hearing loss&#xD;
	&#xD;
	&#xD;
	ESRD= End stage renal disease&#xD;
	&#xD;
	&#xD;
	LFT=&#xA0;&#xA0;&#xA0;&#xA0; Liver function test&#xD;
	&#xD;
	&#xD;
	RFT&#xA0; =&#xA0; Renal function test&#xD;
	&#xD;
	&#xD;
	Hz&#xA0;&#xA0;&#xA0;&#xA0; = Hertz&#xD;
	&#xD;
	&#xD;
	CVA =Cerebro vascular accident&#xD;
	&#xD;
	&#xD;
	Db&#xA0;&#xA0;&#xA0; =&#xA0; Decibel&#xD;
	&#xD;
	&#xD;
	BUN= Blood urea nitrogen.&#xD;
	&#xD;
&#xD;
</Fulltext><FulltextLanguage>English</FulltextLanguage><URLs><Abstract>http://ijcrr.com/abstract.php?article_id=2654</Abstract><Fulltext>http://ijcrr.com/article_html.php?did=2654</Fulltext></URLs><References>&#xD;
	&#xD;
	Joseph O. Boateng et al Hearing impairment among chronic kidney disease patients on haemodialysis at a tertiary hospital in Ghana. &#xA0;Ghana Medical Journal. Volume 53 Number 3 September 2019; 53(3): 197-203.&#xD;
	&#xD;
	&#xD;
	C Balasubramanian et al A Study of Hearing Loss in Chronic Renal Failure.&#xA0; International Journal of Scientific Study | January 2018 | Vol 5 | Issue 10.&#xA0; Print ISSN: 2321-6379.Online ISSN: 2321-595X&#xD;
	&#xD;
	&#xD;
	Haider K. Saeed&#xA0; et al Sensorineural hearing loss in patients with chronic renal failure on hemodialysis in Basrah, Iraq. Tzu Chi Medical Journal 2018; 30(4): 216&#x2013;220.&#xD;
	&#xD;
	&#xD;
	E. K. Reddy et al Proportion of hearing loss in chronic renal failure: Our experience. 2016, Indian Journal of Otology. 22:4-9. IP: [110.227.81.227] &#xD;
	&#xD;
	&#xD;
	Jishana Jamaldeen et al Prevelence and pattern of hearing loss chronic kidney disease patients undergoing haemodialysis. Australian Medical Journal. [AMJ] 2015;8(2):41&#x2013;46.&#xD;
	&#xD;
	&#xD;
	Young Joon Seo et al Association of hearing impairment with chronic kidney disease: a cross-sectional study of the Korean general population.&#xA0; BMC Nephrology. 2015. 16:154 .DOI 10.1186/s12882-015-0151-0.&#xD;
	&#xD;
	&#xD;
	Somashekara KG et al Etiological evaluation of hearing loss in chronic renal failure. Indian Journal of Basic and Applied Medical Research, 2015; 4(2):194-199.&#xD;
	&#xD;
	&#xD;
	Sahin C &amp; Varim C. Hearing loss in geriatric hemodialysis patients. Med J DY Patil Univ, 2015; 8:734-8&#xD;
	&#xD;
	&#xD;
	Peyvandi A et al Hearing loss in chronic renal failure patient undergoing hemodialysis. Indian J Otolaryngol Head Neck Surgery 2013 Dec;65(Suppl 3):537&#x2013;40.&#xD;
	&#xD;
	&#xD;
	&#xA0;Klagenberg KF et al Vestibular dysfunction in adolescents and young adults after kidney transplant. Int Tinnitus J. 2013; 18(2):149-155 &#xD;
	&#xD;
	&#xD;
	Meena RS et al Hearing loss in patients of chronic renal failure: a study of 100 cases. Indian J Otolaryngol Head Neck Surg. 2012 .Dec;64(4):356&#x2013;9.&#xD;
	&#xD;
	&#xD;
	Adekwu A et al Prevalence of hearing loss in chronic kidney disease, stages 3-5 patients in a teaching hospital in Nigeria. J Med Res Pract, 2012; 1(2): 74-76&#xD;
	&#xD;
	&#xD;
	Sharma R et al A study on hearing evaluation in patients of chronic renal failure. Indian J Otol. 2011; 17: 109&#x2013;12.&#xD;
	&#xD;
	&#xD;
	&#xA0;&#xA0;Pandey S et al Audiometric profile in patients with chronic renal failure. J Otolaryngol Head Neck Surg 2011;40:131?6.&#xD;
	&#xD;
	&#xD;
	&#xA0;Vilayur E et al The association between reduced GFR and hearing loss: a cross-sectional population-based study. Am J Kidney Dis. 2010 Oct;56(4):661&#x2013;9.&#xD;
	&#xD;
	&#xD;
	&#xA0;Jakic M et al Sensorineural hearing loss in hemodialysis. patients. Coll Antropol. 2010 Mar;34 Suppl 1:165&#x2013;71.&#xD;
	&#xD;
	&#xD;
	&#xA0;Lasisi AO et al Hearing threshold in patients with chronic renal failure. Saudi Med J. 2007 May;28(5):744&#x2013;6.&#xD;
	&#xD;
	&#xD;
	&#xA0;&#xA0;Bains KS et al Cochlear function in chronic kidney disease and renal transplantation: A longitudinal study. Transplant Proc 2007; 39:1465-8.&#xD;
	&#xD;
	&#xD;
	&#xA0;Lasisi AO, Salako BL, Kadiri S, Arije A, Oko-Jaja R, Ipadeola A, Olatoke F. Sudden sensorineural hearing loss and heamodialysis. Ear, Nose &amp; Throat Journal,2006; 85: 819-821.&#xD;
	&#xD;
	&#xD;
	&#xA0;Thodi C et al Hearing in renal failure. Nephrol Dial Transplant 2006;21:3023?30.&#xD;
	&#xD;
	&#xD;
	&#xA0;Qin Y et al Application of extended high frequency audiometry in the patients with chronic renal failure treated by hemodialysis. Lin Chuang Er Bi Yan Hou Ke Za Zhi&#xA0; 2005;19:17-8.&#xD;
	&#xD;
	&#xD;
	Zeigelboim BS et al High frequency audiometry and chronic renal failure. Acta Otolaryngol 2001;121:245-8.&#xD;
	&#xD;
	&#xD;
	&#xA0;&#xA0;Serbet&#xE7;ioglu MB et al Effects of a single session of hemodialysis on hearing abilities. Acta Otolaryngol 2001;121:836?8&#xD;
	&#xD;
	&#xD;
	&#xA0;Stavroulaki P et al Hearing evaluation with distortion?product otoacoustic emissions in young patients undergoing haemodialysis. Clin Otolaryngol Allied Sci 2001;26:235?42.&#xD;
	&#xD;
	&#xD;
	&#xA0;Hutter JC et al Acute onset of decreased vision and hearing traced to hemodialysis treatment with aged dialyzers. JAMA 2000;283:2128?34.&#xD;
	&#xD;
&#xD;
</References></Article></ArticleSet></xml>
