Author Login

Correspondence to Author: Mossein Najar Jahromi 

Student Research Center, Faculty of Medicine, Tarbiat Modares University, Tehran, Iran.

Abstract:

A bacteria called Helicobacter Pylori inhabits human stomach mucous and naturally colonises people. There is ample evidence linking stomach H. pylori colonisation to gastric cancer, peptic ulcer disease, and chronic gastritis. The purpose of this study was to use PCR to detect the presence of H. pylori in the faeces of HIV-positive patients. Subjects included forty-three patients with verified HIV infection. Precise primers for hpaA (flagellar sheath adhesin) and ureB (urea amidohydrolase) of Helicobacter pylori were created, and the existence of the Helicobacter genome was examined using the PCR technique. Thirty patients (69.76%) had H. pylori, while 35 patients (81.39%) had a CD4+ count < 200. The results of screening HIV-positive patients’ stool for H. pylori bacteria indicate that this bacterium is highly prevalent in these patients. This prevalence is comparable to that of H. pylori in the population that is not HIV-positive.

Keywords: Helicobacter pylori, HIV, flagellar sheath adhesin (hpaA), urea amidohydrolase (ureB), gastric.

The clinical presentation might vary and two hundredth stay well. Most patients gift with imprecise symptoms like early repletion, abdominal pain, and weight loss. Another common symptom could also be injury that is said to erosion of the neoplasm into the canal lumen. we tend to gift a case of extra-gastrointestinal stromal neoplasm in viral hepatitis patient that was ab initio misdiagnosed as pathology and later treated with Imatinib once getting adequate biomarkers. consent was obtained from the patient.

INTRODUCTIONThe helical, flagellate, gram-negative bacillus Helicobacter pylori (H. pylori) inhabits the gastrointestinal mucous of humans by nature. According to Frenck et al. (2003), the prevalence of H. pylori infection among teenagers in the United States is 20%, but infection rates in poor nations surpass 90%. There is ample evidence linking stomach H. pylori colonisation to gastric can cer, peptic ulcer disease, and chronic gastritis (Everhart, 2000). Even so, only a small percentage of infected people progress beyond gastritis to form peptic ulcers or stomach cancers, despite the high rate of infection. Eighty percent of people in Iran have H. pylori infection. H. pylori-related gastritis has been reported to occur less frequently (that is, in 5 to 59% of cases) in adult patients with acquired immunodeficiency syndrome (AIDS) than in immunocompetent subjects in HIV-infected patients.

MATERIALS AND METHODS
43 patients with proven HIV infection who were either hospitalised or routinely visited the hospital for infection monitoring were included in this study. Every sample was taken from the Imam Khomeini Hospital’s sexual infection control centre in Tehran, Iran. We encountered difficulties compiling all demographic data due to hospital privacy policies restricting access to patient data. Formalin and sterile containers were used to collect patient stools for sample collection. A positive control, H. pylori 26695, was employed. The stool was suspended in 400 millilitres of TE buffer (pH 8.0, 10 mM Tris-HCL, 1 mM EDTA, or ethylenediaminetetraacetic acid), filtered, and then DNA extraction was performed.

RESULTS
The age range of the 43 patients (20–52 years old; 38 men and 5 women) included a history of stomach ulcers as well as proven HIV infection. Patients’ peripheral CD4+ lymphocyte counts were recorded from their medical records; 81.39% of the patients, or 35, had counts below 200. Seventy-five percent of the patients had received antibiotic therapy. The presence of H. pylori and CD4+ count did not significantly correlate (P value > 0.05). Through the use of hpaA and ureB screening, 30 patients (69.76%) with HIV infection had H. pylori detected in their stool. Both ureB and hpaA were present, which supported the results.

DISCUSSION
Over 33.2 million individuals worldwide are presently infected with HIV/AIDS, and the disease has already claimed almost 21 million lives (UNAIDS, 2008). There is debate on the prevalence of H. pylori in HIV patients, however reports indicate that it is significantly lower than in non-HIV infected people (Chiu et al., 2004; Blondon et al., 1998; Nielsen et al., 1995; Fabris et al., 1997). The purpose of this study was to determine whether HIV-positive individuals who were admitted to our hospital or just visited would have H. pylori. In order to identify H. pylori in the faeces of HIV-positive patients, we amplified two of the bacteria’s conserved genes. It is yet unknown what the decreased rates’ results mean (Shelton et al., 1998; Benz et al., 1993). A causative agent in some studies is thought to be the variation in the ratio of CD4\CD8 in the gastric mucosa between HIV patients with and without H. pylori infection. The concept states that a distinct presentation of H. pylori infection may be linked to CD4 cells, which are reduced in AIDS patients (Yamaoka et al., 2002; Scarpellini et al., 2001; Bamford et al., 1998). Another theory explains the reduced incidence observed in this population: HIV-positive patients’ regular use of antibiotics may cause H. pylori to be eradicated from the stomach mucosa. According to recent research, screening for the presence of H. pylori by culture revealed that the infection has spread from 48.9% of people. H. pylori was also discovered in 41.1 to 51% of patients in another study (Olmos et al., 2004; Fabris et al., 1997). Patients with advanced immunosuppression from HIV/AIDS had a greater risk of H. pylori infection. Previous investigations found that 80% of the examined region had H. pylori (Massarrat et al., 1995). In our investigation, we employed the PCR method to test for the presence of H. pylori in the stool of HIV-positive patients, particularly those who were immunosuppressed. We detected H. pylori in 69.76% of the patients. This finding was quite similar to our population’s H. pylori prevalence. In an attempt to eliminate any false positives, we attempted to employ two conserved H. pylori genes, and the existence of both genes supported every result. There are many different HIV strains, which are grouped into two main categories: HIV-1 is the most common type of the virus worldwide. HIV-2 was mostly found in West Africa, Asia, and Europe. It is possible for one HIV-positive person to carry multiple different strains of the virus at the same time. HIV continues to be one of the most serious global health threats in recent memory. 1.8 million people tested positive for HIV in 2017, and 940,000 of them passed away from AIDS-related illnesses. We agree that the AIDS epidemic can be stopped. There has been a 35% decrease in AIDS-related deaths in the area of reality where we work since 2010. More people than ever before are receiving therapy.

CONCLUSION
Finally, by testing the faeces of HIV-positive individuals for the presence of H. pylori, our findings demonstrated a significant prevalence of this bacterium in these patients. In actuality, this prevalence is comparable to that of H. pylori in the general population; nevertheless, it is unclear why this bacterium does not cause stomach symptoms in these people, and further research is required to address this issue.

REFERENCES
1. Asgharzadeh M, Kafil HS, Roudsary AA, Hanifi GR (2011). Tuberculosis transmission in Northwest of Iran: Using MIRU-VNTR, ETR-VNTR and IS6110-RFLP methods. Infect. Genet. Evol., 11(1): 124-131.
2. Asgharzadeh M, Kafil HS, Khakpour M (2008). Comparison of mycobacterial interspersed repetitive unit-variable number tandem repeat and IS6110–RFLP methods in identifying epidemiological links in patients with tuberculosis in Northwest of Iran. Ann. Microbiol., 58: 333-339.
3. Bamford KB, Fan X, Crowe SE, Leary JF, Gourley WK, Luthra GK, Brooks EG, Graham DY, Reyes VE, Ernst PB (1998). Lymphocytes in the human gastric mucosa during Helicobacter pylori have a T helper cell 1 phenotype. Gastroenterology, 114(3): 482-492.
4. Battan R, Raviglione MC, Palagiano A, Boyle JF, Sabatini MT, Sayad K, Ottaviano LJ (1990). Helicobacter pylori infection in patients with acquired immunedeficiency syndrome. Am. J. Gastroenterol., 85(12): 1576-1579.
5. Benz J, Hasbach H, Brenden M, Eidt S, Fätkenheuer G, Schrappe M, Geisel J, Goossens H, Mauff G (1993). Humoral and cellular immunity in HIV positive and HIVnegative Helicobacter pylori infected patients. Zentralbl. Bakteriol., 280(1-2): 186-196.
6. Blondon H, Tsakiris L, Coste T (1996). Helicobacter pylori, gastric acid secretion, ulcer disease and HIV infection. Gastroenterol. Clin. Biol., 20(3):248-253.
7. Chiu HM, Wu MS, Hung CC, Shun CT, Lin JT (2004). Low prevalence of Helicobacter pylori but high prevalence of cytomegalovirus- associated peptic ulcer disease in AIDS patients: Comparative study of symptomatic subjects evaluated by endoscopy and CD4 counts. J. Gastroenterol. Hepatol., 19(4): 423-428.
8. Edwards PD, Carrick J, Turner J, Lee A, Mitchell H, Cooper DA (1991). Helicobacter pylori-associated gastritis is rare in AIDS: antibiotic effect or a consequence of immunodeficiency? Am. J. Gastroenterol., 86(12): 1761-1764.
9. Everhart JE (2000). Recent developments in the epidemiology of Helicobacter pylori. Gastroenterol. Clin. North. Am., 29(3): 559-578.
10. Fabris P, Bozzola L, Benedetti P, Scagnelli M, Nicolin R, Manfrin V, Scarparo C, De Lalla F (1997). H. pylori infection in HIV-positive patients. A serohistological study. Dig. Dis. Sci., 42(2): 289-292.
11. Francis ND, Logan RP, Walker MM, Polson RJ, Boylston AW, Pinching AJ, HarrisJR, Baron JH (1990). Campylobacter pylori in the upper gastrointestinal tract of patients with HIV-1 infection. J. Clin. Pathol., 43(1): 60-62.
12. Frenck RW, Clemens J (2003). Helicobacter in the developing world.Microbes Infect., 5(8):705-713.
13. Isomoto H, Mizuta Y, Fukushima K, Takeshima F, Miyazaki M, Murase K, Omagari K, Maeda T, Kamihira S, Tomonaga M, Kohno S (1999). Low prevalence of Helicobacter pylori in individuals with HTLV-I infection. Eur. J. Gastroenterol. Hepatol., 11(5): 497-502.
14. Lake-Bakaar G, Quadros E, Beidas S, Elsakr M, Tom W, Wilson DE, Dincsoy HP, Cohen P, Straus EW (1988). Gastric secretory failure in patients with the acquired immunodeficiency syndrome (AIDS). Ann. Intern. Med., 109(6): 502-504.
15. Marano BJ Jr, Smith F, Bonanno CA (1993). Helicobacter pylori prevalence in acquired immunodeficiency syndrome. Am. J. Gastroenterol., 88(5): 687-690.
16. Massarrat S, Saberi-Firoozi M, Soleimani A, Himmelmann GW, Hitzges M, Keshavarz H (1995). Peptic ulcer disease, irritable bowel syndrome and constipation in two populations in Iran. Eur. J. Gastroenterol. Hepatol., 7(5): 427-433.
17. Nielsen H, Andersen LP (1995). Serodiagnosis of Helicobacter pylori infection in patients with human immunodeficiency virus infection. APMIS, 103(10): 689-692.
18. Olmos M, Araya V, Pskorz E, Quesada EC, Concetti H, Perez H, Cahn P (2004). Coinfection: Helicobacter pylori/ human immunodeficiency virus. Dig. Dis. Sci., 49(11-12): 1836-1839.
19. Scarpellini P, Carrera P, Cavallero A, Cernuschi M, Mezzi G, Testoni PA,Zingale A, Lazzarin A (2002). Direct detection of Helicobacter pylori mutations associated with macrolide resistance in gastric biopsy material taken from human immunodeficiency virus-infected subjects. J. Clin. Microbiol., 40(6): 2234-2237.
20. Shelton MJ, Adams JM, Hewitt RG, Morse GD (1998). Previous infection with Helicobacter pylori is the primary determinant of spontaneous gastric hypoacidityin human immunodeficiency virus- infected outpatients. Clin. Infect. Dis., 27(4): 739-745.
21. UNAIDS (2008). Report on the global AIDS epidemic (July 2008) http://data.unaids.org/pub/epislides/2007/2007epiupdate.en.pdf.
22. Urdez HE, Reglín NH, Escamilla AE, Manríquez MA (2004). Prevalence of Helicobacter pylori among Patients Infected with HIV. Rev. Med. IMSS, 42 (3): 211-210.
23. Welage LS, Carver PL, Revankar S, Pierson C, Kauffman CA (1995). Alterations in gastric acidity in patients infected with human immunodeficiency virus. Clin. Infect. Dis., 21(6):1431-1438.
24. Yamaoka Y, Kikuchi S, el-Zimaity HM, Gutierrez O, Osato MS, Graham DY (2002). Importance of Helicobacter pylori oipA in clinical presentation, gastricinflammation, and mucosal interleukin 8 production. Gastroenterology, 123(2): 414-424.

Citation:

Mossein Najar Jahromi. Screening positive for the virus patients’ stool components for Infection with Helicobacter. Journal of HIV/AIDS Research 2024.