<i>Helicobacter</i><i>pylori</i> in Kidney Allograft Recipients: High Prevalence of Colonization and Low Incidence of Active Inflammatory Lesions

Abstract

Since kidney transplant recipients are at enhanced risk for developing severe upper gastrointestinal disease and Helicobacter pylori (Hp) is an important pathogen in active gastritis and peptic ulcer, we performed gastroduodenoscopic examination, coupled with assessment of Hp colonization in 29 renal allograft recipients complaining of recurrent dyspepsia. Results were compared with those of 25 chronically hemodialyzed patients and 16 subjects free from renal disease, also suffering from upper gastrointestinal symptoms of similar severity. We found that while transplant recipients have had a high prevalence of Hp infection (62 vs. 34.6% in dialysis and 43.6% in control dyspeptic patients), active gastritis was clearly less frequently seen in these patients than in control subjects (transplant group: 6.9%, dialysis 3.8%, control 31.3%) and peptic ulceration was totally absent. Prevalence of Hp colonization was even higher in renal graft recipients on triple posttransplant immunosuppression (82%). In dyspeptic transplant and dialysis patients, colonization with Hp did not account for development of active inflammatory lesions, an association frequently seen in subjects free from renal disease and immunosuppressive therapy.

Eradication and Follow-Up of Helicobacter pylori Infection in Hemodialysis Patients

“…Depending on different studies and methods, the prevalence ranges from 34 to 75% [3, 4, 5, 6, 7]. The 13 C Urea Breath Test ( 13 C UBT) is a new diagnostic approach with a sensitivity of 90–100% and a specificity that ranges from 78 to 100% [8].…”

“…In fact, different cutoff points must be adopted according to several demographic and clinical variables in order to provide different levels of specificity and sensitivity. Although there are several reports on Hp prevalence in uremic patients determined by serology [3, 7, 11], there is scarce information regarding its utility for diagnosis of Hp infection in these patients [3]. Moreover, its usefulness for monitoring eradication therapy on hemodialysis (HD) patients is yet to be established.…”

Helicobacter pylori in solid-organ transplant recipient

“…When the prevalence in transplant recipients is compared with that in the control groups, four [4,6,9,12] of six studies showed no significant difference between renal transplant recipients and nonrenal disease individuals. In contrast, one study [8] showed a lower prevalence and one [10] showed a higher prevalence in renal transplant recipients than in nonrenal disease individuals and hemodialysis patients, but on the whole the prevalence of H. pylori infection in organ transplant recipients appears to be similar to that in control individuals. Interestingly, some studies showed that the prevalence of H. pylori infection decreased after transplantation.…”

“…To clarify the relationship between H. pylori infection and peptic ulcer disease after solid-organ transplantation, the reported prevalence of gastric ulcers and duodenal ulcers and H. pylori status are also summarized in Table 1 and Table 2. The prevalence of peptic ulcer in renal transplant recipients was similar [4,6,10] or slightly lower [9] than in nonrenal disease patients, hemodialysis patients, or both. In renal transplant recipients, H. pylori-positive patients had a higher prevalence of peptic ulcer than H. pylori-negative recipients in three studies [3 ,7,11], whereas one study [5] showed no significant difference between H. pylori-positive and H. pylori-negative patients.…”

Onset of Crohnʼs disease after Helicobacter pylori eradication

“…How the Th2 profile may be important in balancing the immune response is demonstrated by other clinical and experimental observations. For example, in pregnancy, the immune system of the mother undergoes a complex modification characterized by a preferential Th2 “switch“ that enables the mother to “tolerate“ her offspring by inhibiting Th1 response, which would otherwise promote fetus rejection 4–6. Whatever the immune mechanism elicited may be, these cases show that the role of H. pylori infection as a trigger or protective factor for the onset of CD should be still clarified.…”