IntroductionThe immunomodulatory properties of mesenchymal stromal cells (MSC) have been well-characterized in in-vitro and in-vivo models. We have previously shown that liver MSC (L-MSC) are superior inhibitors of T-cell activation/proliferation, NK cell cytolytic function, and macrophage activation compared to adipose (A-MSC) and bone marrow MSC (BM-MSC) in-vitro.MethodTo test these observations in-vivo, we infused these types of MSC into mice with unilateral renal artery stenosis (RAS), an established model of kidney inflammation. Unilateral RAS was induced via laparotomy in 11-week-old, male 129-S1 mice under general anesthesia. Control mice had sham operations. Human L-MSC, AMSC, and BM-MSC (5x105 cells each) or PBS vehicle were injected intra-arterially 2 weeks after surgery. Kidney morphology was studied 2 weeks after infusion using micro-MRI imaging. Renal inflammation, apoptosis, fibrosis, and MSC retention were studied ex-vivo utilizing western blot, immunofluorescence, and immunohistological analyses.ResultsThe stenotic kidney volume was smaller in all RAS mice, confirming significant injury, and was improved by infusion of all MSC types. All MSC-infused groups had lower levels of plasma renin and proteinuria compared to untreated RAS. Serum creatinine improved in micetreated with BM- and L-MSC. All types of MSC located to and were retained within the stenotic kidneys, but L-MSC retention was significantly higher than A- and BM-MSC. While all groups of MSC-treated mice displayed reduced overall inflammation and macrophage counts, L-MSC showed superior potency in-vivo at localizing to the site of inflammation and inducing M2 (reparative) macrophage polarization to reduce inflammatory changes.DiscussionThese in-vivo findings extend our in-vitro studies and suggest that L-MSC possess unique anti-inflammatory properties that may play a role in liver-induced tolerance and lend further support to their use as therapeutic agents for diseases with underlying inflammatory pathophysiology.

Chronic liver disease incidence is increasing among children worldwide due to a multitude of epidemiological changes. Most of these chronic insults to the pediatric liver progress to fibrosis and cirrhosis to different degrees. Liver and immune physiology differs significantly in children from adults. Because most of pediatric liver diseases have no definitive therapy, a better understanding of population and disease-specific fibrogenesis is mandatory. Furthermore, fibrosis development has prognostic significance and often guide treatment. Evaluation of liver fibrosis continues to rely on the gold-standard liver biopsy. However, many high-quality studies put forward the high diagnostic accuracy of numerous diagnostic modalities in this setting. Herein, we summarize and discuss the recent literature on fibrogenesis with an emphasis on pediatric physiology along with a detailed outline of disease-specific signatures, noninvasive diagnostic modalities, and the potential for antifibrotic therapies.

Liver-resident mesenchymal stem cells (L-MSCs) are superior inhibitors of alloreactive T cell responses compared to their counterparts from bone marrow (BM-MSCs) or adipose tissue (A-MSCs), suggesting a role in liver’s overall tolerogenic microenvironment. Whether L-MSCs also impact NK cell functions differently than other MSCs is not known. We generated and characterized L-MSCs, A-MSCs and BM-MSCs from human tissues. The mass spectrometry analysis demonstrated that L-MSC secretome is uniquely different than that of A-MSC/BM-MSC, with enriched protein sets involved in IFNγ responses and signaling. When co-cultured with primary human NK cells, L-MSCs but not other MSCs, decreased surface expression of activating receptors NKp44 and NKG2D. L-MSCs also decreased IFNγ secretion by IL-2-stimulated NK cells more effectively than other MSCs. Cytolytic function of NK cells were reduced significantly when co-cultured with L-MSCs, whereas A-MSCs or BM-MSCs did not have a major impact. Mechanistic studies showed that the L-MSC-mediated reduction in NK cell cytotoxicity is not through changes in secretion of the cytotoxic proteins Perforin, Granzyme A or B, but through increased production of HLA-C1 found in L-MSC secretome that inhibits NK cells by stimulating their inhibitory receptor KIRDL2/3. L-MSCs are more potent inhibitors of NK cell functions than A-MSC or BM-MSC. Combined with their T cell inhibitory features, these results suggest L-MSCs contribute to the tolerogenic liver microenvironment and liver-induced systemic tolerance often observed after liver transplantation.

Bone marrow-derived long-lived plasma cells (LLPCs) are thought to be a major source of alloantibody in sensitized transplant patients. However, studies of LLPCs have been hampered not only by the fact that they are rare and difficult to isolate and culture but also due to the lack of consensus regarding a definitive cell-surface phenotype. The goal of the current study was to determine if LLPCs have a specific, stable cell-surface phenotype. PCs were isolated from high-volume (120cc) bone marrow aspirates that were enriched first by negative selection then positive selection using anti-CD38 antibody-coated beads and purified by cell sorting. A typical isolation resulted in >100,000 PCs that were sorted into 4 populations with variable numbers of PCs: CD19+/CD138+/ CD38Hi (64.1% of the PCs), CD19-/CD138+/CD38Hi (20.9%), CD19+/CD138-/CD38Hi (10.7%), and CD19-/ CD138-/CD38Hi (4.3%). The purity of each subset was 96-99%. Each subset contained PCs secreting IgG and IgA. Measles-and tetanus-specific PCs (i.e. putative IgG secreting, antigen-specific LLPCs). LLPCs were identified in both the CD19+/CD138+/CD38Hi and CD19-/CD138+/CD38Hi subsets and in the smaller CD138-subsets (when pooled). Thus, all CD38Hi subsets contained LLPCs. Cultured PCs maintained viability (>50%) and function and could be retrieved for analyses. During 7 days of culture, cell surface expression changed from baseline in many PCs. For example, approximately 20% of CD19 + CD138+/CD38Hi cells (the largest PC subset) became CD19-. CFSE assays showed no division and only a small percentage of LLPCs were Ki-67 positive suggesting that the cells did not divide in culture and that the antibody detected was not from plasmablasts. We conclude that human bone marrow LLPCs have a heterogeneous expression of CD19 and CD138, which can change during cell culture. The fact that LLPCs were found in all four subsets raises the possibility that a large percentage of PCs in the bone marrow may be LLPCs.

Background. Previous studies demonstrated critical deficits in diagnosis and management of childhood food allergy (FA), and recent developments in FA research support adopting a proactive approach in FA management. Our objective was to describe FA knowledge and management patterns of pediatricians. Method. We applied a 24-item survey to 170 general pediatricians, pediatric allergists and pediatric gastroenterologists practicing in Turkey. Results. Some IgE-mediated symptoms of FA such as cough, urticaria, wheezing and anaphylaxis were falsely recognized as symptoms of non-IgE-mediated FA by 30%, 29%, 25% and 19% of the participants, respectively. By contrast, 50% of the participants falsely recognized bloody stool, a finding of IgE-mediated FA. Most frequently and least frequently used diagnostic tools were specific IgE (30.5%) and oral food challenge test (1.7%), respectively. Maternal diet restrictions and infant diet restrictions were advised by 82% and 82%, respectively. Percentages of physicians eliminating only 1 food were 21%, 19%; 2 foods were 15%, 11%; 3 foods were 7%, 8%; 4-5 foods were 8%, 11%; 5 to 10 foods were 21%, 26%; and > 10 foods were 28%, 25% from the maternal and infant diet, respectively. Cow`s milk, cheese, butter, yoghurt, baked milk products and hen`s egg were the most commonly restricted items. Conclusion. Overall, FA knowledge of pediatricians was fair. Pediatricians utilize an overly restrictive approach when advising diet eliminations in FA. Recent developments favor a more proactive approach to induce immune tolerance and need to be encouraged in pediatric clinical practice. Future educational efforts should focus on emphasizing the deleterious effects of injudicious and extensive eliminations.

Antibody-mediated rejection (ABMR) is one of the most common causes of renal allograft loss. This review aims to outline the different clinical scenarios of ABMR with an emphasis on the cellular sources of antibody. Studies of human plasma cells (PC) and memory B cells have been limited, but existing data suggest that both can contribute to ABMR. Hyperacute ABMR is due to pre-existing anti-HLA antibodies. Early acute ABMR likely involves the stimulation of memory B cells and can lead to new long-lived plasma cells. Late acute ABMR involves the de novo development of new memory B cells and PCs that are resistant to conventional immunosuppression. Chronic active ABMR involves not only antibodies (either pre-existing or de novo) but also effector cells such as NK cells, T cells, and macrophages. Cellular processes underlying ABMR involve interactions between memory B cells, plasmablasts, plasma cells, and various effectors. Understanding these cellular processes is needed to improve therapies for ABMR.

INTRODUCTIONTo describe the clinical and laboratory profile, natural course, treatment outcome, and risk factors of posttransplant esophageal and nonesophageal eosinophilic gastrointestinal disorders (EGIDs).METHODSAll children (aged <18 years) who underwent liver transplantation, between 2011 and 2019, in a single transplant center with a follow-up period of 1 year or more posttransplant and with a history of posttransplant endoscopic evaluation were included in this study.RESULTSDuring the study period, 89 children met the inclusion criteria. Patients were followed for a median of 8.0 years. A total of 39 (44%) patients were diagnosed with EGID after transplantation. Of these, 29 (33%) had eosinophilic esophagitis (EoE), and 10 (11%) had eosinophilic gastritis, gastroenteritis or enterocolitis. In comparison with the non-EGID group, patients with EGID were younger at transplant (P ≤ 0.0001), transplanted more frequently due to biliary atresia (P ≤ 0.0001), and had higher rates of pretransplant allergy (P = 0.019). In the posttransplant period, they had higher rates of mammalian Target of Rapamycin inhibitor use (P = 0.006), Epstein-Barr virus viremia (P = 0.03), post-transplant lymphoproliferative disease (P = 0.005), and allergen sensitization (P ≤ 0.0001). In regression analysis, young age at transplant, age at diagnosis, pretransplant atopic dermatitis, and post-transplant lymphoproliferative disease were associated with an increased risk of EGID or EoE. Laboratory abnormalities such as anemia (P = 0.007), thrombocytosis (P = 0.012), and hypoalbuminemia (P = 0.031) were more commonly observed in the eosinophilic gastritis, gastroenteritis or enterocolitis group than in the EoE group. Following treatment, most patients had symptomatic resolution at 3 months and histologic resolution at 6 months postdiagnosis. Among the patients who had 5 years of follow-up, none recurred.DISCUSSIONEGID is a common posttransplant diagnosis, which seems to affect patients who are transplanted earlier and who have pretransplant atopy. Posttransplant EGID is responsive to treatment, but as histologic remission occurs after symptomatic resolution, the decision to perform control endoscopy should be delayed.

Biallelic mutations in neuroblastoma amplified sequence gene (NBAS) is a rare disease which is characterized by recurrent liver failure (RALF). We reported the novel mutations, clinical characteristics and long-term outcomes of 5 patients with novel biallelic NBAS variants. Four patients (80%) had acute, episodic liver crises (LC) triggered by fever, with a median age of onset of 8.5 months. The median age in the last episode was 34 months. Median number of liver episodes was 4. The course of ALF was complicated by hepatic encephalopathy and hypoglycaemia in all patients with ALF. Two patients recovered with conservative treatment, 2 required liver transplantation (LT) and 1 died during the fourth episode. Long-term post-transplant follow-up showed normal liver function and histology. There is no hepatic or extrahepatic recurrence after LT. Non-transplanted patients exhibited fibrosis in either biopsy or elastography. Despite a reduction in the frequency of clinically significant episodes, patients may exhibit ongoing liver injury and fibrosis. An acute on chronic liver failure with predominant cholestasis can be an alternative presentation.

Gastrointestinal bleeding is a rare but potentially life-threatening manifestation of eosinophilic gastrointestinal disorders (EGIDs). Here, we describe a case series comprising 5 pediatric patients between 7 and 12 years of age, who presented to the emergency department with hematemesis and were subsequently diagnosed with EGID. Accompanying allergic history, peripheral eosinophilia, and total IgE elevation were common. Despite a more severe presentation, response to medical and dietary therapy was favorable. A comprehensive review of the literature revealed 26 other cases with similar findings that reinforced the importance of prompt recognition and early dietary and immunomodulating therapy in the control of this disease.

Contrast-induced nephropathy (CIN) is a relatively common complication following primary coronary angiography (CAG) or percutaneous coronary intervention (PCI), especially in at-risk patients. The goal of this study is to evaluate the role of pre-procedural serum osmolarity as a risk factor for CIN in patients undergoing elective CAG for stable coronary artery disease (CAD). A total of 356 stable CAD patients scheduled to undergo CAG or PCI were included in this two-center study. Serum osmolarity was calculated on admission. CIN was defined according to the KDIGO criteria. There were 45 (12.6%) patients who developed CIN 48–72 h after CAG or PCI. CIN patients had a higher prevalence of diabetes (51.1% in those with CIN vs 24.4% in those without CIN, p < 0.001), higher serum glucose (129 mg/dL in those with CIN vs 108 mg/dL in those without CIN, p < 0.001), blood urea nitrogen (22.4 mg/dL in those with CIN vs 19.0 mg/dL in those without CIN, p = 0.01) and serum osmolarity (294.2 mOsm in those with CIN vs 290.1 mOsm in those without CIN, p < 0.001) levels, had received a higher dose of contrast (250 mL in those with CIN vs 200 mL in those without CIN, p = 0.03) but had lower hemoglobin (12.9 g/dL in those with CIN vs 13.6 g/dL in those without CIN, p = 0.04) level. In multivariate analysis, serum osmolarity [odds ratio (OR) 1.11; 95% confidence interval (CI) 1.04–1.18 for each mOsm/L increase; p = 0.001], diabetes (OR 2.43, 95% CI 1.26–4.71; p = 0.01), C-reactive protein (OR 1.04, 95% CI 1.01–1.08 for each mg/dL increase; p = 0.02) and contrast volume (OR 34.66, 95% CI 1.25–962.22 for each L increase; p = 0.04) remained as independent predictors of CIN. Serum sodium, glucose and blood urea nitrogen contributed to the excess serum osmolarity of CIN patients. Serum osmolarity is a cheap and widely available marker that can reliably predict CIN after CAG or PCI. Future research should focus on determining a clinically optimal cutoff for serum osmolarity that would warrant preventive interventions. Furthermore, later research may investigate the role of serum osmolarity not only as a risk factor but also as a pathogenetic mechanism underlying CIN.

Intradialytic hypotension (IDH) is a frequent and serious complication of chronic haemodialysis, linked to adverse longterm outcomes including increased cardiovascular and all-cause mortality. IDH is the end result of the interaction between ultrafiltration rate (UFR), cardiac output and arteriolar tone. Thus excessive ultrafiltration may decrease the cardiac output, especially when compensatory mechanisms (heart rate, myocardial contractility, vascular tone and splanchnic flow shifts) fail to be optimally recruited. The repeated disruption of end-organ perfusion in IDH may lead to various adverse clinical outcomes affecting the heart, central nervous system, kidney and gastrointestinal system. Potential interventions to decrease the incidence or severity of IDH include optimization of the dialysis prescription (cool dialysate, UFR, sodium profiling and high-flux haemofiltration), interventions during the dialysis session (midodrine, mannitol, food intake, intradialytic exercise and intermittent pneumatic compression of the lower limbs) and interventions in the interdialysis period (lower interdialytic weight gain and blood pressure-lowering drugs). However, the evidence base for many of these interventions is thin and optimal prevention and management of IDH awaits further clinical investigation. Developing a consensus definition of IDH will facilitate clinical research. We review the most recent findings on risk factors, pathophysiology and management of IDH and, based on this, we call for a new consensus definition of IDH based on clinical outcomes and define a roadmap for IDH research.

Liver TransplantationVolume 27, Issue 7 p. 1061-1065 Brief Report Posttransplant Hemophagocytic Lymphohistiocytosis in Pediatric Liver Transplant Recipients Cigdem Arikan M.D, Corresponding Author Cigdem Arikan M.D ciarikan@ku.edu.tr Department of Pediatric Gastroenterology, Hepatology, and Nutrition, Istanbul, Turkey Research Center for Translational Medicine (Koc Universitesi Translasyonel Tıp Araştırma Merkezi), Istanbul, Turkey Address reprint requests to Cigdem Arikan, M.D., Department of Pediatric Gastroenterology, Hepatology, and Nutrition, Koc University School of Medicine, Davutpasa Cd., No: 4, 34010, Zeytinburnu, Istanbul, Turkey. Telephone: 00905336227698; FAX: +90 212 311 34 10; E-mail: ciarikan@ku.edu.trSearch for more papers by this authorFatih Erbey M.D, Fatih Erbey M.D Departments of Pediatric Hematology and Oncology, Koc University School of Medicine, Istanbul, TurkeySearch for more papers by this authorElif Ozdogan M.D, Elif Ozdogan M.D Department of Pediatric Gastroenterology, Hepatology, and Nutrition, Istanbul, Turkey Research Center for Translational Medicine (Koc Universitesi Translasyonel Tıp Araştırma Merkezi), Istanbul, TurkeySearch for more papers by this authorMurat Akyildiz, Murat Akyildiz Department of Gastroenterology and Hepatology, Istanbul, TurkeySearch for more papers by this author Cigdem Arikan M.D, Corresponding Author Cigdem Arikan M.D ciarikan@ku.edu.tr Department of Pediatric Gastroenterology, Hepatology, and Nutrition, Istanbul, Turkey Research Center for Translational Medicine (Koc Universitesi Translasyonel Tıp Araştırma Merkezi), Istanbul, Turkey Address reprint requests to Cigdem Arikan, M.D., Department of Pediatric Gastroenterology, Hepatology, and Nutrition, Koc University School of Medicine, Davutpasa Cd., No: 4, 34010, Zeytinburnu, Istanbul, Turkey. Telephone: 00905336227698; FAX: +90 212 311 34 10; E-mail: ciarikan@ku.edu.trSearch for more papers by this authorFatih Erbey M.D, Fatih Erbey M.D Departments of Pediatric Hematology and Oncology, Koc University School of Medicine, Istanbul, TurkeySearch for more papers by this authorElif Ozdogan M.D, Elif Ozdogan M.D Department of Pediatric Gastroenterology, Hepatology, and Nutrition, Istanbul, Turkey Research Center for Translational Medicine (Koc Universitesi Translasyonel Tıp Araştırma Merkezi), Istanbul, TurkeySearch for more papers by this authorMurat Akyildiz, Murat Akyildiz Department of Gastroenterology and Hepatology, Istanbul, TurkeySearch for more papers by this author First published: 22 November 2020 https://doi.org/10.1002/lt.25951Citations: 1 Potential conflict of interest: Nothing to report. Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Supporting Information Filename Description lt25951-sup-0001-TableS1.docxWord document, 22.7 KB Table S1 lt25951-sup-0002-Supinfo.docxWord document, 18.9 KB Supplementary Material Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article. Volume27, Issue7July 2021Pages 1061-1065 RelatedInformation

What is known and objective Erlotinib is a small molecule tyrosine kinase inhibitor which blocks the activation of epidermal growth factor receptor (EGFR), a transmembrane receptor that is upregulated in many cancer types. Inhibition of angiogenesis with consequent impairments in intratumoral microcirculation is one of the mechanisms through which EGFR inhibition halts the progression of cancer. A consequence of impaired microcirculation is intratumoral hypoxia, which results in increases in serum uric acid levels. The goal of this study was to investigate the relationship between serum uric acid levels and response to erlotinib in metastatic non-small-cell lung cancer (NSCLC). Methods A total of 56 patients with metastatic non-small-cell lung cancer who received erlotinib for a duration of at least 3 months were included in this retrospective cohort study. Demographic characteristics, progression status, baseline serum uric levels and 3-month serum uric acid levels were recorded and analysed. Results and discussion Of the study population, 21 (37.5%) were female and 35 (62.5%) were male patients. No significant difference in above demographic characteristics was observed among exitus, survivor with progression and survivor without progression groups. Patients who responded favourably to erlotinib with no progression of their disease had significantly increased uric acid levels at 3-month follow-up (P = .01). Such a correlation was not observed if the patient was exitus (P = .47) or had progressed on erlotinib therapy (P = .19). What is new and conclusion In conclusion, this study is the first to demonstrate significant increases in serum uric acid levels in patients with metastatic NSCLC who responded favourably to erlotinib and had no progression under erlotinib therapy. Further studies are required to confirm and characterize serum uric acid as a novel biomarker in predicting the outcome in those with metastatic NSCLC.

This essay interprets and analyses the painting called “Dioscoridesdescribing the mandrake”, which is currently located in apermanent exhibition at Wellcome Collection in London, UK.The painting features Pedanius Dioscorides, a Greek botanistand pharmacologist who practiced in the Roman Empire duringthe rule of Nero. Dioscorides is known for his influential DeMateria Medica, a five-volume book on medicinal uses of variousplants and herbs. What makes this script special and influentialis that it included a vast amount of herbs, detailed descriptions,scientific observations, as well as a scientific classification andorder. Upon reflection on this piece of art, I am reminded of themedical realm that we are gradually becoming a part of as medicalstudents. There is immense passion, knowledge and intelligencein how medicine became modern medicine today. For me, thepainting on Dioscorides’ De Materia Medica is a compelling visualrepresentation of centuries – long endeavor.

Renal hyperfiltration, defined as an increased glomerular filtration rate above normal values, is associated with early phases of kidney disease in the setting of various conditions such as obesity and diabetes. Although it is recognized that glomerular hyperfiltration, that is, increased filtration per nephron unit (usually studied at low glomerular filtration levels and often referred to as single nephron hyperfiltration), is a risk factor for the progression of chronic kidney disease, the implications of having renal hyperfiltration for cardiovascular disease and mortality risk are incompletely understood. Recent evidence from diverse populations, including healthy individuals and patients with diabetes or established cardiovascular disease, suggests that renal hyperfiltration is associated with a higher risk of cardiovascular disease and all-cause mortality. In this review, we critically summarize the existing studies, discuss possible mechanisms, and describe the remaining gaps in our knowledge regarding the association of renal hyperfiltration with cardiovascular disease and mortality risk.

Acute alcoholic hepatitis is a syndrome of jaundice and hepatic decompensation that occurs with excessive alcohol consumption. The diagnosis can be made with a combination of clinical characteristics and laboratory studies, though biopsy may be required in unclear cases. Acute alcoholic hepatitis can range from mild to severe disease, as determined by a Maddrey discriminant function ≥32. Mild forms can be managed with supportive care and abstinence from alcohol. While mild form has an overall good prognosis, severe alcoholic hepatitis is associated with an extremely high short-term mortality of up to 50%. Additional complications of severe alcoholic hepatitis can include hepatic encephalopathy, gastrointestinal bleeding, renal failure, and infection; these patients frequently require intensive care unit admission. Corticosteroids may have short-term benefit in this group of patients if there are no contraindications; however, a subset of patients do not respond to steroids. New emerging therapies, which target hepatic regeneration, bile acid metabolism, and extracorporeal liver support, are being investigated. Liver transplantation for alcoholic liver disease was traditionally only considered in patients who have achieved 6 months of abstinence, in part due to social and ethical concerns regarding the use of a limited resource. However, the majority of patients with severe alcoholic hepatitis who fail medical therapy will not live long enough to meet this requirement. Recent studies have demonstrated that early liver transplantation in carefully selected patients with severe alcoholic hepatitis who fail medical therapy can provide a significant survival benefit and yields survival outcomes comparable to liver transplantation for other indications, with 6-month survival rates ranging from 77% to 100%. Alcohol relapse posttransplantation remains an important challenge, and heavy consumption can contribute to graft loss and mortality. Future investigation should address the substantial post-liver transplantation recidivism rate, from improving selection criteria to increasing posttransplantation substance abuse treatment resources.

Ö Z E T Bu çalışmada antrai gastrit ve peptik ülser patogenezinde suçlanan Helicobacter pylori (Hp) enfeksiyonunun dializ ve transplantasyon hastalarındaki sıklığı ve bu en­ feksiyonda rol oynayabilecek faktörlerin araştırılması amaçlanmıştır. Çalışmamızda dializ grubunda 47 (22 er­ kek, 25 kadın) transplantasyon grubunda 57 hasta (39 erkek, 18 kadın) ve kontrol grubunda 298 olgu (155 er­ kek, 143 kadın) incelemeye alınmıştır. Hastaların ortala­ ma yaşı dializ grubunda 36.6+15.1 (18 ile 83 yaş arasın­ da), transplantasyon grubunda 36.8+10.1 (19 ile 60 yaş arasında) ve kontrol grubunda 30.6±10.0 (16 ile 66 ara­ sında) bulundu. Transplantasyon grubundaki hastaların 41 "ı canlı, 16'sı kadavra donör kaynakladır. Ortalama dia­ liz sûresi 32,5 ±27,7 (1 ila 100 ay arasında ortalama transplantasyon süresi 31.9+38.0 (1 ile 162 ay arasında) idi. Hp enfeksiyonu serumda ELİSA ile antikor tayini ya­ pılarak araştırıldı. Hp enfeksiyou ile yaş, cins, primer has­ talık, dializ sıklığı, transplantasyon cinsi ve süresi, kulla­ nılan immunosupresif tedavi arasında anlamlı ilişki sap­ tanmadı (p>0.05). Ancak dializ süresi ile arasında anlamlı ilişki saptandı (p-0.038). Dializ grubundaki 47 hastanın 31'inde (%65.9), transplantasyon grubunda 57 hastanın 22'sinde ( %38.6) Hp antikoru saptanırken, kontrol gru­ bunda 298 hastanın 216'sında (%72.5) bulunmuştur. Hp enfeksiyonu sıklığı, dializ grubunda transplantasyon gru­ bundan daha yüksek bulunmasına rağmen, her iki grupta kontrol grubundan istatistiki anlamlı olarak daha düşük bulunmuştur (p<0.005). Sonuç olarak; Hp infeksiyonu dializ hastalarında transplantasyon hastalarına göre daha yüksek sıklıkta saptanmıştır. Kontrol grubundaki Hp sıklığı ise hem dializ hem de transplantasyon grubundaki hastalardan daha yüksek bulunmuştur. Bu enfeksiyonun sıklığının daha