scholarly journals Contribution of Lynch syndrome to early onset malignancy in Ireland.

2018 ◽  
Vol 36 (4_suppl) ◽  
pp. 586-586
Author(s):  
Alice Talbot ◽  
David James Gallagher
Keyword(s):  
Lynch Syndrome ◽  
Cancer Diagnosis ◽  
Early Onset ◽  
Cancer Genetics ◽  
Statistical Significance ◽  
Hereditary Cancer Syndrome ◽  
Carrier Status ◽  
Mutation Carriers ◽  
Significant Difference ◽  
First Diagnosis

586 Background: Lynch syndrome (LS) is an autosomal dominant hereditary cancer syndrome responsible for 2 -6% of hereditary colorectal cancers. LS is caused by germ-line mutations in mismatch repair genes (MMR): MLH1, MSH2, MSH6, PMS2 or EPCAM. This results in microsatellite instability, a phenotypic hallmark of LS-associated colorectal cancer. The aim of this study was to construct and analyse a database of Irish MMR mutation carriers. Methods: Records were from two of the three existing cancer genetics clinics in Ireland. Clinicopathological data of all probands (n=57) including names, dates of birth and death, carrier status and phenotype were recorded. Death certificates were used to confirm information regarding deceased mutation carriers. An ANOVA test was used to establish statistical significance of variations in age by gene. Length of survival based on stage was assessed using Kaplain Meier curves. Results: 345 affected individuals were identified. The most common cancers recorded were colorectal (53%), breast (12%) and endometrial (10%). 138 confirmed carriers were identified: 65 MLH1 (47%), 43 MSH2 (31%), 11 MSH6 (8%), 17 PMS2 (12%), and 2 EPCAM (1%). 22 patients have died since confirmation of Lynch Syndrome, 50% of whom died within 2.5 years of first diagnosis. All deceased carriers had at least one cancer diagnosis and 50% had developed multiple cancers. 59% of deaths were directly related to cancer. 7 of these patients had Stage 4 cancer at diagnosis. There was a significant difference in length of survival based on stage. (p=.048) Phenotype frequencies varied significantly by gene. (see table 1) Median age of first diagnosis of any cancer was 44.5 years (range 23-81). There was no difference in age at presentation by gene mutated. Conclusions: Under-diagnosis of LS misses a powerful preventive and therapeutic opportunity. LS causes early onset cancer diagnosis with substantial societal impact. A significant number of Lynch Syndrome cases have poor clinical outcomes. Genotype/Phenotype frequencies. [Table: see text]

scholarly journals The contribution of Lynch syndrome to early onset malignancy in Ireland

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Alice Talbot ◽  
Emily O’Donovan ◽  
Eileen Berkley ◽  
Carmel Nolan ◽  
Roisin Clarke ◽  
...  
Keyword(s):  
Lynch Syndrome ◽  
Early Onset ◽  
Cancer Genetics ◽  
Poor Response ◽  
Hereditary Cancer Syndrome ◽  
Cancer Type ◽  
Cancer Syndrome ◽  
Repair Protein ◽  
Therapeutic Opportunity ◽  
First Diagnosis

Abstract Background Lynch syndrome (LS) is an autosomal dominant hereditary cancer syndrome responsible for 2–4% of hereditary colorectal cancers (CRC). Mismatch repair protein deficiency (dMMR) is a characteristic feature of LS. It has been associated with a poor response to standard chemotherapy in metastatic colorectal cancer (mCRC). There is currently no LS database to monitor trends of disease in Ireland. We aim to centralise LS data in Ireland to assess the burden of LS in Ireland and guide improvements in prevention and treatment of LS-associated cancer. Methods A retrospective review was carried out including all medical records for LS patients from two of the three cancer genetics clinics in Ireland between 2000 and 2018 was carried out. Clinicopathological data of probands (n = 57) and affected family members including demographics, mutation status, cancer diagnosis and outcome was recorded. Statistical analysis was carried out using SPSS software. Results Fifty-seven families including three-hundred and forty-five individuals affected by cancer were identified. The most common cancers recorded were colorectal (53%), breast (12%) and endometrial (10%). One-hundred and thirty-eight confirmed carriers were identified: 65 path_MLH1 (47%), 43 path_MSH2 (31%), 11 path_MSH6 (8%), 17 path_PMS2 (12%) and two path_EPCAM (1%). Cancer type varied significantly by gene. Median age of first diagnosis was 44.5 years (range 23–81). Half of all deceased patients (n = 11) in this group died within 2.5 years of first diagnosis. These deaths were directly related to cancer in 59% of cases. Conclusions Under diagnosis of LS misses a powerful preventive and therapeutic opportunity. LS causes early onset dMMR cancer diagnoses with substantial societal impact. Implementation of ICBs into treatment policy for this small cohort of dMMR mCRC is an achievable therapeutic goal that may significantly improve survival. A prospective database for LS in Ireland is necessary to maximise prevention in this population.

Gastrointestinal cancer risk in Irish hereditary breast ovarian cancer families.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. e12565-e12565
Author(s):  
Tomas G Lyons ◽  
Darragh S Gogarty ◽  
Michael P. Farrell ◽  
Naoise Maria Dorman ◽  
Andrew J Green ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Colorectal Cancer ◽  
Ovarian Cancer ◽  
Cancer Risk ◽  
Cancer Diagnosis ◽  
Early Onset ◽  
Age At Diagnosis ◽  
Carrier Status ◽  
Hereditary Breast Ovarian Cancer ◽  
Mutation Carriers

e12565 Background: Colorectal and breast cancer are linked in certain predisposition syndromes such as Cowden and Peutz-Jegers syndrome. Breast cancer risk also appears increased in certain Lynch Syndrome kindreds. Original reports suggested an increased risk of gastrointestinal malignancies in BRCA1 or 2 mutation carriers. Two large studies in Ashkenazi Jewish populations subsequently contradicted this evidence, although only the three founder mutations were included in these studies. We report the Irish experience of colorectal and gastro-oesophageal (GE) cancer in Irish hereditary breast ovarian cancer (HBOC) families. Methods: 104 HBOC families at two tertiary referral centres were reviewed for the presence of early onset gastrointestinal (GI) malignancies. The medical records of individuals with GI cancer were reviewed to determine carrier status. Clinical data including age at diagnosis, stage, treatment and outcome were extracted. Median age of diagnosis and outcome were compared among BRCA1/2 mutation carriers and non-carriers. Results: We identified 33 individuals with GI malignancies in 102 HBOC families (22 with colorectal, 11 with gastric). Definitive carrier status was available on 8 individuals. An additional 7 individuals were obligate carriers. Age at diagnosis ranged from 27-84 years (median=60). Median age of colorectal cancer diagnosis among carriers was 54 compared with 61 among non-carriers. Median age of gastric cancer diagnosis among carriers was 66 compared with 53 among non-carriers. Conclusions: Early onset colorectal cancer occurs in certain HBOC families and may be related to mutation status. No genotype-phenotype association was identified in this study. An additional 60 Irish HBOC families are being screened for GI malignancies and updated data will be presented at the meeting.

Gastrointestinal cancer risk in Irish hereditary breast ovarian cancer families.

2013 ◽  
Vol 31 (4_suppl) ◽  
pp. 413-413
Author(s):  
Darragh S Gogarty ◽  
Tomas Lyons ◽  
Michael P. Farrell ◽  
Naoise Maria Dorman ◽  
Andrew J Green ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Ovarian Cancer ◽  
Cancer Risk ◽  
Lynch Syndrome ◽  
Early Onset ◽  
Carrier Status ◽  
Hereditary Breast Ovarian Cancer ◽  
Mutation Carriers ◽  
Increased Risk ◽  
Age Of Diagnosis

413 Background: Colorectal and breast cancer are linked in certain predisposition syndromes such as Cowden and Peutz-Jegers syndrome. Breast cancer risk also appears increased in certain Lynch syndrome kindreds. Original reports suggested an increased risk of colorectal malignancies in BRCA1/2 mutation carriers. Two large studies in Ashkenazi Jewish populations subsequently contradicted this early evidence, although neither study was powered to address effects if each gene independently, or other modifier effects in certain families. We report the Irish experience of colorectal and gastro-esophageal (GE) cancer in hereditary breast ovarian cancer (HBOC) families. Methods: 97 HBOC families at two tertiary referral centres were reviewed for the presence of early onset GE malignancies. The medical records of individuals with GE cancer were reviewed to determine carrier status. Clinical data including age of diagnosis, stage, treatment and outcome were extracted. Median age of diagnosis and outcome were compared among BRCA1/2 mutation carriers and non-carriers. Results: We identified 30 individuals with GE malignancies in 97 HBOC families (19 with colorectal, 11 with gastric). Two families were excluded as Lynch syndrome was also diagnosed in these families. Definitive carrier status was available on 8 individuals. Additional 7 individuals were obligate carriers. Age at diagnosis ranged from 27-84 years (median=60). Median age of CRC diagnosis among carriers was 54 compared with 61 among non-carriers (p=0.20). Median age of gastric diagnosis among carriers was 66 compared with 53 among non-carriers. Conclusions: Early onset colorectal cancer occurs in certain HBOC families and may be related to mutation status. No genotype-phenotype association was identified in this study. An additional 150 Irish HBOC families are being screened for early onset GI malignancies and updated data will be presented at the meeting.

scholarly journals Lynch Syndrome Caused by Germline PMS2 Mutations: Delineating the Cancer Risk

2015 ◽  
Vol 33 (4) ◽  
pp. 319-325 ◽  
Author(s):  
Sanne W. ten Broeke ◽  
Richard M. Brohet ◽  
Carli M. Tops ◽  
Heleen M. van der Klift ◽  
Mary E. Velthuizen ◽  
...  
Keyword(s):  
Cancer Risk ◽  
Lynch Syndrome ◽  
Family Members ◽  
Cumulative Risk ◽  
Mismatch Repair Gene ◽  
Genetic Modifiers ◽  
Analysis Model ◽  
Repair Gene ◽  
Mutation Carriers ◽  
Significant Difference

Purpose The clinical consequences of PMS2 germline mutations are poorly understood compared with other Lynch-associated mismatch repair gene (MMR) mutations. The aim of this European cohort study was to define the cancer risk faced by PMS2 mutation carriers. Methods Data were collected from 98 PMS2 families ascertained from family cancer clinics that included a total of 2,548 family members and 377 proven mutation carriers. To adjust for potential ascertainment bias, a modified segregation analysis model was used to calculate colorectal cancer (CRC) and endometrial cancer (EC) risks. Standardized incidence ratios (SIRs) were calculated to estimate risks for other Lynch syndrome–associated cancers. Results The cumulative risk (CR) of CRC for male mutation carriers by age 70 years was 19%. The CR among female carriers was 11% for CRC and 12% for EC. The mean age of CRC development was 52 years, and there was a significant difference in mean age of CRC between the probands (mean, 47 years; range, 26 to 68 years) and other family members with a PMS2 mutation (mean, 58 years; range, 31 to 86 years; P < .001). Significant SIRs were observed for cancers of the small bowel, ovaries, breast, and renal pelvis. Conclusion CRC and EC risks were found to be markedly lower than those previously reported for the other MMR. However, these risks embody the isolated risk of carrying a PMS2 mutation, and it should be noted that we observed a substantial variation in cancer phenotype within and between families, suggesting the influence of genetic modifiers and lifestyle factors on cancer risks.

Comparison of Lynch predictive models for identification of MLH1/MSH2 mutation carriers in a Spanish multicentre clinic- based cohort

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. e22077-e22077
Author(s):  
I. Valenzuela ◽  
J. Balmaña ◽  
M. Rue ◽  
I. Blanco ◽  
A. Torres ◽  
...  
Keyword(s):  
Genetic Testing ◽  
Lynch Syndrome ◽  
Predictive Models ◽  
Carrier Status ◽  
Operating Characteristics ◽  
Comparative Performance ◽  
Large Rearrangement ◽  
Clinical Criteria ◽  
Msh2 Mutation ◽  
Mutation Carriers

e22077 Background: Different predictive models for Lynch syndrome have recently been developed and their comparative performance in a clinic-based cohort has not been assessed. We aimed to analyze the accuracy of the MMRpro, Barnetson, and PREMM1,2 models to predict MLH1/MSH2 mutation carrier status in 564 unrelated probands with clinical suspicion of hereditary colorectal cancer and compare it with Wijnen model and clinical criteria. Methods: Overall, 538 individuals (95%) underwent mismatch repair (MMR) deficiency screening before germline genetic testing (sequencing with or without large rearrangement analysis) and 26 (5%) performed direct genetic testing. Prediction scores for all individuals were calculated by each model. Sensitivity, specificity, positive predictive value (PPV), and the areas under the receiver operating characteristics curves (AUC) for all models were calculated and compared with the Revised Bethesda Guidelines (RBG). Results: 114 individuals (20%) were mutation carriers (63 MLH1, 51 MSH2). The AUC was 0.95 (95% CI: 0.93–0.97) for MMRpro, 0.87 (95% CI 0.83–0.91) for the Barnetson model, 0.87 (95% CI 0.83–0.91) for PREMM1,2, and 0.75 (95% CI 0.69–0.80) for the Wijnen model (p<0.001). Testing thresholds and specificity at 100% and 90% sensitivity for each model were: 0.001/17% and 0.33/89% for MMRpro, 0.01/9% and 0.07/59% for Barnetson, 0.05/5% and 0.11/58% for PREMM1,2. Sensitivity and specificity of RBG were 86% and 14%, respectively. Calibration was 0.92, 1.05, 0.50, and 1.25 for PREMM1,2,Barnetson, Wijnen, and MMRpro, respectively. Conclusions: In a population of individuals at risk of Lynch syndrome, the MMRpro model has the largest AUC, although the Barnetson and PREMM1,2 model also show adequate discrimination. Any of the models perform better than the RBG and provide quantitative risk estimation of finding a MLH1/MSH2 mutation useful in genetic counselling. No significant financial relationships to disclose.

scholarly journals Assessment of oxidative damage and enzymatic antioxidant system activity on the umbilical cord blood and saliva from preterm newborns with risk factors for early-onset neonatal sepsis

2018 ◽  
Vol 64 (10) ◽  
pp. 888-895 ◽  
Author(s):  
Fábio Gonçalves Coutinho ◽  
Edna Maria de Albuquerque Diniz ◽  
Ingrid Kandler ◽  
Marco Antônio Cianciarullo ◽  
Natália Rodrigues dos Santos
Keyword(s):  
Risk Factors ◽  
Cord Blood ◽  
Umbilical Cord ◽  
Umbilical Cord Blood ◽  
Neonatal Sepsis ◽  
Early Onset ◽  
Umbilical Vein ◽  
Statistical Significance ◽  
Cross Sectional ◽  
Significant Difference

SUMMARY BACKGROUND: To determine the concentration of the Lipid Peroxidation Marker: Malondialdehyde (MDA), and Antioxidant Markers: Superoxide Dismutase (SOD), Glutathione Peroxidase (GPX), Catalase (CAL) in umbilical cord blood and in unstimulated saliva in the first 24 and 48 hours of life in the PTNB of mothers with and without risk factors for early-onset neonatal sepsis. METHODS: Cross-sectional study with the signing of informed consent by the pregnant women and application of a standard questionnaire classifying the PTNB in Group 1 or 2. RESULTS: Twenty-one PTNB were studied. Regarding gender, birth weight, need for oxygen, use of phototherapy, diagnosis of assumed sepsis, presence of fetal distress, number of pregnancies, type of delivery, use of corticosteroids, premature rupture of membranes, maternal fever, chorioamnionitis, APGAR at the 5th and 10th minute of life. Statistical analysis was performed with the Mann-Whitney test (p = 0.019) on the GPX variable of umbilical cord blood in the group of mothers with risk factors for early-onset neonatal sepsis. There was no statistical difference in the MDA, SOD, and CAT variables of the group with risk factors and in any variable of the group without risk factors. CONCLUSION: There was an increase of the GPX concentration in the blood from the umbilical vein in the group with risk factors for early-onset neonatal sepsis. There was no statistical significance in the comparison of saliva and umbilical cord blood. There was no statistically significant difference in MDA, SOD, CAT.

High prevalence of pathogenic variants in individuals with colorectal cancer ≤ age 35.

2018 ◽  
Vol 36 (4_suppl) ◽  
pp. 576-576 ◽  
Author(s):  
Megan L. Marshall ◽  
Maegan Roberts ◽  
Lisa R. Susswein ◽  
Anna K. McGill ◽  
Zhixiong Xu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Lynch Syndrome ◽  
Early Onset ◽  
Statistical Significance ◽  
Age At Onset ◽  
Tumor Location ◽  
Panel Testing ◽  
Pathogenic Variants ◽  
Gene Panel Testing ◽  
Tumor Studies

576 Background: Young age at onset is a hallmark feature of an inherited predisposition to cancer. Recent evidence suggests that the incidence of pathogenic/likely pathogenic variants (PV) in cancer predisposition genes among individuals diagnosed with colorectal cancer (CRC) ≤ age 35 is high, but few studies have examined the frequency identified by multi-gene hereditary cancer panel testing. We report on PV yield and clinical presentation of individuals diagnosed with CRC ≤ 35 years (y). Methods: We retrospectively reviewed test requisition forms and provided pathology reports for 4,727 individuals with CRC who underwent panel testing of, at a minimum, MLH1, MSH2, MSH6, PMS2, EPCAM, APC, and MUTYH. Two-tailed Fisher’s exact tests were used to determine statistically significant differences between groups. Results: Of the 691 individuals diagnosed with CRC ≤35y, 137 PV were identified in 126 individuals (126/691, 18.2%), including 72 with Lynch syndrome, 16 with familial adenomatous polyposis (FAP), five with MUTYH-associated polyposis, four with constitutional mismatch repair deficiency, one with juvenile polyposis syndrome, and one with Peutz-Jeghers syndrome. Thirty-eight additional PVs were identified in other non-CRC genes. Microsatellite instability (MSI) and immunohistochemistry (IHC) results were reported for 277 individuals and were reportedly abnormal in 63. The yield of PV in individuals with abnormal tumor studies was 52.4% (33/63); PV in genes other than the Lynch syndrome-associated genes were identified, commonly in the MSI-H group. While statistical significance was not observed, the positive rate was higher for individuals with non-rectal cancers (colon cancer: 104/534, 19.5%; rectal cancer: 22/157, 14.0%, p = 0.13). Conclusions: In our cohort, 18.2% of individuals diagnosed with CRC ≤35y were found to harbor a PV. Yield increased in those with abnormal MSI/IHC as well as non-rectal tumor location. Hereditary predispositions in patients diagnosed with very early-onset CRC are not limited to Lynch syndrome and FAP. Therefore, individuals with very early-onset CRC may benefit from multi-gene panel testing rather than syndromic-based testing.

Emerging value of multigene panels for germline testing in patients with neuroendocrine tumors.

2018 ◽  
Vol 36 (4_suppl) ◽  
pp. 226-226
Author(s):  
Julia Whitman ◽  
Brandon Shih ◽  
Amie Blanco ◽  
Salina Chan ◽  
Alan Paciorek ◽  
...  
Keyword(s):  
Neuroendocrine Tumors ◽  
Cancer Genetics ◽  
Statistical Significance ◽  
Single Gene ◽  
Logistic Models ◽  
Germline Mutations ◽  
Significant Difference ◽  
Multigene Panels ◽  
Over Time ◽  
Germline Testing

226 Background: Neuroendocrine tumors (NETs) are known to be associated with hereditary syndromes stemming from MEN1, VHL, SDH or TSC mutations. Recent data suggest that additional germline mutations may be relevant, implying a role of germline testing with multigene panels. We examined genetic counseling (GC) referral and testing patterns, test results, and their changes over time in NET patients (pts). Methods: Retrospective chart review was conducted in 236 NET pts referred to UCSF Cancer Genetics and Prevention Program 2004-2017. Univariate logistic models were used to assess relationship between binary outcome and covariate. STATA was used for analysis and statistical significance was based on p < 0.05. Results: 139 referred pts (59%) followed up with GC. Pts with >1 family members diagnosed with cancer were more likely to attend GC [OR=2.75, p=0.010]. Among 107 pts tested, small bowel NETs were less associated with testing than pancreatic NETs [OR=0.15, p=0.001]. Single-gene tests were routine until 2015, when panels up to 130 genes became standard. Overall, 31 pts (29% of 107 tested) had a pathogenic/likely pathogenic (P/LP) result. There was no significant difference between single and multi-gene tests in identifying P/LP mutations (likely due to changes in threshold for testing over time), but greater diversity in P/LP mutations was noted with larger panels. Functional tumors showed lower rate of P/LP mutations than non-functional [OR=0.17, p=0.037]. Conclusions: Only 59% of referred pts followed up with GC, suggesting significant barriers to testing exist. Of those tested, 29% harbored a P/LP mutation. Germline mutations not traditionally associated with NETs were identified, highlighting the potential importance of larger panels to detect rare mutations. [Table: see text]

LRRK2, GBA and SMPD1 Founder Mutations and Parkinson's Disease in Ashkenazi Jews

2016 ◽  
Vol 42 (1-2) ◽  
pp. 1-6 ◽  
Author(s):  
Efrat Dagan ◽  
Ilana Schlesinger ◽  
Alina Kurolap ◽  
Mareemar Ayoub ◽  
Maria Nassar ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Clinical Characteristics ◽  
Statistical Significance ◽  
Clinical Manifestations ◽  
Age At Diagnosis ◽  
Carrier Status ◽  
Ashkenazi Jews ◽  
Founder Mutations ◽  
Mutation Carriers

Background/Aim: Parkinson's disease (PD) is associated with mutations in LRRK2, GBA, and SMPD1 genes. We describe the clinical characteristics of PD patients related to their carrier status of the Ashkenazi founder mutations in the aforementioned genes. Methods: Ashkenazi PD patients (n = 270) were recruited following informed consent, and tested for the founder Ashkenazi mutations in the above genes. Clinical characteristics were compared between carriers and noncarriers. Homozygotes for mutations in GBA or LRRK2, and those who carried mutations in two causative genes were excluded from the analysis. Results: Five (1.85%), 54 (20%), and 22 (8.1%) PD patients carried mutations in SMPD1, GBA or LRRK2, respectively. By post hoc Bonferroni analysis, GBA carriers were singled at a significantly earlier age at diagnosis compared to noncarriers (58.06 ± 10.84 and 62.65 ± 10.86 years, respectively; p = 0.036), and due to bilateral manifestation at diagnosis compared to all other PD groups (n = 8, 15.7% compared to n = 2, 1.1%, respectively; p < 0.001). Other clinical manifestations were comparable between groups. Conclusion: Although only GBA mutation carriers, compared to noncarriers, reached statistical significance regarding age at diagnosis, it appears that LRRK2 and SMPD1 mutation carriers may reach significance with larger group numbers.

Comparative study of Clinical Characteristics in Patients with Mild and Severe Reflux Esophagitis

2020 ◽  
Vol 66 (1) ◽  
pp. 19-22
Author(s):  
Melania Macarie ◽  
Simona Maria Bataga ◽  
Monica Pantea ◽  
Razvan Opaschi ◽  
Simona Mocan ◽  
...  
Keyword(s):  
Risk Factors ◽  
Sex Ratio ◽  
Hiatal Hernia ◽  
Statistical Significance ◽  
Erosive Esophagitis ◽  
Male Gender ◽  
Consecutive Series ◽  
Study Group ◽  
Entire Study ◽  
Significant Difference

AbstractObjective: This study aims to determine the correlation between risk factors and erosive esophagitis development.Methods: We conducted a retrospective observational study on a consecutive series of 19.672 patients who underwent upper gastrointestinal endoscopy between 01.01.2011-31.12.2017. A total of 3005 patients, diagnosed with erosive esophagitis, were included in the present study and stratified according to Los Angeles classification.Results: During the studied period we found 3005 patients with erosive esophagitis, sex ratio male to female was 1.3/1, the most common forms of esophagitis being grade A and B: 74.54% patients with esophagitis grade A, 14.80% patients with grade B; 5.29% patients were with grade C and 5.35% patients with esophagitis grade D. In severe esophagitis the male predominance was more prevalent (249 males, 71 female), with a sex ratio 3.50/1. The correlation of male gender with severe esophagitis was highly statistically significant (p < 0.0001, OR 2.97; 95% CI 2.25-3.91). Hiatal hernia was diagnosed in 1171 patients, the presence of large hiatal hernias, being an important predictor, with statistical significance (p < 0.0001, OR 3.41; 95% CI 2.22-5.21), for severe esophagitis development. Incidence of Helicobacter pylori infection was 11.51%, in the entire study group, with no statistical significant difference between patients with mild or severe esophagitis (12.02% vs 7.18%).Conclusion: Erosive esophagitis is a frequent disease, the most common forms being grade A and B. Male gender and the presence of hiatal hernia are the most important risk factors for erosive esophagitis development, in our study group.

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