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1.
Gulf J Oncolog ; 1(42): 61-69, 2023 May.
Article in English | MEDLINE | ID: mdl-37283262

ABSTRACT

BACKGROUND AND OBJECTIVE: Pancreatic cancer (PC) is the seventh leading cause of death among cancers mortality. Pancreatic carcinogenesis remains poorly understood. There is still an urge to allocate other related risk factors that may help in better recognition of this pathogenesis. There is increasing evidence suggested that peptic ulcer disease (PUD), and its treatment might affect the development of PC however, studies findings reported conflicting results. Our meta-analysis aimed to study the association between PUD and its treatments (proton pump inhibitors [PPIs] and histamine-2 receptor antagonists [H2RAs]) and risk of PC. METHODS: We searched PubMed/MEDLINE, Embase, and Cochrane library databases from inception through January 2022. We included case-control studies, cohort, and randomized control trials which reported the association between PUD, PPIs, and H2RAs and the risk of PC. Odds ratio (OR) were used to calculate pooled estimates for PC risk. The association were evaluated using random-effects models, in two sided statistical tests. RESULTS: A total of 22 publications were retained for the meta-analysis. PUD was associated with a significant increase in PC risk (OR 1.26, 95% CI= 1.01-1.57, P= 0.038, I2= 92%). The risk of developing PC were significant in patients receiving PPIs (OR 1.76, 95% CI= 1.26-2.46, P=0.001, I2= 98%) and H2RAs (OR 1.25, 95% CI = 1.042- 1.49, P= 0.016, I2= 80%). CONCLUSIONS: There is a 1.26-fold increase risk of PC in patients with PUD. The elevated PC is also attributable to 1.76-fold greater risk in PPIs group compared to 1.25-fold in H2RAs group.


Subject(s)
Pancreatic Neoplasms , Peptic Ulcer , Humans , Peptic Ulcer/chemically induced , Histamine H2 Antagonists/adverse effects , Proton Pump Inhibitors/adverse effects , Risk Factors , Pancreatic Neoplasms/etiology
2.
Geospat Health ; 15(1)2020 06 22.
Article in English | MEDLINE | ID: mdl-32575972

ABSTRACT

Although Antimicrobial Resistance (AMR) is a worldwide threat, local AMR databases do not exist. Unlike other health disasters, developing containment strategies for AMR cannot be started without a representative, local, updated AMR data. However, Geographical Information Systems (GIS) mapping technology is capable of visualizing AMR data integrated with geographical regions. Due to the absence of AMR databases in Saudi Arabia, we searched Medline and Embase databases from inception until May 28, 2018, including literature that reported AMR data on the most prevalent gram-negative bacterial strains in Saudi Arabia. These data were extracted into Microsoft Excel file and inserted into STATA software, version 13 and ArcMap 10.6 software platform for mapping. We found particularly high levels of AMR in Makkah (Mecca), possibly due to high antibiotic consumption because of the influx of pilgrims, with Pseudomonas aeruginosa isolates showing the highest resistance rate against amikacin, aztreonam, cefepime, ceftazidime, ciprolfloxacin, gentamicin, imipenem, meropenem and pipracillin/tazobactam, and Enterobacteriaceae isolates against cefuroxime, ciprofloxacin, ampicillin, imipenem and ertapenem. The cause is, however, multifactorial since Acinetobacter baumannii isolates showed a variable resistance rate throughout the country. The employment of mapping technology in displaying AMR data extracted from published literature is a practically useful approach, and advanced GIS analyses should help stakeholders create containment strategies and allocate resources to slow down the emergence of AMR.


Subject(s)
Anti-Bacterial Agents , Drug Resistance, Bacterial , Geographic Information Systems , Acinetobacter baumannii/drug effects , Anti-Bacterial Agents/pharmacology , Drug Resistance, Bacterial/drug effects , Gram-Negative Bacteria/drug effects , Humans , Pseudomonas aeruginosa/drug effects , Saudi Arabia , Technology
3.
Expert Opin Drug Saf ; 19(3): 327-334, 2020 03.
Article in English | MEDLINE | ID: mdl-31928106

ABSTRACT

Objectives: To estimate the pancreatic cancer risk among subjects exposed versus not exposed to proton pump inhibitors.Methods: The authors searched PubMed, EMBASE, Scopus, Cochrane Library, and clinicaltrials.gov to identify relevant studies. The authors quantified pancreatic cancer risk among subjects exposed versus not exposed to PPIs, expressed as the pooled (adjusted) odds ratio (OR/aOR) and 95% confidence interval (95%CI) in overall and sensitivity analyses.Results: One randomized trial, two cohort, four case-control, and five nested case-control studies with 700,178 subjects (73,985 cases; 626,193 controls) were retained. PPI exposure was associated with pancreatic cancer risk (OR = 1.75, 95%CI = 1.12-2.72, I2 = 99%); confirmed in sensitivity analyses for high-quality studies, observational studies, case-control studies, studies with pancreatic cancer as the primary outcome, and in sensitivity analyses for diabetes and obesity but not for pancreatitis and smoking. This association was independent of the duration and Defined Daily Dose of PPI exposure. Rabeprazole had a singular significant association with pancreatic cancer (OR = 5.40, 95%CI = 1.98-14.703, I2 = 87.9%).Conclusion: The class of PPIs is associated with a 1.75-fold increase in pancreatic cancer risk, confirmed in sensitivity analyses.


Subject(s)
Pancreatic Neoplasms/chemically induced , Proton Pump Inhibitors/adverse effects , Humans , Risk Factors
4.
Prostate ; 79(8): 880-895, 2019 06.
Article in English | MEDLINE | ID: mdl-30900310

ABSTRACT

BACKGROUND: A prior meta-analysis found no association between BRCA1 mutation and prostate cancer (PCa). Subsequent BRCA2 mutation studies have shown an association with PCa risk and mortality. We conducted a meta-analysis of overall BRCA mutation carriers and in subgroups to (1) estimate PCa risk in BRCA mutation carriers, (2) evaluate the frequency of BRCA mutation carriers in patients with PCa, and (3) compare cancer-specific survival (CSS) and overall survival (OS) among BRCA mutation carriers and noncarriers. METHODS: We searched the PubMed/MEDLINE, Embase, and Cochrane databases. Unadjusted odds ratio (OR), percentage (%), and hazard ratio (HR) were used to calculate pooled estimates for PCa risk, frequency, and survival, respectively. Subgroup analyses by mutation type ( BRCA1 or BRCA2) were conducted for the three objectives. Further subgroup analyses by study design (age-sex-adjusted or crude), ascertainment method (ascertained or inferred genotyping), population (Ashkenazi Jewish or general population), and survival outcomes (CSS or OS) were conducted. The associations were evaluated using random-effects models, in two-sided statistical tests. RESULTS: A total of 8 cohort, 7 case-control, 4 case-series, 28 frequency, and 11 survival studies were included. Being a BRCA mutation carrier ( BRCA1 and/or BRCA2) was associated with a significant increase in PCa risk (OR = 1.90, 95% CI = 1.58-2.29), with BRCA2 mutation being associated with a greater risk of PCa (OR = 2.64, 95% CI = 2.03-3.47) than BRCA1 (OR = 1.35, 95% CI = 1.03-1.76). The frequency of BRCA1 and BRCA2 carriers in patients with PCa was 0.9% and 2.2%, respectively. OS (HR = 2.21, 95% CI = 1.64-2.30) and CSS (HR = 2.63, 95% CI = 2.00-3.45) were significantly worse among BRCA2 carriers compared to noncarriers, whereas OS (HR = 0.47, 95% CI = 0.11-1.99) and CSS (HR = 1.07, 95% CI = 0.38-2.96) were statistically not significant when comparing BRCA1 carriers and noncarriers. CONCLUSIONS: There is a 1.90-fold greater risk of PCa in overall BRCA mutation carriers. This elevated PCa risk is attributable mainly to a 2.64-fold greater risk of PCa in BRCA2 carriers compared to a moderate 1.35-fold greater risk in BRCA1 carriers. The frequency of BRCA2 mutations was higher than BRCA1 mutations among patients with PCa. BRCA2 but not BRCA1 mutations were associated with higher PCa mortality. The BRCA mutation may be a clinical factor to stratify high-risk patients and guide clinical strategies for more effective treatments for patients with PCa.


Subject(s)
Genes, BRCA1 , Genes, BRCA2 , Mutation , Prostatic Neoplasms/genetics , Prostatic Neoplasms/mortality , BRCA1 Protein/genetics , BRCA2 Protein/genetics , Case-Control Studies , Cohort Studies , Humans , Male
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