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Background: Radical excision (RE) for rectal cancer carries a higher risk of mortality and morbidity, while local excision (LE) could decrease these postoperative risks. However, the long-term benefit of LE is still debatable. Aim: To study the effectiveness of LE versus RE in T1 and T2 rectal cancer. Methods: A systematic review and meta-analysis was conducted using key databases like PubMed and ClinicalTrials.gov. Only cohort studies and randomized controlled trials were included. RevMan 5.4 tool was used for data analysis. Both clinical and statistical heterogeneity of the studies were assessed, and I2 >75% was considered as highly heterogeneous. The primary outcomes being measured were 5-year overall survival (OS) and 5-year disease free survival (DFS). A subgroup analysis of patients with T1-only was also conducted, without adjuvant chemo/radiotherapy. Results: A total of 18 studies were included for final meta-analysis. Four were RCTs, while the other 15 were retrospective cohort studies. One included study had data from both RCT and non-RCT study groups. Nine studies were multicentered or national studies while nine were unicentral.There was no difference in risk ratio (RR) between OS: RR 0.95, 95% Confidence Interval (CI) [0.91, 0.99] and DFS: RR 0.93, 95% CI [0.87, 1.01]. There were lower hazards ratios in OS: RR 1.41, 95% CI [1.14, 1.74] and DFS: RR 1.95, 95% CI [1.36, 2.78] with radical, as compared to LE. Lower recurrence rate was associated with RE. Random effect model was used due to clinical heterogeneity between studies (different surgical procedures, tumor staging, adjuvant chemo or radiotherapy). Conclusions: LE for early-stage rectal cancer has lower 5-year OS and DFS than RE, with higher local recurrence rate. However, LE is associated with lower early postoperative mortality, morbidity and length of stay as compared to RE.
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BACKGROUND: The relationship between Helicobacter pylori (H. pylori) and hepatocellular carcinoma (HCC) was firstly proposed in 1994 after Ward et al demonstrated the role of Helicobacter hepaticus in the development of HCC in mice. Studies also investigated the role of hepatitis B virus (HBV) and hepatitis C virus (HCV) coexisting with H. pylori in causing HCC. A causal relationship was never confirmed, and the relationship remains controversial. This meta-analysis aimed to summarize the research on this topic and investigate if a relationship exists between H. pylori infection and the development of HCC and if the presence of HCV and HBV along with H. pylori plays a role in liver carcinogenesis. METHODS: Following PRISMA guidelines, we performed a systematic review of all relevant studies published in the literature using the keywords "Helicobacter pylori" and "hepatocellular carcinoma" on major literature databases, including PubMed, EMBASE, Web of Science, and Cochrane controlled trials register. A total of 656 research studies were identified between 1994 and 2020. Of those, 26 qualified under our selection criteria. Patients who were positive for HCC were classified as cases and those who did not have HCC were classified as controls. The H. pylori status and HCV status, if available, were identified for both groups. Statistical analysis was carried out by a biostatistician according to the Cochrane reviewer's handbook. RESULTS: Out of the 26 studies included in the final analysis, 13 were retrospective case-control studies, 11 were cross-sectional studies, and two were prospective case-control and cohort studies. Overall, the prevalence of H. pylori infection was 64.78% (561 of 866) amongst HCC cases and 47.92% (1,718 of 3,585) in the non-HCC control group. The summary odds ratio (OR) for the association of H. pylori infection with the risk for HCC (using the random-effects model, which accounted for the heterogeneity across the 26 studies) was determined to be 4.75 (95% confidence interval (CI): 3.06 - 7.37, I2 = 63%). We also performed a subgroup analysis to determine the odds of developing HCC in the presence of H. pylori and HCV coinfection. The summary OR of it was 12.76 (95% CI: 4.13 - 39.41, I2 = 78%). The summary OR for the risk of developing HCC in the presence of HCV infection without H. pylori infection was 2.21 (95% CI: 0.70 - 6.94, I2 = 79%). Whereas, the odds of developing HCC in the presence of only H. pylori infection without HCV was found to be 0.54 (95% CI: 0.11 - 2.63, I2 = 80%). There was inconsistency in the data presented in some studies regarding HCV infection status. Since data were extracted from different study designs, subgroup analysis by study design was performed which showed no significant difference between the study groups (P = 0.5705). CONCLUSION: This meta-analysis demonstrates a positive association between H. pylori infection and the development of HCC. There is a significantly higher risk of developing HCC in the presence of HCV infection along with H. pylori. Further prospective cohort studies are needed to prove the causal relationship, especially in cases of HBV and HCV coinfection, and cirrhotic patients.
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Background: Globally Esophageal cancer is a common cancer arising from human esophageal mucosal tissue. Epidemiological studies suggest inverse correlation between carotenoid intake and incident risk of this devastating malignancy. Methods: In an effort to examine the modulatory role of carotenoids in human esophageal carcinogenesis at a cellular level, we examined the effects of α-carotene and ß-carotenes, on cell proliferation and DNA synthesis in human esophageal epithelial (HEE) cells and human esophageal squamous cancer (HESC) cells in in-vitro cultures. HEE and HESC cells were incubated with different concentrations of α- and ß-carotenes both individually and in combination. Results: Both Carotenes significantly inhibited (p<0.05) cellular proliferation and decreased DNA synthesis in HEE and HESC cells. The effect of α- and ß-carotene together on DNA synthesis in HEE and HESC cells was significantly greater than either carotenoid alone, suggesting a synergistic effect. Greater magnitude of cellular inhibition of DNA synthesis was observed on HEE cells than HESC cells. Conclusion: Our results suggest that a combination of α-and ß-carotene may provide a novel strategy for prevention and treatment of esophageal and upper aero digestive tract cancer in humans.
Assuntos
Carcinoma de Células Escamosas/tratamento farmacológico , Carotenoides/farmacologia , Proliferação de Células/efeitos dos fármacos , Células Epiteliais/efeitos dos fármacos , Neoplasias Esofágicas/tratamento farmacológico , Carcinoma de Células Escamosas/patologia , Células Cultivadas , Células Epiteliais/patologia , Neoplasias Esofágicas/patologia , HumanosRESUMO
Extramedullary plasmacytomas (EMP) are a subcategory of plasma cell neoplasm that involves organs outside the bone marrow. Involvement of the pancreas is relatively rare, reported in only 2.3% of autopsies. Radiologic findings in plasmacytoma are nonspecific, but endoscopic ultrasound fine-needle aspiration is a fast and reliable technique to acquire a histologic sample for initial diagnosis. Recently, the use of fluorine-18 fluorodeoxyglucose PET/CT has been recommended in patients with active multiple myeloma and solitary plasmacytoma. We present an interesting case of primary EMP in the pancreatic body encasing the portal vein as well as the celiac artery, which was detected before the patient was diagnosed of multiple myeloma.