The relationship between hepatitis B virus (HBV) and nonhepatocellular cancers remains inconclusive. This large case‐control study aimed to assess the associations between HBV infection status and ...multiple cancers. Cases (n = 50 392) and controls (n = 11 361) were consecutively recruited from 2008 to 2016 at the First Affiliated Hospital of Nanjing Medical University. Multivariable adjusted odds ratios (aORs) and 95% confidence intervals (95% CIs) were estimated using logistic regression by adjusting age and gender. A meta‐analysis based on published studies was also performed to verify the associations. Of these, 12.1% of cases and 5.5% of controls were hepatitis B surface antigen (HBsAg) seropositive. We observed significant associations between HBsAg seropositivity and esophagus cancer (aOR 95% CI = 1.32 1.13‐1.54), stomach cancer (1.46 1.30‐1.65), hepatocellular carcinoma (HCC; 39.11 35.08‐43.59), intrahepatic and extrahepatic bile duct carcinoma (ICC and ECC; 3.83 2.58‐5.67 and 1.72 1.28‐2.31), pancreatic cancer (PaC; 1.37 1.13‐1.65), non‐Hodgkin lymphoma (NHL; 1.88 1.61‐2.20) and leukemia (11.48 4.05‐32.56). Additionally, compared to participants with HBsAg−/anti‐HBs−/anti‐HBc−, participants with HBsAg−/anti‐HBs−/anti‐HBc+, indicating past HBV‐infected, had an increased risk of esophagus cancer (aOR 95% CI = 1.46 1.24‐1.73), stomach cancer (1.20 1.04‐1.39), HCC (4.80 3.95‐5.84) and leukemia (15.62 2.05‐119.17). Then the overall meta‐analysis also verified that HBsAg seropositivity was significantly associated with stomach cancer (OR 95% CI = 1.23 1.14‐1.33), ICC (4.05 2.78‐5.90), ECC (1.73 1.30‐2.30), PaC (1.26 1.09‐1.46), NHL (1.95 1.55‐2.44) and leukemia (1.54 1.26‐1.88). In conclusion, both our case‐control study and meta‐analysis confirmed the significant association of HBsAg seropositivity with stomach cancer, ICC, ECC, PaC, NHL and leukemia. Of note, our findings also suggested that the risk of stomach cancer elevated for people whoever exposed to HBV.
What's new?
Infection with hepatitis B virus (HBV) is an important cause of hepatocelluar carcinoma and may be linked to certain non‐hepatocellular cancers as well, including colon cancer and stomach cancer. This case‐control investigation of cancer patients in China shows that positivity for hepatitis B surface antigen (HBsAg) is significantly higher in cancer patients overall than in controls. Among Chinese patients, HBsAg seropositivity was associated particularly with stomach cancer, pancreatic cancer, intrahepatic and extrahepatic bile duct carcinoma, non‐Hodgkin lymphoma, and leukemia. These observations were consistent with meta‐analysis of previous studies exploring possible associations between HBV and non‐hepatocellular cancers.
Background and purpose
Specific respiratory tract infections, including COVID‐19, may cause smell and/or taste disorders (STDs) with increased frequency. The aim was to determine whether new‐onset ...STDs are more frequent amongst COVID‐19 patients than influenza patients.
Method
This was a case–control study including hospitalized patients of two tertiary care centres. Consecutive patients positive for COVID‐19 polymerase chain reaction (cases) and patients positive for influenza polymerase chain reaction (historical control sample) were assessed during specific periods, employing a self‐reported STD questionnaire.
Results
Seventy‐nine cases and 40 controls were included. No significant differences were found in basal features between the two groups. New‐onset STDs were significantly more frequent amongst cases (31, 39.2%) than in the control group (5, 12.5 %) adjusted odds ratio 21.4 (2.77–165.4, P = 0.003). COVID‐19 patients with new‐onset STDs were significantly younger than COVID‐19 patients without STDs (52.6 ± 17.2 vs. 67.4 ± 15.1, P < 0.001). Amongst COVID‐19 patients who presented STDs, 22 (70.9%) recalled an acute onset and it was an initial manifestation in 11 (35.5%). Twenty‐five (80.6%) presented smell disorders (mostly anosmia, 14, 45.2%) and 28 (90.3%) taste disorders (mostly ageusia, 14, 45.2%). Only four (12.9 %) reported concomitant nasal obstruction. The mean duration of STD was 7.5 ± 3.2 days and 12 patients (40%) manifested complete recovery after 7.4 ± 2.3 days of onset.
Conclusion
New‐onset STDs were significantly more frequent amongst COVID‐19 patients than influenza patients; they usually had an acute onset and were commonly an initial manifestation. The use of STD assessment in anamnesis as a hint for COVID‐19 and to support individuals’ self‐isolation in the current epidemic context is suggested.
Background
Resolution and prevention of peri‐implant mucositis are a key in preventing peri‐implantitis. This case–control study aims to assess the modifying effect of a deep mucosal tunnel (DMT) on ...the induction and resolution phases of experimental peri‐implant mucositis.
Methods
Nineteen subjects with a tissue level implant were assigned to cases (DMT, depth ≥3 mm) or controls (shallow mucosal tunnel ≤1 mm, SMT). Subjects underwent a standard experimental peri‐implant mucositis protocol characterized by an oral hygiene optimization phase, a 3‐week induction phase using an acrylic stent to prevent self‐performed oral hygiene at the experimental implant, and a 3 + 2 weeks resolution phase. Modified plaque (mPI), gingival index (mGI) and peri‐implant sulcus fluid IL‐1β concentrations were measured over time. Differences between DMT and SMT were assessed with the Mann–Whitney test.
Results
Modified plaque index and mGI increased in parallel during the induction phase. After resumption of oral hygiene practice, mPI and mGI resolved towards baseline values in the SMT group. In DMT, mPI and mGI values diverged: plaque resolved but resolution of inflammation was delayed and of smaller magnitude during the first 3 weeks after resumption of oral hygiene. IL‐1β concentrations were significantly higher in DMT at 21 days (end of induction) and during the resolution phase corroborating the clinical findings. Removal of the crown and submucosal professional cleaning were needed to revert mGI to baseline values in DMT implants.
Conclusions
The depth of the mucosal tunnel modifies the resolution of experimental peri‐implant mucositis at transmucosal implants. This observation raises important questions on the effectiveness of self‐performed oral hygiene in cases where implants are placed deeper and the ability to resolve mucositis and effectively prevent peri‐implantitis in such situations.
Some studies suggest that periodontal diseases increase the risk of oral cancer, but contradictory results also exist. Inadequate control of confounders, including life course exposures, may have ...influenced prior findings. We estimate the extent to which high levels of periodontal diseases, measured by gingival inflammation and recession, are associated with oral cancer risk using a comprehensive subset of potential confounders and applying a stringent adjustment approach. In a hospital‐based case‐control study, incident oral cancer cases (N = 350) were recruited from two major referral hospitals in Kerala, South India, from 2008 to 2012. Controls (N = 371), frequency‐matched by age and sex, were recruited from clinics at the same hospitals. Structured interviews collected information on several domains of exposure via a detailed life course questionnaire. Periodontal diseases, as measured by gingival inflammation and gingival recession, were evaluated visually by qualified dentists following a detailed protocol. The relationship between periodontal diseases and oral cancer risk was assessed by unconditional logistic regression using a stringent empirical selection of potential confounders corresponding to a 1% change‐in‐estimates. Generalized gingival recession was significantly associated with oral cancer risk (Odds Ratio = 1.83, 95% Confidence Interval: 1.10–3.04). No significant association was observed between gingival inflammation and oral cancer. Our findings support the hypothesis that high levels of periodontal diseases increase the risk of oral cancer.
What's new?
Can gum disease predict the onset of oral cancer? As with many such questions, there's data supporting both sides. A new report comes down on the side of yes—periodontal disease is associated with risk of oral cancer. It's a complex question, because both gum disease and oral cancer share certain established risk factors, such as smoking. These authors applied stringent criteria to correct for potential confounders. They evaluated periodontal disease by measuring inflammation and recession of the gums and determined that gingival recession—but not inflammation—did significantly associate with oral cancer risk.
Selenium for preventing cancer Vinceti, Marco; Filippini, Tommaso; Del Giovane, Cinzia ...
Cochrane database of systematic reviews,
01/2018, Letnik:
2020, Številka:
2
Journal Article
Recenzirano
Odprti dostop
Background
This review is the third update of the Cochrane review "Selenium for preventing cancer". Selenium is a naturally occurring element with both nutritional and toxicological properties. ...Higher selenium exposure and selenium supplements have been suggested to protect against several types of cancer.
Objectives
To gather and present evidence needed to address two research questions:
1. What is the aetiological relationship between selenium exposure and cancer risk in humans?
2. Describe the efficacy of selenium supplementation for cancer prevention in humans.
Search methods
We updated electronic searches of the Cochrane Central Register of Controlled Trials (CENTRAL; 2017, Issue 2), MEDLINE (Ovid, 2013 to January 2017, week 4), and Embase (2013 to 2017, week 6), as well as searches of clinical trial registries.
Selection criteria
We included randomised controlled trials (RCTs) and longitudinal observational studies that enrolled adult participants.
Data collection and analysis
We performed random‐effects (RE) meta‐analyses when two or more RCTs were available for a specific outcome. We conducted RE meta‐analyses when five or more observational studies were available for a specific outcome. We assessed risk of bias in RCTs and in observational studies using Cochrane's risk assessment tool and the Newcastle‐Ottawa Scale, respectively. We considered in the primary analysis data pooled from RCTs with low risk of bias. We assessed the certainty of evidence by using the GRADE approach.
Main results
We included 83 studies in this updated review: two additional RCTs (10 in total) and a few additional trial reports for previously included studies. RCTs involved 27,232 participants allocated to either selenium supplements or placebo. For analyses of RCTs with low risk of bias, the summary risk ratio (RR) for any cancer incidence was 1.01 (95% confidence interval (CI) 0.93 to 1.10; 3 studies, 19,475 participants; high‐certainty evidence). The RR for estimated cancer mortality was 1.02 (95% CI 0.80 to 1.30; 1 study, 17,448 participants). For the most frequently investigated site‐specific cancers, investigators provided little evidence of any effect of selenium supplementation. Two RCTs with 19,009 participants indicated that colorectal cancer was unaffected by selenium administration (RR 0.99, 95% CI 0.69 to 1.43), as were non‐melanoma skin cancer (RR 1.16, 95% CI 0.30 to 4.42; 2 studies, 2027 participants), lung cancer (RR 1.16, 95% CI 0.89 to 1.50; 2 studies, 19,009 participants), breast cancer (RR 2.04, 95% CI 0.44 to 9.55; 1 study, 802 participants), bladder cancer (RR 1.07, 95% CI 0.76 to 1.52; 2 studies, 19,009 participants), and prostate cancer (RR 1.01, 95% CI 0.90 to 1.14; 4 studies, 18,942 participants). Certainty of the evidence was high for all of these cancer sites, except for breast cancer, which was of moderate certainty owing to imprecision, and non‐melanoma skin cancer, which we judged as moderate certainty owing to high heterogeneity. RCTs with low risk of bias suggested increased melanoma risk.
Results for most outcomes were similar when we included all RCTs in the meta‐analysis, regardless of risk of bias. Selenium supplementation did not reduce overall cancer incidence (RR 0.99, 95% CI 0.86 to 1.14; 5 studies, 21,860 participants) nor mortality (RR 0.81, 95% CI 0.49 to 1.32; 2 studies, 18,698 participants). Summary RRs for site‐specific cancers showed limited changes compared with estimates from high‐quality studies alone, except for liver cancer, for which results were reversed.
In the largest trial, the Selenium and Vitamin E Cancer Trial, selenium supplementation increased risks of alopecia and dermatitis, and for participants with highest background selenium status, supplementation also increased risk of high‐grade prostate cancer. RCTs showed a slightly increased risk of type 2 diabetes associated with supplementation. A hypothesis generated by the Nutritional Prevention of Cancer Trial ‐ that individuals with low blood selenium levels could reduce their risk of cancer (particularly prostate cancer) by increasing selenium intake ‐ has not been confirmed. As RCT participants have been overwhelmingly male (88%), we could not assess the potential influence of sex or gender.
We included 15 additional observational cohort studies (70 in total; over 2,360,000 participants). We found that lower cancer incidence (summary odds ratio (OR) 0.72, 95% CI 0.55 to 0.93; 7 studies, 76,239 participants) and lower cancer mortality (OR 0.76, 95% CI 0.59 to 0.97; 7 studies, 183,863 participants) were associated with the highest category of selenium exposure compared with the lowest. Cancer incidence was lower in men (OR 0.72, 95% CI 0.46 to 1.14, 4 studies, 29,365 men) than in women (OR 0.90, 95% CI 0.45 to 1.77, 2 studies, 18,244 women). Data show a decrease in risk of site‐specific cancers for stomach, colorectal, lung, breast, bladder, and prostate cancers. However, these studies have major weaknesses due to study design, exposure misclassification, and potential unmeasured confounding due to lifestyle or nutritional factors covarying with selenium exposure beyond those taken into account in multi‐variable analyses. In addition, no evidence of a dose‐response relation between selenium status and cancer risk emerged. Certainty of evidence was very low for each outcome. Some studies suggested that genetic factors might modify the relation between selenium and cancer risk ‐ an issue that merits further investigation.
Authors' conclusions
Well‐designed and well‐conducted RCTs have shown no beneficial effect of selenium supplements in reducing cancer risk (high certainty of evidence). Some RCTs have raised concerns by reporting a higher incidence of high‐grade prostate cancer and type 2 diabetes in participants with selenium supplementation. No clear evidence of an influence of baseline participant selenium status on outcomes has emerged in these studies.
Observational longitudinal studies have shown an inverse association between selenium exposure and risk of some cancer types, but null and direct relations have also been reported, and no systematic pattern suggesting dose‐response relations has emerged. These studies suffer from limitations inherent to the observational design, including exposure misclassification and unmeasured confounding.
Overall, there is no evidence to suggest that increasing selenium intake through diet or supplementation prevents cancer in humans. However, more research is needed to assess whether selenium may modify the risk of cancer in individuals with a specific genetic background or nutritional status, and to investigate possible differential effects of various forms of selenium.
Background. Infants with pertussis infection are at risk of severe clinical illness and death. Several countries, including the United Kingdom, have introduced maternal pertussis vaccination during ...pregnancy to protect infants from infection following national increases in pertussis notifications. The objective of this study was to estimate the effectiveness of maternal pertussis vaccination in protecting infants against laboratory-confirmed pertussis infection. Methods. A case-control study was undertaken in England and Wales between October 2012 and July 2013. Cases were infants aged <8 weeks at onset with pertussis infection tested by real-time polymerase chain reaction or culture. Family doctors of each case were asked to identify healthy infants born consecutively after the case in each practice, to act as controls. Fifty-eight cases and 55 controls were included in this study. Odds ratios (ORs) were calculated for the association between maternal vaccination and infant pertussis infection. The vaccine effectiveness (VE) was calculated as 1 – OR. This was adjusted for sex, geographical region, and birth period. Results. Mothers of 10 cases (17%) and 39 controls (71%) received pertussis vaccine in pregnancy. This gave an unadjusted VE of 91% (95% confidence interval CI, 77%–97%). Adjusted VE was 93% (95% CI, 81%–97%). Conclusions. Maternal pertussis vaccination is effective in preventing pertussis infection in infants aged <8 weeks and may be considered in other countries experiencing high levels of pertussis notifications.
Background
Diseases caused by Streptococcus pneumoniae (S. pneumoniae) continue to cause substantial morbidity and mortality globally. Whilst pneumococcal polysaccharide vaccines (PPVs) have the ...potential to prevent disease and death, the degree of protection afforded against various clinical endpoints and within different populations is uncertain.
Objectives
To assess the efficacy and effectiveness of PPVs in preventing pneumococcal disease or death in adults. We did not assess adverse events.
Search methods
We searched CENTRAL 2012, Issue 6, MEDLINE (January 1966 to June Week 2, 2012) and EMBASE (1974 to June 2012).
Selection criteria
We considered randomised controlled trials (RCTs) in adults, provided the study outcome met the definition of the outcome considered in the review. We also considered non‐RCTs in adults, where the study assessed PPV effectiveness against culture‐confirmed invasive pneumococcal disease (IPD), provided the study controlled for important confounding factors.
Data collection and analysis
Two review authors assessed trial quality of RCTs and three review authors extracted the data. We estimated odds ratios (ORs) and 95% confidence intervals (CIs) using a random‐effects model. Two review authors assessed study quality and extracted data for non‐RCTs. We calculated ORs and 95% CIs using a random‐effects model following the conversion of each study outcome to a log OR and standard error (SE).
Main results
Twenty‐five studies met our inclusion criteria (18 RCTs involving 64,852 participants and seven non‐RCTs involving 62,294 participants). Meta‐analysis of the RCTs found strong evidence of PPV efficacy against IPD with no statistical heterogeneity (OR 0.26, 95% CI 0.14 to 0.45; random‐effects model, I2 statistic = 0%). There was efficacy against all‐cause pneumonia in low‐income (OR 0.54, 95% CI 0.43 to 0.67, I2 statistic = 19%) but not high‐income countries in either the general population (OR 0.71, 95% CI 0.45 to 1.12, I2 statistic = 93%) or in adults with chronic illness (OR 0.93, 95% CI 0.73 to 1.19, I2 statistic = 10%). PPV was not associated with substantial reductions in all‐cause mortality (OR 0.90, 95% CI 0.74 to 1.09; random‐effects model, I2 statistic = 69%). Vaccine efficacy against primary outcomes appeared poorer in adults with chronic illness. Non‐RCTs provided evidence for protection against IPD in populations for whom the vaccine is currently utilised (OR 0.48, 95% CI 0.37 to 0.61; random‐effects model, I2 statistic = 31%). This review did not consider adverse events as it was outside the scope of the review.
Authors' conclusions
This meta‐analysis provides evidence supporting the recommendation for PPV to prevent IPD in adults. The evidence from RCTs is less clear with respect to adults with chronic illness. This might be because of lack of effect or lack of power in the studies. The meta‐analysis does not provide evidence to support the routine use of PPV to prevent all‐cause pneumonia or mortality.
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