Background: Nonmelanoma skin cancer (NMSC) is the most common malignancy. Basal cell carcinoma (BCC) comprises about 80% of all NMSCs and its incidence continues to rise. Although BCC rarely leads to metastases or increased mortality, its effects on healthcare costs and quality of life are substantial. Aspirin may prevent the development of basal cell carcinoma (BCC) by the inhibition of cyclooxygenase (COX) enzymes, which are associated with carcinogenesis and inflammation. This study therefore examined the effect of aspirin on the risk of BCC, its clinical outcomes, and its treatment costs.Methods: A retrospective study (2010 -2018) was conducted using the Humana Health Insurance Database. International Classification of Disease ninth and 10th codes and National Drug Codes were used to identify BCC diagnoses and aspirin prescriptions. Patients were matched for age, sex, Charlson Comorbidity Score (CCI), and region of residence. Chi-squared, logistic regression, and odds ratio (OR) analyses were utilized to test for significance and to estimate relative risk.Results: Aspirin use was associated with a decreased incidence of BCC in unmatched (OR = 0.658, 95% confidence interval (CI) 0.526 -0.820) and matched (OR = 0.54, 95% CI 0.47 -0.61) analyses. Aspirin was also associated with a decreased BCC risk when stratified by hypertension (P = 3.888 × 10 -5 ), chronic obstructive pulmonary disease (COPD) (P = 0.014), diabetes (P = 0.049) and tobacco use (P = 0.017). Aspirin use was not associated with risk of BCC when stratified by obesity (P = 0.408). The average paid per patient for BCC treatment was significantly higher for patients in the aspirin use group than in the aspirin nonuse group (P = 0.0087).Conclusions: While the high incidence and cost of treatment of BCC are demanding both clinically and financially, the low cost of aspirin and its widespread use may have vital implications for its preventative role in this disease. This study concluded that aspirin use was associated with a significantly decreased risk of BCC.
Background Hemophilus influenzae is a gram-negative coccobacillus. Non-typeable H. influenzae infection is a significant cause of disease that activates the inflammatory pathway involving the nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome. A gain-of-function mutation in NLRP3 results in cryopyrin-associated periodic syndromes characterized by inflammatory conditions in the lungs, skin, joints, and eyes but not in the gut. This leads to homeostasis of the gut microbiota, which reduces inflammation and may have protective effect against colorectal cancer (CRC). This study aimed to evaluate the correlation between H. influenzae infection and the incidence of CRC. Methods A retrospective study was conducted from 2010 to 2019 using a HIPAA-compliant national database. ICD-10, ICD-9, CPT, and National Drug Codes were used to identify patients with or without a history of H. influenzae infection. Standard statistical methods were used to analyze the outcomes. Results The query was analyzed and matched, resulting in 13,610 patients in both groups. The incidence of CRC was 167 and 446 in the H. influenzae and control groups, respectively. The difference was statistically significant with P < 2.2 ×10 -16 and an odds ratio of 0.41 (95% confidence interval: 0.36 - 0.47). Additionally, the groups were further evaluated and matched by treatment, which resulted in a statistically significant decrease in CRC incidence in the H. influenzae group. Conclusion This study showed a statistically significant correlation between H. influenzae and the reduced incidence of CRC. This reduction in CRC in patients with a history of H. influenzae infection suggests a potential link to the NLRP3 inflammasome, which should be further studied.
Background: Enterococci role in the microbiome remains controversial, and researches regarding enterococcal infection (EI) and its sequelae are limited. The gut microbiome has shown to play an important role in immunology and cancer. Recent data have suggested a relationship between the gut microbiome and breast cancer (BC).Methods: Patients in a Health Insurance Portability and Accountability Act (HIPAA) compliant national database (2010 -2020) were used for this retrospective study. International Classification of Disease (ICD) Ninth and Tenth Codes, Current Procedural Terminology (CPT), and National Drug Codes were used to identify BC diagnosis and EI. Patients were matched for age, sex, Charlson comorbidity index (CCI), antibiotic treatment, obesity, and region of residence. Statistical analyses were implemented to assess significance and estimate odds ratio (OR).Results: EI was associated with a decreased incidence of BC (OR = 0.60, 95% confidence interval (CI): 0.57 -0.63) and the difference was statistically significant (P < 2.2 × 10 -16 ). Treatment for EI was controlled for in both EI and noninfected populations. Patients with a prior EI and treated with antibiotics were compared to patients with no history of EI and received antibiotics. Both populations subsequently developed BC. Results remained statistically significant (P < 2.2 × 10 -16 ) with an OR of 0.57 (95% CI: 0.54 -0.60). In addition to standard matching protocol, obesity was controlled for in both groups by exclusively containing obese patients, but one group with prior EI and the other without. In obese patients, a lower incidence of BC was shown in the infected group compared to the noninfected group. Results were statistically significant (P < 2.2 × 10 -16 ) with an OR of 0.56 (95% CI: 0.53 -0.58). Age of BC diagnosis with and without a prior EI was analyzed and demonstrated increased BC incidence with increasing age in both groups, but less in the EI group. Incidence of BC based on region was analyzed, which showed lower BC incidence across all regions in the EI group. Conclusion:This study shows a statistically significant correlation between EI and decreased incidence of BC. Further exploration is needed to identify and understand not only the role of enterococcus in the microbiome, but also the protective mechanism(s) and impact of EI on BC development.
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