The effects of smoking and alcoholism in acute coronary syndrome

Funding Acknowledgements Type of funding sources: None. Introduction Several studies have concluded that smoking increases mortality in patients with coronary disease. On the other hand, a J-shaped dose-effect curve has been used to describe the relationship between alcohol and cardiovascular mortality. According to the majority of studies, a moderate intake of alcohol is associated with a decrease in mortality, while an excessive alcohol intake appears to increase mortality. Aim To evaluate the effect of smoking and excessive alcohol intake in hospital mortality and 1-year mortality in patients hospitalized due to acute coronary syndrome (ACS). Methods A single-centre retrospective study was conducted, with inclusion of all consecutive patients admitted in the Cardiology Department due to ACS. Follow-up started after hospital admission and ended upon hospital death, death within the following 12 months or 12 months after study entry. Patients were divided in two groups: smokers (Group-A) and non-smokers (Group-B), to analyse the effect of smoking in hospital mortality and 1-year mortality. To analyse the effect of excessive alcohol intake, patients were also divided in other two groups: Group-C (excessive drinkers) and Group-D (non-excessive drinkers). Statistical analysis was performed with SPSS and a p value < 0.05 was considered statistically significant. Results 1120 patients (68.9% male, mean age 69.12 ± 12.67 years) were included in this study. 20.5% were smokers and 3.2% had a previous excessive alcohol intake. Between Group-A and Group-B, a statistically significant difference was observed in gender (93.1% male in Group-A vs 62.9% male in Group-B, p = 0.002), but not in age (p = 0.116). Hospital mortality rates in Group-A and Group-B were respectively 6.0% and 8.7% (p = 0.191) and 1-year mortality rates were 3.1% vs 5.1% (p = 0.239). Between Group-C and Group-D, a statistically significant difference was observed in gender (94.4% male in Group-C vs 69.8% male in Group-B, p < 0.001), but not in age (p = 0.730). Hospital mortality rates in Group-C and Group-D were respectively 25% and 9.6% (p = 0.003) and 1-year mortality were 3.8% vs 6.6% (p = 0.577). Conclusions Smoking did not have a positive or negative effect in hospital mortality and 1-year mortality. However, excessive alcohol intake was associated with increased hospital mortality in this population.

Alcohol Intake and Alcohol–SNP Interactions Associated with Prostate Cancer Aggressiveness

Excessive alcohol intake is a well-known modifiable risk factor for many cancers. It is still unclear whether genetic variants or single nucleotide polymorphisms (SNPs) can modify alcohol intake’s impact on prostate cancer (PCa) aggressiveness. The objective is to test the alcohol–SNP interactions of the 7501 SNPs in the four pathways (angiogenesis, mitochondria, miRNA, and androgen metabolism-related pathways) associated with PCa aggressiveness. We evaluated the impacts of three excessive alcohol intake behaviors in 3306 PCa patients with European ancestry from the PCa Consortium. We tested the alcohol–SNP interactions using logistic models with the discovery-validation study design. All three excessive alcohol intake behaviors were not significantly associated with PCa aggressiveness. However, the interactions of excessive alcohol intake and three SNPs (rs13107662 [CAMK2D, p = 6.2 × 10−6], rs9907521 [PRKCA,p = 7.1 × 10−5], and rs11925452 [ROBO1, p = 8.2 × 10−4]) were significantly associated with PCa aggressiveness. These alcohol–SNP interactions revealed contrasting effects of excessive alcohol intake on PCa aggressiveness according to the genotypes in the identified SNPs. We identified PCa patients with the rs13107662 (CAMK2D) AA genotype, the rs11925452 (ROBO1) AA genotype, and the rs9907521 (PRKCA) AG genotype were more vulnerable to excessive alcohol intake for developing aggressive PCa. Our findings support that the impact of excessive alcohol intake on PCa aggressiveness was varied by the selected genetic profiles.

Hepatic steatosis associated with exposure to elvitegravir and raltegravir

Moderate-to-severe hepatic steatosis in people living with HIV without viral hepatitis or excessive alcohol intake was associated with cumulative exposure to stavudine, elvitegravir and raltegravir. Prospective trials are required to establish a causal association.

Inflammation in Primary and Metastatic Liver Tumorigenesis–Under the Influence of Alcohol and High-Fat Diets

The liver plays an outsized role in oncology. Liver tumors are one of the most frequently found tumors in cancer patients and these arise from either primary or metastatic disease. Hepatocellular carcinoma (HCC), the most prevalent form of primary liver cancer and the 6th most common cancer type overall, is expected to become the 3rd leading cause of cancer mortality in the US by the year 2030. The liver is also the most common site of distant metastasis from solid tumors. For instance, colorectal cancer (CRC) metastasizes to the liver in two-thirds of cases, and CRC liver metastasis is the leading cause of mortality in these patients. The interplay between inflammation and cancer is unmistakably evident in the liver. In nearly every case, HCC is diagnosed in chronic liver disease (CLD) and cirrhosis background. The consumption of a Western-style high-fat diet is a major risk factor for the development of non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH), both of which are becoming more prevalent in parallel with the obesity epidemic. Excessive alcohol intake also contributes significantly to the CLD burden in the form of alcoholic liver disease (ALD). Inflammation is a key component in the development of all CLDs. Additionally, during the development of liver metastasis, pro-inflammatory signaling is crucial in eliminating invading cancer cells but ironically also helps foster a pro-metastatic environment that supports metastatic seeding and colonization. Here we review how Westernized high-fat diets and excessive alcohol intake can influence inflammation within the liver microenvironment, stimulating both primary and metastatic liver tumorigenesis.