Alcohol consumption and risk of deep venous thrombosis and pulmonary embolism in older persons

Alcohol consumption and risk of deep venous thrombosis and pulmonary embolism in older persons

The effect of alcohol on the outcome and fibrinolysis phenotype in trauma patients remains unclear. Hence, we performed this study to determine whether alcohol is a risk factor for mortality and fibrinolysis shutdown in trauma patients. The dose–response association between alcohol intake and venous thromboembolism risk. The solid line and the long dash line represent the estimated risk estimates and their 95% CIs.

Therefore, physicians should carefully estimate the risk of VTE in patients with AI. Alcohol consumption may decrease the amount of fibrinogen in the blood. The liver produces this protein, which plays an important role in controlling blood flow and promoting blood clotting. Healthline has strict sourcing guidelines and relies on peer-reviewed studies, academic research institutions, and medical associations.

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Cox proportional hazard regression analysis was conducted to determine the risk of VTE in the patients with AI compared with the controls. In our study, patients in the alcohol positive group had lower GCS, lower SBP, higher head AIS and higher lactic blood thinners and alcohol acid levels compared to those in the alcohol negative group. We believe that the reason for lower GCS was not just alcohol, but also the effects of head trauma and the state of shock. Alcohol has the potential to induce metabolic acidosis.

How much alcohol can you drink while on blood thinners?

Moderate alcohol use is generally safe while taking most blood thinners. For healthy adults, doctors recommend limiting alcohol intake to a maximum of two drinks a day for males and one drink a day for females.

Similar to the previous studies, we reported that prothrombin time INR was not different in the alcohol-positive and alcohol-negative groups, but EXTEM CT was significantly different. Even though our report is one of the first to investigate a broad range of haemostatic markers in relation to alcohol consumption and to take genetic factors into consideration, we dealt with certain limitations. Using the QFFQ method could result in over- or under-reporting of alcohol consumption and cannot discern between binge or moderate drinkers. However, our findings are validated by also observing associations and interactions with biomarkers reflecting alcohol intake. While we included two FXIII SNPs, we could unfortunately not measure FXIII levels to provide supporting evidence for the effect of FXIII levels on fibrin clot structure.

Comparison of the alcohol-positive and alcohol-negative groups

However, effects of alcohol on the outcome in trauma patients remain unclear, and several studies have shown that the outcome of alcohol intoxicated patients is superior to that of patients who are not intoxicated [2, 10–12]. Fourteen fibrinogen and two SNPs in the FXIII gene were genotyped to determine their influence. Although our results do not reveal the mechanism for this association, according to our literature review, we suggest that several possible explanations exist for the mechanism for this association. Stasis, hypercoagulability, and endothelial dysfunction, known as the Virchow triad, are believed to contribute to thrombosis. Heavy alcohol consumption may be an independent risk factor for endothelial dysfunction.

  • However, more research is necessary to determine whether alcohol use is directly responsible for these possible heart benefits.
  • Future research should investigate the mechanisms behind the interactions we observed per loci.
  • Both alcohol and blood thinners like warfarin thin your blood.

Some authorities insist that—even in small quantities—the harmful effects of alcohol outweigh the benefits, because alcohol-related liver disease remains the main cause of liver-related mortality worldwide . Our research shows that, in terms of haemostasis, modest amounts of alcohol seem to be beneficial. From a genetics viewpoint, we show here that for individuals harbouring certain genotypes, alcohol intake may be more beneficial than for others. A better understanding of diet-gene interactions has important implications for therapeutic decision making and lifestyle education. Nevertheless, drinking alcohol should never be recommended to improve health status; and for current drinkers, the prevailing evidence supports the adoption of even lower limits of consumption than are presently in most guidelines.


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