Study: Use of NSAID and risk of hepatocellular carcinoma and chronic liver disease

Die Studie untersucht den Zusammenhang zwischen der Verwendung nichtsteroidaler entzündungshemmender Medikamente (NSAIDs), chronischer Lebererkrankung und hepatozellulärem Karzinom (HCC). Es handelt sich um eine prospektive Beobachtungsstudie, bei der Teilnehmer einen Fragebogen zu Risikofaktoren ausfüllten und ihren NSAID-Konsum angeben mussten. Es wurde festgestellt, dass die Verwendung von NSAIDs das Risiko sowohl für HCC als auch für die Sterblichkeit durch chronische Lebererkrankungen verringert. Insbesondere die Verwendung von Aspirin wurde mit einer größeren Risikominderung in Bezug auf HCC in Verbindung gebracht. Es wird vermutet, dass die Hemmung des Enzyms COX-2 durch NSAIDs eine Rolle bei der Risikominderung spielen könnte. Weitere Forschung in diesem Bereich …
The study examines the connection between the use of non -steroidal anti -inflammatory drugs (NSAIDS), chronic liver disease and hepatocellular carcinoma (HCC). It is a prospective observation study in which participants had to fill out a questionnaire to risk factors and specify their NSAID consumption. It was found that the use of NSAIDS reduces the risk for both HCC and mortality from chronic liver diseases. In particular, the use of aspirin was associated with a greater risk reduction in terms of HCC. It is believed that the inhibition of the enzyme COX-2 by NSAIDS could play a role in risk reduction. Further research in this area ... (Symbolbild/natur.wiki)

Study: Use of NSAID and risk of hepatocellular carcinoma and chronic liver disease

The study examines the connection between the use of non -steroidal anti -inflammatory drugs (NSAIDS), chronic liver disease and hepatocellular carcinoma (HCC). It is a prospective observation study in which participants had to fill out a questionnaire to risk factors and specify their NSAID consumption. It was found that the use of NSAIDS reduces the risk for both HCC and mortality from chronic liver diseases. In particular, the use of aspirin was associated with a greater risk reduction in terms of HCC. It is believed that the inhibition of the enzyme COX-2 by NSAIDS could play a role in risk reduction. However, further research in this area is required.

Details of the study:

Reference

Sahasrabuddhe VV, Gunja Mz, Graubard Bi, et al. Use of non -steroidal anti -inflammatory medication, chronic liver disease and hepatocellular carcinoma. J Natl Cancer Inst . December 5, 2012; 104 (23): 1808-1814.

Design

prospective observation study, in which a self -completed questionnaire was used to assess the demographic characteristics, the nutrition and the lifestyle of the participants. Six months later, a questionnaire became risk factors, which contained questions both about the use of aspirin and non-aspirin-containing non-steroidal anti-inflammatory drugs (NSAID), to participants who had not themselves reported on a history of colon, breast or prostate cancer. The self-reported consumption of aspirin and non-aspirin-nsar was associated with diagnoses and the risk of hepato cellular carcinoma (HCC) and death due to chronic liver disease (CLD). CLD was observed in patients without HCC.

participant

330,504 men and women between the ages of 50 and 71, who participated in the National Institute for Health-American Association of Retired Personal (NIH-AARP), filled out the questionnaire to risk factors and filled the inclusion criteria.

target parameter

Reduction of the risk of developing HCC and reducing the risk of dying to CLD.

most important knowledge

Those who used any kind of NSAID reduced their risk of falling ill (rr = 0.63; 95 %-KI: 0.46–0.87) and reduced their risk to die to CLD (rr = 0.49; 95 %-KI: 0.39–0,61) compared to those who have no NSAIDS used.

In the restriction to the use of aspirin, with or without non-aspirin-nsaids, there was a statistically significant reduction in the risk of HCC development (rr = 0.59; 95 %KI: 0.45–0.77) and mortality due to CLD (rr = 0.55 %). AI: 0.45–0.67) compared to non -users. Statistically

Nur-Aspirin user showed the greatest risk reduction in HCC development (RR = 0.51; 95 %-KI: 0.35–0.75) and a similar risk reduction in mortality due to CLD compared to those that income (rr = 0.50; 95 %). AI: 0.38–0.65).

Those who have non-aspirin-nsar (regardless of aspirin) had no less risk of developing HCC, but had a lower risk of dying from CLD compared to non-users. This finding was only significant for those who are not-aspirin naids per month (RR = 0.60; 95 %-KI: 0.47–0.76) and not every week or daily. The use of non-aspirin-containing NSAIDs reduced the risk of HCC or death by CLD not significantly compared to those that did not use any of the two types of NSAIDS.

effects on practice

Many published studies show a connection between aspirin consumption and a reduced risk of liver cancer and cancer in general. A meta-analysis of 51 randomized controlled studies, of which 34 information on cancer deaths contained, showed that daily aspirin reduced the number of cancer-related deaths compared to control (OR = 0.85; 95 %KI: 0.76–0.96; p = 0.008). ). Six of these studies showed that the daily intake of low-dose aspirin lowered the risk of cancer compared to the control group (HR = 0.88; 95 %-KI: 0.80–0.98; p = 0.017). 1 Two studies came to the conclusion that aspirin reduces the liability of the cells and apoptosis in human hepato cellular Carcinoma cell lines induced. 2.3 In addition, the daily intake of aspirin reduced tumor growth in a rodent model (Hepg2-Xeno transplant).

Why does Aspirin seem to reduce the risk of HCC and death by CLD more effectively than the use of NSAIDs without aspirin? Why did a study from 2012 come to the conclusion that the taking of Aspirin reduced the risk of prostate cancer, but taking prescription of prescription NSAIDs increased the risk?

Aspirin and possibly other non-selective NSAIDS and selective COX-2-NSAAIDs can reduce the risk of HCC and death by CLD.

Aspirin is a dual inhibitor, which means that it does not selectively inhibit both COX-1 and COX-2. Indomethacin, naproxen and ibuprofen are also dual inhibitors. However, other NSAIDs favor COX-1 compared to COX-2 and vice versa. In most fabric types, COX-1 is expressed in relatively constant quantities, while COX-2 is induced by bacteria, cytokines and growth factors. 6 It has been determined that COX-2 is overexpressed in chronic hepatitis, liver cirrhosis and HCC, with the expression more pronounced at low-level HCC Is than with high -grade HCC. Koga and others explain that COX-2 may play a role in the early stages of the HCC, but not in advanced stages. 7.8 A positive correlation between Cox-2 and the vascular endothelial growth factor (VEGF) was also observed.

The authors of this study presented stated that the questionnaire sent to the subject did not ask them to indicate which non-aspirin-nsaids they took. The non-aspirin NSAIDs examined in this study had different degrees of COX inhibition. The authors also pointed out the curiosity that non-aspirin-NSAIDS reduced the risk of dying from CLD, only in the case of monthly and not in the event of a weekly or daily intake. This can be attributed to a disruptive factor that was not taken into account. The information provided suggests that aspirin and possibly other non-selective NSAIDS and selective COX-2-NSAIDs can reduce the risk of HCC and death by CLD.

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