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Results would
be higher if those studies that included the low-dose aspirin (85 mg) were
excluded. All NSAIDs but aspirin increase very significantly the risk
for heart attacks--but for aspirin--by accelerating atherosclerosis (American Heart Association
warning) MI increased 50% for daily use of Naproxen after 2 years for the
elderly (Advantage Study)--jk. 2005, vol. 13, no4, pp. 559-583 [25
page(s) (article)] (264 ref.) Oncology
reports ISSN 1021-335X 2005, vol. 13, no4, pp. 559-583 [25
page(s) (article)] (264 ref.) Titre
du document / Document title Aspirin, ibuprofen, and other
non-steroidal anti-inflammatory drugs in cancer prevention: A critical review
of non-selective COX-2 blockade (Review) Résumé
/ Abstract We
comprehensively reviewed the published scientific literature on non-steroidal
anti-inflammatory drugs (NSAIDs) and cancer and evaluated results based upon
epidemiologic criteria of judgment: consistency of results, strength of
association, dose response, molecular specificity, and biological plausibility.
Sufficient data from 91 epidemiologic studies were available to examine the
dose response of relative risk and level of NSAID intake for ten human
malignancies. Dose response curves were fitted by exponential regression. Results showed a significant exponential decline in the risk
with increasing intake of NSAIDs (primarily aspirin or ibuprofen) for 7-10
malignancies including the four major types: colon, breast, lung, and prostate
cancer. Daily
intake of NSAIDs,
primarily aspirin, produced risk reductions of 63% for colon, 39% for breast,
36% for lung, and 39% for prostate cancer. Significant risk reductions were
also observed for esophageal (73%), stomach (62%), and ovarian cancer (47%). NSAID effects became apparent after
five or more years of use and were stronger with longer duration. Observed protective effects were
also consistently stronger for gastrointestinal malignancies (esophagus,
stomach, and colon). Results for pancreatic, urinary bladder, and renal cancer
were inconsistent. Initial epidemiologic
studies of malignant melanoma, Hodgkin's disease, and adult leukemia also found
that NSAIDs are protective. A few studies suggest that ibuprofen has
stronger anticancer effects than aspirin, particularly against breast and lung
cancer. Overexpression of
cyclooxygenase-2 (COX-2) and increased prostaglandin biosynthesis correlates
with carcinogenesis and metastasis at most anatomic sites. Preclinical
investigations provide consistent evidence that both selective and
non-selective NSAIDs effectively inhibit chemically-induced carcinogenesis of
epithelial tumors. This review provides compelling and converging evidence
that regular intake of NSAIDs that non-selectively block COX-2 protects against
the development of many types of cancer. ^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^ |
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Aspirin lowers risk of
Hodgkin’s lymphoma 60% (acetaminophen
increased risk 72%, non-aspirin NSAIDs decreased risk 5%). Criterion for use was those taking 2 or more
aspirin per week for 5 years or longer.
Therefor it is likely that higher dose of aspirin per week would confer
a greater reduction of Hodgkin’s lymphoma.
Aspirin and the Risk of
Hodgkin's Lymphoma in a Population-Based Case–Control Study Journal of the National Cancer Institute:
·
Oxford Journals, ·
Medicine ·
JNCI
J Natl Cancer Inst ·
Volume96, Issue4 ·
Pp. 305-315, Background:
Regular use of nonsteroidal anti-inflammatory
drugs (NSAIDs) is associated with decreased risk of several malignancies.
NSAIDs may prevent cancer development by blocking the cyclooxygenase-catalyzed
synthesis of proinflammatory prostaglandins. Aspirin may also protect against
Hodgkin's lymphoma by inhibiting transcription factor nuclear factor κB
(NF-κB), which is necessary for immune function and the survival of Hodgkin's
lymphoma cells. We examined the association between regular analgesic use and
the risk of Hodgkin's lymphoma. Methods: A population-based
case–control study of 565 case patients with Hodgkin's lymphoma and 679 control
subjects was conducted in the metropolitan area of Boston, Massachusetts, and
in the state of Connecticut. Participants reported their average use of
aspirin, non-aspirin NSAIDs, and acetaminophen over the previous 5 years. Regular analgesic use was defined as
consumption of at least two tablets per week on average over the preceding 5
years; non-regular use was defined as consumption of fewer than two tablets
per week. Results: The risk of Hodgkin's lymphoma associated with
regular aspirin use was statistically significantly lower (odds ratio [OR] = 0.60, 95%
confidence interval [CI] = 0.42 to 0.85) than that associated with non-regular
aspirin use. The risk was not associated with use of other non-aspirin NSAIDs
(OR = 0.97, 95% CI = 0.73 to 1.30). However, the risk associated with regular
acetaminophen use was statistically significantly higher (OR = 1.72, 95% CI =
1.29 to 2.31) than that associated with non-regular use. Conclusion:
The inverse association between aspirin, but not other NSAIDs, and Hodgkin's
lymphoma suggests that NF-κB signaling may play a key role in Hodgkin's
lymphoma pathogenesis.
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