Ian Field wrote:
> Is there any reason a diabetic shouldn't use aspirin?
>
> Thanks.
If you have diabetes *And* a high blood glucose your chance of
cardiovascular events is increased. Aspirin won't help because the glucose
in your blood and the Aspirin compete for the same reaction. The best thing
left is to lower your HbA1c to a reasonable level (< 8% if older) by
exercise and diet. After which you nolonger need Aspirin.
<
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2777137/>
Cardiovasc Diabetol. 2009 Oct 30;8:57. doi: 10.1186/1475-2840-8-57.
Lack of benefits for prevention of cardiovascular disease with aspirin
therapy in type 2 diabetic patients--a longitudinal observational study.
BACKGROUND: The risk-benefit ratio of aspirin therapy in prevention of
cardiovascular disease (CVD) remains contentious, especially in type 2
diabetes. This study examined the benefit and harm of low-dose aspirin
(daily dose < 300 mg) in patients with type 2 diabetes. METHODS: This is a
longitudinal observational study with primary and secondary prevention
cohorts based on history of CVD at enrollment. We compared the occurrence of
primary composite (non-fatal myocardial infarction or stroke and vascular
death) and secondary endpoints (upper GI bleeding and haemorrhagic stroke)
between aspirin users and non-users between January 1995 and July 2005.
RESULTS: Of the 6,454 patients (mean follow-up: median [IQR]: 4.7 [4.4]
years), usage of aspirin was 18% (n = 1,034) in the primary prevention
cohort (n = 5731) and 81% (n = 585) in the secondary prevention cohort (n =
723). After adjustment for covariates, in the primary prevention cohort,
aspirin use was associated with a hazard-ratio of 2.07 (95% CI: 1.66, 2.59,
p < 0.001) for primary endpoint. There was no difference in CVD event rate
in the secondary prevention cohort. Overall, aspirin use was associated with
a hazard-ratio of 2.2 (1.53, 3.15, p < 0.001) of GI bleeding and 1.71 (1.00,
2.95, p = 0.051) of haemorrhagic stroke. The absolute risk of
aspirin-related GI bleeding was 10.7 events per 1,000 person-years of
treatment. CONCLUSION: In Chinese type 2 diabetic patients, low dose aspirin
was associated with a paradoxical increase in CVD risk in primary prevention
and did not confer benefits in secondary prevention. In addition, the risk
of GI bleeding in aspirin users was rather high.
PMID: 19878541
<
http://jama.jamanetwork.com/article.aspx?articleid=182877>
JAMA. 2008 Nov 12;300(18):2134-41. doi: 10.1001/jama.2008.623. Epub 2008 Nov
9.
Low-dose aspirin for primary prevention of atherosclerotic events in
patients with type 2 diabetes: a randomized controlled trial.
CONTEXT: Previous trials have investigated the effects of low-dose aspirin
on primary prevention of cardiovascular events, but not in patients with
type 2 diabetes. OBJECTIVE: To examine the efficacy of low-dose aspirin for
the primary prevention of atherosclerotic events in patients with type 2
diabetes. DESIGN, SETTING, AND PARTICIPANTS: Multicenter, prospective,
randomized, open-label, blinded, end-point trial conducted from December
2002 through April 2008 at 163 institutions throughout Japan, which enrolled
2539 patients with type 2 diabetes without a history of atherosclerotic
disease and had a median follow-up of 4.37 years. INTERVENTIONS: Patients
were assigned to the low-dose aspirin group (81 or 100 mg per day) or the
nonaspirin group. MAIN OUTCOME MEASURES: Primary end points were
atherosclerotic events, including fatal or nonfatal ischemic heart disease,
fatal or nonfatal stroke, and peripheral arterial disease. Secondary end
points included each primary end point and combinations of primary end
points as well as death from any cause. RESULTS: A total of 154
atherosclerotic events occurred: 68 in the aspirin group (13.6 per 1000
person-years) and 86 in the nonaspirin group (17.0 per 1000 person-years)
(hazard ratio [HR], 0.80; 95% confidence interval [CI], 0.58-1.10; log-rank
test, P = .16). The combined end point of fatal coronary events and fatal
cerebrovascular events occurred in 1 patient (stroke) in the aspirin group
and 10 patients (5 fatal myocardial infarctions and 5 fatal strokes) in the
nonaspirin group (HR, 0.10; 95% CI, 0.01-0.79; P = .0037). A total of 34
patients in the aspirin group and 38 patients in the nonaspirin group died
from any cause (HR, 0.90; 95% CI, 0.57-1.14; log-rank test, P = .67). The
composite of hemorrhagic stroke and significant gastrointestinal bleeding
was not significantly different between the aspirin and nonaspirin groups.
CONCLUSION: In this study of patients with type 2 diabetes, low-dose aspirin
as primary prevention did not reduce the risk of cardiovascular events.
TRIAL REGISTRATION:
clinicaltrials.gov Identifier: NCT00110448.
PMID: 18997198
J Mol Med (Berl). 2005 Feb;83(2):148-58. Epub 2004 Nov 10.
Increased protein glycation in diabetes mellitus is associated with
decreased aspirin-mediated protein acetylation and reduced sensitivity of
blood platelets to aspirin.
Reduced effectiveness of the most common antiplatelet drug, acetylsalicylic
acid (ASA, aspirin), in diabetes mellitus has been associated with a lowered
platelet sensitivity to ASA and related to glycemic control in diabetic
patients. Our objectives were (a) to monitor the chemical background of how
chronic hyperglycemia affects platelet response to ASA in diabetes and (b)
to study a chemical competition between the amount of bound acetyl residues
and the extent of protein glycation in blood platelets. Using whole-blood
impedance aggregometry and platelet function analyzer (PFA-100) we observed
a reduced platelet response to ASA in diabetic patients (14% vs. 79% for
PFA-100 collagen-epinephrine occlusion time) and an association between the
index of glycemic control and platelet refractoriness to ASA (r(S)
= -0.378). Impaired platelet response to ASA was related to enhanced
platelet protein glycation (3.6+/-0.4 in diabetes vs. 2.3+/-0.4 micromol
fructosamine/microg protein in control) and reduced incorporation of acetyl
residue into proteins of platelets from diabetic patients (47.4+/-2.0 in
control vs. 33.1+/-0.7 micromol acetyl/microg protein in diabetic subjects).
Incubation of blood platelets with increasing concentrations of glucose and
ASA under in vitro conditions led to excessive modification in protein amino
groups: glucose and ASA competed with each other in the course of
nonenzymatic modifications, glycosylation, or acetylation, and their
contributions to the occupancy of protein amino groups (R2 = 0.22 for
glucose, R2 = 0.43 for ASA) were dependent upon the concentrations of
glucose and ASA. Overall the effects of high glucose and high ASA on the
overall occupancy of protein free amino groups are not additive. While at
higher concentrations ASA overcomes the effects of hyperglycemia and retards
glycation, high glucose makes acetylation less efficient, and therefore the
resultant chemical modification becomes greatly reduced. In conclusion,
diminished susceptibility of various platelet proteins and receptors on
blood platelet membranes to acetylation and high ambient glucose might
underlie the apparently differentiated sensitivity of blood platelets to ASA
and determine platelet "insensitivity to aspirin" in diabetic patients.
PMID: 15723265