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ASPIRIN SAFEST NSAIDS ULCERS--& Coated aspirin sucknte


The standard does of 325 mg of coated aspirin does not significantly cause gastro-intestinal bleeding except for those with an existing problem—which is brought on by H. pylori.


Omeprazole (Prilosec OTC), also in the PPI family are Nexium, Esomeparzole magnesium, Zegerid, Prevacid, Iansopravole, Pantoprazole, Protonix, Rabaprazole, Aciphex, and Biaxin.  They are protein pump inhibitors.  Current wisdom is to avoid this more dangerous, high-priced way of treating heartburn, and take an old-fashioned anti-acid medication.     See  


Stomach Bleeding Comparison to Aspirin, other NSAIDs 9 times higher (1.9:18.8)

Omeprazole is a proton pump inhibitor (blocks the production of HCl in the stomach 80-95%).  Ulcers are caused by a stomach bacteria H. pylori.  Treatment consists of eradication the bacteria.  Following this half were given the proton pump inhibitor.  Both groups then resumed taking either aspirin or other NSAIDs as befores.  The aspirin group faired much better:  they had half the stomach bleeds if on Omeprazole, and 1/9th the bleeds without Omeprazole.  This is more evidence concerning the disinformation big PhARMA has put out about the relative risk of aspirin to other NSAIDs. 


NEGM (New England Journal of Medicine)

Volume 344:967-973

March 29, 2001

Number 13


Preventing Recurrent Upper Gastrointestinal Bleeding in Patients with Helicobacter pylori Infection Who Are Taking Low-Dose Aspirin or Naproxen

Francis K.L. Chan, M.D., S.C. Sydney Chung, M.D., Bing Yee Suen, R.N., Yuk Tong Lee, M.D., Wai Keung Leung, M.D., Vincent K.S. Leung, M.D., Justin C.Y. Wu, M.D., James Y.W. Lau, M.D., Yui Hui, M.D., Moon Sing Lai, M.D., Henry L.Y. Chan, M.D., and Joseph J.Y. Sung, M.D., Ph.D.



Background Many patients who have had upper gastrointestinal bleeding continue to take low-dose aspirin for cardiovascular prophylaxis or other nonsteroidal antiinflammatory drugs (NSAIDs) for musculoskeletal pain. It is uncertain whether infection with Helicobacter pylori is a risk factor for bleeding in such patients.

Methods We studied patients with a history of upper gastrointestinal bleeding who were infected with H. pylori and who were taking low-dose aspirin or other NSAIDs. We evaluated whether eradication of the infection or omeprazole treatment was more effective in preventing recurrent bleeding. We recruited patients who presented with upper gastrointestinal bleeding that was confirmed by endoscopy. Their ulcers were healed by daily treatment with 20 mg of omeprazole for eight weeks or longer. Then, those who had been taking aspirin were given 80 mg of aspirin daily, and those who had been taking other NSAIDs were given 500 mg of naproxen twice daily for six months. The patients in each group were then randomly assigned separately to receive 20 mg of omeprazole daily for six months or one week of eradication therapy, consisting of 120 mg of bismuth subcitrate, 500 mg of tetracycline, and 400 mg of metronidazole, all given four times daily, followed by placebo for six months.

Results We enrolled 400 patients (250 of whom were taking aspirin and 150 of whom were taking other NSAIDs). Among those taking aspirin, the probability of recurrent bleeding during the six-month period was 1.9 percent for patients who received eradication therapy and 0.9 percent for patients who received omeprazole (absolute difference, 1.0 percent; 95 percent confidence interval for the difference, –1.9 to 3.9 percent). Among users of other NSAIDs, the probability of recurrent bleeding was 18.8 percent for patients receiving eradication therapy and 4.4 percent for those treated with omeprazole (absolute difference, 14.4 percent; 95 percent confidence interval for the difference, 4.4 to 24.4 percent; P=0.005).

Conclusions Among patients with H. pylori infection and a history of upper gastrointestinal bleeding who are taking low-dose aspirin, the eradication of H. pylori is equivalent to treatment with omeprazole in preventing recurrent bleeding. Omeprazole is superior to the eradication of H. pylori in preventing recurrent bleeding in patients who are taking other NSAIDs, such as naproxen.


Coated Aspirin lowers gatric mucosal damage


Two problems, often the research has been funded by PHARMA, which in the drive for profits is eager to publicize bleeding with aspirin, but not with the other NSAIDS.  They often use lesions to support their findings; however, these lesion are not a good The results are often contaminated by the use of other NSAIDs in addition to aspirin.  These greatly increase the incident of gastrointestinal bleeding.  For example a Madrid study (pre-publication edition on web, by Francisco J. De Abajo, MD, M.P.H, Division de Farmacoepidemoligia y Farmacovigilamcia Agencia Espanola del Medicamento, Madrid found for 2,195 UGIC (upper gastrointestional complications) that the concomitant use of aspirin with high-dose NSAIDs caused a 3 fold increase.  “The concomitant use of low-does aspirin & NSAIDs at high dose put patients at higher risk of UGIC.  Published November of 2000. Another problem with PHARMA studies are that they rely upon endoscopic examination for lesions, “However, it is known that these lesions are not good predictors of major upper gastro-intestinal bleeding, yielding apparently opposite results” (at p. 4).  Of interest was the find that there was no dose relationship in the 75 to 300 mg range. A drug which causes a side effect will cause more at a higher dose.  It is my recommendation that the higher dose be taken so as to potentate the cancer protective effect.--JK 

Enteric Aspirin

Pharma is pushing low dose enteric coated aspirin with meals.  Reason it doesn’t work!

Think of wearing the hat of the CEO of Pfizer, duty is to follow the tobacco ethics to maximize quarterly profit.  Aspirin with regular long-term usage at 325 mg or higher, lower the risk of 6 out of 7 of the most profitable classes of drug treatments (cancer, heart attacks, diabetes, Alzheimer’s disease and other dementia, and blood clots, and hypertension by preventing atherosclerosis—see above, doesn’t have a major benefit for the neurotic).  Thus the war on aspirin by bad pharma is consistent with their corporate tobacco ethics.  They thus teach doctors to prescribe low dose coated aspirin to be taken with a meal.  At one year tolerance develops so that it doesn’t even prevent heart attacks, let alone caner and other conditions listed above.  The coated aspirin with a meal takes 8 hours to reach peak blood level and that is well below the level of a plain aspirin at 30 minutes on an empty stomach. 


“The variable absorption of drugs in enteric-coated tablets appears to be due to wide differences in gastric retention time of solid objects…. it constitutes an inherent limitation in the absorption efficacy of all enteric-coated tablets” This was contrasted with the absorption of aspirin in solution which produced consistent rapid results. 7/12/65.  July 12, 1965

The delay in aspirin absorption from an enteric-coated tablet is directly related to its GRT [gastric residue time—time to clearance since it doesn’t dissolve], which is gender related and greatly affected by food.”  Compared to an uncoated aspirin the start of absorption with food  averaged 0.8 hours, the enteric start averaged 5.9 hours.  For after feeding the time for peak serum concentration was 2.7 hours, but for the enteric it was 8.9 hours.  Thus for relief of acute pain the enteric aspirin is useless, and the uncoated aspirin should be taken without food—contrary to common belief.  Jan 15,1987


For example, the t 50% for serum TxB2 inhibition was 5.0 0.6 minutes with the chewed tablet versus 12.0 2.3 minutes when the tablet was swallowed (p = 0.01). A 50% decrease in serum TxB2 occurred 7.6 1.2 minutes after Alka Seltzer solution (p = 0.04 vs chewing a tablet; p = 0.13 vs swallowing a whole tablet). Chewing an aspirin tablet is the most effective way of accelerating absorption of aspirin into the blood and shortening the time required for an antiplatelet effect.  15 August 1999

This study showed that there was a 17% increase risk of upper stomach bleeding with  enteric coated aspirin compared to uncoated aspirin (relative risk of 2.6 vs. 3.1), which is a reduction of 0.5 bleed episodes per year with enteric aspirin.   Several problems with this study. The control population was not adjusted for contravening variables such as use of other medications, alcohol, hot peppers, cigarettes, etc.  Thus a questionnaire of 7-day prior usage of aspirin does not compare apples to apples.   Second problem is that 75% of ulcers (bleeding) occur in the duodenum, for which given the basic PH is not increased by aspirin.  Thus the overall risk of an ulcer compared to the total risk is again inflated. 



^^^^^^^^^^^^^^^^^^^^^^^^^^some bad pharma funded studies

r J Clin Pharmacol. 1991 Jul;32(1):77-

Related Articles, Links


Journal of Clinical Pharmacology July 1991, 32(1):77-83
Aspirin-induced gastric mucosal damage: prevention by enteric-coating and relation to prostaglandin synthesis.

Hawthorne AB, Mahida YR, Cole AT, Hawkey CJ.

Department of Therapeutics,
University Hospital, Nottingham.

Hawthorne AB, Mahida YR, Cole AT, Hawkey CJ.

Department of Therapeutics, University Hospital, Nottingham.

1. Gastric damage induced by low-dose aspirin and the protective effect of enteric-coating was assessed in healthy volunteers in a double-blind placebo-controlled cross-over trial using Latin square design. Each was administered placebo, plain aspirin 300 mg daily, plain aspirin 600 mg four times daily, enteric-coated aspirin 300 mg daily, or enteric-coated aspirin 600 mg four times daily for 5 days. Gastric damage was assessed endoscopically, and gastric mucosal bleeding measured. 2. Aspirin 300 mg daily and 600 mg four times daily caused significant increases in gastric injury compared with placebo. Gastric mucosal bleeding was significantly more with the high dose, with a trend towards increased gastric erosions, compared with the low dose. 3. Enteric-coating of aspirin eliminated the injury caused by low dose aspirin and substantially reduced that caused by the higher dose. 4. All dosages and formulations caused similar inhibition of gastric mucosal prostaglandin E2 synthesis. 5. Serum thromboxane levels were suppressed equally with plain and enteric-coated aspirin. 6. In this short-term study in healthy volunteers, gastric toxicity from aspirin was largely topical, independent of inhibition of prostaglandin synthesis, and could be virtually eliminated by the use of an enteric-coated preparation.




Regular, high dosage usage of aspirin for rheumatic disease; the ulcer incidents was only one fourth for those who took enteric aspirin.


Ann Intern Med. 1979 Oct;91(4):517-20.

Related Articles, Links

Incidence of gastric lesions in patients with rheumatic disease on chronic aspirin therapy.

Silvoso GR, Ivey KJ, Butt JH, Lockard OO, Holt SD, Sisk C, Baskin WN, Mackercher PA, Hewett J.

Endoscopy was done in 82 patients with rheumatic disease who were receiving chronic aspirin therapy. Fifty-eight patients were taking at least eight aspirin tablets daily for 3 or more months; 24 patients were taking, in addition to the aspirin, a maximum of one other antiinflammatory, nonsteroidal medication. Endoscopy in 45 normal subjects not taking aspirin showed no ulcers or erosions and a 4% incidence of gastric erythema. In the 82 patients with rheumatic disease, 14 (17%) had gastric ulcers, 33 (40%) had gastric erosions, and 62 (76%) had gastric erythema. Regular aspirin and buffered aspirin users had an ulcer incidence of 23% and 31% respectively, compared with a 6% incidence in enteric-coated aspirin users (P less than 0.05). One third of all patients with gastric ulcer had no gastrointestinal symptoms. Patients taking chronic aspirin therapy for rheumatic diseases have a higher than suspected incidence of gastric ulcer and erosions. Gastric ulcer may exist without symptoms in such patients.


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Disclaimer:  The information, facts, and opinions provided here is not a substitute for professional advice.  It only indicates what JK believes, does, or would do.  Always consult your primary care physician for any medical advice, diagnosis, and treatment.