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Non steroidal anti inflammatory drugs (NSAIDs),risks?

Can NSAIDs be lethal?
Can NSAIDs be lethal?
Chris Hill

There are presently two common OTC, non narcotic forms of pain medications, acetaminophen-based which includes drugs like Tylenol, and NSAIDs , ibuprofen-based, which includes drugs like Advil, Motrin, and Aspirin. Non steroidal anti inflammatory drugs (NSAIDs) in low, over the counter (OTC) doses can help reduce joint pain and inflammation, but these same drugs in higher doses can be lethal, adversely affecting kidney functions, up to the point of renal failure and possibly death. Tylenol is a different class of drug, and can adversely affect liver functions.

In both types of drugs, the dosage varies for adults and children. A dose of 10 mg in an adult weighing approximately 160lbs is nearly twice the same dose at 10 mg in a child weighing only 80lbs. In all cases, the lowest effective (short-term) dose, is usually considered safest. Use of any drug over longer term, can result in intolerance with complications, and sometimes resulting in death. Then there is also the age of an adult to consider. A dose deemed safe and effective for a healthy 35 year old adult, may prove to be excessive in older adults or in the elderly, since the ability for the human body’s organs to eliminate toxins reduces as people age.

NSAIDs are a class of anti inflammatory pain killer that should be taken with copious amounts of fluid, such as water. Toxic effects of these drugs increase rapidly during dehydration, and NSAIDs and dehydration together can have an adverse affects on kidney function. This can occur under many circumstances, including active sports in hot weather. For example, it is not uncommon for a triathlon runner, bike racer, or back country mountaineer to take NSAID pills to reduce inflammation and pain following a long day of extreme exertion. Such conditions can be particularly hard on kidneys, if a person is also dehydrated at the time of taking multiple doses of NSAIDs.

Ten people were randomly interviewed in two countries for this article. Of these ten, three were doctors. Of the ten people interviewed, regarding their particular NSAID use and experience, all ten had used some form of NSAID, and six of ten knew of a person who had either experienced organ failure, was hospitalized, or knew someone who had died from a NSAID related complication. Four of the ten had experienced moderate pain relief. It is not surprising that everyone interviewed had used an NSAID; what was somewhat surprising were stories of ‘graver’ complications, as they did not match (word for word) side effects of published annual NSAID risk factors, but were consistent with NSAID affected organs. Further, of the ten people interviewed, four had experienced a mild form of gastro intestinal (GI) side effect, such as stomach upset or indigestion. Statistics show that roughly 60 million persons in the United States regularly use some form of NSAID, each year. Considering that approximately 16,500 U.S. arthritis sufferers are estimated to die annually from using NSAIDs, that is a fairly small percentage of the estimated 60 million reported user population. If you are part of the 99 percent of NSAID users, you are expected to benefit from ‘moderate use’ of an NSAID, but if you become part of the other percentage, your experience may have dire or even fatal consequences.

Common NSAIDs include: Aspirin, Indomethacin (Indocin), Ibuprofen (Advil, Motrin), Naproxen (Naprosyn), Piroxicam (Feldene), and, Nabumetone (Relafen). ( Reference, COX-2_Inhibitors ) NSAIDs, as a class of drugs, tend to inhibit cyclooxygenase and reduce prostaglandin synthesis.

A closer study shows that NSAIDs are referred to as COX-1 or COX-2 inhibitors. “In the 1990s, researchers discovered that two different COX enzymes existed, now known as COX-1 and COX-2. Cyclooxygenase-1 (COX-1) is known to be present in most tissues. In the gastrointestinal tract, COX-1 maintains the normal lining of the stomach. The enzyme is also involved in kidney and platelet function. Cyclooxygenase-2 (COX-2) is primarily present at sites of inflammation.”1 (Reference:, Cyclooxygenase explained.)” (Reference: For this reason, pain medication research has focused much attention on developing drugs that block COX-2 enzyme processes. However, COX 2 selective inhibitors can cause other, even more serious complications. For example, "In the United States alone, Vioxx (a COX-2 inhibitor) killed 60,000 Americans, due to heart attacks induced by the drug. Aside from these 60,000 Vioxx deaths, those who suffered from heart attacks and strokes were around 88,000 to 140,000. Since the product was used in over 80 countries, the total fatalities would be far greater than these numbers. (Reference: VIOXX" According to the American Nutrition Association: “a July 1998 issue of The American Journal of Medicine (AJM) indicates the following: “Conservative calculations estimate that approximately 107,000 patients are hospitalized annually for nonsteroidal anti-inflammatory drug (NSAID)-related gastrointestinal (GI) complications, and at least 16,500 NSAID-related deaths occur each year among arthritis patients alone.” Statistics also indicate NSAIDs use by elderly patients doubles the odds of being admitted to hospital for cardiac arrest, and roughly 10 percent of people admitted to a hospital for NSAID cardiac issues result in deaths.

Clearly the risk of using NSAIDs varies significantly from person to person, and tends to increase with age.
There are classes of drugs that have the effect of reducing pain through other mechanisms, such as influencing opioid receptors, including use of moderate forms of exercise, physical rehab, and diet. It is up to each individual to find a healthy balance between pain tolerance and pain reduction strategies.

Whelton A.; Nephrotoxicity of nonsteroidal anti-inflammatory drugs. physiologic foundations and clinical implications. Am J Med. 105 1999:13S-24S.

Mukherjee D., Nissen S.E., Topol E.J.; Risk of cardiovascular events associated with selective COX-2 inhibitors. JAMA. 286 2001:954-959.

Yamamoto T., Kakar N.R., Vina E.R., Johnson P.E., Bing R.J.; Effect of cyclooxygenase-2 inhibitor (celecoxib) on the infarcted heart in situ. Pharmacology. 63 2001:28-33.

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