Aspirin
(acetylsalicylic acid) and ibuprofen are the more popular over-the-counter
(OTC) non-steroidal anti-inflammatory drugs (NSAIDs) seen in many outpatientclinics. Hauser (2010) reported that globally,
especially in the more developed countries, over 25% of geriatric patients suffering
from osteoarthritis (OA) will take NSAIDs to address pain (p. 305). According to Ciccone (2007, p. 199), aspirin
is classified as a salicylate, but is the most representative example of NSAIDs
due to its anti-inflammatory, moderate analgesic, antipyretic and
anticoagulation properties. He reports
the anti-inflammatory property of acetylsalicyclic acid results from the inhibited
synthesis of prostaglandins, an endogenous lipid-like substance that regulates
cellular function (p. 200). Hauser (2010)
agrees the mechanism of NSAIDs is caused by the inhibition of both cyclooxygenase-1
(COX 1) and cyclooxygenase-2 (COX 2) enzymes, with COX 2 being the newer and kinder
on the gastrointestinal tract, but both limiting the prostaglandin messenger
necessary for inflammation . He expressed strong concerns over the treatment of
osteoarthritis (OA) with NSAIDs and suggested focusing the medical intervention
on the articular cartilage breakdown or pain of OA versus swelling, favoring a
more conservative approach to NSAIDs with lower dosages and shorter durations (p.
311).
There are other pro-inflammatory
lipid-like substances that are similar to prostaglandins called leukotrienes
and thromboxanes, with all three being collectively known as eicosanoids (Ciccone,
2007, pp. 200-201). Eicosanoids are
powerful at regulating issues like inflammation, but their exact action on the
immune system is still not totally understood (Pratt & Brown, 2014, p.
3). However, it is known that in the
presence of dysfunctional regulation of inflammatory and anti-inflammatory
mediators or eicosanoids, this mechanism has a direct impact on the course of a
disease (Pratt & Brown, 2014, p. 5).
Hauser (2010) found that prostaglandins stimulate the proliferation of
chondrocytes, a very beneficial aspect of cartilage healing, but also a
mechanism that gets blocked by NSAIDs. According
to Nasjletti (1998), the same is true for blood pressure regulation, where
eicosanoids mediate angiotensin-dependent hypertension through the balancing of
prohypertensive and antihypertensive functions that may be hindered by NSAIDs (p.194).
Hauser (2010) feels strongly that the adverse
long term side effect of aspirin is the degradation of articular cartilage caused
by the degenerative impact on the cartilage matrix and possibly the reduced compensatory/protective
joint strategies caused by local analgesia (p. 316). He believes in situations of osteoarthritis,
oftentimes characterized as a condition of joint degeneration that is usually without
swelling or heat, the use of anti-inflammatory drugs like NSAIDs for a
non-inflammatory condition can be very problematic to the individual’s
cellular healing (p. 311). He found in
some cases where matrix alterations or internal changes to mechanical
properties of the cartilage had occurred, the result was consistent with an
increased incidence of bone cysts, nodules or spurs (p. 308). However, on a more positive note, Wang et al.
(2003) had an in vitro study showing aspirin’s promise of inhibiting growth of H pylori, as well as value in increasing
the organism’s susceptibility to antimicrobials, however suggesting further in
vivo research aimed at drug resistance and virulence was needed (p. 494).
Adverse drug
reactions (ADR) or side effects of acetylsalicylic acid commonly seen in my
clinic are tinnitus, gastric distress and easy bruising. Ciccone (2013) finds the most severe
reactions are gastric bleeding, anaphylaxis and laryngeal swelling, but to a
lesser degree a skin rash, anemia and abdominal pain (p. 80). Caution must be taken during physical therapy
to minimize bruising during manual therapy and therapeutic exercises, carefully
monitoring for rashes, blood pressure, shortness of breath, nausea or abdominal
pain as it may be related to an allergic reaction or bleeding associated with
acetylsalicylic acid (p.80).
The ugly side of
drug to drug interactions must now be written on the front of prescription labels,
mandated by the FDA, stating that any prescription and OTC drug containing
NSAIDs, blood thinners or steroids may cause bleeding or stomach ulcers with
this product (Hauser, 2010, p. 318).
Ciccone (2013) further highlighted that ibuprofen may decrease the
antiplatelet effect, pencillins and oral hypoglycemics may be potentiated, sulfonamides
and methotrexate may be potentiated, ACE inhibitors may be limited and antacids
may limit the salicylate effect. This
drug is well absorbed in the small intestine and rapidly distributed
throughout, crossing the placenta and entering breast milk, so it should not be
used in children, new mothers or in pregnancy (p. 81).
The main food to
drug interaction occurs during the over-consumption of foods that increase the
acidity of urine as this may increase serum salicylate levels (Ciccone, 2013,
p. 81). Herbals that increase the risk
of bleeding are arnica, chamomile, clove, garlic, gingko, ginseng and ginger
(p. 81). Hauser (2010) also believes
limiting alcohol consumption is necessary to minimize the risk of bleeding and
ulcers (p.318).
Finally, according to Scott, Khan, Roberts,
Cook and Duronio (2004), inflammation is a complex, integrated cellular phenomenon
that encompasses many mechanisms from cell death and cellular debridement to tissue
proliferation and cellular regeneration, so having assumptions that pain
directly correlates with inflammation is misguided and may even be harmful to
the healing process (p. 372-375). The use
of NSAIDs must be prescribed or taken with great caution and accuracy,
utilizing physical therapy modalities, complementary and alternative medicine,
exercise, proper body and joint mechanics, as well as good nutrition and
hydration to achieve the goal of pain relief and improved function.
References
Ciccone, C. D. (2007). Pharmacology
in rehabilitation (4th ed). Philadelphia, PA: F. A. Davis
Company.
Ciccone, C. D. (2013). Drug
guide for rehabilitation professionals. Philadelphia, PA: F. A.
Davis Company.
Hauser, R. A. (2010). The acceleration of articular
cartilage degeneration in osteoarthritis by
nonsteroidal
anti-inflammatory drugs. Journal of Prolotherapy, 2(1), 305-322. Retrieved from
Nasjletti, A. (1998). Hypertension,
31, 194-200. doi: 10.1161/01.HYP.31.1.194
Pratt, C. & Brown, C. (2014). The role of eicosanoids in
experimental Lyme arthritis. Frontiers in cellular
and infection
microbiology, 469. doi:10.3389/fcimb.2014.00069
Scott, A., Khan, K. M., Roberts, C. R., Cook, J. L. &
Duronio, V. (2004). What do we mean by the term
‘‘inflammation’’? A contemporary basic science update for sports
medicine. Br J Sports Med, 38,
372–380. doi: 10.1136/bjsm.2004.011312
Wang, W. H., Wong, W. M., Dailidiene, D., Berg, D. E., Gu,
Q., Lai, K. C.,…Wong, B. C. Y. (2003).
Aspirin
inhibits the
growth of Helicobacter pylori and enhances its susceptibility to antimicrobial
agents.
Gut, 52, 490-495. doi:10.1136/gut.52.4.490
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