The Discovery of Acetaminophen
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Acetaminophen was discovered accidentally, it is used for reducing pain and fever. It does not restrain platelet aggregation (Ayoub et al, 2004; Josephy, 2005). However, the mechanism of action of acetaminophen is yet to be understood properly (Josephy, 2005). Prostaglandin (PGs) causes a lot of the symptoms of inflammation, which are produced by the inducible cyclooxygenase (COX)-2. PGs that are created by a constitutive enzyme (COX-1), helps in protecting the stomach mucosal lining and instigate platelet aggregation when necessary. Inhibition of PGs production by acetaminophen fluctuates in different tissues, thus reducing the activity of brain COX to a greater degree than the activity of COX in the stomach mucosa (Ayoub et al, 2004). A research study has shown that the production of PGs activity in dog brain inhibited more compared to that of rabbit spleen. The finding suggests that the presence of elevated peroxide levels such as the ones in inflamed tissues eliminates acetaminophen inhibitory activity on COX-1 or COX-2. Thus, acetaminophen inhibitory activity of COX-1 or COX-2 can only transpire in cells and tissues with low concentrations of peroxides such as brain cells (Ayoub et al, 2004; Josephy, 2005).
Acetaminophen became popular in 1960 as a lesser toxic, analgesic antipyretic agent than aspirin (Ayoub et al, 2004; Gyamlani and Parikh, 2002). Paradoxically, it is now the second leading source of toxic drug intake in the United States (Gyamlani and Parikh, 2002). According to the father of modern toxicology Paracelsus who stated that “The dose makes the poison” (Richards, 2008, p.7) In other words, the amount of acetaminophen an individual consumes is as important as how toxic the acetaminophen effect would be.
Acetaminophen overdose problem is due to the fact that it is a common medication, which is frequently consumed nonchalantly, and it can only take few days to exceed the maximum dose for it to damage the liver. Thus, liver damage due to an overdose of acetaminophen tends to be the most serious side effect which varies from mild to severe ( Mayhew, 2007). Some extremes of acute liver failure include “coagulopathy and encephalopathy” ( Mayhew, 2007). As a public health professional, I would create an awareness program, educate the public about the significance of taking this common medication, and enlighten about the potential problems related to acetaminophen overdose.
References:
- Ayoub, S.S., Botting, R.M., Goorha, S., Colville-Nash, P.R., Willoughby, D. A., and Ballou, L.R. (2004). Acetaminophen-induced hypothermia in mice is mediated by a prostaglandin endoperoxide synthase 1 gene-derived protein. vol. 101 no. 30 11165-11169. doi: 10.1073/pnas.0404185101 PNAS. Retrieved January 24, 2010, from, http://www.pnas.org/content/101/30/11165.full
- Gyamlani, G.G., and Parikh, C.R. (2002). Acetaminophen toxicity: suicidal vs accidental. Critical Care 6:155-159;doi:10.1186/cc1475. Retrieved January 24, 2010, from http://ccforum.com/content/6/2/155
- Josephy, P. (2005). The molecular toxicology of acetaminophen. Drug Metabolism Reviews, 37, 581-594. DOI: 10.1080/03602530500205200; Retrieved January 27, 2010 from http://web.ebscohost.com.ezp.waldenulibrary.org/ehost/pdf?vid=3&hid=7&sid=502535c8-fcd5-4832-a155-79ae43ed996e%40sessionmgr4
- Richards, I. S. (2008). Principles and Practice of Toxicology in Public Health
- Maren Mayhew, M.(2007). Acetaminophen Toxicity. Journal for Nurse Practitioners.3(3):186-188.Retrieved January 23, 2010 from http://www.medscape.com/viewarticle/557074
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