Tampa Tylenol Lawsuit

TYLENOL – Danger and Misplaced Trust

Brief history of Tylenol:

To fully understand why McNEIL has been able to get away with its advertising campaign and not fully reveal the dangers of Tylenol, you must first look into the history of the product. Acetaminophen has been available in over-the-counter (OTC) pain relievers since the 1950’s and was first marketed in the United Stated under the trademark name of Tylenol in 1951.[1] [2]

Tylenol is manufactured by McNEIL, a subsidiary of Johnson & Johnson. As of the date of this article there are approximately 23 different types of over-the-counter (OTC) Tylenol products available in the United States. [3]Tylenol is available in three different dosages by adults: regular, extra strength and extended release. The regular strength has 325 mg of acetaminophen per dose; extra strength has 500 mg of acetaminophen per dose and the extended release has 650 mg of acetaminophen per dose. [4]Acetaminophen is the most commonly used over-the-counter (OTC) pain reliever in the U.S. with “19% of adults reporting taking the drug in any given week.”[5]

Acetaminophen & Acute Liver Failure:

Acetaminophen is a well-established liver toxin. The mechanism by which acetaminophen can cause acute liver failure has been thoroughly studied over the past few decades. As Acetaminophen is metabolized in the liver, approximately 5 percent to 6 percent of the acetaminophen is turned into liver toxin referred to by the acronym “NAPQI”. In order the NAPQI not to destroy one’s liver it must bind with a substance called glutathione. When glutathione binds with the NAPQI, the NAPQI is detoxified and released from the body in urine. However, if there are either inadequate amounts of glutathione present in the liver or too much NAPQI present, then NAPQI attacks the liver, which results in acute liver failure.[6]

The link between Tylenol and acute liver failure is undeniable. Beginning in the late 90’s, research began to emerge indicating that “acetaminophen hepatrotoxicity was a major cause of acute liver failure (ALF) in the United States”, accounting for approximately 40% of acute liver failure hospitalizations.[7] Acetaminophen-related hepatotoxicity remains the “leading cause of acute liver failure (ALF) in the United States, Great Britain and most of Europe.”[8] In fact, the “incidence of acetaminophen-related ALF exceeds by at least three-fold that due to all other idiosyncratic drug reactions combined.”[9]

There is also no doubt that acetaminophen-induced acute liver failure is a serious and potentially life-threatening medical condition. The condition carries with it a 30% mortality rate.[10]  Additionally, more than “100,000 calls to Poison Control Centers, 56,000 emergency room visits, 2,600 hospitalizations and nearly 500 deaths are attributed to acetaminophen in this country annually.”[11] Additionally, there is data that demonstrates that the number of acetaminophen-related acute liver failure cases has increased since 1998.[12]

It has been demonstrated since 1975 that Tylenol can cause acute liver failure. In 1975, an article in The Lancet included the following statement:

The hepatotoxicity of paracetamol [acetaminophen] remains a serious problem, and liver damage has been observed after absorption of as little as 6.2 G. – not much more than the recommended dosage…Surely the time has come to replace paracetamol with an effective analogue that cannot cause liver damage.[13]

Scores of additional articles have also been written in the decades after this Lancet article was published. These articles established Tylenol’s propensity to cause acute liver failure. By 2002, the FDA found it necessary to convene an Advisory Committee meeting to discuss the growing epidemic.[14] The FDA recommendations prompted public comments, including hepatic experts at the American Association for the Study of Liver Diseases (“AASLD”). The AASLD took the unprecedented step of recommending sweeping label changes to acetaminophen-containing OTC products, including Tylenol. Among other recommendations, the following specific language was proposed by the AASLD:

This product can cause severe or even fatal liver injury: The chance is higher if you:

1. Use the drug at the maximum recommended dose (4 grams/day) for 5 or more consecutive days;
2. Use this drug at the maximum recommended dose (4 grams/day) when food intake is restricted or prohibited[15] (emphasis added)

The AASLD further voiced concerns that the “acetaminophen has a narrow therapeutic-to-toxic window”, which simply means that exceeding the recommended daily dose of Tylenol by even a small amount can expose the taker to a substantial increased risk of acute liver failure.[16] The AASLD’s discussion of the narrow therapeutic-to-toxic windown with acetaminophen is certainly alarming, given that Tylenol is available for use without a prescription and without physician supervision. This concern was echoed by the FDA Acetaminophen Hepatotoxicity Working Group:

The Working group was also impressed with the fact that current dosing recommendations and tablet sizes of acetaminophen leave little room for error. The 4 gram per day recommended dose is also the maximum safe dose, one that must not be exceeded, an unusual situation for any drug, particularly an OTC drug, one placing a large fraction of users close to a toxic dose in the ordinary course of use.[17]

McNEIL has been keenly aware that patients taking Tylenol routinely and unintentionally ingested more than the recommended dose. Some of McNEIL’s own studies show that many people taking Tylenol used more than the recommended daily dose. Similar findings have been seen in other publications.[18] In fact, widespread unintentional misuse of Tylenol has been cited as a “serious public health threat requiring urgent attention”[19] Despite having this information, McNEIL has done little to ensure that people taking Tylenol did so without exceeding the recommended daily dose.

Unfortunately, many people who have suffered acetaminophen-induced acute liver failure have not exceeded the recommended daily dose of Tylenol.  

While the exact number is unclear, some in the medical community have estimated that approximately 10 percent of the acetaminophen-induced acute liver failure cases have occurred in patients that have not exceeded the recommended daily dose.[20] What is clear is that the exact dose of acetaminophen that will lead to acute liver failure is so “highly variable and unpredictable” that it is difficult to ascertain “what is a perfectly safe dose of acetaminophen, especially when taken for more than a day or two.”[21]

As noted above, the AASLD, as part of its 2007 recommendation for updated labeling for acetaminophen containing products, urged manufacturers to include warnings that the risk of acute liver failure increased “when food intake is restricted or prohibited.”[22] This increased risk involved those taking Tylenol in situations where they are fasting, usually because they are suffering from the flu, migraine, recovering from dental surgery, or some other similar pain causing condition, which necessitates Tylenol use.   Unfortunately, many of these conditions prevent food consumption. This leads to people who are taking Tylenol for the actual reason it is intended to be used, as a pain reliever, to potentially be more at risk by taking the recommended daily dose. Again, the data supporting this proposed label change was available long before 2007.

The FDA medical researchers have consistently concluded that acute liver failure among patients taking acetaminophen products, including Tylenol, is a serious problem requiring immediate attention. The FDA cited the “significant public health problem” of the continued occurrence of acetaminophen hepatotoxicity as being the driving force of the formation of the FDA Acetaminophen Hepatotoxicity Working Group.[23] Due to the massive amounts of documentations, medical journal articles, studies and FDA recommendations, one would expect that McNEIL would do anything possible to prevent further Tylenol induced liver injuries and deaths. Unfortunately, McNEIL’s actions indicate that it was more interested in protecting its bottom line than the health of those taking Tylenol.

McNEIL’s Marketing of Tylenol:

McNEIL has spent tens maybe even hundreds of millions of dollars on various marketing campaigns to market Tylenol. Phrases printing frequently in Tylenol advertising and repeatedly seen by most Americans include Tylenol is “most trusted” and “the #1 choice of doctors”. MCNEIL has shown the intent to portray Tylenol to the public as a medication that is safe. However, they have done little or nothing to talk about the risk of Tylenol or the risk of liver failure in Tylenol and instead they have taken every chance they can to prevent the public from gaining this information from trusted sources. An example is that in 2004 the FDA decided to engage in a public education campaign focusing on their concerns about liver failure caused by Tylenol. McNEIL moved quickly asking the FDA to stop the campaign or take other corrective action. The FDA rejected McNEIL’s request stating “we do not believe the education campaign taken as a whole, or in any of its parts”, were false or misleading. [24]

McNEIL has taken no action to inform the public about Tylenol’s increased risk of acute liver failure while fasting. Nor has McNEIL used its immense advertising budget to warn the public not to exceed the daily recommended dose under any circumstances. What makes this incredibly dangerous is the paper thin therapeutic-to-toxic window for Tylenol and McNEIL’s knowledge that many people routinely exceed the recommended daily dose.

Tylenol’s Inadequate Warnings:

Project Protect:

In addition to the alarming nature of McNEIL’s failure to warn patients about the risks and dangers of taking Tylenol, it is even more outrageous that McNEIL knew of and even studied a second compound that could be added to Tylenol that would counter Tylenol’s toxic effect on the liver. As early as 1991, McNEIL entered into an investigation titled “Project Protect”, whose purpose was to find a compound that could be added to Tylenol that would reduce its liver toxicity.

As there is generally no physician overseeing the use of Tylenol among individuals and the fact that McNEIL knows this, it is clear that McNEIL waited too long to add any warning about liver damage to its Tylenol packaging and that the warnings in place, even today, are woefuly inadequate. It was until 2005 that McNEIL first added a warning to its Tylenol packaging concerning liver damage occurring in patients taking Tylenol. Also, the warning merely told the user that “taking more than the recommended dose of Tylenol may lead to liver damage.” In 2010, McNEIL slightly changed the language of its warning to provide the language available today. Again, this “warning” is woefully inadequate. For example, absent is any reference of Tylenol “causing” acute liver failure. In fact, the term “liver failure” does not even appear on the label. Additionally, it doesn’t even make any statements about its potential for “severe liver damage”, which can be fatal. Again, the label is still silent about the increased risk of acute liver failure while taking Tylenol while fasting and this is an unequivocal and clear recommendation made by the AASLD in 2007. The egregious conduct of McNEIL is clearly demonstrated by the inadequacies in its warning and unending marketing campaign expressing how “safe” Tylenol is.

However, by 1995 McNEIL abruptly stopped “Project Protect” because they were concerned that if they added the compound it would be admitting that Tylenol was in fact a dangerous liver toxin – contrary to their long standing marketing claims. This is especially egregious considering:

1. McNEIL could potentially have minimized the toxic effects of Tylenol in the liver, but choose to abandon its efforts;
2. The FDA was not notified by McNEIL that “Project Protect” was ever being considered, much less that it was undertaken and a promising protective compound was discovered.

Status of Litigation:

On April 2, 2013, the United States Judicial Panel in the Middle District established MDL No. 2436, which centralized the Tylenol litigation in the United States District Court for the Eastern District of Pennsylvania. Currently there are dozens of actions pending in MDL 2436. Additionally, there are approximately 16 cases currently pending in state court with 15 filed in the Superior Court of the State of New Jersey in Atlantic County and one case pending in the Philadelphia Court of Common Pleas.

An unknown number of Americans and people around the world and what they use everyday is probably what they believed before you read the above article; Tylenol was a harmless over-the-counter medication. The truth is entirely different and certainly can be very frightening.

If you have any questions on how TYLENOL could be dangerous to you or your family, please feel free to call my office at any time. Additionally, please remember if you or someone you know has been injured in an Auto, Motorcycle, Trucking, Slip/Fall… accident or suffered an injury, please call my office at any time at #877-444-2929 or log onto www.LigoriLaw.com and inquire on the website.

[1] Due to the fact that Tylenol entered the marketplace in the 1950’s it was not subject to the FDA’s current approval process for over-the-counter (OTC) medications. (William M. Lee, Acetaminophen Toxicity: Changing Perceptions on a Social/Medical Issue, 46(4) Hepatology 966, 966 (2007).

[2] The FDA’s approval process requires various levels of proof of both safety and efficacy.&nbsp; (Acetaminophen is referred to in many countries outside the United States as paracetamol)</p>

[3] www.tylenol.com/products

[4] Id. Tylenol is also available in various children’s formulations.

[5] Michael S. Wolf, Risk of Unintentional Overdose with Non-Prescription Acetaminophen Products, 27(12) J. Gen. Intern. Med. 1587, 1587 (2012).

[6] See JR Mitchell et al., Acetaminophen-induced hepatic injury; protective role of glutathione in man and rationale for therapy, 16(4) Clin. Pharmacol. Ther., 676-84 (1974); Paracetamol Hepatotoxicity, 2 (7946) The Lancet 1189-91 (1975).

[7] The Acetaminophen Hepatotoxicity Working Group, Recommendations for FDA Interventions to Decrease the Occurrence of Acetaminophen Hepatotoxicity, at 3 (Feb. 26, 2008).

[8] William M. Lee, Acetaminophen Toxicity: Changing Perceptions on a Social/Medical Issue, 46(4) Hepatology 966, 966 (2007).

[9] Id.

[10] Id.

[11] Id.

[12] Id.

[13] Paracetamol Hepatotoxicity, 2(7946) The Lancet 1189-91, 1191 (1975).

[14] The Acetaminophen Hepatotoxiticy Working Group, Recommendations for FDA Interventions to Decrease the Occurrence of Acetaminophen Hepatotoxicity, at 3 (Feb. 26, 2008).

[15] American Association for the Study of Livr Diseases (AASLD), Public Comment Regarding the Proposed Amendment of the Tentative Final Monograph of Internal Analgesic, Antipyretic and Antirheumatic Drug Products for Over-the-Cunter Human Use, at 2 (Apr. 27, 2007).

[16] Id.

[17] The Acetaminophen Hepatotoxicity Working Group, Recommendations for FDA Interventions to Decrease the Occurrence of Acetaminophen Hepatotoxicity, at 5 (Feb. 26, 2008).

[18] Michael S. Wolf, Risk of Unintentional Overdose with Non-Prescription Acetaminophen Products, 27(12) J. Gen. Intern. Med. 1587 (2012).

[19] Id. at 1590.

[20] William M. Lee, Acetaminophen Toxicity: Changing Perceptions on a Socal/Medical Issue, 46(4) Hepatology 966, 967 (2007).

[21] Neil Kaplowitz, Acetaminophen Hepatotoxicity: What Do We Know, What don’t We Know, and What do We Do Next? 40(1) Hepatology 23, 23, 25 (2004).

[22] American Association for the Study of Liver Diseases (AASLD), Public Comment Regarding the Proposed Amendment of the Tentative Final Monograph of Internal Analgesic, Antipyretic and Antirheumatic Drug Products for Over-the-Counter Human Use, at 2 (Apr. 27, 2007).

[23] The Acetaminophen Hepatotoxicity Working Group, Recommendations for FDA Interventions to Decrease the Occurrence of Acetaminophen Hepatotoxicity, at 4 (Feb. 26, 2008).

[24] Letter from Department of Health &amp; Human Services to Ms. Nancy L. Buc and Ms. Kate C. Beardsley, (Aug. 25, 2004).