Flexible Resources for Mass Tort Firm

Nexium (esomeprazole magnesium) belongs to a class of drugs called proton pump inhibitors (PPIs), which include Prilosec (omeprazole), Prevacid (lansoprazole) and Protonix (pantoprazole), Aciphex (rabeprazole) and Dexilant (dexlansoprazole). These drugs are used to treat heartburn, gastroesophageal reflux disease (GERD), stomach ulcers and inflammation of the esophagus by lowering the amount of acid produced in the stomach.

PPIs have been linked to an increased risk of heart attack, bone fracture, hypomagnesemia (low magnesium levels), birth defects, acquired infections and short-term kidney failure, including inflammatory kidney disease and acute interstitial nephritis (AIN)—a kidney disorder in which the spaces between the kidney tubules become swollen. The acute form of AIN occurs most often due to side effects from certain drugs. While AIN can only be definitively diagnosed by renal biopsy, side effects include fever, fatigue, lethargy, weight loss, nausea and vomiting. PPIs now appear to also be linked to long-term kidney damage, which can potentially lead to kidney failure, necessitating regular dialysis and a kidney transplant.

Concern that omeprazole users (i.e. Prilosec) could be subject to an increased risk of AIN was first raised in 1992 when a 74-year-old woman reportedly developed fatigue, malaise, hematuria, proteninuria and eosinophiluria after taking omeprazole for six months. The case report prompted studies on the risks of PPIs, the results of which suggested that all PPIs were linked to the occurrence of AIN.

In a 2004 case series, researchers identified 24 AIN diagnoses from Norwich University Hospital in the United Kingdom from 1995 to 1999. Of those, six instances of AIN were due to the patient’s use of omeprazole and two from lansoprazole. All of the patients recovered kidney function, but 75% were left with “some degree of chronic kidney disease.” A 2006 study performed in Auckland, New Zealand found 15 cases of PPI-induced AIN, 12 of which were proven through biopsies. The patients had been taking the medication anywhere from 10 days to 18 months when the symptoms developed.

An Australian study published in Clinical Gastroenterology and Hepatology in May 2006 became the first to connect all commercially available PPIs to AIN. Researchers examined potential cases of PPI-induced AIN by retrospectively reviewing records from two teaching hospitals and data from the Therapeutic Goods Administration of Australia’s registry. The study determined that there were 49 cases of biopsy-proven, PPI-induced AIN, 18 of which caused acute renal failure, 20 cases of unclassified acute renal failure, 26 cases of renal impairment, and 10 cases of suspected interstitial nephritis. Researchers felt that PPI-induced AIN will become more frequent considering the widespread use of the drugs; they concluded that the study’s results suggested a class effect with potentially “catastrophic long-term consequences including chronic kidney disease.”

A 2007 study from the Netherlands published in the British Journal of Clinical Pharmacology reported seven additional cases of PPI-induced AIN, five of which were biopsy-proven. The patients exhibited symptoms anywhere from hours after taking the PPI to four months. All but one patient recovered after being taken off the medication; the other patient recovered after being treated with prednisolone. One patient began taking the PPI again nine days after the initial event, and developed symptoms of AIN within 12 hours of exposure. The authors of the Netherlandic study also queried the World Health Organization Collaborating Center for International Drug Monitoring Database and identified an additional 150 cases that practicing clinicians reported to the registry.

Authors of another 2007 critical review published in Clinical Nephrology noted that PPIs are listed as the most common cause of drug-induced AIN on several registries of adverse drug events. They concluded their review by stating, “the PPI drug class is clearly associated with the development of AIN…As such, AIN from PPIs should be suspected as a potential cause of AKI in patients without an obvious cause of kidney dysfunction.”

In a 2013 case-control study published in BMC Nephrology, determined that “renal disease was positively associated with PPI use.” Researchers looked at 184,480 patients from the Midwest, age 18 and older, who were enrolled with a private insurer for at least two years between September 2002 and November 2005. They identified 854 cases with at least two claims for acute renal disease, and those cases were matched to a control group based on demographics. It was determined that those who were diagnosed with renal disease were twice as likely to have previously taken a PPI.

Another 2013 study published in the Indian Journal of Nephrology described four cases of PPI-induced AIN, concluding that because of the non-specific symptoms of AIN, PPI-induced AIN was “likely to be under-recognized and undertreated in India.” Researchers suggest that if AIN is suspected, the physician should stop treatment, perform a renal biopsy and start steroid therapy if needed to halt the renal disease.

A March 2014 study published in Kidney International looked at 572,661 patients, who had taken at least one course of PPI treatment from May 2005 to August 2009, had correctly linked data and did not have history of renal disease prior to taking the drug. Of those patients, 72 presented with AIN. The study determined that current PPI users were at a substantially greater risk of AIN than past users; the results also showed that the absolute risk increased for users who were age 60 and older.

In December 2014, the FDA approved a label change for Nexium delayed-release capsules and Nexium delayed-release oral suspension to include AIN, among other things, to the label. The label states “acute interstitial nephritis may occur at any point during PPI therapy and is generally attributed to idiopathic hypersensitivity reaction.”

In April 2015, CMAJ Open published the results of a study involving 290,592 Ontario residents, age 66 and older, who began PPI therapy, comparing them to an equal-sized control group. Researchers determined that those taking PPIs were three times more likely to develop interstitial nephritis and 2.5 times more likely to develop acute kidney injury than the control group. Researchers suggest that patients need to be monitored for AIN during treatment and should “discourage the indiscriminate use of these drugs.”

A January 2016 study published in JAMA Internal Medicine examined the data from self-reported PPI use among over 10,000 patients who took part in a national study; they also examined data from about 250,000 outpatient PPI prescriptions in a Pennsylvania healthcare system. Although the study was not a clinical trial and could not establish a direct cause-and-effect relationship between the drugs and chronic kidney disease, it does suggest that the two are interrelated. Researchers also stated that the medication is overprescribed, determining that 25 percent of long-term PPI users could stop taking the prescription medication without suffering from any increased effects of heartburn or acid reflux.

According to the results of the 2016 JAMA study, PPI users have a 20 to 50 percent higher risk of chronic kidney disease as compared to nonusers, with an increased risk associated with an increased dosage. Those who took the medication twice daily had a 46 percent increased risk, as opposed to those who took the medication once a day that had a 15 percent increased risk. The study also addressed concerns that PPI users suffer from chronic kidney disease due to overall poor health, as subjects of the study were found to have health problems such as obesity, high blood pressure and heart problems. Researchers compared PPI users to patients using another type of heartburn medication called H2 blockers, which include Pepcid, Tagamet and Zantac. In doing so, they found that PPI users had a 39 percent higher risk of developing chronic kidney disease as compared to patients taking H2 blockers.

On April 14, 2016, the Journal of the American Society of Nephrology published another study connecting PPI use to long-term kidney damage. By examining five years of data from national databases consisting of 173,321 new users of PPIs and 20,270 new users of H2 blockers, researchers determined that PPI users were 96 percent more likely to develop kidney failure and 28 percent more likely to develop chronic kidney disease than users of H2 blockers. This study also found “a graded association between the duration of PPI exposure and the risk of renal outcomes among those exposed to PPI for 31-90, 91-180, 181-360, and 391-720 days compared to those exposed for…30 days [or less].”

Despite making changes to Nexium’s label to include AIN in 2014, the FDA has not yet taken action regarding the risk of chronic kidney disease and kidney failure.

Thousands of lawsuits involving claims that talcum powder causes ovarian cancer have been filed—mostly in St. Louis and New Jersey. The defendants named in the litigation are: the manufacturer of the products, Johnson & Johnson; its parent company, Johnson & Johnson Consumer Companies; the company that mines the talc for the manufacturer, Imerys Talc America f/k/a Luzenac America; and the trade associate responsible for representing industry interest and lobbying on against regulation of talc.

Talcum powder is made from the mineral talc, which is combination of the elements magnesium, silicon, and oxygen. Talcum powder has been used in cosmetic products for decades and was commonly marketed as a useful way to absorb moisture, keep skin dry, and to prevent friction and rashes.

According to the FDA, talc is used in over 4,200 different cosmetic products and 40,000 pharmaceutical products in the United States. Currently there is no FDA warning concerning the negative physical side effects of talcum powder in products like Johnson & Johnson’s Baby Powder or Shower-to-Shower products because “under the Federal Food, Drug and Cosmetic Act (“FD&C Act”), cosmetic products and ingredients, with the exception of color additives, do not have to undergo FDA review or approval before they go on the market.” The FDA needs “sound scientific data” before it issues a warning that a cosmetic product is harmful under its intended use.

The first study linking talcum powder usage to ovarian cancer was published in 1971. Scientists took a microscopic analysis of 13 ovarian tumors and discovered that 10 of the tumors had talc particles deeply embedded in the tissue.

Then, in 1982, the Journal of Cancer published a case-controlled study of the links between ovarian cancer and intimate talcum powder use. The study involved 215 women diagnosed as having ovarian cancer in Boston hospitals from November 1978 to September 1981. Of the women, approximately 43 percent “said they dusted talc on their genitals or on sanitary napkins, against about 28 percent of a control group of similar background, age and marital status who said they did not use talc.”

In 1994, the Cancer Prevention Coalition petitioned the FDA to require cosmetic products containing talc to bear the warning: “Talcum powder causes cancer in laboratory animals. Frequent talc application in the female genital area increases the risk of ovarian cancer.” However, the FDA did not mandate a warning on the product because it determined that the scientific studies linking talc to ovarian cancer were not substantial enough to warrant such a warning.

In 2005, the National Toxicology Program (a part of the U.S.  Department of Health and Human Services) decided not to list talc as a cancer-causing agent because, like the FDA, it found the data insufficient to support a warning. However, in 2006, the International Agency for Research on Cancer, a branch of the World Health Organization, classified talc as a Group 2B agent, which means it is “possibly carcinogenic to humans.”

In 2007, the year the first talc lawsuit was filed, the Cancer Registry of Norway published a report after conducting one cohort study and 20 case controlled studies. The Cancer Registry of Norway cited mixed results regarding the link between perineal region talc use and ovarian cancer. The cohort study, which the report suggested was the strongest, revealed “there was no association between cosmetic talc use and risk of all subtypes of ovarian cancer combined.” The case controlled studies were split down the middle with half showing an increased risk and half showing non significant excess risk.

Plaintiffs in this litigation assert that the defendants knew that talc-based products could cause ovarian cancer when used for personal hygiene, but failed to warn consumers of such increased risk.

Risperdal is the brand name for Risperidone, an atypical or “second generation” antipsychotic drug prescribed to treat schizophrenia and other manifestations of psychotic disorders. The defendants named in the litigation are the designers, developers, manufacturers, marketers, advertisers, distributors and/or sellers of the drug, including Johnson & Johnson (“J&J”) and its subsidiary, Janssen Pharmaceutica (“Janssen”). 

On December 29, 1993, the FDA approved Janssen’s New Drug Application for Risperdal as a prescription drug used for the treatment of adults suffering from schizophrenia. In 2006, the FDA approved the use of Risperdal in children, specifically for the treatment of irritability associated with autistic disorders. The product label was also changed to state that Risperdal was “associated with higher levels of prolactin elevation than other antipsychotic agents.” Then, in 2007, FDA once more expanded the approved use of Risperdal to treat schizophrenia in adolescents ages 13-17, and for the short-term treatment of manic or mixed episodes of bipolar I disorder for children ages 10 to 17.

In addition to prescribing Risperdal in accordance with FDA approval, The defendants also promoted the drug’s off-label use. From the late 1990s and early 2000s, Janssen and J&J endorsed its product as a cure for stuttering, Tourette's syndrome, obsessive-compulsive disorder, attention deficit hyperactivity disorder (ADHD), OCD, anxiety, sleep difficulties, dementia, anger management, and depression. This was done despite the lack of FDA approval for use with children or adolescents for any purpose until 2006 and generic usage not beginning until approximately 2008. 

Risperdal has been linked to several serious side effects, most notably gynecomastia, the development of male breasts. This is because the drug has been found to increase a hormone called prolactin, which stimulates breast growth. Many young boys with Risperdal-associated gynecomastia undergo breast reduction and even mastectomies to correct the problem.

The plaintiffs in this litigation allege that the defendants were aware of the known health risks to children and adolescents while marketing this drug, including for off-label usage. Further, the plaintiffs claim that that the defendants knew of various studies showing that Risperdal patients had significantly elevated prolactin levels. Despite such knowledge, the plaintiffs argue that J&J/Janssen continued to actively market the drug to children and adolescents and failed to warn of the likelihood of gynecomastia as a serious side effect.

Risperdal actions have been filed in two separate state court coordinated actions—one in Philadelphia and another in Los Angeles.

Actos is a prescription Type 2 diabetes drug that has only one active ingredient, pioglitazone, and is part of a class of drugs known as thiazoldidinediones (“TZDs”). TZDs are oral anti-diabetic agents that decrease insulin resistance. The other TZDs are Avandia (rosiglitazone) and Rezulin (troglitazone).

After the FDA-approval of Actos in 1999, Takeda and Eli Lilly jointly launched the drug into the U.S. market. In 2006, Takeda took over the marketing Actos (Eli Lilly continued to receive residual royalties from Actos sales until 2009).

In 2007, the FDA and manufacturers of TZDs agreed to add stronger warnings of the risk of heart failure after taking certain drugs approved to treat Type 2 diabetes. The information was included in the form of a black box warning (the FDA’s strongest form of a warning). In an alert specific to Actos, the FDA stated that Actos might cause or exacerbate congestive heart failure in some patients. Nevertheless, in 2010, Actos was the 11th top selling drug in the U.S, with sales exceeding $2.6 billion and in March 2011, sales of the drug peaked at $4.5 billion.

In June 2011, the FDA issued a warning informing the public that use of Actos for more than one year may be associated with an increased risk of bladder cancer. The FDA based its conclusion on data from a 5-year interim analysis of an ongoing 10-year epidemiological study. The 5-year results showed that “although there was no overall increased risk of bladder cancer with pioglitazone use, an increased risk of bladder cancer was noted among patients with the longest exposure to pioglitazone.”

In June 2013, 23 experts from 9 countries met at the International Agency for Research on Cancer (IARC) to assess the carcinogenicity of fourteen drugs and herbal products. After a detailed review of one large randomized controlled study, 4 cohort studies, and 3 case controlled studies, the Agency determined that pioglitazone should be classified as probably carcinogenic to humans based on the evidence that it causes bladder cancer.

Moreover, the British Journal of Clinical Pharmacology published a study in December 2013 that linked the use of TZDs, including Actos, to the development of bladder cancer. Researchers discovered that there was “an increased risk of bladder cancer in patients with the highest doses of pioglitazone and in patients who either took Actos between 12 and 24 months or more than 24 months.” In addition, the researchers noted that there was a higher overall risk of bladder cancer in patients who used Actos than those who used Avandia.

Plaintiffs in the litigation involving Actos allege that they purchased and ingested Actos believing it to be safe based upon the promotions, advertising, marketing and labeling by the defendants. Further, the plaintiffs contend that the ingestion of Actos posed significant safety risks, including the development of bladder cancer, due to design defects and inadequate testing.

On December 29, 2011, the federal Actos cases were consolidated into a multi-district litigation in the Western District of Louisiana, assigned to Hon. Rebecca F. Doherty. Several thousand cases were also filed in state courts, mainly in California and Illinois.

Hundreds of lawsuits have been filed against Xarelto manufacturers Johnson & Johnson and Bayer Healthcare alleging that the manufacturers failed to warn consumers of the gravity of the risks involved in taking the blood-thinning drug.

Xarelto, generically known as rivaroxaban, is an anticoagulant or blood thinner developed by Bayer and Janssen Pharmaceuticals, a subsidiary of Johnson & Johnson. The FDA approved the drug for use in 2011 for individuals suffering from Atrial Fibrillation (Afib), Pulmonary Embolism (PE), and Deep Vein Thrombosis (DVT).

Xarelto belongs to a class of drugs called direct thrombin inhibitors and functions by inhibiting the Factor Xa, which is an enzyme needed for blood clots to form. The drug functions differently from traditional blood thinners, like Coumadin (Warfin), which instead interferes with vitamin K.

Manufacturers of Xarelto have promoted the product to the public as a more convenient alternative to the popular Coumadin because, unlike patients taking Coumadin, Xarelto users do not need to undergo regular blood tests to continually adjust their dosage. Patients taking Coumadin are also advised to stay away from leafy greens in order to keep vitamin K levels low, whereas Xarelto users have no dietary restrictions.

However, Xarelto, unlike Coumadin has no antidote to stop hemorrhaging. Xarelto has a low therapeutic index, which means that the difference between safe levels of the drug does not significantly differ from dangerous dosages. If severe hemorrhaging occurs while using Xarelto doctors are left with no other solution than to perform a blood transfusion.

Just one year after the FDA approved Xarelto for public use, the agency revealed that three times as many people died as a result of adverse events caused by Xarelto as compared to patients using Coumadin. QuarterWatch the quarterly adverse drug event report published by the Institute for Safe Medication Practices reported that in the first quarter of 2012 alone there were 356 reports of serious, disabling, or fatal injury involving Xarelto use.

In August 2013, the FDA sent a warning letter to Janssen advising the drug maker that changes to the labeling of Xarleto had to be made immediately. Specifically, the FDA stated that the labeling on Xarelto medication boxes was misleading to consumers, as were the Xarelto advertisements running at the time.  The labeling and advertisements in question at the time minimized the risks associated with the drug. Out of six possible categories of safety labeling listed by the FDA in 2013 Janssen had to alter four categories—boxed warnings, precautions, adverse reactions, and warnings in general. In 2014, the FDA once again notified Janssen that it had to alter the Xarelto box warnings.

Plaintiffs in the Xarleto lawsuits allege that defendants, Bayer Healthcare and Johnson & Johnson, recklessly placed Xarelto on the market and knowingly promoted the drug despite being aware that no antidote was available once a patient started hemorrhaging. Plaintiffs also allege that had they been made aware of the true extent of the serious risks involved with Xarelto they would not have taken the drug. The injuries alleged by the plaintiffs in the litigation include: gastrointestinal bleeding, brain hemorrhage, subdural hematoma, epidural hematoma, pulmonary hematoma, heart attack, stroke, blood clots, rectal bleeding, and liver issues.