Today we bring you a terrific Daubert defense win. But, we’ll be honest it’s long. Really long. Thorough, but long. So, we’re going to hit the highlights.
The case is Davis v. McKesson Corp., 2019 WL 3532179 (D. Ariz. Aug. 2, 2019). It is a multi-plaintiff case against manufacturers and distributors of gadolinium-based contrast agents (“GBCA”) – used in MRIs. GBCAs were the subject of an MDL several years involving allegations that when administered to patients with advanced kidney disease they caused a disease known as nephrogenic systemic fibrosis (“NSF”). Id. at *2. Plaintiffs in the current action allege that they have been exposed to GBCAs but that they do not have impaired kidneys and they have not been diagnosed with NSF. Rather, they contend that after receiving GBCAs they developed “a range of symptoms [that] has not been recognized as a disease by regulatory authorities or medical associations, but the collection of symptoms has been referred to in some literature as “gadolinium deposition disease” (“GDD”). Id. In fact, the FDA convened an advisory committee in 2017 to explore the very issue of any connection between the retention of GBCAs in the body and the various symptoms reported by patients with healthy kidneys. The board “unanimously concluded that the medical and scientific evidence does not establish that GBCAs cause GDD.” Id. at *6. Many other foreign regulatory bodies and medical societies have reached the same conclusion. Id.
So, the court decided that the issue of general causation should be decided first and plaintiffs served expert reports from four experts, three on medical causation. And if we had to sum it all up, what plaintiffs’ experts offer are “theories” or “hypotheses” – that still need to be tested – but are not reliable science that establish that the symptoms associated with GDD are an actual illness or that the illness is caused by GCBAs. Id. at *10. But, the court provides a lot more detail.
For instance, one of plaintiffs’ experts’ opinions is that GBCAs cause a “continuum” of symptoms the most severe of which cause NSF in renal impaired patients and less severe symptoms in patients with healthy kidneys. Id. at *11. This would basically impute the general medical causation of NSF to GDD because they are simply different ends of the same continuum. “But this leap rests on nothing more than [plaintiff’s expert’s] say so.” Id. at *12.
Plaintiffs try to bridge the gap by relying on case reports and surveys – the experiences of single patients without a formal study or control group. Id. at *14. But, “case reports are not reliable scientific evidence of causation,” id. at *14, and “[s]urveys are even less reliable.” Id. at *15. At least some case reports are made by physicians, whereas surveys “consist of unscreened answers from people who believe they suffer from GBCA-caused illnesses, often provided anonymously.” Id. All of plaintiffs’ causation experts relied on both case reports and surveys with no acknowledgement of their limitations.
From there, plaintiffs’ experts moved on to animal studies which while not inadmissible, “there must be a basis for extrapolating them to the human population.” Id. at *16. Plaintiffs’ experts did not provide any such basis. In fact, several of the animal studies plaintiffs’ experts relied on involved rodents whose kidneys had been removed – making them less relevant to plaintiffs’ allegations that GBCAs cause GDD in humans with healthy kidneys. Id. The connection between the animal studies and plaintiffs’ experts’ opinions is based only on the experts’ “say-so.” Id. at *17.
Plaintiffs’ experts similarly cite in vitro studies but do not discuss “the doses used in the studies or explain how those doses can reliably be extrapolated to the effects of GBCAs in humans with healthy kidneys.” Id. Further, plaintiffs’ experts’ “principles and methods for finding GBCA causation of GDD have not been accepted by other experts, regulatory bodies, or professional associations” and at least two of the experts “have not done [independent] research and their opinions appear to have been prepared solely for this litigation.” Id. Indeed, one of plaintiffs’ experts was a keynote speaker at the FDA advisory board where “he made several statements quite inconsistent with his current opinions” but nowhere in his report does he cite any data to support his changed opinions. Id. at *25-26.
The bulk of the rest of the decision is filled with example after example of the specific ways in which plaintiffs’ experts fail in each of the above ways to satisfy the standard for admissibility under Daubert and Rule 702. For instance:
- Plaintiffs’ expert “never explains why the transfer of gadolinium from pregnant mice to their pups, or the accidental injection of GBCAs into the spinal canals of patients, or two case reports with their wide and differing range of symptoms can, through reliable scientific principles and methods, be extrapolated to show that GBCAs cause GDD in patients with healthy kidneys.” at *19
- Plaintiffs’ expert “does not explain how the in utero exposure relates to patients with healthy kidneys, nor does he address why the in vitro study of skin growth, and its doses, can be reliably extrapolated to humans with no renal impairment.” at *22.
- Plaintiffs’ expert “does not explain why case reports from NSF patients can reliably be applied to reach any conclusions, including conclusions regarding patients who have healthy kidneys and do not have NSF; why the use of a survey or the effects on a dog can be applied reliably to the same patients; or, for that matter, why heart, respiratory, and liver effects have anything to do with Plaintiffs, none of whom claim such ill effects.”
- Plaintiffs’ expert “cites no evidence that retention in patients with normal renal function is equal in method or quantity to the accumulation in renally-impaired patients, and he merely assumes as probable that ‘tissue injury that occurs from GBCAs in renally impaired patients shares the same mechanisms of toxic injury with patients who have normal kidney function.’” Id. at *30.
- Plaintiffs’ expert “offers only one-line conclusions summarizing the results of these studies with no explanation about why these studies can reliably be applied to the causation issue in this case or how they relate to his opinions.” at *31.
And then there is plaintiffs’ experts’ application of the Bradford Hill criteria. The Bradford Hill criteria are used by epidemiologists in differentiating between a mere association and a causal connection. While the court conducts a thorough analysis of all nine criteria, we really only need to examine the first one – strength of association. An observed association is the starting point for the Bradford Hill analysis. And the association that starts the analysis is normally an epidemiologic study – which plaintiffs admit doesn’t exist for the relation between GBCAs and GDD. Id. at *33. At best plaintiffs’ experts can cite the causal link between GBCA and NSF, but that doesn’t establish a relationship to GDD – and you can’t assume a relationship. Id.
Finally, the court explains why plaintiffs’ case law doesn’t save their argument. First, plaintiffs rely on Wendell v. GlaxoSmithKline, LLC, 858 F.3d 1227 (9th Cir. 2017) – one of our worst decisions that year and discussed in more detail here. Fortunately, the court quickly distinguished it as a specific causation case and while we think there are many more reasons not to follow it, we’ll take it. Davis, at *44-45. Second, plaintiffs tried to analogize to the Daubert decision in the NSF MDL, but for all the reasons plaintiffs’ experts couldn’t rely on NSF science, the court wasn’t going to rely on NSF law. Id. at *45.
The court gave the parties two weeks to submit a “plan” for what happens next. Without an expert on general causation, the only route we see as viable is dismissal.