[Drug and Device Law] What Does Pharmacogenomics Have To Do With Product Liability? - Potentially Everything
Recently, Bexis attended the DRI drug and device committee spring conference. Among other things he heard a bang-up presentation on genomics and personalized (also known as “precision”) medicine from Paige Sensenbrenner. On that same day, co-blogger Steve Boranian alerted Bexis to a new defense argument in asbestos/mesothelioma cases that also utilizes genomics – certain mutations in a gene called “BAP1” – to identify persons at greater risk of idiopathic (that is, not related to asbestos) mesothelioma. Here’s a link to that article. A verifiable alternative cause could be a game-changer for asbestos litigation. The statement we quoted back in 2009, uttered by the first person ever to have his genome individually sequenced, that “individual genes are just not very informative,” appears in the process of being disproven by ongoing scientific events.
Both items, as informative as they were on scientific facts, were rather short on the law. That’s where we come in. We thought we’d take a look at what law exists concerning the intersection of pharmacogenomics, personalized medicine, and prescription medical product liability litigation. We’ve touched on these issues back in 2011, when we blogged about Mills v. Bristol-Myers Squibb Co., 2011 WL 4708850 (D. Ariz. Oct. 7, 2011), one of the first cases in which the plaintiff made allegations about pharmacogenomically-based risks. Back then we said:
The plaintiff is claiming that a drug is defective, not because of anything inherent in the drug itself, but solely because it is less effective (and therefore has a different risk-benefit profile) due to the plaintiff’s peculiar genetic makeup. Essentially, the allegations seek to impose a non-FDA-approved contraindication, using state law, based upon human genetic variability. With advances in computer technology making genetic testing exponentially cheaper and more detailed as times passes (see Moore’s law), more and more genetic variability in the efficacy of prescription drugs is bound to be discovered. Eventually - certainly within some of our lifetimes - we'll be able to carry our entire individual genetic code around with us on a chip, should we so choose….
The complaint in Mills is a bare genetic susceptibility claim, frankly based on an allegation of “variant” genetic characteristics shared by only a minority of the population. In our view, unless and until – and only to the extent that – the FDA decides to assess drug approvals and contraindications on the basis of genetic subgrouping, this type of tort claim should not be recognized, because it is flatly contrary to the criteria by which the intended uses of drugs are currently determined. Claims such as in Mills, which are at loggerheads with FDA criteria for drug development, are precisely those with the most potential for making pharmaceutical manufacturers into “sitting ducks” for litigation, in this instance litigation based on extraneous genetic factors.
It may well be that the coming (and to some extent existing) revolution in genetically individualized medical therapy will require changes in how drugs are evaluated, labeled, etc., but this is a singularity-driven issue that needs to be addressed by the policy branches of our government, and not haphazardly in product liability litigation.
(Emphasis added).
FDA Regulation of Pharmacogenomic Information
We still feel the same way, but now with the caveat that the FDA is starting to lay the regulatory foundation for drug warnings in the coming age of personalized medicine. Way back in 2005, the FDA allowed voluntary addition of pharmacogenomic information in drug labeling:
The pharmacogenomic data and resulting test or tests may be intended to be included in the drug labeling to choose a dose and dose schedule, to identify patients at risk, or to identify patient responders. Inclusion of a pharmacogenomic test in the labeling would be contingent upon its performance characteristics.
FDA, Guidance for Industry, Pharmacogenomic Data Submissions, at 5 (March 2005) (available here). Under the heading “Clinical Pharmacology,” drug labeling can now contain a subsection specifically devoted to pharmacogenomics. As of last year, over 100 drugs contained such information, according to the FDA.
Since our post in 2011, the FDA has released several additional guidance documents in this field. This one, the most basic, simply defines the relevant terminology, particularly in the area of clinical investigations. This one addresses how to incorporate genetic variation into the design and implementation of clinical investigations. This one concerns inventing tools to identify biomarkers in the course of drug development. This one concerns how to report pharmacogenomic data to the Agency. The FDA’s online pharmacogenomics resources offer links to scads of other stuff. We don’t purport to be either scientists or regulatory lawyers, so now we’ll turn to the underlying purpose of this post, which is the legal precedent involving pharmacogenomics and product liability.
Pharmacogenomic Product Liability Claims
Pharmacogenomics is a double-edged sword. There will be some cases in which the results of genetic testing might assist plaintiffs (for example, in the absence of an adequate warning) and others in which the results of genetic testing will indisputably aid defendants – such as the mesothelioma alternative cause scenario mentioned above:
In the ideal plaintiff’s case, a person with an allele that made him or her specifically susceptible to the action of some toxin would be exposed to that toxin, which would cause a unique and detectable biochemical change, which in turn would be shown to cause an extremely high likelihood of contracting the plaintiff's disease. The ideal defendant’s case might occur in several ways: similar biomarker evidence would point a finger at a purely genetic cause or at some other (perhaps voluntary or non-anthropogenic) exposure; or, a person exposed to a toxin known to cause the person's disease in susceptible people might have a gene that completely neutralized the toxic effect and also might lack a biomarker that is uniformly found in people whose disease was caused by exposure.
Steve C. Gold, “The More We Know, the Less Intelligent We Are? − How Genomic Information Should, and Should Not, Change Toxic Tort Causation Doctrine,” 34 Harv. Envtl. L. Rev. 369, 392 (2010) (footnote omitted).
The plaintiffs’ side has sporadically argued that genetic markers should be warned about or, in some cases designed around, although we doubt the latter is even possible. So far many plaintiffs have had trouble coming up with factual support to back such allegations – and sometimes we’re not even sure why they’re making them. In the latter category we place Newman v. McNeil Consumer Healthcare, 2013 WL 9936293 (N.D. Ill. March 29, 2013), a case we blogged about a couple of years ago. Newman involved SJS/TEN, the autoimmune diseases (or different forms of the same disease) Stevens Johnson Syndrome and Toxic Epidural Necrosis. SJS/TEN is somewhat analogous in our sandbox to mesothelioma in asbestos cases, since plaintiffs often work backwards from the diagnosis to look for some drug company to sue. We mentioned in a recent post the wide variety of drugs that plaintiffs have claimed to cause these conditions. Perhaps to bolster the often weak SJS/TEN causation testimony, in Newman the plaintiff’s expert sought to discuss pharmacogenomics. However, the testimony about purported genetic predisposition to the disease was rejected as speculative, because no genetic link to SJS/TEN has yet been discovered:
Defendants are correct that [the expert] testimony on the subject would be speculative and irrelevant. First of all, Plaintiffs’ argument admits that the relevance and helpfulness of the information is conditioned on the discovery of a genetic link, which may not happen. Secondly, even if such a link were discovered, Plaintiffs fail to explain how it rebuts Defendants claim that SJS/TEN was unpredictable during the relevant time frame.
Id. at *8. As of the time of trial, the state of the art did not include a genetic marker for SJS/TEN. “That SJS/TEN may be more predictable in the future if a particular discovery is made says nothing about Defendants’ negligence.” Id. While the genetic testimony in Newman was offered by the plaintiff, should an SJS/TEN marker be discovered, we believe that overall such a development would help defendants far more than plaintiffs by exonerating most, and maybe all – if the marker is not drug related – of the plethora of drugs that plaintiffs have alleged as causitive agents.
Then there’s the Mills case itself. Mills was similar to Newman in that the plaintiff once again made baseless allegations about possibly carrying a genetic marker. In Mills, the plaintiff claimed that, due to a variant gene (“CYP”), she could not metabolize the defendant’s drug as well as most other people. The presence of this adverse genetic marker purportedly supported a design defect theory:
Plaintiff alleges that the chemical structure of [the drug] is defective because it carries a higher risk of adverse events for patients who carry the genetic variant CYP, who are poor metabolizers of the drug. Plaintiff contends that [the drug] is the proximate cause of her injuries because, “[u]pon information and belief,” she is a CYP carrier.
Mills, 2011 WL 4708850, at *2. As in Newman, the court in Mills did not let the plaintiff get away with this subterfuge. A plaintiff’s own genetic markers, and genome generally, is something the plaintiff is uniquely in possession of. “Plaintiff’s genetic makeup is a fact solely within her control. Tests are available that can reveal whether plaintiff in fact possesses CYP.” Id. Where the plaintiff is asserting a claim based on pharmacogenomics, s/he is responsible for producing the evidence to prove it. Id.
Similar – and similarly unsupported – allegations of “genetic predisposition” to being a “poor metabolizer” of a drug contributed to the rejection of the plaintiff’s expert report in Rimbert v. Eli Lilly & Co., 2009 WL 2208570 (D.N.M. July 21, 2009), aff’d, 647 F.3d 1247 (10th Cir. 2011) (which we blogged about here).
Ultimately, almost everything in [the expert’s] specific causation opinion is hypothetical and speculative, except for her conclusion. She wrote that “it is unknown” whether [the plaintiff’s decedent] may have been among the small percentage of Caucasians who are poor metabolizers of [the drug], [and] that he “may have” been vulnerable to a rise in blood and brain levels of [the drug].
Id. at *19. See also Tamraz v. Lincoln Electric Co., 620 F.3d 665, 670-71 (6th Cir. 2010) (expert opinion founded on speculation about undiagnosed “genetic predisposition” to injury from product exposure was not admissible); In re TMI Litigation, 193 F.3d 613, 622 (3d Cir. 1999) (recognizing use of genetic markers as “an accepted method” of evaluating radiation exposure, but rejecting as unreliable a sample taken 15 years after the event in question); Munro v. Regents of University of California, 263 Cal. Rptr. 878, 882-83 (Cal. App. 1989) (summary judgment affirmed against claim that “certain rare and isolated groups” were genetically at higher risk of a disease due to lack of expert testimony); Easter v. Aventis Pasteur, Inc., 358 F. Supp.2d 574, 575 (E.D. Tex. 2005) (precluding expert testimony that “some children are genetically susceptible to mercury poisoning” in vaccine case where the minor-plaintiff “not meet th[at] genetic profile”); Agee v. Purdue Pharmaceuticals, Inc., 2004 WL 5352989, at *3 (W.D. Okla. Nov. 22, 2004) (plaintiff’s expert “did not have any basis for concluding that [plaintiff] was a ‘slow metabolizer’”), aff’d, 242 F. Appx. 512 (10th Cir. 2007); Trainer v. Sec’y of HHS, 2013 WL 4505803, at *7 (Fed. Cl. July 24, 2013) (“[p]etitioner, however, fails to present any evidence indicating that he has a mitochondrial DNA mutation that would make him more susceptible”); Kolakowski v. Sec’y of HHS, 2010 WL 5672753, at *43 (Fed. Cl. Nov. 23, 2010) (absent any testing showing “genetic predisposition,” plaintiff could not prove claim).
These cases are all well and good, but with continuing advances in genetic screening, sooner or later at least some plaintiffs should be able to support claims of pharmacogenomic injury with the necessary evidence. When that happens, defendants must be on the lookout to prevent warning claims about genetic markers and pharmacogenomic susceptabilities from becoming so detailed that they seek to tell physicians how to practice medicine. We’ve discussed those principles (outside the genetic context) here.
If and when plaintiffs are able support claims based on peculiar genetic susceptibility to injury, they will seek to convert pharmacogenomic claims into the 21st Century version of the “eggshell” plaintiff rule – that a tortfeasor is liable for aggravated injuries due to a “preexisting physical or mental condition.” See Restatement (Third) of Torts, Liability for Physical & Emotional Harm §31 (2010); Restatement (Second) of Torts §461 (1965). This principle has already cropped up in some cases involving genetic conditions. Most recently, in Vanslembrouck v. Halperin, 2014 WL 5462596 (Mich. App. Oct. 28, 2014) (unpublished), the defendants asserted a “genetic abnormality” as an alternative cause. Id. at *2. The plaintiffs sought, and received, an “eggshell” plaintiff charge, which the court held appropriate under the loose “clear error” standard, because the defendant made no objection. Id. at *58-59. The same sort of unobjected-to instruction about genetic susceptability was given in Rite Aid Corp. v. Levy-Gray, 876 A.2d 115, 140 (Md. App. 2005), aff’d, 894 A.2d 563 (Md. 2006).
The Vaccine Court has applied “eggshell” plaintiff principles to reject allegations that genetic predispositions were a superseding cause of vaccine-related injuries, but only “[s]o long as the [product] was a substantial factor” cause. Zeller v. Sec’y of HHS, 2008 WL 3845155, at *26 (Fed. Cl. July 30, 2008).
Respondent proffered evidence and arguments that [plaintiff’s] genetic predisposition was a superseding cause of her injury, rendering irrelevant the vaccine as a substantial cause. . . . [I]f the administration of the vaccine(s) to [plaintiff] creates or increases the foreseeable risk of harm that preexisted and coexisted in her genetic predisposition . . ., and the vaccine is found to be a substantial factor in causing her injury, then the genetic predisposition cannot constitute a superseding cause. . . . Applying the general rule from the common law of torts, compensation is appropriate even when the vaccine operates upon a concealed physical condition, such as a latent disease, or susceptibility to disease, to produce consequences incapable of reasonable anticipation. . . . As every aspiring attorney learns, a defendant takes a plaintiff as he finds him.
Sucher v. Sec’y of HHS, 2010 WL 1370627, at *43 (Fed. Cl. Mar. 15, 2010) (citations and quotation marks omitted); accord Byers v. Sec’y of HHS, 2010 WL 5663019, at *26 (Fed. Cl. Nov. 30, 2010) (same rationale). The possibility of a latent or otherwise unknown genetic condition is only a damages principle, however, and does not affect either the standard of care or the causation requirement. Garcia v. United States, 2010 WL 2977611, at *20 n.10 (D.N.M. June 15, 2010) (discussing example of the “genetic disorder” of osteogenesis imperfecta).
Pharmacogenomic Claims Concerning Efficacy Rather Than Safety
Pharmacogenomics can identify not only genetic markers that increase risk of adverse drug reactions, but also those that reduce a drug’s effectiveness. This latter situation – that a drug allegedly didn’t work as well as it was supposed to due to genetic variation − has not been considered a legitimate product liability claim, since the plaintiff is not asserting that the drug caused any injury that the would not have happened anyway. Several cases from the Plavix MDL establish this principle. In the first of these, Solomon v. Bristol-Myers Squibb Co., 916 F. Supp.2d 556 (D.N.J. 2013) (blogged about here), the plaintiff claimed that he “should have been genetically tested to determine his genetic response” to the drug because it was ineffective in some people due to genetic variation. The court first found that the effectiveness evidence didn’t relate to this plaintiff’s particular facts, id. at 566-67, and went on to reject the very idea of product liability due to lack of effectiveness:
[I]t appears that Plaintiff’s efficacy arguments are not relevant in the context of a failure-to-warn analysis. . . . [A] drug manufacturer is required to provide an adequate warning of its product if it knows of any potential harm that may result from the use of its product. In other words, a proper warning should adequately alert any danger or harm that may result from ingesting the drug. Permitting Plaintiff to pursue his failure-to-warn claim on an efficacy theory would, as has been found in other jurisdictions with similar laws, impermissibly expand liability under Texas law on the adequacy of pharmaceutical warning labels.
Id. at 564 (citations omitted) (emphasis original). Other cases rejecting mere effectiveness/efficacy claims are: LaBarre v. Bristol Myers Squibb Co., 544 F. Appx. 120, 125 (3d Cir. 2013) (“efficacy is not relevant to a failure to warn claim”; a warning “duty does not extend to a warning about a drug’s efficacy”) (discussed here); Tobin v. Astra Pharmaceutical Products, Inc., 993 F.2d 528, 536 (6th Cir. 1993) (rejecting warning “argument . . . relat[ing] to the studies on efficacy”; efficacy only relevant to design claim); Needham v. White Laboratories, Inc., 639 F.2d 394, 402 (7th Cir. 1981) (where plaintiff alleged only that defendant “failed to warn, comment k could not apply . . ., and evidence of the efficacy, or inefficacy, of [the drug] was irrelevant”); In re Fosamax (Alendronate Sodium): Products Liability Litigation, 2014 WL 1266994, at *15 (D.N.J. March 26, 2014) (“omission of efficacy information does not constitute a failure to warn about a drug’s risks and therefore, does not raise a genuine issue of material fact”); Carr-Davis v. Bristol Myers-Squibb Co., 2013 WL 322616, at *6 (D.N.J. Jan. 28, 2013) (“studies based on the efficacy of [the drug] . . . fail to raise a genuine issue of material fact on the question of whether [its] warnings were adequate”) (discussed here); Begley v. Bristol-Myers Squibb Co., 2013 WL 144177, at *6 (D.N.J. Jan. 11, 2013) (“although the efficacy of a drug may play a role in a physician’s decision to prescribe, the failure-to-warn doctrine is not primarily concerned with a drug’s efficacy”) (discussed here), aff’d, 544 F. Appx. 120 (3d Cir. 2013); In re Fosamax Products Liability Litigation, 2010 WL 1257299, at *5 (S.D.N.Y. Mar. 26, 2010) (“[t]o allow Plaintiff to pursue a claim for the ‘failure to warn’ of the efficacy of a drug would be an expansion of liability”) (discussed here).
Using Pharmacogenomic Conditions As Alternative Cause
Pharmacogenomics can also assist the defense of prescription medical product cases by establishing alternative cause. Many of the most thoughtful cases doing so involve federal vaccine litigation. For example, an exhaustive discussion of the genetic underpinnings of autism is found in Snyder v. Sec’y of Dept. of HHS, 2009 WL 332044, at *45-50 (Fed. Cl. Feb. 12, 2009). Ultimately, the vaccine court concluded, “[t]he evidence for autism’s genetic basis and prenatal origin renders petitioners’ [vaccine-related] theory of causation improbable. Id. at *52. Similarly, in Simanski v. Sec’y of HHS, 115 Fed. Cl. 407 (Fed. Cl. 2014), aff’d, 2015 WL 795060 (Fed. Cir. Feb. 26, 2015), an inherited genetic condition was advanced as an alternative non-vaccine-related cause for the injury being alleged. The plaintiffs’ position was rejected in part because “have done very little to refute these conclusions, including allowing genetic testing” that would have confirmed or denied the alternative cause. Id. at 427. In another vaccine case, Waters v. Sec’y HHS, 2014 WL 300936 (Fed. Cl. Jan. 7, 2014), genetic testing had occurred, and it had revealed an alternative genetic cause that precluded a finding of vaccine-related causation:
Petitioners have failed to show by a preponderance of the evidence that [minor plaintiff’s] current condition constitutes a significant aggravation of his condition prior to vaccination. He had the SCN1A mutation before his vaccinations, his clinical course developed consistent with that condition, and his current condition is a result of his genetic mutation.
Id. at *23. See also Chapman v. Procter & Gamble Distributing, LLC, 766 F.3d 1296, 1310 & n.16 (11th Cir. 2014) (defendant successfully established a genetic condition as alternative cause); Kane v. Motorola, Inc., 779 N.E.2d 302, 309 (Ill. App. 2002) (plaintiff’s expert properly excluded because he “could not rule out any other cause of [plaintiff’s injury], including genetics”); Hendrix v. Evenflo Co., 255 F.R.D. 568, 598 (N.D. Fla. 2009) (plaintiff’s expert’s causation opinion excluded because he “ignore[d] the possibility of other genetic conditions as a cause”), aff’d, 609 F.3d 1183 (11th Cir. 2010); Schenk v. Novartis Pharmaceuticals Corp., 2014 WL 3656904, at *4-5 (D. Ariz. July 23, 2014) (plaintiff’s expert excluded for lack of good grounds for excluding plaintiff’s known genetic condition as causative factor); Blackmon v. American Home Products Corp., 346 F. Supp.2d 907, 919 (S.D. Tex. 2004) (plaintiff’s expert excluded for lack of good grounds for excluding “other known causes . . ., such as genetics”); Medalen v. Tiger Drylac U.S.A., Inc., 269 F. Supp.2d 1118, 1139 (D. Minn. 2003) (plaintiff’s expert testified “I didn’t really evaluate the genetic aspect of that”; Daubert motion granted).
Defense-side pharmacogenomics alternative cause evidence should be adequately supported by both known facts and expert testimony. Otherwise, a defendant’s assertion of a genetically-based alternative cause runs the risk of failing for essentially the same reasons as the plaintiffs in the cases already discussed. See In re Prempro Products Liability Litigation, 586 F.3d 547, 566 (8th Cir. 2009) (pointing out that the plaintiff “submitted to every available genetic test” without any positive result); Levy-Gray, 876 A.2d at 139-40 (no evidence of genetic marker for alternative cause). However, in Roberti v. Andy’s Termite & Pest Control, Inc., 2011 WL 635369 (Cal. App. Feb. 23, 2011) (unpublished), a defense expert was allowed to give testimony that the plaintiff could well have a “genetic abnormality” responsible for his condition that had not yet been discovered:
[The expert’s] opinion was not speculative or devoid of foundation. He merely pointed out that the current state of medical science does not allow him to confirm, or to rule out, a genetic or chromosomal abnormality as the cause of plaintiff’s condition. It was a factually accurate statement to say that often birth defects are linked to genetic abnormalities, but that relatively little is known about identifying the precise genetic defect responsible for various conditions. . . . [H]e simply said that it was possible that a genetic cause was responsible. This was not speculation; it was a statement relevant to [the expert’s] opinion regarding causation based on his scientific knowledge. In addition, we note that the opinion was offered to refute plaintiff’s counsel’s attempt to definitively confirm that plaintiff did not have a genetic disorder. . . . Merely suggesting that the injury could have another cause that cannot be verified is hardly prejudicial or likely to mislead the jury.
Id. at *13.
Using Pharmacogenomic Conditions To Defeat Medical Monitoring Claims
Genetic markers can also defeat claims for medical monitoring. In Sheridan v. NGK Metals Corp., 609 F.3d 239 (3d Cir. 2010), “exposure [to the defendant’s product] itself appears to be insufficient because only persons who have a particular genetic ‘marker’” went on to develop the medical condition at issue. Id. at 244. The evidence established that “only a small percentage of the population with the known genetic marker . . . is at risk of becoming sensitized.” Id. at 252. Since only that small percentage was therefore at risk of eventually developing the disease for which monitoring was being demanded, the class-wide monitoring claim failed as a matter of law:
[P]laintiffs did not prove they were at a significantly increased risk of developing [the disease] and thus did not present sufficient evidence to make out a prima facie cause of action for medical monitoring.
Id. Accord Pohl v. NGK Metals Corp., 936 A.2d 43, 51 (Pa. Super. 2007) (affirming summary judgment against medical monitoring claim on similar facts; “[a]ppellants cannot show they are even susceptible . . ., because [such] susceptibility cannot be determined by a test”). Although Sheridan and Pohl did not involve class certification, the same logic should apply in that context as well, since any risk dependent on the presence of genetic markers – by definition not common to the entire population – would require individualized evidence to establish for every purported class member. See Norwood v. Raytheon Co., 237 F.R.D. 581, 592 (W.D. Tex. 2006) (individual “genetic makeup” one of factors cited in denying class certification in radiation case).
Using Pharmacogenomic Conditions To Defeat Failure-To-Recall Claims
Another way that pharmacogenomics can help defendants is in those relatively rare cases where the plaintiff claims that the drug should have been recalled. These claims have mostly been preempted, but Lance v. Wyeth, 85 A.3d 434 (Pa. 2014) (discussed on several occasions, most notably here), remains. Lance, however was based in significant part on Restatement (Third) of Torts, Products Liability §6(c) (1998), which Lance indicated “at the very least overlaps or intersects” with Pennsylvania negligence law. 85 A.3d at 459 n. 37. This section, however, is only applicable where the risk/benefit ratio is such that “reasonable” physicians, aware of such risks, “would not prescribe the drug or medical device for any class of patients.” Id. (emphasis added). Advances in genomics and individualized genetic markers should narrow this already small exception concerning prescription drug design even further, since such markers will create precisely those “classes of patients” so benefitted. In Mills, for example, the court rejected a §6(c) claim because “nowhere does plaintiff allege that [the drug] would not be prescribed for any class of patients” besides those allegedly carrying the adverse genetic marker. 2011 WL 4708850, at *3.
Using Pharmacogenomic Conditions To Support the Statute of Limitations
Genetic testing has also proven relevant to the operation of the discovery rule where the timeliness of the suit under the applicable statute of limitations is at issue. See D.D. v. Idant Laboratories, 374 F. Appx. 319, 322-23 (3d Cir. 2010) (plaintiff deciding to undergo genetic testing showed sufficient awareness of possible external cause to satisfy discovery rule).
Pharmacogenomic Discovery
Finally, discovery. As mentioned in Mills, plaintiffs are in sole possession of their genome. Along the same lines, we have often seen plaintiff’s experts get away with blowing off the entire subject of genomics with the flippant statement that the plaintiff has “no known history” of genetic issues, without any affirmative investigation. E.g., Junk v. Terminix International Co., 577 F. Supp.2d 1086, 1096 (S.D. Iowa 2008); Colville v. Pharmacia & Upjohn Co. LLC, 565 F. Supp.2d 1314, 1319 (N.D. Fla. 2008). That should stop, and if the plaintiffs won’t do genetic testing themselves, it’s increasingly feasible for defendants to fill that gap with court-ordered discovery. Each year, more genomic research identifies more genetic markers for drug (and other) reactions that were previously considered idiopathic. Thus, going forward, pharmacogenomics and identification of genetic markers will become increasingly relevant to product liability (and other) litigation. Simultaneously, the cost of genetic sequencing and testing continues to drop dramatically.
For all these reasons the discovery of genetic information should become, for plaintiffs, what ediscovery has been for defendants – only without the exorbitant cost. In ten years it is likely that the submission of genetic samples by plaintiffs will be as commonplace in MDLs as the completion of a preliminary questionnaire is today. Cf. In re Welding Fume Products Liability Litigation, 2006 WL 2505891, at *1 (N.D. Ohio Aug. 28, 2006) (MDL discovery order requiring plaintiff’s counsel to search medical records for “known genetic or familial susceptibility” to the conditions at issue).
Back in 2008, we had a guest post that addressed discovery of genetic information. That post cited Cruz v. Superior Court, 17 Cal. Rptr. 3d 368, 369 (Cal. App. 2004), affirming compelled genetic testing of the plaintiff mother in a birth defect case to determine if the injury was, in fact, a pre-existing genetic condition unrelated to the defendant; and Bowen v. E.I. DuPont de Nemours & Co., 2005 WL 1952859, at *5 (Del. Super. June 23, 2005), aff’d, 906 A.2d 787 (Del. 2006), relying upon compelled genetic testing to exclude as unreliable the plaintiff’s expert witnesses testimony as to non-genetic cause. See also Harris v. Mercy Hospital, 596 N.E.2d 160, 163 (Ill. App. 1992) (although “the blood test may not conclusively determine whether [plaintiff] has a genetic disorder, we conclude that the trial court did not abuse its discretion in ordering . . . the blood test since the probative value of this evidence is outweighed by the potential risk”); Bennett v. Fieser, 1994 WL 542089, at *2 (D. Kan. Feb. 25, 1994) (plaintiff ordered to provide blood sample under Fed. R. Civ. P. 35 for genetic testing); Dodd-Anderson v. Stevens, 1993 WL 273373, at *1 (D. Kan. May 4, 1993) (same).
Looking at the issue anew, we’ve found more cases in which the court has ordered recalcitrant plaintiffs to undergo genetic testing. See Vanslembrouck, 2014 WL 5462596, at *37 (noting trial court order requiring genetic testing); Cutting v. United States, 2008 WL 5064267, at *1 (D. Colo. Nov. 24, 2008) (court ordered genetic testing of plaintiff, but held that Rule 35 did not apply to non-party relatives); see also Kirk v. Schaeffler Group USA, Inc., 2014 WL 2807681, at *3 (W.D. Mo. June 20, 2014) (requiring plaintiff seeking recovery for auto-immune condition to identify “medical providers who provided treatment . . . for autoimmune illnesses or disorders”).
To those, we would also add Johnson v. Superior Court, 95 Cal. Rptr. 2d 864 (Cal. App. 2000), which ordered considerable genetic-related discovery against a non-party witness – albeit not outright testing − an anonymous sperm donor. The rationale in Johnson was:
There may be instances under which a child conceived by artificial insemination may need his or her family’s genetic and medical history for important medical decisions. For example, such genetic and medical history can lead to an early detection of certain diseases and an increased chance of curing them. . . . While in most situations the donor’s genetic and medical information may be furnished without the need of disclosing the donor’s identity, there may be other situations that require disclosure of the donor's identity in order to obtain the needed information.
Id. at 875 (citations omitted). If genetic discovery can be demanded from an third-party who had been promised anonymity, then a fortiori it can be ordered from a plaintiff that initiated the very litigation to which that person’s genetic information is relevant.
Given privacy rights, the question of court-ordered genetic testing of third parties is a dicey one, however, with respect to plaintiffs themselves, we believe that any such interests were surrendered when they chose to file suit – at least insofar as the particular test results are relevant to a claim or defense in the case. For plaintiffs, privacy concerns are addressable by protective orders, and “fishing expedition” arguments manageable by only looking for genetic markers already identified by science as pertinent to the claim to alternative causes. If extraneous results are generated, plaintiffs’ counsel can decide, on a client-by-client basis, whether the client wants to/should know those results. Compared to ediscovery, discovery concerning pharmacogenomics will be much easier, cheaper, and (most importantly) relevant.
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Posted By Bexis to Drug and Device Law at 5/26/2015 10:42:00 AM --
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