We write this as key elements of the Drug and Device Law Passover Feast languish in the oven. Tomorrow, the Drug and Device Law Bubbie will force four generations of our family – the devout and the not and everyone in between – to read (aloud) the lengthy prayer service that precedes the meal. The ritual includes much laughter, enthusiastic (if discordant) singing, and predicable misbehavior from those of us at the “kids’ table” (the 50- and 60-year-olds, as distinguished from our parents) that provokes sharp rebukes from the elders. And, these days, the gathering is a little bit bittersweet (cue “Sunrise, Sunset”), as time’s toll on the eldest members of the clan is softened by the presence, each year, of more of our babies’ babies. We complain about the cooking. We grouse about the most troublesome relatives. But we wouldn’t miss it for the world, though we should mention that “feast” is something of a misnomer, as many Passover staples are notorious for barely crossing the line into “palatable.”
Speaking of misnomers, earlier this week, one of our co-bloggers termed causation the “MVP” of mass tort practice. While we heartily agree in principle, we have read (and participated in) too many scenarios in which a passive judge “benched” this “player” to allow meritless cases to queue up in settlement inventories. On the flip side, we are heartened by the increase in Lone Pine orders demanding early causation evidence and by judges who refuse to allow plaintiffs lacking proof of causation to escape summary judgment.
Such was the result of today’s case, a Risperdal case out of the Northern District of Alabama. In Drake v. Ortho-McNeil-Janssen Pharms., 2018 U.S. Dist. LEXIS 47164 (N.D. Ala. Mar. 22, 2018), the plaintiff was an obese 36-year-old man who was diagnosed as schizophrenic at age 17. He was initially prescribed Risperdal but was switched to other drugs several months later. He was switched back to Risperdal about two years after that and then remained on the drug for about thirteen years before different drugs were again substituted.
Shortly after the plaintiff stopped taking Risperdal, a social worker noticed that he had large breasts and told his mother that he should be tested for gynecomastia, benign enlargement of glandular breast tissue in males. Antipsychotic medications have been associated with gynecomastia, which “is distinct from pseudo-gynecomastia, which is breast enlargement due to fat deposits in overweight males. The two conditions may be differentiated only with a physical exam.” Drake, 2018 U.S. Dist. LEXIS 47164 at *4. No exam took place. The plaintiff was never diagnosed with gynecomastia, though his levels of prolactin were elevated. Proclactin is a hormone that induces lactation, but it “does not have a direct grown-stimulating effect on the breast glandular tissue.” Id. at *6 (citation omitted). Many of the drugs prescribed to the plaintiff were known to cause prolactin elevation.
The plaintiff’s complaint, asserting all of the usual causes of action, alleged that Risperdal caused him to develop gynecomastia. The defendant moved for summary judgement, arguing that the plaintiff could not meet his burden of establishing causation. The judge emphasized that the plaintiff was required to prove both general and specific causation and that expert testimony was required for both. The plaintiff’s expert was a certain former FDA commissioner who has testified that the risk of gynecomastia in children and adolescents was higher than Risperdal’s labeling represented. But, as the court pointed out, while the expert’s “report and deposition testimony from other cases might be sufficient to raise a question of fact regarding general causation, . . . his report and testimony contain[ed] no evidence regarding the cause of [the plaintiff’s] alleged injuries. Id. at *13. And the plaintiff had no other causation expert.
As such, as the court put it, “the plaintiff’s evidence concerning specific causation [was] threadbare.” Id. There was no evidence that the plaintiff had even been diagnosed with gynecomastia. And while the plaintiff argued that, if his elevated prolactin level had caused “testosterone level drops leading to estrogen expression,” then Risperdal could “theoretically [have caused] gynecomastia,” there was “no evidence in the record regarding [the plaintiff’s] testosterone or estrogen levels, and evidence that Risperdal could theoretically cause gynecomastia [was] not sufficient to raise a disputed issue of material fact concerning specific causation.” Id. The court concluded, “In the absence of medical or expert evidence, a fact finder must speculate about the cause of [the plaintiff’s] enlarged breasts, and a verdict may not rest on speculation.” Id.
In other words, maybes on top of maybes do not proof of causation make. If the plaintiff cannot be bothered to get a diagnosis or an expert, that plaintiff should not be in court. Unassailable, although we’ve all seen too many such “easy” decisions go wrong. We like this case. We will continue to keep you posted on the good and the bad, and we wish happy gatherings to all celebrating any holiday this week.