Philadelphia Inquirer<\/font><\/strong>
by David Sell
September 20, 2012<\/div>\n
<\/p>\n
The plaintiff is a 17-year-old boy from Sherman, Tex. He was prescribed Risperdal and began taking it when he was five years old. He began growing breasts when he was 12. Jury selection began Thursday, with the trial scheduled to begin Monday. This the second of a string of Risperdal cases filed by Philadelphia attorneys Stephen Sheller and Brian McCormick in which they hoped to put Gorsky on the stand.<\/p>\n
The first one was to begin on Sept. 10. In that one, a 21-year-old man, prescribed Risperdal as a child, had to have a double mastectomy in which tissue was suctioned out of the breast he grew. With a jury waiting, J&J settled with the man rather than have a judge potentially rule that Gorsky must testify. In the second case, the J&J defense team, led by Drinker Biddle attorney Kenneth Murphy, had argued that the subpoena for Gorsky to testify should be quashed because Gorsky was scheduled to be in Asia on business. In support of the motion to quash, defense attorneys submitted an affidavit from Gorsky’s administrative assistant, who outlined his travel plans.<\/p>\n
Gorsky was ordered to sit for a deposition in May. The transcript of that deposition is here<\/font><\/u><\/a><\/strong>. J&J faces hundreds of individual suits over its marketing practices related to Risperdal. So far, at least, it is also on the losing side of multi-million judgments in state-led Medicaid cases in Louisiana, South Carolina and Arkansas. It paid $158 million to stop a trial in Texas. The company is also negotiating with the federal government in a separate case that might involve payments of $2 billion.<\/sup><\/div>\n<\/blockquote>\n Given that we won’t be hearing from Gorsky directly, I thought I’d extract a piece from his deposition that is the kind of thing I’d like to hear from him directly on the witness stand. This is a case of gynocomastia [breast growth] in a teenaged boy who was put on Risperdal at 5 years old [somewhere about 2000+<\/u>]. In the first part, Gorsky is questioned about an email he sent out suggesting that they accentuate the positives and defend against the negatives. Case in point – elevations in Prolactin levels. It follows a discussion of meeting minutes in 1998 about Prolactin elevations in which they conclude they don’t need any further study[reference<\/font><\/strong><\/u><\/a>]<\/sub>. It’s too long to quote and too evasive to follow: <\/p>\n <\/p>\n <\/p>\n\n
Q. Do you see that on January 20th, 2001 you sent an email to a number of individuals at Janssen US and Janssen Belgium, including Ivo Caers, Janet Vergis, Ludwig Hantson and Ramy Mahmoud?
A. Yes, I did.
Q. And the subject line is "Competitive Activity"?
A. Yes, it is.
Q. And does this email concern Risperdal and competition from other antipsychotics?
A. Yes, it covers my thoughts around our clinical developments programs.
Q. If we turn to page two of the document, which is a continuation of your email, looking at the third bullet point where you say "While we cannot respond to each and every competitive jab…we should expect that we will be challenged on a number of fronts due to our market position…therefore we need to be proactive in expanding on our strengths (efficacy long and short term, agitation, weight gain, etc) and defending our weak spots (prolactin, QTc, EPS)" and then an elliptical or ellipsis. Do you see – did I read that correctly?
A. Yes, you did read that correctly.
Q. And in here you identify prolactin as one of Risperdal’s weak spots, correct?
A. Identified it as one of our weak spots relative to our competitors and our positioning in the marketplace at the time.
Q. In January of 2001, Mr. Gorsky, you would have still been vice-president of sales and marketing for Janssen US. Is that correct?
A. Yes, that’s correct.
Q. And even then you knew that prolactin was a weak spot for Risperdal. Is that correct?
A. I believe what I was referring to at that time, there was a major promotional battle taking place between the various antipsychotics and their relative positioning, and this was the way that the — the result of what our competitors were saying and information in the marketplace. So yes, that was generally, I think, an accepted point of view, as I put in the paragraph.
Q. And what was a generally accepted point of view?
A. Regarding the relative strengths and weaknesses. I don’t think it was necessarily based — it was based on perceptions that had been developed over the previous years.
Q. Well, Risperdal caused prolactin to be more elevated than other antipsychotics, right?
MR. MURPHY: Objection to the form. You may answer.
THE WITNESS: While I was working on the brand, I don’t remember that ever being concluded with statistically significant data.<\/sup><\/div>\n<\/blockquote>\n\n
Q. And the title of that is "Double-blind evaluation of Risperidone versus haloperidol on the long-term morbidity of early psychotic patients." Do you see that?
A. Yes.
Q. The date is May 17th, 2002 in the top left-hand corner?
A. Yes
…
Q. And then next under that they say there was a statistically significant difference between the treatment groups and the number of patients with prolactin-related adverse events, too. Is that correct?
A. That’s correct.
Q. And what was the percentage of prolactin-related adverse events for Risperdal?
A. It says five percent.
Q. And what was it for haloperidol?
A. 0.4 percent.
Q. So, let’s turn back to page 8779, please. Do you see in the middle there 3.1.3, it has "Prolactin-related adverse events"?
A. Yes, I do.
Q. And then it has the same percentages down there in the third or fourth row, the total number of patients with prolactin-related AEs? It has five percent for risperidone and 0.4 for Haloperidol?
A. Yes, it does.
Q. And that’s fourteen patients out of 278 had prolactin-related adverse events in this clinical trial. Is that right?
A. That’s correct.<\/sup><\/div>\n<\/blockquote>\n\n
Hyperprolactinemia
As with other drugs that antagonize dopamine D2 receptors, risperidone elevates prolactin levels and the elevation persists during chronic administration. Tissue culture experiments indicate that approximately one-third of human breast cancers are prolactin dependent in vitro, a factor of potential importance if the prescription of these drugs is contemplated in a patient with previously detected breast cancer. Although disturbances such as galactorrhea, amenorrhea, gynecomastia, and impotence have been reported with prolactin-elevating compounds, the clinical significance of elevated serum prolactin levels is unknown for most patients.<\/font><\/strong> As is common with compounds which increase prolactin release, an increase in pituitary gland, mammary gland, and pancreatic islet cell hyperplasia and\/or neoplasia was observed in the risperidone carcinogenicity studies conducted in mice and rats. However, neither clinical studies nor epidemiologic studies conducted to date have shown an association between chronic administration of this class of drugs and tumorigenesis in humans; the available evidence is considered too limited to be conclusive at this time.<\/sup><\/div>\n<\/blockquote>\n\n
5.6 Hyperprolactinemia <\/font><\/strong>
As with other drugs that antagonize dopamine D2 receptors, RISPERDAL elevates prolactin levels and the elevation persists during chronic administration.<\/font> RISPERDAL® is associated with higher levels of prolactin elevation than other antipsychotic agents.<\/font><\/strong> Hyperprolactinemia may suppress hypothalamic GnRH, resulting in reduced pituitary gonadotropin secretion. This, in turn, may inhibit reproductive function by impairing gonadal steroidogenesis in both female and male patients. Galactorrhea, amenorrhea, gynecomastia, and impotence have been reported in patients receiving prolactin-elevating compounds. Long-standing hyperprolactinemia when associated with hypogonadism may lead to decreased bone density in both female and male subjects.<\/font><\/strong><\/sup><\/div>\n
Hyperprolactinemia, Growth, and Sexual Maturation<\/font><\/strong>
RISPERDAL® has been shown to elevate prolactin levels in children and adolescents as well as in adults [see Warnings and Precautions (5.6)]. In double-blind, placebo-controlled studies of up to 8 weeks duration in children and adolescents (aged 5 to 17 years) with autistic disorder or psychiatric disorders other than autistic disorder, schizophrenia, or bipolar mania, 49% of patients who received RISPERDAL® had elevated prolactin levels compared to 2% of patients who received placebo. Similarly, in placebo-controlled trials in children and adolescents (aged 10 to 17 years) with bipolar disorder, or adolescents (aged 13 to 17 years) with schizophrenia, 82–87% of patients who received RISPERDAL® had elevated levels of prolactin compared to 3-7% of patients on placebo.<\/font><\/strong> Increases were dose-dependent and generally greater in females than in males across indications. In clinical trials in 1885 children and adolescents, galactorrhea was reported in 0.8% of RISPERDAL®-treated patients and gynecomastia was reported in 2.3% of RISPERDAL®-treated patients.<\/font><\/strong><\/sup><\/div>\n<\/blockquote>\nto know it<\/strike> it known].<\/div>\n![](\"http:\/\/1boringoldman.com\/images\/ssri-3.gif\")
<\/div>\n
\n\n