Larson v. Abbott Labs., Inc.

KAREN LARSON, as Guardian for KRAIG LARSON v. ABBOTT LABORATORIES, INC.

No. 2260

COURT OF SPECIAL APPEALS OF MARYLAND

September Term, 2016

July 19, 2018

Circuit Court for Baltimore City

Case No. 24C13000002

UNREPORTED

Meredith, Nazarian, Zarnoch, Robert A. (Senior Judge, Specially Assigned), JJ.

Opinion by Zarnoch, J.

*This is an unreported opinion, and it may not be cited in any paper, brief, motion, or other document filed in this Court or any other Maryland Court as either precedent within the rule of stare decisis or as persuasive authority. Md. Rule 1-104.

This appeal arises out of product liability claims involving the prescription biologic, HUMIRA (adalimumab), which was manufactured by Abbott Laboratories, Inc. and is now manufactured by AbbVie, Inc. (collectively "Abbott"). Kraig Larson ("Mr. Larson") -- formerly a highly-educated space engineer -- suffered permanent brain injuries associated with his development of progressive multifocal leukoencephalopathy (PML) a few months after beginning treatment for his psoriasis with HUMIRA. Although Mr. Larson survived, he was left with permanent cognitive impairments, mobility issues, and the inability to care for his basic needs.

Mr. Larson was diagnosed as positive for human immunodeficiency virus ("HIV+") in 2004, but his immune status was considered "well-controlled" until November 2009. Appellant Karen Larson ("Ms. Larson"), Mr. Larson's sister and guardian, brought product liability claims against Abbott, alleging that Mr. Larson's development of PML was caused by Abbott's failure to include adequate warnings of the risks of prescribing it to HIV+ patients. The Circuit Court for Baltimore City (Fletcher-Hill, J.) granted summary judgment in favor of Abbott after finding that Ms. Larson could not prove that HUMIRA was a substantial factor in Mr. Larson's development of PML, and alternatively, that the warning Abbott included was adequate as a matter of law. Ms. Larson timely appealed and asks that we review the following list of issues:

1. Did the trial court err by assuming that Frye-Reed applied even though the causation opinions were not novel?

2. Did the trial court err by excluding the causation opinions of an expert the court described as having "superior training and experience in the field of infections disease, focusedespecially on HIV" and for whom "[t]he court has no reservations about . . . qualifications or with methodology of his theorizing?"¹

3. Did the trial court err by prohibiting Johns Hopkins physicians from opining as to medical causation when they formed their causation opinions during their regular care and treatment of the patient and used ordinary processes?

4. Did the trial court err by prohibiting Plaintiff from proving causation by demonstrating that Plaintiff would not have been injured if the product contained an adequate label?

5. Did the trial court err by ruling that the product label was adequate as a matter of law given that the prescribing physician's knowledge is in dispute?

6. Did the trial court err in granting Defendant's motion to bar the testimony of Plaintiff's causation experts and granting summary judgment?

Paragraphs 1 through 3, however, are resolved by our review of the issues contained in paragraph 6 -- whether the circuit court erred in finding that Abbott was entitled to summary judgment based on the inadmissibility of Ms. Larson's expert causation witnesses. Without sufficient evidence that Mr. Larson's use of HUMIRA was a proximate cause of his development of PML, Ms. Larson could not prevail on any of her claims. Accordingly, if the circuit court's decision with respect to the inadmissibility of Ms. Larson's causation experts is correct, we need not answer the questions contained inparagraphs 4 and 5, related to whether Abbott's warnings were adequate as a matter of law, or whether the question of proximate causation was for the finder of fact.

BACKGROUND & PROCEDURAL HISTORY

History of Mr. Larson's Medical Treatment Prior to PML Diagnosis

In early 2009, Mr. Larson was a thirty-nine year old space engineer working at NASA's Goddard Space Flight Center. After he was diagnosed as HIV+ in 2004 until the spring of 2010, Mr. Larson's HIV condition and immune health was monitored by infectious disease specialist Dr. Ellen Yang, M.D. at Annapolis Infectious Disease Associates, LLP ("AIDA"). For the first five years after his diagnosis, his HIV condition remained "well-controlled," as indicated by blood tests monitoring his level of "T cells" or "CD4 count" and viral load.²

Mr. Larson also suffered from the inflammatory skin condition, plaque psoriasis, since 1995. Psoriasis is a genetic, immunological disorder in which "the cytokines that regulate function in the skin are abnormal," and typically manifests as red or scaly patches of skin. For several years, Mr. Larson treated his psoriasis with at-home remedies, but he eventually found his condition to be unmanageable and sought treatment with dermatologists. In 2007, he began seeing physician's assistant Julie Catlin, P.A. ("Ms. Catlin"). Mr. Larson tried prescription treatments for his psoriasis, such as topical corticosteroids, UVB therapy, and laser therapy, but he was not satisfied with his progress.At a routine infectious disease appointment in October 2009, Dr. Yang noted that Mr. Larson's plaque psoriasis had worsened since his last visit in March 2009. Dr. Yang informed him that his HIV appeared asymptomatic, but she had not yet received his lab results to evaluate his CD4 count and viral load.

In November 2009, after researching other psoriasis treatments, Mr. Larson asked Ms. Catlin about treatment with HUMIRA. Because Ms. Catlin did not have experience prescribing biologics to HIV+ patients, but believed it could be used in some circumstances, she agreed to look into a referral. On November 24, 2009, at a lunch meeting with two Abbott sales representatives at her office, Ms. Catlin asked the representatives to recommend a dermatologist that treated HIV+ patients with HUMIRA. The representatives recommended Monte S. Meltzer, M.D., who was the director of the dermatology clinic at Union Memorial Health Services, Inc. ("Union Memorial") and maintained a private practice -- Monte S. Meltzer, M.D., LLC.³

The representatives also arranged for Ms. Catlin to receive a Medical Information Letter ("Letter") from Abbott's medical department containing information about prescribing HUMIRA to HIV+ patients. The Letter, dated November 24, 2009, said, in pertinent part, the following:

Our representative, Laura Rose, has informed us of your request. We are responding to your inquiry regardingHumira® (adalimumab, Abbott) and use in patients with concomitant [HIV].

Abbott has not specifically evaluated the safety or efficacy of adalimumab therapy in patients with comorbid [HIV] infection. The effect of adalimumab therapy, if any, on HIV is unknown. [ . . . ] [P]atients with a known history of HIV infection were excluded from participating in the adalimumab clinical trials . . . . [ . . . ]

The possibility exists for tumor necrosis factor (TNF) blocking agents, including adalimumab, to affect host defenses against infections since TNF mediates inflammation and modulates cellular immune responses. The impact of treatment with adalimumab on the development and course of chronic infections is not fully understood.

* * *

Very limited data suggest that the use of TNF blockers in patients with well-controlled HIV infection, who are not severely immunocompromised, does not appear to exacerbate HIV viral load or adversely [a]ffect CD₄ cell counts.

* * *

MONITORING AND PATIENT MANAGEMENT

Since the safety and efficacy of TNF blockers in patients with comorbid HIV infection has not been established, recommendations regarding specific monitoring parameters of HIV such as CD₄ cell count or viral load are not available. Such monitoring is at the discretion of the healthcare professional. Since the potential exists for TNF blocker therapy to reactivate HIV replication and induce opportunistic infections, suppression of HIV with antiretroviral therapy prior to initiation of TNF blockers and close monitoring of clinical and laboratory parameters by physicians knowledgeable in HIV management is recommended in the published literature.

(Endnotes omitted). The Letter also described a "retrospective, open-label case series," which examined the safety of the use of "TNF blocker therapy . . . in 8 HIV-1 infected patients with various rheumatic conditions." According to the letter, because "TNF blockertherapy was generally well-tolerated and did not adversely [a]ffect HIV viral load or CD₄ cell count," the results of the case series suggested that,

if a patient's HIV infection is controlled and they are not severely immunocompromised (CD₄ count of >200 mm³ and HIV viral load of <60,000 copies/mm³ ), TNF blocker therapy may be administered with a reasonable ratio of benefits to risks profile in patients refractory to standard therapy for rheumatic diseases.

Abbott's medical department did not send the letter to Dr. Meltzer.

On December 10, 2009, Ms. Catlin referred Mr. Larson to Dr. Meltzer based on the information she received from Abbott. Dr. Meltzer saw Mr. Larson on January 6, 2010 at his private practice and diagnosed him with moderate-to-severe plaque psoriasis. Mr. Larson told Dr. Meltzer that he was HIV+, the status of his HIV was "well-controlled," he was not on HAART, and he was being monitored by an infectious disease doctor. Dr. Meltzer reviewed Mr. Larson's medication list and observed that "he wasn't on [HAART] therapy and he wasn't on antibiotic prophylaxis for opportunistic infection." He did not ask for the name of Mr. Larson's infectious disease doctor, attempt to consult with Dr. Yang, or look into other information related to the state of Mr. Larson's HIV. He did, however, perform a tuberculosis skin test, as recommended by the prescribing information. Dr. Meltzer then prescribed HUMIRA.

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