MINDY MICHAELS ROTH, Special Master.
On September 29, 2014, C.P. ("petitioner") timely filed a petition for compensation under the National Vaccine Injury Compensation Program, 42 U.S.C. § 300aa-10, et seq.
Many of the facts relevant to this case are undisputed. The parties agree that petitioner was diagnosed with PMR months after his influenza vaccination and that he was subsequently diagnosed with seronegative RA. The issues in dispute are whether the flu vaccine can cause and/or trigger PMR and/or seronegative RA, whether it did so in this case, and whether the timing is medically appropriate.
An entitlement hearing was held on December 11-12, 2017 in Washington, D.C. Petitioner failed to meet his burden to show, by a preponderance of evidence, that it was more likely than not that he developed PMR and/or RA as a result of receiving the flu vaccine. For the reasons detailed below, I find that petitioner is not entitled to compensation.
Petitioner filed his petition on September 29, 2014. Petition, ECF No. 1. This case was initially assigned to Special Master Hamilton-Fieldman on September 29, 2014 and was reassigned to me on January 14, 2016. ECF Nos. 4, 32.
Petitioner filed several medical records on October 2, 2014 and a Statement of Completion on October 3, 2014. Petitioner's Exhibits ("Pet. Ex.") 1-18, ECF Nos. 6-9. Respondent filed a status report on November 24, 2014, advising that he had reviewed the medical records that were filed and determined the records to be sufficient to complete his Rule 4(c) Report. Respondent's Status Report ("Resp. S.R.") at 1, ECF No. 13.
On December 29, 2014, respondent filed his Rule 4(c) Report which contained a detailed review of petitioner's medical history. Respondent's Report at 1-8, ECF No. 14. Respondent stated that petitioner failed to provide evidence that he suffered PMR or RA as a result of the flu vaccine. Id. at 10. Respondent noted that in May 2013, petitioner's primary care physician recommended that petitioner receive a flu shot in the fall of that year. Id. Respondent reasoned that this suggested petitioner's primary care physician did not associate petitioner's PMR and/or RA with the flu vaccine. Id. (citing Pet. Ex. 2 at 2-3). Respondent argued petitioner was not entitled to compensation based on his medical records and that without more proof, petitioner's claim should be dismissed. Id. Petitioner filed a response to respondent's Rule 4(c) Report on January 7, 2015. Response, ECF No. 15.
A status conference was held on January 21, 2015, after which petitioner was ordered to file an expert report by March 25, 2015. Order, ECF No. 16. After three extensions of time, petitioner filed an expert report from Dr. Kristin Gowin, a rheumatologist, along with supporting medical literature on July 27, 2015. Pet. Ex. 20-21, ECF No. 25. Respondent filed a responsive expert report authored by Dr. Mehrdad Matloubian, an immunologist and rheumatologist, on November 3, 2015 and supporting medical literature on November 13, 2015. Respondent's Exhibit ("Resp. Ex.") A1-A17, ECF Nos. 28-30.
A status conference was held on November 19, 2015 during which Special Master Hamilton-Fieldman requested that, if petitioner decided to file a supplemental expert report, the expert address the triggering action in this case, the homology of RA, the nature of petitioner's pre-clinical RA, and the issues outlined in respondent's Rule 4(c) Report. Order, ECF No. 30. Petitioner was ordered to file either a supplemental expert report or a status report by January 22, 2016. Id. This case was reassigned to me on January 14, 2016. ECF No. 32.
After an extension of time, petitioner filed a supplemental expert report from Dr. Gowin and an expert report with supporting literature from Dr. Michael Gurish, an immunologist, on February 5, 2016. Pet. Ex. 22-24, ECF No. 35. Respondent filed a responsive expert report from Dr. Matloubian and supporting medical literature, on May 4, 2016. Resp. Ex. C1-14, ECF No. 38-40.
A status conference was held on June 30, 2016, during which petitioner advised he intended to file an additional responsive expert report. Order, ECF No. 41. The parties also discussed scheduling an entitlement hearing for October or November 2017. Id. Petitioner was ordered to file a responsive expert report by August 1, 2016, and a joint status report proposing entitlement hearing dates by August 29, 2016. Id.
On August 29, 2016, petitioner filed a joint status report proposing entitlement hearing dates. Joint S.R., ECF No. 43. An entitlement hearing was scheduled for October 2 and 3, 2017. Prehearing Order, ECF No. 44.
After three extensions of time, petitioner filed a supplemental expert report from Dr. Gurish on October 13, 2016. Pet. Ex. 25, ECF No. 47. Petitioner filed additional medical records on February 8, 2017. Pet. Ex. 26-32, ECF No. 49.
On August 7, 2017, the entitlement hearing was rescheduled for December 11 and 12, 2017. Pre-Hearing Order, ECF No. 50. On October 13, 2017, petitioner filed updated medical records. Pet. Ex. 33-40, ECF No. 51. Petitioner filed his prehearing brief on October 16, 2017, and additional medical literature on November 6, 2017. Prehearing Submission, ECF No. 53; Pet. Ex. 41-44, ECF No. 56.
Respondent filed his prehearing brief and additional medical literature on November 9, 2017. Prehearing Submission, ECF No. 58; Resp. Ex. D-J, ECF No. 59. Petitioner filed a response to respondent's prehearing brief on November 20, 2017. Response, ECF No. 60. The parties filed their joint prehearing submission on December 4, 2017. ECF No. 63. A prehearing status conference was held on December 5, 2017, during which the parties discussed the logistics of the entitlement hearing. Order, ECF No. 64.
An entitlement hearing was held on December 11 and 12, 2017. Order, ECF No. 69. Dr. Gowin and Dr. Gurish testified on behalf of petitioner and Dr. Matloubian testified on behalf of respondent. Id. Petitioner's co-counsel appeared via video conference from California, along with petitioner, C.P., and his wife, [REDACTED/], who also testified at the hearing. Id. At the conclusion of the hearing, petitioner was ordered to file all pharmacy records from 2010 through 2012, all rheumatology records since March 2017, and all records related to petitioner's November 2017 back surgery, by March 12, 2018. Id. Respondent was ordered to file an article referenced by Dr. Matloubian during the hearing that discussed the effect of trauma on the autoimmune system by March 12, 2018. Id.
Petitioner filed some of the requested medical records on February 27, 2018, and March 8, 2018. See Pet. Ex. 45-50, ECF Nos. 74, 77. On March 12, 2018, petitioner filed a status report advising he needed additional time to obtain the remaining outstanding medical records. Pet. S.R., ECF No. 79. Petitioner was ordered to file all outstanding records, along with a status report advising that the record was complete, by April 16, 2018. Order at 1, ECF No. 80. On March 14, 2018, petitioner filed the outstanding records and a status report advising that the record was complete. See Pet. Ex. 51, ECF No. 81; Pet. S.R. at 1, ECF No. 83. The parties were ordered to file their post-hearing briefs by May 14, 2018. Non-PDF Order, dated March 14, 2018. Petitioner and respondent filed their post-hearing briefs on June 20, 2018. See ECF Nos. 86-87.
This matter is now ripe for determination.
Petitioner was born on August 22, 1956. Petitioner has a complicated medical history both before and after his vaccination which includes type II diabetes, hypertension, high cholesterol, neck pain, tendonitis of the left shoulder, left arm pain, torn rotator cuff of the right shoulder, chronic lower back pain with sciatic pain, numbness and weakness in his legs, hip pain, two arthroscopic surgeries of the left knee, total left knee replacement with resulting deep vein thrombosis ("DVT"), left foot surgery, neuropathic pain, and diabetic neuropathy. See generally Pet. Ex. 12-13, 29, 36-38, 40. Over the years, petitioner has undergone chiropractic care, physical therapy, acupuncture and pain management, and received multiple pain injections and pain blocks for his lower back and hip pain. Id. He is under the routine care of an ophthalmologist due to his diabetes. See generally Pet. Ex. 31. Both petitioner and his wife stated that petitioner was in relatively good health prior to his vaccine and remained physically active due to his physically demanding job as a maintenance worker for a school district. Tr. 6, 27-28; Pet. Ex. 17 at 1; Pet. Ex. 19 at 1. While all of petitioner's medical records were reviewed in this matter, only his relevant medical history is discussed below.
On February 6, 2009, petitioner fell from a ladder onto his left leg while at work as a maintenance worker for his city's school district. Tr. 6; Pet. Ex. 3 at 40-48. An MRI of his left leg revealed a medial meniscus tear of his left knee. Pet. Ex. 3 at 40. Following a course of physical therapy, petitioner underwent arthroscopic surgery of the left knee on June 11, 2009. Id. Petitioner filed a workers' compensation claim following his fall from the ladder. Tr. 24.
In the months following petitioner's left knee surgery, he presented multiple times to his primary care physician ("PCP") and orthopedist with continued complaints of worsening knee pain. See Pet. Ex. 3 at 32-38, 40-48.
On August 6, 2010, petitioner presented to his PCP with complaints of ongoing left knee pain as well as lower back pain. Pet. Ex. 2 at 25. He had recently been diagnosed with diabetes and was taking Metformin to control his diabetes along with cholesterol and blood pressure medication. Id. Due to his continued knee pain, he had been receiving joint injections and a total knee replacement surgery was discussed. Id. An MRI performed in September 2010 revealed a medial meniscus tear, so petitioner's total left knee replacement was scheduled for May 2011. Pet. Ex. 3 at 27. Petitioner's workers' compensation case was reopened in March 2011 due to his progressively worsening knee injury. Id. at 32.
A total left knee replacement was performed on May 27, 2011.
On June 21, 2011, petitioner was admitted to Huntington Hospital with complaints of weakness and pain in his left leg. Pet. Ex. 5 at 41-43; Pet. Ex. 13 at 77. He had developed deep vein thrombosis ("DVT")
On June 30, 2011, petitioner presented to his orthopedist, Dr. Dietrick, for follow up of his left knee replacement and DVT surgery. Pet. Ex. 3 at 2-3. He was taking narcotics for pain management and remained unable to return to work. Id. at 3.
On July 25, 2011, Dr. Dietrick issued a report regarding petitioner's work-related left knee injury. Pet. Ex. 6 at 34-37. The report stated that following a fall from a ladder in 2009, petitioner was diagnosed with osteoarthritis, effusion, and probable loose body. Id. at 34. He underwent a total knee replacement for his degenerative arthritic condition on May 27, 2011 and his post-operative course was complicated by a blood clot the following month. Id. Petitioner had also developed sciatic pain in his lower back after surgery for which he received two epidural injections and was prescribed Dilaudid and Percocet for pain management. Id.
From July to September 2011, petitioner presented to his primary care physician and Dr. Dietrick for follow up of his left knee and DVT surgeries. See Pet. Ex. 2 at 19; Pet. Ex. 6 at 32-33. At these visits, petitioner continued to complain of sciatica
On October 14, 2011, petitioner presented to his PCP with complaints of right thigh burning, tingling, and numbness that had persisted for approximately one month. Tr. 8; Pet. Ex. 2 at 16; Pet. Ex. 17 at 1. He was diagnosed with entrapment of the lateral cutaneous nerve of the thigh and given Voltaren
On October 28, 2011, petitioner presented to Dr. Dietrick for follow up of his left knee replacement. Pet. Ex. 6 at 28. Petitioner was still experiencing numbness and constant pain in his left knee. Id. He was noted to walk with an antalgic gait favoring his left leg. Id. Dr. Dietrick reported no nerve root tension signs in the left leg but noted atrophy and tenderness on the lateral patella facets with slight lateral tracking of the patellofemoral joint. Id. Dr. Dietrick recommended that petitioner attend physical therapy. Id. at 29.
Petitioner and his wife testified that in late November 2011, petitioner began experiencing progressive weakness, fatigue, and aches in his shoulders, groin, and back. Tr. 8, 28-29. Petitioner attributed these symptoms to his recent return to work, stating "I was dreading going back to work because I had the major muscle issues . . . It was really hard just getting up and getting started . . . I did physical labor, manual labor, I climbed ladders and everything. It was a killer." Tr. 8-9. Petitioner's wife added he had never complained that way prior to the flu vaccine. Tr. 29; Pet. Ex. 19 at 1-2.
Petitioner returned to Dr. Dietrick on December 7, 2011 with complaints of continued knee pain, popping, stabbing, and numbness. Pet. Ex. 6 at 26. He reported no improvement with physical therapy and at-home exercises. Id. Dr. Dietrick advised petitioner to continue with physical therapy but if his pain and discomfort continued, possible arthroscopic surgery or a lateral patellar facetectomy would be considered. Id. at 26-27. Petitioner made no additional complaints at this visit. However, he testified that he was experiencing shoulder and hip pain at this visit and at the October 28, 2011 visit but did not mention it to Dr. Dietrick because he was only treating with Dr. Dietrick for his knee. Tr. 24-25.
Petitioner's wife recalled that petitioner called her on December 9, 2011 while she was at work and told her he thought he had the flu. Pet. Ex. 19 at 2. On December 10, 2011, petitioner continued to feel poorly but accompanied her to her employer's holiday party. Id. Petitioner was typically very social at these events, but Mrs. [REDACTED/] remembered that petitioner was very quiet at this event; he sat in a corner for most of the event and then left early to go to bed. Id.; Tr. 32. Petitioner recalled that he had difficulty walking at this event. Pet. Ex. 17 at 2.
While petitioner stated that he had returned to work in November, Mrs. [REDACTED/] testified that he returned to work in mid-December and worked through the pain until the school district's Christmas break began. Pet. Ex. 19 at 2-3. She remembered him having difficulty sleeping and being very anxious about working in pain. Id. at 3. Mrs. [REDACTED/] stated that petitioner was unable to attend a New Year's Eve party and a family wedding in January 2012 due to his pain and discomfort. Id.
Petitioner returned to his PCP on December 29, 2011 with complaints of continued right leg numbness and progressive pain in his legs, shoulders, and groin. Pet. Ex. 2 at 13. He reported that the Voltaren was not working to relieve his pain and discomfort. Id. He was noted to have normal range of motion in his upper and lower extremities and diffuse pain over both shoulders and thighs. Id. His PCP questioned whether petitioner's myalgias
Petitioner completed a form entitled "History of Work Related Accident/Injury" on January 2, 2012 in which he indicated he had aches and pains outside and in the rear of his left knee, tenderness on the outside and front of the knee, and sharp, stabbing pain on the outside and back of the left knee. Pet. Ex. 6 at 49. No other complaints were reported. See id. Petitioner testified that he was experiencing PMR-like symptoms at this time but he did not include those symptoms on this form. Tr. 25.
On January 16, 2012, petitioner presented to Dr. O'Connor, a rheumatologist, with complaints of bilateral shoulder pain, hip pain, stiffness, and low energy which he reported he had been experiencing since December 2011. Pet. Ex. 7 at 65. His family history was significant for diabetes, hypertension, and myasthenia gravis. Id. 65-66. Petitioner had a history of alcohol use but quit drinking in 2011. Id. at 66. Petitioner had previously been given a Medrol dose pack
On January 20, 2012, petitioner returned to Dr. Dietrick reporting that he had tried to return to work but the squatting, kneeling, and climbing ladders and stairs had caused a flare up of his knee pain. Pet. Ex. 6 at 24. He rated his current knee pain as 5-/8/10 and noted his knee pain had actually worsened before he had returned to work. Id. Dr. Dietrick's assessment of petitioner's condition was lateral retinacular left knee pain, status post-knee replacement, left knee synovitis with overuse, and IT band syndrome. Id. Dr. Dietrick recommended that petitioner modify his job duties as he had "overdone it." Id. at 25. Petitioner made no complaints of hip or shoulder pain or stiffness during this examination and Dr. Dietrick's examination revealed normal hip range of motion. Id. at 24-25.
On February 6, 2012, petitioner returned to Dr. O'Connor reporting his symptoms were alleviated by prednisone but advising he continued to have osteoarthritic pain in his shoulders. Pet. Ex. 7 at 62. Bloodwork revealed an elevated C-reactive protein ("CRP")
Petitioner presented for a CT scan of his left knee and follow up with Dr. Dietrick on February 27, 2012. Pet. Ex. 6 at 22-23. Due to petitioner's continued complaints of left knee pain, Dr. Dietrick requested the disc of the CT scan to review it to determine if rotation of petitioner's knee implant was the cause. Id. at 23.
On March 1, 2012, petitioner returned to Dr. O'Connor. Pet. Ex. 7 at 59. It was noted that at his February 2012 visit, prednisone had been tapered to 15 mg per day and Mobic
On March 14, 2012, petitioner returned to Dr. Dietrick reporting continued numbness and stabbing pain on the outside of his knee with sharp and aching pain in the front and back of his knee. Pet. Ex. 6 at 20. Dr. Dietrick discussed his review of the CT scan as showing mild internal rotation of the femoral component only, with lateral subluxation of the patella. Id. at 21. Dr. Dietrick suggested left arthroscopy and debridement with possible lateral retinacular release and lateral patellar facetectomy. Id.
Petitioner recalled that during this time, he developed pain in his wrists, hands, feet, and toes that was different from his PMR symptoms. Tr. 10. He described constant aching and tingling in his bones and specifically remembered that in March 2012, his hands were so stiff when he woke up in the morning that he was unable to make a fist. Tr. 11.
On April 5, 2012, petitioner returned to Dr. O'Connor reporting he had decreased his prednisone usage to 10 mg per day was feeling better and believed the methotrexate was unnecessary. Pet. Ex. 7 at 56. Upon examination, Dr. O'Connor noted no joint deformity, heat, swelling, erythema, or effusion of the hands and no edema or cyanosis in petitioner's extremities. Id. at 57. Petitioner's seronegative RA was noted to be stable and he was advised to taper his prednisone usage to 5 mg per day for one week and then discontinue use completely. Id. at 58.
On April 30, 2012, petitioner presented to Dr. Dietrick for pre-operative examination for lateral patellofemoral compression syndrome. Pet. Ex. 6 at 18. Dr. Dietrick recommended arthroscopic debridement and lateral release in addition to lateral patellar facet patelloplasty, rather than full revision. Id. at 19.
On May 2, 2012, petitioner presented to Dr. Wallace, a rheumatologist, for a second opinion. Pet. Ex. 10 at 13. He reported being in good health until the previous year when he underwent a routine left knee replacement that was immediately followed by the development of acute sciatica and a blood clot that required petitioner to take anticoagulants. Id. Petitioner reported that in December 2012, he had a sudden onset of achiness in his upper back and neck and "could not move." Id. He reported that his bloodwork in January 2012 revealed an elevated ESR level
Petitioner underwent total knee arthroplasty for patellofemoral malalignment and lateral plica on May 7, 2012. Pet. Ex. 6 at 38-40.
Petitioner returned to Dr. Dietrick and his PCP three times over the following months for follow up of his left knee surgery. Pet. Ex. 6 at 14-16; Pet. Ex. 7 at 53. He reported persistent knee pain that was relieved by increasing his prednisone dosage to 15 mg per day. Pet. Ex. 7 at 53. He remained out of work due to knee pain. Pet. Ex. 6 at 14-15.
On July 12, 2012, petitioner returned to Dr. O'Connor with continued PMR complaints. Pet. Ex. 7 at 50. Petitioner had been taking methotrexate and prednisone. Id. He reported his symptoms worsened when he tapered the prednisone dosage to 5 mg per day, so he increased the dose to 10 mg per day. Id. Dr. O'Connor noted that petitioner's recent ESR and CRP levels were normal and there was no joint symptoms or inflammatory synovitis present. Id. Petitioner was still out of work due to his ongoing knee pain. Id. Dr. O'Connor directed petitioner to taper his prednisone dosage and remain on the methotrexate. Id. at 51.
On July 25, 2012, petitioner returned to Dr. Dietrick reporting no change or improvement in his left knee. Pet. Ex. 6 at 12. Dr. Dietrick documented that petitioner had not yet reached maximum medical improvement in his knee. Id. He advised petitioner it was unlikely that petitioner could ever return to his current occupation and job duties due to the severe restrictions on his physical abilities related to his knee. Id. at 13.
On August 9, 2012, petitioner returned to Dr. O'Connor. At this visit, Dr. O'Connor documented rheumatoid arthritis ("RA") symptoms along with joint swelling, hand pain, bilateral carpal tunnel, and PMR. Pet. Ex. 7 at 47. Dr. O'Connor discovered polysynovitis
Between September and December 2012, petitioner returned to Drs. Dietrick and O'Connor on five occasions with complaints of aches and pains around his left knee. See Pet. Ex. 2 at 5; Pet. Ex. 6 at 10; Pet. Ex. 7 at 36-38, 42, 45. He was ordered to taper his prednisone prescription and continue his meloxicam and leflunomide
On January 9, 2013, petitioner received a final disability rating for his work-related knee injury. Pet. Ex. 6 at 1-5. He completed a form on that date noting aching in the front, outside and rear of his left knee, sharp pain on the outside and rear of his left knee and up and down his leg, with tenderness in the front and outside of his left knee. Id. at 42. Dr. Dietrick concluded that due to his work-related knee injury, petitioner was permanently disabled from his current job and issued a disability rating of 20% of his whole person and 50% of his lower left extremity.
On February 21, 2013, petitioner presented to Dr. O'Connor with complaints of tingling in his hands and thighs and minimal joint swelling. Pet. Ex. 7 at 30. Dr. O'Connor documented that petitioner's sciatic pain had never been evaluated for neuropathy and he was prescribed Neurontin but was unable to take it due to central nervous system changes. Id. Petitioner's RA symptoms were noted to be stable with no inflammatory arthritis in petitioner's feet and/or hands noted. Id. at 31-32. Dr. O'Connor wrote that there was little development of petitioner's RA or PMR symptoms and his ESR and CRP levels continued to be normal. Id. at 32. Dr. O'Connor documented that many of petitioner's complaints were related to his peripheral neuropathy from his diabetes and sciatica. Id.
On March 4, 2013, an MRI of petitioner's lumbar spine revealed bulging annuli at L2-3, L4-5, and L5-S1 without impingement. Pet. Ex. 5 at 38-40. On March 7, 2013, an MRI of petitioner's left shoulder revealed a labrum injury with a cyst over the humeral head.
On March 20, 2013, petitioner returned to Dr. O'Connor. Pet. Ex. 7 at 18. Petitioner was taking methotrexate, low dose prednisone, and Lyrica with lessened pain in his hands. Id. Petitioner's bloodwork was normal, and his RA was noted to be stable. Id. Dr. O'Connor directed petitioner to increase his Lyrica prescription, but the record contained no explanation for this increase. Id. at 20.
On April 8, 2013, petitioner underwent EMG and a nerve conduction study ("NCS") of the upper extremities. Pet. Ex. 5 at 5-18. The EMG/NCS revealed generalized diabetic peripheral neuropathy which had progressed since 2010 and petitioner's diagnosis of diabetes four years prior. Id. at 8-9. The doctor opined peripheral neuropathies are predisposed to entrapment neuropathies at the cubital and carpal tunnels as well as subclinical electrical slowing across these regions. Id. at 9. Petitioner was noted to have moderate left carpal tunnel syndrome and mild to moderate right carpal tunnel syndrome superimposed on peripheral neuropathy. Id. His doctor concluded that all of petitioner's symptoms discussed at this visit were unrelated to PMR and/or RA. See id. (emphasis added).
On April 24, 2013, petitioner presented to Dr. O'Connor for follow up. His RA symptoms were noted to be stable. He was directed to continue his current medications. Pet. Ex. 7 at 12.
On May 3, 2013, petitioner underwent caudal epidural and lumbar facet injections at L1-2, L2-3, L4-5, and L5-S1 for sciatic pain. Pet. Ex. 5 at 2-3.
Petitioner presented to his PCP on May 29, 2013 with dermatologic symptoms and skin lesions with abscesses. Pet. Ex. 2 at 2. Petitioner complained of possible shingles on his left shoulder and neck that had persisted for four days. Id. He had begun acyclovir the previous day to alleviate his symptoms. Id. Upon examination, hypersensitivity along the left shoulder blade was noted but no active rash was present. Id. Petitioner was diagnosed with likely prodromal shingles. Id. Petitioner's RA was noted to be stable. Id.
On June 19, 2013, petitioner received a shingles vaccination without event. Id. at 1.
On July 15, 2013, petitioner presented to Dr. O'Connor for instructions on using the Enbrel Sure Clinic Pen.
On February 20, 2014, petitioner was diagnosed with a multinodular goiter on his thyroid by his endocrinologist. Pet. Ex. 8 at 44.
On June 23, 2014, petitioner presented to Inland Neurosurgery and Spine with bilateral leg, left ankle, and foot pain. Pet. Ex. 15 at 1-3. He had several epidural injections and had developed burning of the right thigh and anterior shin two years prior. Id. at 1. Petitioner also reported his EMG/NCS performed the previous year revealed muscle atrophy that began following his knee replacement in 2011. Id. Petitioner reported being diagnosed with RA in 2012 and that his hands constantly ached. Id. Petitioner's symptoms were noted to be related to his peripheral neuropathy that had never been worked up for a treatable cause. Id. at 3.
In July 2014, petitioner presented to his rheumatologist with tenderness and swelling at the wrists and MCPs. Pet. Ex. 7 at 130-33. His ankles and toes were tender, and he was noted to have symptomatic RA. Id. at 132. He was prescribed Remicade.
On July 22, 2014, petitioner underwent additional EMG/NCS testing due to bilateral upper extremity numbness and tingling. Pet. Ex. 16 at 5-6. He was noted to have mild carpal and cubital tunnel syndrome, mild right C6 radiculopathy, and no brachial plexopathy or myopathy. Id. at 5.
On July 29, 2014, petitioner presented to the neurologist with complaints of neck pain, back pain, numbness and tingling of the upper and lower extremities, RA, and PMR. Id. at 1. The opinion was petitioner's neuropathy could have been caused by his diabetes. Id. at 1. Right C6 radiculopathy and L4-5 root irritation were noted. Id. at 2.
Petitioner returned to Inland Neurosurgery on August 12, 2014 for follow up. Pet. Ex. 15 at 23. Petitioner was noted to have a history of demyelinating and axonal peripheral neuropathy and cervical and lumbar degenerative disc disease with shooting pain in his leg. Id. Petitioner was diagnosed with peripheral neuropathy, mild right C6 radiculopathy, and a possible torn rotator cuff in his right shoulder. Id. at 24. He was directed to continue with Remicade for RA and PMR. Id.
On December 10, 2014, petitioner presented for pre-operative examination of his right shoulder. Pet. Ex. 30 at 30. Petitioner was cleared for surgery that was scheduled to take place the following week. Id.
On December 11, 2014, petitioner presented for follow up of his RA. Id. at 144. He was doing well on Remicade and leflunomide and reported a pain severity level of 2/10. Id.
On December 19, 2014, petitioner underwent right shoulder surgery for a torn rotator cuff reportedly resulting from lifting a couch. Pet. Ex. 32 at 66-68. Petitioner subsequently underwent extensive physical therapy for his shoulder following this surgery. See generally Pet. Ex. 29.
Between June and September 2015, petitioner presented for follow up of his RA on three occasions. Pet. Ex. 30 at 26, 111, 121. At each visit, petitioner's CRP and ESR levels were normal and his RA was noted to be under control. Id.
On September 25, 2015, petitioner underwent dual energy x-ray absorptiometry
On October 2, 2015, petitioner presented to rheumatologist, Dr. Shinada, at Keck Medicine of USC for additional evaluation of his RA and PMR diagnoses. Pet. Ex. 26 at 8. His history was noted to be significant for diabetes, seronegative RA that began in August 2012, and PMR that began in January 2012. Id. Petitioner complained of pain in his hands, wrists, shoulders, and arms with stiffness in the mornings. Id. at 17. Petitioner stated he had previously taken Enbrel and methotrexate and was currently taking Arava daily and Remicade infusions every eight weeks. Id. He also took Nexium, metformin, glimepiride, Januvia, Invokana, atorvastatin, lisinopril, Lyrica, prednisone 5 mg every other day, various vitamins, and used Andro gel. Id. at 16-18. On examination, he had good range of motion in his shoulders, elbows, wrists, and hands with no synovitis or edema noted and good range of motion in his hips and knees with some effusion of the left knee and some crepitus and effusion of the right knee. Id. at 18. Reduction of prednisone was suggested. Id.
On January 18, 2016 petitioner underwent left foot surgery which included distal chevron osteotomy, second plantar plate repair, hammertoe correction with proximal interphalangeal joint arthrodesis, extensor tendon lengthening, and repair of the second extensor tendon plantar with condylectomy around the second metatarsophalangeal joint. Pet. Ex. 32 at 55-57.
Petitioner presented for follow up of his RA twice in March 2016. Pet. Ex. 26 at 69; Pet. Ex. 30 at 22. He complained of increased stiffness at each visit due to inability to receive Remicade injections following his foot surgery. Id. He reported taking prednisone and Percocet for pain. Id.
On April 5, 2016, petitioner presented to Loma Linda Hospital Pain Management for assessment of his left foot. Pet. Ex. 28 at 13. He had complex regional pain syndrome of the left foot, lumbar radiculopathy, myalgias, arthralgias, stiffness, back pain, and redness and swelling of joints. Id. Petitioner was noted to be dependent on opioid therapy and could not function or perform daily activities of living without them. Id. at 18. He was ultimately diagnosed with idiopathic progressive polyneuropathy. Id. at 21, 36.
Petitioner presented for follow up related to his left foot surgery on April 19, 2016. Pet. Ex. 32 at 20. Petitioner continued to complain of persistent pain despite a sympathetic nerve block performed on April 5, 2016. He continued to experience burning in his forefoot, but he could walk with a substantial amount of pain. Id.
Between May 11, 2016 and August 24, 2016, petitioner followed up for his RA on three occasions. See Pet. Ex. 30 at 6, 10, 21.
On September 15, 2016, petitioner presented to the orthopedist with complaints of left shoulder and lumbar spine pain. Pet. Ex. 32 at 11. He reported a previous repair of his right shoulder for labral tear with debridement, subacromial decompression, and distal clavicle excision. Id. At this visit, he complained of left shoulder pain with reaching in different directions and back pain. Id. He was diagnosed with rotator cuff tendinopathy of the left shoulder and degenerative lumbar spondylosis. Id.
An MRI of petitioner's lower back performed on September 23, 2016 revealed loss of disc space at L2-3 with new moderate endplate degenerative changes and prominent endplate signal abnormality. Pet. Ex. 30 at 90. There was a progression of retrolisthesis
On October 3, 2016, petitioner presented to his orthopedist with complaints of lower back pain. Pet. Ex. 32 at 5. It was noted that petitioner's pain seemed to be mechanical rather than neurologic. Id. Muscle spasms from T10 to L3 were noted. Id. MRIs revealed severe degenerative disc changes, stenosis, and tightness. Id. Voltaren and physical therapy were recommended. Id. at 6.
On October 24, 2016, petitioner returned to the orthopedist with complaints of episodic acute back pain. Id. at 3. He had previously seen improvement with physical therapy and Voltaren. Id. He was sent back to physical therapy and directed to continue with Voltaren. Id. If necessary, a bilateral L2-L3 root block would be discussed. Id.
On October 26, 2016, petitioner returned to his PCP. Pet. Ex. 30 at 1. He was noted to have been initially diagnosed with PMR in January 2012 and treated with prednisone and methotrexate. Id. He was ultimately diagnosed with seronegative rheumatoid arthritis after worsening of joint pain and was treated with Enbrel for a year, then switched to leflunomide and Remicade infusions. Id. He had a left bunionectomy and tendon repair with continued burning of the left foot and ankle. Id. He was taking Percocet for pain and had tendinosis of the left shoulder. Id. His active problems at this visit were RA, bicipital tendinitis of the left shoulder, type II diabetes, hypertension, hyperlipidemia, lower back pain, neuropathy, rosacea, PMR, sciatica, and history of shoulder joint pain. Id. at 1-2. He was directed to continue his current medications and return in two months for follow up. Id. at 5.
As of 2017, petitioner continued to have severe pain in his foot and was diagnosed with reflex dystrophy syndrome of the left foot as well as diabetic neuropathy. Pet. Ex. 34 at 3-4. Sympathetic nerve blocks, Voltaren, and Robaxin were used for pain. Id. at 4.
Dr. Gowin earned a Bachelor of Arts in Zoology from the University of Miami, an M.D. from the University of Cincinnati College of Medicine, and a Master of Science in clinical epidemiology from the University of Pennsylvania School of Medicine. Tr. 42; Pet. Ex. 21 at 1. In 1990, Dr. Gowin became a resident in internal medicine at the Hershey Medical Center and spent a year on the faculty there as an instructor in the Division of General Internal Medicine. Pet. Ex. 21 at 1. In 1994, she went to the University of Pennsylvania, where she was a fellow in rheumatology and did her degree in clinical epidemiology while there. Id.; Tr. 42. She left the University of Pennsylvania in 1999 to pursue private practice. Tr. 42. Dr. Gowin is board certified in rheumatology and was board certified in internal medicine but chose not to re-certify. Id.
Dr. Gowin is currently a partner at the Asheville Arthritis and Osteoporosis Center and a sub-investigator in their clinical trial unit. Tr. 41-42, 66; Pet. Ex. 21 at 1. Dr. Gowin actively sees approximately 1,000 patients, the frequency depends on the condition for which they are being seen. Tr. 42-43. Her patients typically suffer from different kinds of arthritis, including rheumatoid arthritis, psoriatic arthritis, and other inflammatory conditions like polymyalgia rheumatica and inflammatory eye disease. Tr. 43. As a sub-investigator, Dr. Gowin contributes patients to clinical trials but is only involved in the clinical gathering of the scientific data, rather than researching and/or writing articles related to the data. Tr. 68. The drug companies oversee the trials, collection of data, analysis, and reporting of the results. Id. The most recent study she is involved in is for the GIACTA trial, researching a treatment for giant cell arteritis. Tr. 69. Dr. Gowin agreed that she has not published a paper since 2001, and the papers she published involved data analysis based on studies of conditions and diseases or statistical analysis of data to assess causal relationship were on gout. Tr. 70-71. Dr. Gowin explained that while she has had some case reports presented at meetings as poster presentations, none were related to the flu vaccine. Tr. 71-72. She has not been involved in cases or investigations related to rheumatic diseases. Tr. 71.
Dr. Gowin opined there is biologic plausibility for the influenza vaccine to cause either onset or flare of RA. Pet. Ex. 20 at 4.
Dr. Gurish
Dr. Gurish opined that molecular mimicry as well as epitope spreading, bystander activation, and polyclonal activation were responsible for petitioner's development of autoimmunity. Pet. Ex. 23 at 3 (citing Pet. Ex. 23-D at 1043-44;
Dr. Matloubian is an Associate Adjunct Professor at the University of California at San Francisco School of Medicine. Resp. Ex. B. at 1. Dr. Matloubian received a Bachelor of Science degree in biochemistry, a Ph.D., and an M.D. from UCLA. Id. He completed his residency in internal medicine and a fellowship in rheumatology. Id.; Tr. 176. Dr. Matloubian is an immunologist and board-certified rheumatologist who actively evaluates and treats patients with complex autoimmune diseases, including rheumatoid arthritis, lupus, mixed connective tissue disease, PMR, different types of inflammatory myositis, and vasculitis. Tr. 182; Resp. Ex. B. at 2. Dr. Matloubian also has a Ph.D. in microbiology and immunology with an emphasis in virology. Resp. Ex. B at 2. His post-doctoral training focused on how lymphocytes, or white blood cells, travel from different tissues and different organs, and immune responses to acute and chronic viral infections focusing on both innate and adaptive immune responses. Tr. 177. He is familiar with the mechanics of immunology and how the immune system responds to various antigens. Id. He has published several articles on immunology, particularly on lymphocyte trafficking, in peer-reviewed journals. Resp. Ex. B at 6-9. His other research interests include autoimmune disease, interferons, plasmacytoid dendritic cells, antibody responses in chronic viral infection, chemokines, and chronic inflammation. Id. at 2.
Dr. Matloubian disagreed that molecular mimicry was the correct mechanism in this case, stating, "For molecular mimicry to be relevant to a disease in question, the natural infection, i.e. influenza virus in this case, should also lead to development of that disease in some people." Resp. Ex. A at 11. He opined there is no evidence associating influenza virus with PMR or RA and that because the components of the vaccine are derived from the influenza virus, "it is highly unlikely that a mechanism such as molecular mimicry can cause arthritis due to this vaccine." Id. Dr. Matloubian further highlighted the absence of a causal relationship between the inactivated flu vaccine and the development of inflammatory arthritis. Id. at 12; Resp. Ex. C at 7. Dr. Matloubian concluded he strongly believed petitioner would have developed PMR and/or RA even if he had not received the flu vaccine on October 14, 2011. Resp. Ex. C at 7.
The opinions of the experts are set forth in greater detail below.
The process for making determinations in Vaccine Program cases regarding factual issues, such as the timing of onset of petitioner's alleged injury, begins with analyzing the medical records, which are required to be filed with the petition. 42 U.S.C. § 300aa-11(c)(2). Medical records created contemporaneously with the events they describe are presumed to be accurate and "complete" such that they present all relevant information on a patient's health problems. Cucuras v. Sec'y of Health & Human Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993); Doe/70 v. Sec'y of Health & Human Servs., 95 Fed. Cl. 598, 608 (2010) ("Given the inconsistencies between petitioner's testimony and his contemporaneous medical records, the special master's decision to rely on petitioner's medical records was rational and consistent with applicable law."). This presumption is based on the linked proposition that (i) sick people visit medical professionals; (ii) sick people honestly report their health problems to those professionals; and (iii) medical professionals record what they are told or observe when examining their patients in an accurate manner, so that they are aware of enough relevant facts to make appropriate treatment decisions. Sanchez v. Sec'y of Health & Human Servs., No. 11-685V, 2013 WL 1880825, at *2 (Fed. Cl. Spec. Mstr. Apr. 10, 2013); Cucuras v. Sec'y of Health & Human Servs., 26 Cl. Ct. 537, 543 (1992), aff'd, 993 F.2d. 1525 (Fed. Cir. 1993) ("[I]t strains reason to conclude that petitioners would fail to accurately report the onset of their daughter's symptoms. It is equally unlikely that pediatric neurologists, who are trained in taking medical histories concerning the onset of neurologically significant symptoms, would consistently but erroneously report the onset of seizures a week after they in fact occurred.").
Where medical records are clear, consistent, and complete, they should be afforded substantial weight. Lowrie v. Sec'y of Health & Human Servs., No. 03-1585V, 2005 WL 6117475, at *20 (Fed. Cl. Spec. Mstr. Dec. 12, 2005). Indeed, contemporaneous medical records are generally found to be deserving of greater evidentiary weight than oral testimony—particularly where such testimony conflicts with the record evidence. Cucuras, 993 F.2d at 1528; see also Murphy v. Sec'y of Health and Human Servs., 23 Cl. Ct. 726, 733 (1991), aff'd per curiam, 968 F.2d 1226 (Fed. Cir. 1992) cert. den'd; Murphy v. Sullivan, 506 U.S. 974 (1992) (citing United States v. United States Gypsum Co., 333 U.S. 364, 396 (1947) ("It has generally been held that oral testimony which is in conflict with contemporaneous documents is entitled to little evidentiary weight.")). In making contemporaneous reports, the declarant's motivation for accurate explication of symptoms is more immediate, as opposed to testimony offered after the events in question, which is considered inherently less reliable. Reusser v. Sec'y of Health & Human Servs., 28 Fed. Cl. 516, 523 (1993).
Despite the weight afforded medical records, special masters are not bound rigidly by those records in determining onset of a petitioner's symptoms. Vallenzuela v. Sec'y of Health & Human Servs., No. 90-1002V, 1991 WL 182241, at *3 (Fed. Cl. Spec. Mstr. Aug. 30, 1991); see also Eng v. Sec'y of Health & Human Servs., No. 90-1754V, 1994 WL 67704, at *3 (Fed. Cl. Spec. Mstr. Feb. 18, 1994) (explaining that §13(b)(2) "must be construed so as to give effect also to §13(b)(1) which directs the special master or court to consider the medical records [reports, diagnosis, conclusions, medical judgment, test reports, etc.] but does not require the special master or court to be bound by them.") (emphasis in original). There are situations in which compelling oral testimony may be more persuasive than written records—for instance, in cases where records are deemed to be incomplete or inaccurate.
Polymyalgia rheumatica ("PMR") is an inflammatory rheumatic disease which commonly presents in patients over the age of 50 with approximately 1 out of every 150 persons over the age of 50 being affected by the disease. Pet. Ex. 43 at 117;
PMR is commonly characterized by startingly abrupt onset of pain and morning stiffness in the shoulders and pelvic girdles. Id. "However, distal manifestations, which include peripheral arthritis and distal extremity swelling with pitting edema, may occur in about half the cases." Resp. Ex. A-2 at 1053. Ultrasound evidence of bilateral subacromial/subdeltoid bursitis in the shoulders may represent a hallmark of PMR. Id. Elevated inflammatory markers of CRP, ESR, and creatine kinase ("CK") levels have been shown to be the hallmark of PMR. Id.; Pet. Ex. 44 at 345-46.
Rheumatoid arthritis ("RA") is a common autoimmune disease associated with progressive disability, systemic complications, early death, and socioeconomic cost. Resp. Ex. A-3 at 2205.
Individuals with RA are considered either seropositive or seronegative. In seropositive RA, the long-established association with the human leukocyte antigen ("HLA")-DRB1 locus has been confirmed in patients who test positive for rheumatoid factor or ACPA; alleles that contain a common amino acid motif, QKRAA, in the HLA-DRB1 regions, termed the "shared epitope," confer particular susceptibility. Resp. Ex. A-3 at 2206. These findings suggest that some predisposing T-cell repertoire selection, antigen presentation, or alteration in peptide affinity has a role in promoting autoreactive adaptive immune responses. Id. Other possible mechanisms include molecular mimicry of the shared epitope by microbial proteins, increased T-cell senescence induced by shared epitope-containing HLA molecules, and a potential proinflammatory signaling function unrelated to the role of the shared epitope in antigen recognition. Id. Infectious agents — Epstein-Barr virus, cytomegalovirus, proteus species and E-coli — and their products have been linked with RA through some form of molecular mimicry. Id.
While seropositive RA has a presence of autoantibodies, none exist or are known for seronegative RA, suggesting that the pathogenesis or mechanisms that lead to the breakdown of tolerance and generation of autoimmunity in each case may be different. Resp. Ex. C at 3 (citing Pet. Ex. 22 at 2). In practice, seronegative RA is determined by clinical diagnosis and no distinction is made for purposes of treatment because the medications prescribed are the same and are limited. Id.
In a new criteria set, classification as "definite RA" is based on the confirmed presence of synovitis in at least one joint, absence of an alternative diagnosis that better explains the synovitis, and achievement of a total score of 6 or greater (of a possible 10) from the individual scores in 4 domains: number and site of involved joints (score range 0-5), serologic abnormality (score range 0-3) elevated acute phase response (score range 0-1), and symptom duration (2 levels; range 0-1). Resp. Ex. A-7 at 2570.
RA and PMR have similar clinical presentations and it is still debated as to whether they are the same entity. Resp. Ex. A-8 at 1021, 1023.
The onset of RA has been associated with adverse life events with molecular explanations emerging from animal models of inflammation which show a link between the hypothalamic-pituitary-adrenal axis and cytokine production. Resp. Ex. A-3 at 2206-07. "The central nervous system is normally involved in immune regulation and homeostasis, and neuroimmunologic interactions regulate disease development in rodent models of arthritis either locally (several neurotransmitters are expressed in synovitis in RA) or centrally (cytokines are rapidly up regulated in the hypothalamus during peripheral inflammation)." Id. Humoral adaptive immunity is integral to RA. Id. at 2209. Plasma cells are more widely distributed in the synovium and juxta-articular bone marrow. Plasma cells are not targeted by anti CD20 antibodies and autoantibody levels are variably altered after treatment, these clinical observations suggest that the role of B cells and their progeny in the pathogenesis of RA goes beyond antibody production to include autoantigen presentation and cytokine production. Id. at 2209-10.
Smoking, alcohol intake, high BMI, high birthweight, lower socioeconomic status, and periodontal disease increase patient's risk of RA. Resp. Ex. C-11 at 523.
The onset of petitioner's symptoms varies between the medical records and the testimony of petitioner and his wife. Petitioner and his wife both testified that he was relatively healthy before his receipt of the flu vaccination in October 2011. Both initially stated that his pain and morning stiffness began in mid- to late-November 2011. Tr. 6, 27-28. Petitioner associated this with his return to work following knee replacement surgery. Tr. 9-10, 29-30; Pet. Ex. 17 at 2; Pet. Ex. 19 at 1-2. However, Mrs. [REDACTED/] affirmed that petitioner did not return to work until mid-December, just before the Christmas break. Pet. Ex. 19 at 2-3. Further, the medical records prior to petitioner's vaccination document ongoing complaints of neck and shoulder pain, sciatic pain with numbness and tingling in his legs. Pet. Ex. 2 at 16; Pet. Ex. 17 at 1; see generally Pet. Ex. 12-13, 29, 36-38, 40. On the day of the allegedly causal vaccination, petitioner presented with complaints of right thigh burning, tingling, and numbness for one month. Pet. Ex. 2 at 16; Pet. Ex. 17 at 1. The medical records after his vaccination consistently document petitioner's reporting onset of PMR symptoms as December 2011, a diagnosis of PMR in January 2012, suspected RA in March 2012 and diagnosis of seronegative RA in August 2012. Pet. Ex. 6 at 67; Pet. Ex. 7 at 47-48; see Pet. Ex. 10 at 13; Pet. Ex. 26 at 8. Notably, both petitioner and his wife avoided any testimony regarding his ongoing left knee issue or his being out of work since May 2011 as a result of his work-related knee injury.
In considering petitioner and his wife's testimony in concert with the contemporaneous medical records, the medical records clearly reference onset of the alleged PMR symptoms in December 2011. See Lowrie, 2005 WL 6117475, at *20. Petitioner and his wife's testimony carried less weight in this matter due to changes in their testimony when confronted with records filed in this matter. Initially, petitioner and his wife postured that petitioner's pain upon his return to work, pain at the Christmas party, inability to walk, inability to participate in New Year's Eve and a family wedding were the results of his PMR symptoms, only to later concede that the pain was actually related to the ongoing debilitating problems associated with his prior knee surgery. Tr. 9-10, 29-30. Petitioner and his wife also suggested that his early retirement was due to the progression of PMR and RA, when in fact he was determined to be unable to return to his job by Dr. Dietrick due to his knee injury, was assessed with a disability rating by workers' compensation, and recovered an award from workers' compensation as a result thereof. See id.; Pet. Ex. 7 at 24. Further, petitioner admitted in his affidavit that he retired early so he could maintain his health insurance because he was out of work for so long with his knee issues. Pet. Ex. 17 at 3.
Ultimately, based on the medical records and testimony, I find that the onset of petitioner's alleged PMR was late December 2011, with seronegative RA suspected in March 2012 and diagnosed in July of 2012.
The Vaccine Act provides two avenues for petitioners to receive compensation. First, a petitioner may demonstrate a "Table" injury—i.e., an injury listed on the Vaccine Injury Table that occurred within the provided time period. 42 U.S.C. § 300aa-11(c)(1)(C)(i). "In such a case, causation is presumed." Capizzano v. Sec'y of Health & Human Servs., 440 F.3d 1317, 1320 (Fed. Cir. 2006); see § 13(a)(1)(B). Second, where the alleged injury is not listed on the Vaccine Injury Table, a petitioner may demonstrate an "off-Table" injury, which requires that the petitioner "prove by a preponderance of the evidence that the vaccine at issue caused the injury." Capizzano, 440 F.3d at 1320; see § 11(c)(1)(C)(ii). A petitioner need not show that the vaccination was the sole cause, or even the predominant cause, of the alleged injury; showing that the vaccination was a "substantial factor" and a "but for" cause of the injury is sufficient for recovery. Pafford v. Sec'y of Health & Human Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006); Shyface v. Sec'y of Health & Human Servs., 165 F.3d 1344, 1352 (Fed. Cir. 1999).
To prove causation, petitioners must satisfy the three-pronged test established in Althen v. Sec'y of Health & Human Servs., 418 F.3d 1274 (Fed. Cir. 2005). Althen requires that petitioners show by preponderant evidence that a vaccination petitioner received caused his or her injury "by providing: (1) a medical theory causally connecting the vaccination and the injury; (2) a logical sequence of cause and effect showing that the vaccination was the reason for the injury; and (3) a showing of a proximate temporal relationship between vaccination and injury." Id. at 1278. Together, these prongs must show "that the vaccine was `not only a but-for cause of the injury but also a substantial factor in bringing about the injury.'" Stone v. Sec'y of Health & Human Servs., 676 F.3d 1373, 1379 (Fed. Cir. 2012) (quoting Shyface, 165 F.3d at 1352-53). Causation is determined on a case-by-case basis, with "no hard and fast per se scientific or medical rules." Knudsen v. Sec'y of Health & Human Servs., 35 F.3d 543, 548 (Fed. Cir. 1994). Petitioners are not required to identify "specific biological mechanisms" to establish causation, nor are they required to present "epidemiologic studies, rechallenge, the presence of pathological markers or genetic disposition, or general acceptance in the scientific or medical communities." Capizzano, 440 F.3d at 1325 (quoting Althen, 418 F.3d at 1280). "[C]lose calls regarding causation are resolved in favor of injured claimants." Althen, 418 F.3d at 1280.
Each of the Althen prongs requires a different showing. Under the first Althen prong, petitioner must provide a "reputable medical theory" demonstrating that the vaccine received can cause the type of injury alleged. Pafford, 451 F.3d at 1355-56 (citation omitted). To satisfy this prong, petitioner's "theory of causation must be supported by a `reputable medical or scientific explanation.'" Andreu, 569 F.3d at 1379 (quoting Althen, 418 F.3d at 1278). This theory need only be "legally probable, not medically or scientifically certain." Id. at 1380 (emphasis omitted) (quoting Knudsen, 35 F.3d at 548). Nevertheless, "petitioners [must] proffer trustworthy testimony from experts who can find support for their theories in medical literature." LaLonde, 746 F.3d at 1341.
The second Althen prong requires proof of a "logical sequence of cause and effect." Capizzano, 440 F.3d at 1326 (quoting Althen, 418 F.3d at 1278). Even if the vaccination can cause the injury, petitioner must show "that it did so in [this] particular case." Hodges v. Sec'y of Health & Human Servs., 9 F.3d 958, 962 n.4 (Fed. Cir. 1993) (citation omitted). "A reputable medical or scientific explanation must support this logical sequence of cause and effect," id. at 961 (citation omitted), and "treating physicians are likely to be in the best position to determine whether a logical sequence of cause and effect show[s] that the vaccination was the reason for the injury," Paluck v. Sec'y of Health & Human Servs., 786 F.3d 1373, 1385 (Fed. Cir. 2015) (quoting Andreu, 569 F.3d at 1375).
However, medical records and/or statements of a treating physician's view do not per se bind the special master to adopt the conclusions of such an individual, even if they must be considered and carefully evaluated. Section 12(b)(1) (providing that "[a]ny such diagnosis, conclusion, judgment, test result, report or summary shall not be binding on the special master or court."); Snyder v. Sec'y of Health & Human Servs., 88 Fed. Cl. 706, 746 n.67 (2009) ("[T]here is nothing...that mandates that the testimony of a treating physician is sacrosanct—that it must be accepted in its entirety and cannot be rebutted"). As with expert testimony offered to establish a theory of causation, the opinions or diagnoses of treating physicians are only as trustworthy as the reasonableness of their suppositions or bases. The views of treating physicians should also be weighed against other, contrary evidence also present in the record — including conflicting opinions among such individuals. Hibbard v. Sec'y of Health & Human Servs., 100 Fed. Cl. 742, 749 (2011) (determining it is not arbitrary or capricious for a special master to weigh competing treating physicians' conclusions against each other), aff'd. 698 F.3d 1355 (Fed. Cir. 2012); Caves v. Sec'y of Health & Human Servs., 100 Fed. Cl. 119, 136 (2011), aff'd, 463 Fed. Appx. 932 (Fed. Cir. 2012); Veryzer v. Sec'y of Health & Human Servs., No. 06-522V, 2011 WL 1935813, at *17 (Fed. Cl. Spec. Mstr. Apr. 229, 2011), mot. for review den'd, 100 Fed. Cl. 344 (Sept. 29, 2011), aff'd, 475 Fed. Appx. 765 (Fed. Cir. 2012).
The third Althen prong requires that petitioner establish a "proximate temporal relationship" between the vaccination and the alleged injury. Althen, 418 F.3d at 1281. This "requires preponderant proof that the onset of symptoms occurred within a timeframe for which, given the medical understanding of the disorder's etiology, it is medically acceptable to infer causation-in-fact." De Bazan v. Sec'y of Health & Human Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). Typically, "a petitioner's failure to satisfy the proximate temporal relationship prong is due to the fact that onset was too late after the administration of a vaccine for the vaccine to be the cause." Id. However, "cases in which onset is too soon" also fail this prong; "in either case, the temporal relationship is not such that it is medically acceptable to conclude that the vaccination and the injury are causally linked." Id.; see also Locane v. Sec'y of Health & Human Servs., 685 F.3d 1375, 1381 (Fed. Cir. 2012) ("[If] the illness was present before the vaccine was administered, logically, the vaccine could not have caused the illness.").
Finally, although this decision discusses many but not all of the literature in detail which was submitted by the parties, I reviewed and considered all of the evidence submitted including all medical records and literature filed in this matter. See Moriarty ex rel. Moriarty v. Sec'y of Health & Human Servs., 844 F.3d 1322, 1328 (Fed. Cir. 2016) ("We generally presume that a special master considered the relevant record evidence even though [s]he does not explicitly reference such evidence in h[er] decision."); Simanski v. Sec'y of Health & Human Servs., 115 Fed. Cl. 407, 436 (2014) ("[A] Special Master is `not required to discuss every piece of evidence or testimony in her decision.'" (citation omitted)), aff'd, 601 F. App'x 982 (Fed. Cir. 2015).
Establishing a sound and reliable medical theory often requires a petitioner to present expert testimony in support of his claim. Lampe v. Sec'y of Health & Human Servs., 219 F.3d 1357, 1361 (Fed. Cir. 2000). Vaccine Program expert testimony is usually evaluated according to the factors for analyzing scientific reliability set forth in Daubert v. Merrell Dow Pharm., Inc., 509 U.S. 579, 594-96 (1991).
The Daubert factors are usually employed by judges in the performance of their evidentiary gatekeeper roles to exclude evidence that is unreliable and/or could confuse the jury. In Vaccine Program cases, by contrast, these factors are used in the weighing of the reliability of scientific evidence proffered. Davis v. Sec'y of Health & Human Servs., 94 Fed. Cl. 53, 66-67 (2010) ("uniquely in this Circuit, the Daubert factors have been employed also as an acceptable evidentiary-gauging tool with respect to persuasiveness of expert testimony already admitted"). The flexible use of the Daubert factors to evaluate the persuasiveness of expert testimony has routinely been upheld. See, e.g., Snyder, 88 Fed. Cl. at 742-45. In this case, as in numerous other Vaccine Program cases, Daubert has not been employed to determine what evidence should be admitted, but rather to determine whether expert testimony offered is reliable and/or persuasive.
Where both sides offer expert testimony, a special master's decision may be "based on the credibility of the experts and the relative persuasiveness of their competing theories." Broekelschen v. Sec'y of Health & Human Servs., 618 F.3d 1339, 1347 (Fed. Cir. 2010) (citing Lampe, 219 F.3d at 1362). However, nothing requires the acceptance of an expert's conclusion, "connected to existing data only by the ipse dixit of the expert," especially if "there is simply too great an analytical gap between the data and the opinion proffered." Snyder, 88 Fed. Cl. at 743 (quoting Gen. Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997)); see also Isaac v. Sec'y of Health & Human Servs., No. 08-601V, 2012 WL 3609993, at *17 (Fed. Cl. Spec. Mstr. July 30, 2012), mot. for review den'd, 108 Fed. Cl. 743 (2013), aff'd, 540 F. App'x. 999 (Fed. Cir. 2013) (citing Cedillo, 617 F.3d at 1339). Weighing the relative persuasiveness of competing expert testimony, based on a particular expert's credibility, is part of the overall reliability analysis to which special masters must subject expert testimony in Vaccine Program cases. Moberly v. Sec'y of Health & Human Servs., 592 F.3d 1315, 1325-26 (Fed. Cir. 2010) ("[a]ssessments as to the reliability of expert testimony often turn on credibility determinations"); see also Porter v. Sec'y of Health & Human Servs., 663 F.3d 1242, 1250 (Fed. Cir. 2011) ("this court has unambiguously explained that special masters are expected to consider the credibility of expert witnesses in evaluating petitions for compensation under the Vaccine Act.").
Because petitioner does not allege an injury listed on the Vaccine Injury Table, his claim is classified as "off-Table." As noted above, for petitioner to prevail on an "off-Table" claim, he must show by preponderant evidence that B.L.'s injury resulted from the vaccination at issue. Capizzano, 440 F.3d at 1320. Doing so shifts the burden to respondent to show that the injury was caused by factors unrelated to the vaccination. Deribeaux, 717 F.3d at 1367.
Application of the Althen prongs reveals evidentiary deficiencies in petitioner's claim: (1) petitioner failed to offer a persuasive or reliable medical theory; (2) the theory provided is not applicable to the facts of petitioner's case; and (3) petitioner has not established a medically acceptable timeframe in which his symptoms could have begun or developed.
To satisfy Althen Prong I, petitioner must present a "sound and reliable medical or scientific explanation" causally connecting the vaccine to his alleged injuries. Knudsen, 35 F.3d at 548. Petitioner's causation theory has several deficiencies.
Dr. Gowin opined there is biologic plausibility for the influenza vaccine to cause either onset or flare of RA. Pet. Ex. 20 at 4. She suggested that the initiating event activating T-lymphocytes could be a vaccine. Id. (citing Pet. Ex. 20-G at 1). Though no single driving antigen has not been identified, there may be several that initiate RA in genetically susceptible individuals by molecular mimicry. Id. (citing Pet. Ex. 20-G at 1). Dr. Gowin submitted an article that stated lymphocytes specific for influenza virus have been found in the joints of patients with RA suggesting that they may participate in onset or flare of the disease. Id. (citing Pet. Ex. 20-G at 4-5). "Immunological changes can be seen even several years prior to the onset of symptoms for patients who will develop rheumatoid arthritis given the appropriate trigger to the immune system. Various viruses or their analogous vaccines have been postulated as triggers for autoimmunity." Id. (citing Pet. Ex. 20-H at 1-2). She did not explain how this relates to petitioner, whose RA is classified as seronegative as he does not have a positive rheumatoid factor or anti-CCP.
Dr. Gowin acknowledged that she is not an immunologist but stated that her training and experience in rheumatology is "pretty good clinical immunology training." Tr. 72-73. Dr. Gowin submitted that molecular mimicry is the mechanism by which the flu vaccine caused and/or triggered petitioner's PMR and subsequent RA, stating molecular mimicry is "one of the things that I think people hang their hat on sometimes...where they talk about molecular mimicry as an autoimmune trigger," it's a reliable and plausible theory; "... molecular mimicry, [which] has been put forth as a mechanism for a lot of these reactive syndromes." Tr. 56, 77.
In support of her opinions, Dr. Gowin submitted a case study of an 85-year-old woman with a prior history of diabetes and dyslipidemia who developed a high fever, tested positive for influenza B by rapid influenza test, and was treated with intravenous peramivir.
Dr. Gowin submitted that multiple case reports show autoimmune disease onset after influenza vaccine, including cases of RA, PMR, systemic lupus, and reactive arthritis "in an HLA-B27 positive patient."
Dr. Gowin discussed the Soriano study, stating that it was a large collection of people with onset of PMR after influenza vaccine and two cases in which there was a recurrence following influenza vaccine. Tr. 63-64; Pet. Ex. 42.
Dr. Gowin testified that the question is not the safety of vaccinations for the general public but whether the vaccine can incite the onset of RA in a susceptible individual. Tr. 88. She agreed that the current studies have discounted the possibility but submitted these would be rare events and the studies are underpowered to detect such rare events. Tr. 81, Pet. Ex. 22 at 2. Dr. Gowin submitted that the literature suggests only seropositive RA was studied, likely due to misclassification or case definition. Tr. 82; Pet. Ex. 22 at 2. If the studies counted only seropositive RA, this would result in an underestimation of the number of cases of RA associated with vaccines. Id.; Pet. Ex. 22 at 2.
Dr. Gowin stated that there is a known connection between PMR and RA. Pet. Ex. 20 at 4. A prospective study of 116 patients after a one year follow up had a diagnosis change to RA in 20% of those initially diagnosed with PMR. Id. (citing Pet. Ex. 20-I at 6-7
Dr. Gurish's theory was based on molecular mimicry, stating that molecular mimicry could cause an interaction by the T cell receptor with that part of the antigen presenting molecule that is exposed. Pet. Ex. 23 at 5.
Dr. Gurish submitted that in addition to molecular mimicry, epitope spreading, bystander activation and polyclonal activation all provide immune responses that could lead to reactivity of self-components.
Dr. Gurish noted that genetics, health, and environmental exposure such as toxins, infections, or vaccinations may contribute to the breakdown of the immune system. Id. (citing Pet. Ex. 23-I at 85-86). Dr. Gurish stated twin studies prove that the individual nature of the genetic composition of every human which is composed of inherited genes and superimposed epigenetic changes make it virtually impossible to predict how any one individual might react. Id. (citing Pet. Ex. 23-H at 978-79
Dr. Gurish cited to literature in support of the view that aging results in more variability of the immune system. Pet. Ex. 25 at 2. The immune system is under constant regulation to allow protective immune response while curtailing autoimmunity. Id. (citing Pet. Ex. 25-B at 225-26
Dr. Gurish agreed with Dr. Gowin's opinions; he discussed a case study of a patient who developed RA two weeks after receiving a flu vaccine.
Dr. Matloubian stated that there is no biological evidence linking influenza virus to RA or any other autoimmune disease. Resp. Ex. A at 8. Dr. Matloubian addressed Dr. Gowin's statements about HLA-B27 positive patients, stating people who are HLA-B27 positive are genetically predisposed to develop this type of arthritis usually a couple of weeks after infection with certain microorganisms. Id. Six percent of the US population has HLA-B27. Id. With the millions of influenza vaccines administered yearly, one would expect to see more cases of vaccine associated rheumatoid arthritis if the association existed. Id.; see Pet. Ex. 20-B at 645. Further, there is no indication in his records that petitioner is HLA-B27 positive.
Dr. Matloubian addressed the same case study submitted by Dr. Gowin of the smoker with a 12-year history of RA who developed vasculitis two weeks after influenza vaccine. Resp. Ex. A at 9 (citing Pet. Ex. 20-C). Dr. Matloubian noted that she was taking medications known to be associated with vasculitis which could have been the cause of the development of vasculitis independent of the vaccine. Id. Dr. Matloubian further pointed out that the authors of the case study concluded that temporal relationship between vaccine and onset of rheumatic disease does not prove cause and effect. Resp. Ex. A at 8-9 (citing Pet. Ex. 20-C at 7).
Dr. Matloubian agreed with Dr. Gowin that epidemiologic studies provide evidence for hypothesis "to ask if there is causal link, mechanistically," between influenza vaccine and PMR/RA and are useful in generating a hypothesis. Tr. 286. However, Dr. Matloubian did not agree that the studies presented in this case were underpowered. Id. He pointed out that the Bengtsson article, for example, discussed multiple studies concluding that in combination there was no signal to say there was an association between vaccinations and development of RA. Tr. 286 (citing Resp. Ex. A-11 at 1833).
Dr. Matloubian stated that despite the "theoretical simplicity" of molecular mimicry, such a mechanism has rarely been persuasively demonstrated as the cause of autoimmunity, except for rheumatic fever after streptococcal bacterial infection. Resp. Ex. A at 10-11. For molecular mimicry to be relevant, the natural infection must lead to the development of the disease. Id. Research of the literature finds no mention of influenza infection being associated with polyarthritis. Id. Therefore, since the components of the vaccine are derived from influenza virus, it is "highly unlikely" that a mechanism such as molecular mimicry can cause arthritis due to vaccine. Id. (citing Pet. Ex. 20-H at 5). Further, hundreds of millions of people worldwide are affected with influenza each year and there is no epidemic of PMR or RA after the virus itself. Therefore, the theory that molecular mimicry caused petitioner's disease is highly speculative in Dr. Matloubian's opinion. Id.
Dr. Matloubian discussed the Pelton article in which lymphocytes specific to a pathogen were found in joints of RA patients as submitted and discussed by both Dr. Gowin and Dr. Gurish. Tr. 251-52; Resp. Ex. C-4. Dr. Matloubian is an expert in lymphocyte trafficking. Resp. Ex. B at 2. He stated that it is not surprising to see a pathogen at an inflammatory site and the findings do not imply the involvement of that pathogen or the lymphocyte specific for it in the pathogenesis of the autoimmune disease. Resp. Ex. A at 11. Natural infections lead to memory lymphocytes, which circulate through the blood and tissues surveying for specific invading pathogens. Tr. 252. The memory lymphocytes would circulate through sites of inflammation such as RA synovium checking to see if their specific pathogen was the culprit. Id. The lymphocytes specific to influenza virus found in the joints of those with RA in the study are irrelevant. Resp. Ex. A at 11. Lymphocytes are bystanders, not the culprits, in the inflammation. Id. They merely migrate to the area of inflammation wherever chemokines are being expressed, explaining why so many lymphocytes with so many specificities are found in the RA synovium and other sites of inflammation. Resp. Ex. C at 5. The Pelton study showed that the lymphocytes migrated to the joints which are already inflamed; they did not cause the inflammation. Resp. Ex. C-4 at 660.
Dr. Matloubian agreed with Dr. Gowin that in practice, no distinction is made between seronegative and seropositive RA, since the medications available for treatment of inflammation are limited. Resp. Ex. C at 3. However, the distinction exists in the pathogenesis of the two diseases. Seropositive RA has a presence of autoantibodies, whereas none exist or are known for seronegative RA, suggesting that mechanisms that lead to the breakdown of tolerance and generation of autoimmunity in each case may be different. Id.
The experts agree that there are no known autoantibodies or antigens identified in PMR or seronegative RA so therefore, no sequence of amino acids can be shown to compare to those in the influenza vaccine. Dr. Matloubian stated that if a pathogen does not contain any molecular mimic that is associated with a specific autoimmune disease, that autoimmune disease will not manifest. Tr. 200-01. Dr. Matloubian discussed a 2017 paper in which Dr. Gurish was a co-author. The paper raised the question of whether B cells even play a role in seronegative RA. Tr. 257 (citing Resp. Ex. F
Petitioner has failed to file any literature in this case to support a finding that influenza or the influenza vaccine can cause and/or trigger PMR or seronegative RA. Though Dr. Gowin criticized many the studies filed in this matter as underpowered, she agreed that none of the studies demonstrated a clinical likelihood of PMR or RA whether seropositive or seronegative following an influenza vaccine or a bout of influenza. Tr. 297-98. She also acknowledged that millions of people receive the flu vaccine every year, but was unable to provide a single example of a case report or study connecting the vaccine to either PMR or RA. Id. Dr. Matloubian pointed out that the literature relied on by petitioner showed an abundance of T-cells in seropositive RA synovium, highlighting the importance of tissue localized T cell/B cell interaction. Tr. 212-13. However, T cells do not exist in seronegative RA, and it is unknown whether there is any T cell/B cell interaction in seronegative RA. Id. Dr. Matloubian concluded that there is no known connection between influenza virus and PMR and/or RA. Tr. 227.
Dr. Matloubian added that it is rarely known what the cause of a patient's RA is, with a few exceptions. Tr. 191. For example, it is known that hepatitis B and C have been associated with arthritis, so testing for both conditions is necessary for treatment. Id. However, aside from rare instances, there is otherwise no known cause for RA and PMR. Tr. 192.
Dr. Matloubian posited that trauma has been considered a cause of RA and submitted an article at the hearing regarding trauma and RA. Tr. 232-33; see generally Resp. Ex. L.
In assessing the reliability and credibility of an expert's opinion, a special master must consider whether the expert offering the opinion is testifying within his training or expertise. Walton v. Sec'y of Health & Human Servs., No. 04-503V, 2007 WL 1467307, at *17-18 (Fed. Cl. Spec. Mstr. Apr. 30, 2007) (otolaryngologist not well suited to testify about disciplines other than her own specialty). In recognizing the liberality with which evidence offered in Vaccine Program cases is treated, I read and evaluated all of the testimony of the experts offered and all of the literature filed in this case and gave appropriate weight to whether certain testimony is beyond a particular expert's purview. See, e.g., King v. Sec'y of Health & Human Servs., No. 03-584V, 2010 WL 892296, at *78-79 (Fed. Cl. Spec. Mstr. Mar. 12, 2010) (finding petitioner's expert far less qualified to offer opinion on general causation issues pertaining to autism than specific issues pertaining to the petitioner's actual medical history, given the nature of the expert's qualifications). Dr. Gowin is a treating rheumatologist who focuses her practice on clinical diagnosis and treatment of rheumatological conditions, including RA. Though Dr. Gowin participates in trials and research related to rheumatological conditions including PMR and RA, she only participates in the clinical side of the trials by recommending patients for a study rather than the research or data gathering. Tr. 43, 67; Pet. Ex. 21 at 1, 8-10. Petitioner's other expert, Dr. Gurish, was an immunologist who focused his practice on mast cell development and the function of innate and adaptive immune responses. Pet. Ex. 24 at 1. Both of petitioner's experts are/were well-credentialed and impressive, but neither expert's practice and research focus on the treatment and development of RA and PMR as heavily as Dr. Matloubian's practice and research. Resp. Ex. B at 2, 6-9. Thus, Dr. Matloubian's testimony and reports were more persuasive than that of Drs. Gowin and Gurish.
PMR, seronegative RA, and seropositive RA are diseases of unknown cause. The literature filed in this matter fails to provide any scientific evidence that either influenza virus or influenza vaccine is associated with PMR, seronegative or seropositive RA. Drs. Gowin and Gurish opined that petitioner's diagnoses of PMR and subsequent seronegative RA are related and were caused by and/or triggered by the influenza vaccine he received. Petitioner provided one case study of an 85-year-old who developed PMR following influenza virus. See Pet. Ex. 44 at 345-46. The case study provides no support epidemiologically or mechanistically for the hypothesis that influenza virus was associated with the development of her PMR. See id. The authors of the study concluded that the relationship, if there was one at all, was temporal and could not say that she would not have developed PMR in any event.
Moreover, seropositive RA and seronegative RA are different diseases, though clinically they are treated the same. Over 55,000 cases of RA are diagnosed each year. PMR is a disease typical in those who are over 50 years of age and has a usual time of onset in the fall and winter months. The prevalence of these diseases and the onset timing makes a temporal relationship to influenza vaccinations more likely a coincidence. More troubling is that there is known cause of PMR or seronegative RA, and no known autoantibody associated with either condition. The experts all agree that petitioner has PMR and seronegative RA. Therefore, though petitioner's experts provided detailed descriptions of the immune system and molecular mimicry, which could explain a plausible theory for seropositive RA with known autoantibodies, the theory does not apply to PMR or seronegative RA. Petitioner has provided no evidence to suggest what in the influenza vaccine was mimicked to cause or trigger PMR/seronegative RA when neither disease has a known cause or a known autoantibody.
As such, petitioner has failed to satisfy Prong I.
In order to sustain his burden under Prong II, petitioner must show that the flu vaccine caused and/or triggered his PMR and/or RA.
Both Drs. Gowin and Gurish opined that molecular mimicry was at play in the development of petitioner's PMR and subsequent seronegative RA diagnoses. Tr. 85-86, 165. However, when asked what in the vaccine was being mimicked in this mechanism, neither expert could provide an answer. Tr. 88, 147-48. Dr. Gowin responded, "I don't think I can give you a specific antigen, Dr. Gurish may be able to do a better job of explaining that." Tr. 88. Dr. Gurish was similarly unable to provide an example of what components in the flu vaccine were being targeted or mimicked during molecular mimicry. Tr. 147-48. Dr. Matloubian stated that while molecular mimicry works in vaccine-associated injuries, since there is no known antibody that causes PMR or seronegative RA, to suggest molecular mimicry as the mechanism in this case would be speculative at best. Tr. 230-31 ("[H]ow do you say something mimics something when you don't know what it is. In [the] case of Guillain-Barre [syndrome], we know the target is the gangliosides on the nerve cells, so then you can say like what mimics ganglioside, but for seronegative RA, we hypothesize that it's some synovial joint antigen, but we don't know what it is.").
Dr. Gowin concluded that petitioner met the diagnosis of PMR based on shoulder and hip girdle pain including arms, shoulders, buttocks, groin and back with stiffness and elevated ESR. Tr. 110. His PMR transitioned into RA with petitioner meeting the 2010 criteria of RA. Other causes of inflammatory arthritis were ruled out. His pre-existing osteoarthritis would not have made him more likely to have an immune reaction to flu vaccine and would not have caused such diffuse pain and elevated markers. His onset was within weeks of the influenza vaccination, consistent with reactive autoimmune syndromes reported in the literature. Petitioner's knee replacement in May of 2011 did not show evidence of synovitis in the joint. In Dr. Gowin's opinion, both temporal relationship and biological possibility exist for the flu vaccine to have triggered the onset of petitioner's RA. Pet. Ex. 20 at 4-5; Pet. Ex. 22 at 2. However, Dr. Gowin's conclusion was not based on accurate information. Petitioner never had an elevated ESR and had only a mildly elevated CRP on one occasion. Pet. Ex. 7 at 62, 64. All of his other blood work was normal. He had constant moderate pain and swelling of his knee following his knee replacement in May 2011, which continued even after Dr. Dietrick did corrective surgery on his knee. Pet. Ex. 7 at 62; see generally Pet. Ex. 7. He had a history of right thigh burning, tingling, and numbness that had persisted for a month prior to the day he received the allegedly causal flu vaccine. Pet. Ex. 2 at 16; Pet. Ex. 17 at 1. Dr. Gowen concluded that onset of symptoms was within weeks of the October 14, 2011 vaccination rather than in December of 2011 as reported by petitioner throughout his medical records.
According to Dr. Gurish, there was no alternative cause for petitioner's development of his rheumatologic condition except the influenza vaccine. Tr. 140. When asked whether a failed knee replacement, with ongoing moderate to severe pain, inflammation and inability to walk would be considered a trauma significant enough to trigger rheumatic disease, he responded that trauma leads to inflammatory response, so he cannot say it could not happen, but he did not see any evidence in this case for that. Tr. 156-57. However, it is the law of the Vaccine Program that evidence of the development of a disease and/or injury temporally following a vaccination is insufficient on its own to establish causation. Grant v. Sec'y of Health & Human Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992). Merely identifying the vaccine as causal because of its existence as a known, pre-onset occurrence is insufficient to establish causation without corroborative record proof demonstrating the "logical sequence of cause and effect" required. Id. A wide variety of indirect and circumstantial evidence can support that determination, whether in the form of test results or witness testimony. Thus, Dr. Gurish and Dr. Gowin's opinions of temporal association between the vaccine and petitioner's development of PMR and RA are insufficient to support a finding of entitlement.
Dr. Gowin opined that the influenza vaccine is an antigen vaccine. Tr. 111. When pushed to give an explanation as to how this caused or triggered PMR or RA, she stated, "I don't know that I can give you the specific antigen on the cell or in the vaccine or the adjuvant that it could have even been." Tr. 112. It is of note that the influenza vaccine petitioner received did not contain any adjuvants. Tr. 205.
Several factors are troublesome in this case. Petitioner presented on the day of his vaccination, October 14, 2011, with complaints of symptoms of tingling, burning, and numbness of the left thigh ongoing for weeks that could have been attributed to PMR. Pet. Ex. 2 at 16. Though petitioner and his wife initially testified to the onset of his symptoms in late November, petitioner's physicians' records more persuasively show that his shoulder pain and hip pain arose in mid-December 2011, following his return to work and after having been sedentary since his May knee surgery. Further, his pain and inability to walk during the holiday events in December were ultimately admitted by petitioners to be more related to his knee injury. Tr. 9-10, 29-30. Petitioner repeatedly reported to all his physicians that his symptoms began in December of 2011. On January 20, 2012, petitioner's CRP level was slightly elevated, but the rest of his bloodwork was normal. Pet. Ex. 6 at 64-65. An elevated CRP level is an indication of general inflammation, which petitioner may have had because of his knee injury. Rapid response to prednisone is typical for pain and inflammation, and in fact, petitioner reported to Dr. Dietrick that he had to increase his prednisone following his corrective knee surgery to deal with the pain. Pet. Ex. 7 at 53.
Later records show that petitioner was suspected of having seronegative RA in March 2012, which was confirmed in July 2012 with only one medical record showing joint swelling by Dr. O'Connor, but that was denied by petitioner himself. Whether petitioner had PMR that evolved into seronegative RA or evolving seronegative RA all along, matters little. As set forth at length above, neither PMR nor seronegative RA has a known cause or autoantibody associated with it and neither has been associated with influenza vaccine or virus. Coupled with the fact that the onset of both is typical in those over 50 years of age, which petitioner was, with 55,000 cases of RA diagnosed each year, the temporal association with the influenza vaccine appears to be more coincidence. Petitioner failed to adequately provide a plausible theory for how the flu vaccine could cause or trigger either disease, or that it did so in this case. Petitioner further failed to provide any literature to support a correlation between influenza virus or vaccine and either PMR or seronegative RA. Thus, petitioner has failed to satisfy the requirements of Prong II.
To satisfy the third Althen prong, petitioner must establish a "proximate temporal relationship" between the vaccination and the alleged injury. Althen, 418 F.3d at 1281. This "requires preponderant proof that the onset of symptoms occurred within a timeframe for which, given the medical understanding of the disorder's etiology, it is medically acceptable to infer causation-in-fact." De Bazan, 539 F.3d at 1352. Typically, "a petitioner's failure to satisfy the proximate temporal relationship prong is due to the fact that onset was too late after the administration of a vaccine for the vaccine to be the cause." Id. However, "cases in which onset is too soon" also fail this prong; "in either case, the temporal relationship is not such that it is medically acceptable to conclude that the vaccination and the injury are causally linked." Id.; see also Locane v. Sec'y of Health & Human Servs., 685 F.3d 1375, 1381 (Fed. Cir. 2012) ("[If] the illness was present before the vaccine was administered, logically, the vaccine could not have caused the illness.").
As set forth above, the medical records clearly show that if petitioner did not already have symptoms of PMR and/or seronegative RA on or before the date of his flu vaccine, he consistently reported onset of symptoms as mid-December 2011, with seronegative RA suspected in March of 2012, over two and five months following his receipt of the flu vaccine, respectively. Therefore, petitioner needed to demonstrate an appropriate timeframe for the development of PMR and RA following the flu vaccine to satisfy his burden under Prong III. Langland, 109 Fed. Cl. at 443 ("[T]o satisfy the `proximate temporal relationship' prong of the Althen test, petitioners must demonstrate, by a preponderance of the evidence, that the onset of symptoms occurred within a time frame for which it is medically acceptable to infer causation-in-fact....With no reputable theory as to how the vaccination could cause the injury, this exercise is not possible.") (citing De Bazan, 539 F.3d at 1352).
The experts' opinions regarding the onset of petitioner's PMR and seronegative RA was at odds with the contemporaneous medical records. Dr. Gowin stated that petitioner's onset was within weeks of his influenza vaccine. Pet. Ex. 20 at 1. Dr. Gurish placed onset at six weeks from vaccination. Pet. Ex. 23 at 5. Thus, both place onset sometime in November of 2011 in reliance on petitioner's affidavit rather than the medical records, which confirm that petitioner reported onset of symptoms to his physician as December 2011 consistently throughout the record. See Pet. Ex. 6 at 65.
Though Dr. Matloubian opined that molecular mimicry was not a plausible biological mechanism for PMR and seronegative RA, he pointed out that generally, it takes T cells 7 to 14 days to reach their peak levels. Resp. Ex. A at 12. During this time, they can provide help to activated B cells, which in turn make antibodies within 7 to 10 days. Id. In infections known to cause autoimmunity, the temporal association between inciting infection and development of disease is a couple of weeks, not more than a month. Resp. Ex. A at 12 (citing Pet. Ex. 20-B).
Further, both Dr. Gowin and Dr. Matloubian agreed that individuals can test positive for seropositive RA for years without any clinical symptoms of disease. Both agreed that it is unknown what may trigger the manifestations of clinical symptoms other than smoking in anti-CCP seropositive RA. Tr. 83-84. Dr. Matloubian questioned when a diagnosis should be made, when the autoantibodies are found in the body or when clinical manifestation of disease begins. Tr. 212-13. Therefore, since neither PMR or seronegative RA has any known autoantibodies, when petitioner's disease may have started is unknown, but petitioner's clinical symptoms of PMR, if they were not already present at the time of his vaccination, began by his own reporting in mid-December of 2011, two months after his vaccination. His seronegative RA was suspected in March of 2012 and diagnosed in July 2012.
Petitioner's prior medical history of back pain with associated sciatic pain, neck pain and diabetic neuropathies before, on the day of, and after receiving the flu vaccine are so undefined and insidious in nature, it is impossible to know when the onset of either PMR or seronegative RA truly began. Arguably, petitioner's complaints on the day of the vaccine could have been symptoms of PMR. Alternatively, based on the medical records and the reports by petitioner upon presentation to his doctors, his symptoms of PMR began in mid-December and were diagnosed in January, while his rheumatologist raised the issue of RA in March but did not diagnose it until July because there was no objective evidence to support it. Moreover, while the experts discussed the immune system, how it works and reacts, and their respective theories regarding the flu vaccine and molecular mimicry, they never discussed a timeframe in which that process would result in the manifestation of either disease. Thus, petitioner has failed to sustain his burden under Prong III, as no timeframe was provided.
Accordingly, I find that petitioner has not established entitlement to compensation and his petition must be dismissed. In the absence of a timely filed motion for review (see Appendix B to the Rules of the Court), the Clerk shall enter judgment in accordance with this decision.
