Age: 44.0
Sex: F
Vaccine: LYME
Symptoms: Cognitive disorder, Confusional state, Fatigue, Headache, Hypoaesthesia
Clinical narrative: This report described the occurrence of arthritic pain in a female patient who received LYMERIX. This report was received as part of litigation proceedings, and was subsequently medically confirmed. The medical history included a viral upper respiratory infection and Eustachian tube dysfunction on 10 March 1999, and "presumed BACTRIM allergy" and allergic rhinitis on 10 may 1999. Additional medical history included mitral valve prolapse for which she received prophylactic amoxicillin, joint pain associated with possible fibromyalgia, whiplash, neck stiffness and occasional pain, low back pain radiating to the groin, and headaches. An arthritis profile was planned in May 1998 for evaluation of possible fibromyalgia. Paternal history was significant for gout and arthritis. The patient was 44 years of age at the time of immunization. The patient received injections of LYMERIX on 27 April 1999(lot "LY21FS"; not a valid lot number)  and 25 May 1999 (lot LY123A9). On 03 September 2003, the patient's attorney alleged that the patient "suffered arthritic pain, fatigue, headaches, myalgias and muscle spasm. The onset of her symptoms is not clear at this time." Treatment and outcomes of the alleged events were not reported. The following information was received via medical records. The patient received her initial LYMERIX injection on 27 April 1999 and the second LYMERIX injection on 25 May 1999. Initial onset of symptoms was noted to be 26 May 1999, the day after the second LYMERIX vaccination. Subsequent to receiving the second LYMERIX vaccination, in the summer of 1999, the patient developed joint pains, headaches, cognitive difficulties, achiness, fatigue of a "diffuse nature," chest spasms, palpitations, and chest pressure. A work-up for possible coronary disease was negative, and she was diagnosed with mitral stenosis of a mild nature. She experienced sharp pain in both knees and flu-like symptoms. Several Lyme tests and rheumatoid testing were "always negative." She developed left trochanter bursitis treated with a cortisone injection. Over 1999, 2000 and 2001, she complained of fatigue, cyclical joint pain, lethargy and headaches. In March 2000, x-rays of the hips and spine were normal. The patient reported feeling better following treatment with Voltaren, but continued to complain of chronic fatigue. The third LYMERIX vaccination, due in April 2000, was not administered. Examination showed painful trigger points in the trapezius muscles with limited neck range of motion. In June 2000, the pt twisted her knee, and since that time experienced persistent achy pain along the medial aspect of the knee, in addition to pain while going up and down stairs, walking and running. Magnetic resonance imaging performed in November 2000 revealed a small tear in the peripheral aspect of the medial meniscus junction. On 04 June 2001, the patient was evaluated for left knee pain. Medical history as of 03 April 2002 was noted to include fibromyalgia and migraines. In June 2002 the patient received a tick bite. Although results of ELISA testing were negative, a blood test was positive for B. henselae which was considered to be indicative of Lyme infection. Treatment for central nervous system Lyme disease and Bartonellosis was initiated and included CEFTIN, BIAXIN, PLAQUENIL, doxycycline, amoxicillin, ROCEPHIN, ZITHROMAX, Rifampin and CLAFORAN. A PICC line was placed for IV Lyme disease therapy. CLAFORAN was stopped after the patient developed bone marrow suppression, and doxycycline therapy was extended. She experienced significant improvement in joint pain following doxycycline therapy. Complaints included cognitive decline, facial numbing and burning, left arm and hand numbness, "squeezing" chest pain, shooting pain in legs, fatigue, muscle and joint pain, and memory problems. She also experienced leg cramps, which were possibly due to dehydration and/ or electrolyte abnormality, left side mid-thoracic spine tenderness, left sciatica, occasional intermittent numbness of the left foot, and left trochanteric bursitis. She was diagnosed with possible central nervous system Lyme disease an Lyme arthritis, associated with back pain accompanied by radicular symptoms. In July and August 2002, she received herbal remedies including Chigong treatment for back and hip pain and arm numbness. In 2003, she had a positive Lyme PCR and positive Lyme ELISA, abnormal MRI showing white matter lesion in the right frontal lobe, abnormal cerebrospinal fluid, and significantly abnormal SPECT scan with hypoperfusion of the left frontal and temporal lobes. Medical records dated 18 March 2003 included an assessment of Lyme disease, headaches, arthritis, fatigue and myalgia. On 15 April 2003 she complained of pain in the hips and knees when standing, but reported improvement in achiness. Intravenous doxycycline was continued for treatment of Lyme disease. Additional complaints included cognitive decline, fatigue and muscle and joint pain. In July 2003, Lyme symptoms including confusion and blurred vision had improved, although she continued to experience knee pain and stiffness. On 12 August 2003, the patient complained of increased pain in her back and neck, palpitations, fatigue, numbness in her face and hands, and headaches, which the pt believed to be stress-related. Following the reported onset of arthritic symptoms, the patient experienced bone marrow suppression with significant neutropenia and atypical lymphocytes associated with CLAFORAN therapy, leg cramps possibly due to electrolyte abnormality and/ or dehydration, acid reflux, vaginal yeast infection, dermatitis, elevated liver function tests, gallstones, chest spasms and pressure, palpitations, "mild" mitral stenosis, sinus tachycardia, and allergies to clarithromycin and azithromycin. These were not reported as adverse events due to vaccine administration, but were found during the course of review of the pt's medical records. Therefore, they are not listed as adverse events. This report described the  On Sept 15 2004, the patients attorney alleged that the patient, now 49 years old, experienced autoimmune arthritis, fatigue, tingling, headaches, muscle pain and spasm with white matter hyperintensity on brain MRI (magnetic resonance imaging scan). Outcomes of these were not reported. Additional information was received from a lawyer on 03 April 2006 in the form of a statement of injuries. The statement of injuries indicted that the patient experienced pain and swelling in her joints, tingling in her extremities, severe pain in her spine, muscle pains and weakness, headaches, fatigue, possible neurological injuries, possible autoimmune disease, and decreased activities of daily life. Follow up information was received on 24 January 2007 via medical records. Medical history included elevated liver function tests including transaminases. Family history included osteopenia. On 01 June 2004, the subject was seen in consultation by a hematologist for evaluation of hypoglobulinemia following a two year history of CNS  Lyme disease and bartonellosis. Assessment included low normal IgG level and significant reductions in total IgA and IgM levels. The hematologist stated "In the context of her history of recurrent infections, other possible immune related phenomena, her failure to respond to the LYMERIX and PNEUMOVAX vaccines, and the positive family history for infectious illnesses. I think it is most likely that the subject has a common form of variable immunodeficiency". A peripheral blood smear showed minor white blood cell abnormalities, "likely congenital". On 08 June 2004, the subject was seen in follow-up by a neurologist, and mild degenerative changes of the cervical spine and some epidural lipomatosis of the dorsal upper thoracic spine were noted. The subject continued to ganglioneuritis, although there was no conclusive evidence of small fiber neuropathy. In January 2005 a bone density examination showed osteopenia of the hips and the spine. In March 2005, the subject was evaluated for osteomiosis. At the time, it was noted that she had experienced chronic Lyme disease post LYMERIX vaccination. The evaluating physician's impression was that the subject "may have primary hyperparathyroidism to account for her osteoporosis". On 11 May 2005, the subject was seen for an initial neurology consultation with complaints of pain in the knees, fatigue, arthralgia, lethargy, headache, hyperpigmentation, and memory disturbance subsequent to LYMERIX administration. Neurological evaluation showed minor abnormalities, including a single focus of frontal lobe hyperintensity, sensory loss in the legs to pinprick/vibrations/light touch stimulation, degenerative disc disease, polyarthralgia/polyneuropathy, imbalance of stance and tandem gait, hypo reflexia of the ankles, and intact cognition, cranial nerves, and limb strength. A punch skin biopsy showed significantly reduced epidermal nerve fiber. A hematology/oncology evaluation showed autoimmune common variable immunodeficiency, and endocrinologic evaluation  showed autoimmune thyroid disease (possibly parathyroid disease). Treatment included intravenous immunoglobulin followed by a "noted" reduction in neuropathic pain. On 17 May 2005, Fosamax was initiated for idiopathic osteoporosis. In a letter to the subject's attorney dated 01 July 2005, the neurologist stated that the subject "has an autoimmune syndrome caused by LYMERIX vaccination including encephalopathy and small fiber neuropathy, elevated IgG MAG antibodies, pancytopenia, arthritis and IgM and IgA immunodeficiency". A complete blood cell count, automated differential, and routine chemistry on 15 December 2005 revealed findings that were within normal limits. On 05 July 2005, she was evaluated in follow up for Lyme disease, and received treatment with normal limits. On 05 July 2005, she was evaluated in follow up for Lyme disease, and received treatment with Bicillin injection. Upon examination, she denied fatigue, fever, headaches, or dizziness. She underwent a rheumatology consultation on 23 September 2005, with a resulting impression of SSA positive polyarthralgia, polyneuropathy with mild symptoms of Sjogren's syndrome, and evidence of autoimmune thyroid disease and mild hyperparathyroidism. Plaquenil was continued. Ac coring to neurologist's letter dated 06 February 2006, repeat electrodiagnostic studies showed evidence of chronic distal demyelinating neuropathy, and a repeat  punch skin biopsy showed normal epidermal fiber density. The case was assessed by GSK upon follow up to be medically significant. The subject was hospitalized from 25 June 2003 to 29 June 2003 for neutropenia and fever associated with an allergic reaction to cefotaxime with associated bone marrow suppression, hemolytic anemia, and fever. She was also diagnosed with hyperparathyroidism, benign intrahepatic cyst, and diverticulitis. These considered to be incidental findings upon review of medical records. Follow-up received on 21 March 2007 via medical records. The subject was evaluated on 01 April 2005 by a neurologist for suspected neuropathy. At this vis tit her chief complaints were chronic fatigue and intermittent joint pains at the ankles, knees, elbows, writs and spine, chronic headaches and lump in throat when she swallows. Physician examination noted diffuse hyperpigmentation of her skin over the upper thoracic spine. The subject reported that a skin biopsy in 2001 revealed "post inflammatory changes." On sensory examination, vibration was mildly to moderately impaired at the large toes and mildly impaired at the ankles. Fingers were also impaired. The impression was that the subject's symptoms may be due to a "mild sensory neuropathy or ganglioneuritis or to central nervous sytem involvement." The cause is unknown but an inflammatory mechanism was considered to be a possibility. On 08 September 2005, she was evaluated by another neurologist who concluded since the start of IVIG therapy, the subject had noted overall less joint pain, intermittent fatigue, numbness, headache, and was able to run however it was not sustained. Neurological examination revealed improved stance and tandem gait. The findings were consistent with autoimmune small fiber sensory neuropathy, SSA seropositivity, IgM hypogammaglobulinemia, parathyroid and thyroid disease, hepatic dysfunction and hepatitis immunity. Future expedited VAERS reports for this LYMERIX case shall be referenced to BB-IND 5420, which is a change from the past reports referencing the voluntarily-revoked license (STN 103757). Follow up information was received on 30 April 2007 via medical records. Between 02 July 2002 and 08 August 2002, the subject was treated via a holistic health practice for pain, including Chinese herbal therapy and Chigong treatment. At the time of evaluation on 23 June 2003 for complaints including neutropenia with "a white count of 1200 white cells total and some abnormal liver function tests", the subject reported a two-day history of fever, shaking, chills , nausea, and vomiting. She was referred to the emergency room for further evaluation. Impression was of a subject with chronic CNS Lyme disease on intravenous antibiotics, who developed neutropenia and fever. On 24 August 2006, hepatology evaluation indicated that the subject had experienced elevations of liver functions test, which appeared to have occurred following initiation of IVIG therapy. Impression on that date was autoimmune syndrome with multiple autoantibodies. Hepatologist's notes indicated "doubt significant liver damage. Possible antibody dependent cytoxicity (ADCC) related to ? cross reacting hepatic antigens". At that time, the subject continued to receive a three -day course of IVIG every four weeks, and liver function tests were reportedly normal. Follow up information was received on 14 May 2007 via medical records. According to a letter written by the subject's neurologist dated 01 April 2005, the subject developed " a flu- like illness with sharp pains in her joints lasting approximately one day" within hours of receiving her second LYMERIX vaccination. She subsequently experienced recurrent diffuse joint pains and fatigue, and in 2001 a skin biopsy of a hyperpigmented macular lesion on her back reportedly showed post-inflammatory changes. In July 2001, "several days following a tick bite", she developed flu-like symptoms including fatigue, headache, joint pain, and short term memory deficits. She was treated with doxycycline, and subsequently with BIAXIN, PLAQUENIL, CEFTIN. In August 2003 she developed numbness of the left side of her face, hand, and leg, which gradually resolved but returned to a "lesser extent" in February 2005. Follow-up via medical records received on 06 June 2007. Through the course of review of the medical records, nausea and epigastric pain of unclear etiology were noted to be incidental findings. Esophagogastroduodenoscopy on 14 December 2004 revealed transitional type gastritic mucosa with minimal chronic non-specific gastritis. Follow up information was received on 14 September 2007 via medical records. On 13 July 2006, it is noted that the subject continued to experience peripheral neuropathy, and had recently "switched to Gamunex". Diagnoses on examination between October 2006 and November 2006 included Lyme disease, migraine, and neuropathy. Treatment included increased rest and fluids, and continued FIORINAL. On 6 January 2007, complaints included joint aches and neuropathy. Gamma guard infusions had been decreased to one day per week "as globulin levels have been high while on 3 days/week infusion." The subject noted headache, abdominal discomfort, and nausea following IVIG infusions. Assessment on that date included "neuropathy and myalgias post-LYMERIX vaccination". A trial of Ultram was initiated on that date to minimize tiredness. On 13 February 2007, she complained of myalgias following intravenous immunoglobulin therapy. Examination revealed full range of motion of major joints, without joint swelling or crepitus. Diagnoses included idiopathic peripheral neuropathy (unspecified) and palpitations as well as ongoing hyperlipidemia. On 27 February 2007, the subject presented with right sided chest pain and complained of having fallen on her ribs while skiing the previous weekend. She was diagnosed with a sprain in the thoracic neuropathy, mixed hyperlipidemia, cellulitis/abscess (leg), and ankle enthesopathy. On 08 May 2007, the subject was receiving continued intravenous immunoglobulin (IVIG) therapy "down to once a month" and experienced persistent weakness and an increase in numbness/paresthesias. Notes indicated "hold the Lipitor x one month and see if paresthesias improve". In November 2006, the subject developed rash on her arms, chest, and trunk which was assessed to be "most likely" a viral rash. She developed cellulitis/phlebitis associated with intravenous therapy, and experienced "severe" myalgias and fatigue following IVIG therapy. These, as well as the diagnoses of sprain (thoracic region), diverticulosis/diverticulitis, and hyperlipidemia were considered to be incidental findings based on medical record review. Follow up information was received on 09 October 2007 via medical records. On an unspecified date, the subject reported sensory dysfunction and mild large fiber sensory dysfunction was observed upon examination by a neurologist. In August 2004, treatment with Malarone and unspecified antibiotics was prescribed, which she interrupted for approximately one week while on vacation. She developed pain along the bilateral ribs, with some involvement from the back to the clavicle, and was diagnosed with costochondritis. In September 2004, the subject quit work and reported exhaustion and fatigue. Upon follow up with her neurologist on 28 January 2005, the subject reported improved joint pains and had not noticed the "sandpaper like sensations along her left face, arm and leg". She complained of some numbness and prickly sensations along her left face, and noted that her left leg was thought to be weaker than the right. Evaluation showed normal mental status functions and normal attention and concentration. Work-up, including skin biopsies, were unremarkable and the neurologist stated "there is no clear indication for [intravenous immunoglobulin] at this time. In 2004, the subject was also diagnosed with gastritis, an ulcer, and cholelithiasis. These were considered to be incidental findings upon medical record review. Follow up information was received on 19 October 2007 via medical records. In October 2004, the subject complained of pain in the region of the right seventh and eighth ribs, although radiographic findings showed no evidence of rib fracture. On 06 January 2005 the subject underwent a bone mineral analysis due to a clinical indication of menopause and osteopenia, and results indicated osteopenia of the hips and spine. A follow up bone mineral analysis in October 2006 showed continued osteopenia with a slight decrease in spinal T-score.