Sex: F
Vaccine: LYME
Symptoms: Compression fracture, Computerised tomogram normal, Cushingoid, Decreased appetite, Dehydration
Clinical narrative: This case was reported by a lawyer via a statement of injuries and described the occurrence of muscle aches in a female subject of unspecified age who was vaccinated with LYMErix for prophylaxis. A physician or other health care professional has not verified this report. On an unspecified date the subject received unspecified dose of Lymerix (unknown). At an unspecified time after vaccination with Lymerix, the subject experienced muscle aches, liver disorders, fatigue, flu-like symptoms, headaches, "possible" memory loss, and decreased activities of daily living. Additionally, the subject experienced "rheumatologic, neurologic, and/or cognitive impairment of an autoimmune, immune-mediated, or other mechanism. At the time of reporting the outcome of the events was unspecified. Follow up information was received on 27 December 2007 via medical records. Medical history included two past episodes of Lyme disease, glaucoma, cataract surgery, atrial trigeminy and sinus arrhythmia, as well as dizzy spells beginning in approximately 1999. In September 1999 and/or November 1999, she experienced a tick bite with a surrounding inflammatory reaction and rash, and was treated with a two week course of amoxicillin. She was reportedly advised that Lyme disease and Ehrlichiosis were excluded. In late November 1999, she developed fatigue. Alanine aminotransferase was approximately 1400 U/L at that time, and aspirate aminotransferase was over 700 U/L. Several weeks after completing amoxicillin therapy, she developed an itchy body rash felt to be allergic dermatitis, and was treated with cortisone injection and a course of doxycylline for Lyme disease. Aminotransferase values were reportedly elevated until mid-January 2000 (ALT approximately 189 and AST approximately 130). Acute viral hepatitis serologies were negative. In early 2000 she presented with hepatitis determined to be autoimmune in nature, and a biopsy on 24 March 2000 revealed hepatitis with fibrosis/early cirrhosis. Prednisone therapy was initiated. Upon follow up on 19 April 2000, the subject reported a "return to feeling of good health" with persistent lightheadedness, which was not attributed to liver disease. In approximately November 2000, she experienced liver enzyme abnormalities initially described as an allergic reaction from antibiotics. In February 2001, a percutaneous liver biopsy revealed features of chronic active hepatitis with bridging necrosis and early fibrosis. She was diagnosed with autoimmune hepatitis and treatment included prednisone and Imuran. Between 04 April 2001 and September 2006, the subject was seen on a regular basis at a nephrology practice. Upon initial examination on 04 April 2001, the 77-year-old subject reported that she had been in "excellent health" prior to 2000. She was being "followed and treated" for autoimmune hepatitis, and also had been diagnosed with osteoarthritis. Complaints included fatigue, a "funny sensation in her head", recurrent transient skin rash, and lightheadedness. Over assessment included chronic active hepatitis with fibrosis, in addition to evanescent skin rash and present facial telangiectasias suggestive of collagen vascular disease. Upon examination on 23 July 2001, complaints included decreased energy, lightheadedness, a "band like sensation around her head", feeling enervated almost always associated with standing or sitting in one position, swelling of hands and limitation of hand function, and morning stiffness. She was significant for a past history of positive antinuclear antibodies (ANA), but past rheumatological studies included rheumatoid factor, lupus panel, and complement levels were all negative. Medications included prednisone, Fosamax, and Citracal. Examination revealed synovial thickening over the proximal interphalangeal joints with normal grip strength. Hands were "close, consistent with Raynaud's phenomenon." Assessment was of autoimmune hepatitis "presumably in the context of systemic illness in this elderly woman". Liver function tests at that time were normal. She was seen for follow up on 09 October 2001 and was continuing to experience fatigue. She was receiving prednisone for her "autoimmune disorder", and it was noted that her liver function tests had been normal since discontinuation of Imuran. She had been diagnosed by x-rays with degenerative arthritis consistent with osteoarthritis on an unspecified date, and reported that her arthritic problems had "pretty much resolved with just mild exercise. She was also reported to have osteoarthritis and autoimmune hepatitis that was "currently stable in apparent remission". On 13 March 2002, she complained of occasional hip pain that was assessed as musculoskeletal rather than renal in origin. Autoimmune hepatitis remained in remission. She returned on 04 June 2002 and reported feeling "the best she has felt in a long time". Her dose of prednisone had been tapered down to 2.5 mg daily, liver enzymes were normal and hepatitis remained in remission, and osteoporosis was stable on Fosamax and calcium. In a letter dated 19 June 2002, her digestive disease specialist expressed the opinion that her autoimmune chronic active hepatitis and early cirrhosis was believed to have been "precipitated by an Amoxicillin reaction in the fall of 1999). On 24 September 2002, she was off prednisone, and complained of tiredness as well as dizzy spells that had "plagued her for the last three years". Overall assessment was chronic active hepatitis in remission and osteoporosis, as well as dizziness that was "possibly vascular related". In an office note dated 30 December 2002, it was noted that osteoporosis was steroid-induced. Dizzy spells were improved that that time. In a letter dated 05 February 2003, a digestive disease physician noted that liver function tests had remained normal, "thus I believe she has resolved her chromic autoimmune hepatitis". On 22 April 2003, it was noted that her autoimmune hepatitis had been in remission for approximately 2 years, and that her physician believed "this well may have been a consequence of amoxicillin and therefore it is out of her system now". The subject was evaluated by neurologists between as early as November 2003 through as recently as December 2004. Upon presentation on 24 November 2003, complaints include fatigue ("predominantly muscular), dizziness ("weakness and lightheaded"), hearing deficiency, upper back pain, balance difficulties, difficulty getting up from a chair at times, nocturia, and swelling and numbness of the right hand. Examination revealed bradykinesia and cogwheeling in the right and left upper extremities, and paucity of facial expression. Impression was of "signs and symptoms that are diagnostic of Parkinson's disease". The neurologist stated "I believe there are no conditions present which may be mimicking that so I am comfortable making a diagnosis of idiopathic Parkinson's disease". Treatment with Mirapex was initiated. Upon follow up on 22 January 2004, she exhibited diminished facial expression and gesturing, difficulty walking with falling/tripping, and apraxia with respect to right handwriting. She continued to experienced neurodegenerative symptoms which were assessed on 12 May 2004 as "probably cortico-basal ganglionic degeneration". The neurologist noted "I think that this (right hand) is developing the alien hand". The subject also reported sporadic memory, word finding difficulties, and fatigue. It was noted that her Parkinsonian plus syndrome was stable at that time. Subsequent diagnostic tests showed normal metabolism of the basal ganglia and thalamus "whereas if she had Parkinson's disease it would be diminished in those areas. She was referred to an expert in movement disorders for further evaluation. In March 2005, antinuclear antibody, rheumatoid factor, and Actin IgG results were positive. On 19 April 2005 she was evaluated at a movement disorders clinic. In addition to previously reported symptoms, she complained of a history of of visual perceptions difficulties starting in approximately 2001, possibly a problem with depth perception, noting an occasion when she had "fallen on stairs because she says these steps look flat". She also excessive daytime sleepiness, motor changes including fine motor difficulties, hand tremor greater in the right hand, and decreased activities of daily living. Examination revealed bradykinesia, decreased pinprick sensation in the distal lower extremities, and resting hand tremors. The movement disorders specialist comment "I suspected that she primarily has a cortical dementia". Recommendations included initiation of Aricept as well as use of a can for ambulation. She was seen for follow up by the nephrologists on 23 August 2005, at which time the subject complained of tremor that had worsened from intermittent to continual, accompanied by daytime drowsiness. She described a weight loss of ten pounds possibly attributable to stress, as well as difficulty concentrating and memory problems. Her physician commented that her sedimentation rate was 7 "so it is hard for me to believe that she still has an active autoimmune hepatitis". Additional complaints included blurred vision, red, dry and itching eyes, and occasional eye droop. Assessment was of "worsening symptoms of Parkinson's disease at this point in conjunction with the rest of her neurological problems", and it was also noted that her drowsiness/"fogginess" were possibly attributable to a sleep disorder. On 04 October 2005, a severe periodic limb movement disorder was observed in combination with mild obstructive sleep apnea, detected by diagnostic polysomnogram. By 05 October 2005, her condition had worsened further with respect to Parkinsonian symptoms, and she appeared cachectic with bitemporal wasting. She exhibited a marked resting tremor in the left and right arms and "quite bradykinetic movements". It was noted that she had received Mirapex on a prior occasion, which was stopped after she developed hallucinations. On 25 November 2005, she was referred for progressive dementia. Increased motor tome (right greater than left), cogwheeling of the wrists, and some decreased muscle bulk were noted on examination. The subject admitted to illusions/hallucinations, and had an "excellent memory for household events". The evaluating physician commented that the subject appeared to have 'diffuse Lewy body disease, with rather classic Lewy body dementia (mainly visuomotor and visual hallucinations), Parkinson's disease, gastrointestinal slowing, orthostatic hypotension, and sleep disorder. Norflex was discontinued for that time (presumably prescribed for tremor), and Seroquel was started. On 30 November 2005, the subject reported that she had been seen by another neurologist who felt "the most likely diagnosis was Lewy body disease" based upon Parkinsonian features as well as a documented rapid eye movement (REM) sleep disorder). Assessment by the nephrologists on that date included "question Parkinson's versus Lewy body disease), as well as sleep disorder with restless leg". Treatment with Seroquel and Sinemet was initiated, followed by improvement of symptoms. On 24 January 2006, she reported improvement in functioning and decreased 'fogginess", although she complained of difficulty dressing herself due to tremulousness, as well as eye irritation which was attributed to lower eyelid retraction. A subsequent bone density study revealed worsening osteoporosis, and on 07 April 2006 assessment included "probable Lewy body disease versus Parkinsonianism", weakness which was attributed to a urinary tract infection, "significant" osteoporosis, and sleep disturbance. On 26 May 2006, progress notes indicated that the subject's cognitive status was much better on Seroquel, but that an increase in Sinemet dosage was needed. She complained of balance that was "not good" and falling; visual hallucinations were resolved. In June 2006, the subject developed "significant orthostatic changes in blood pressure with lightheadedness and dizziness, which were attributed to an increase in Sinemet and Seroquel dosages. On 07 June 2006, the subject reported no improvement in tremulousness or involuntary limb movement despite changes to dosages of Seroquel and Sinemet. The dose of Sinemet was reduced. She was subsequently evaluated on 29 June 2006, and assessment included autoimmune hepatitis "apparently in biochemical remission", Lewy Body disease with Parkinsonian features, mild dementia "which appears to have stabilized", and osteoporosis that was stable on Fosamax. Orthostatic hypotension was resolved on that date. On 19 September 2006, complaints included profound excessive daytime drowsiness, attributed to obstructive sleep apnea and periodic limb movement disorder, and difficulty hearing. At that time she was receiving Aricept as well as "the anti-Parkinsonian drugs", and reported that her head was clearer although tremors had worsened. The subject was admitted to the hospital on 06 October 2006 due to severe right hip pain following a fall, without evidence of fracture. Other diagnosis included left pleural effusion and possible pneumonia with fever and chills, an "old fracture" of the left third and fifth ribs", Lewy body disease with dementia and Parkinsonian features, chronic autoimmune hepatitis, and osteoarthritis. Medications included Aricept, Citracal, Sinemet, and Seroquel, and she had recently discontinued Florinef. She improved and was able to resume walking, and was discharged on 06 October 2006. On 09 January 2007, the subject was hospitalized after falling and complaining of severe lower back pain. Overall assessment included acute compression fracture of L1, Lewy body disease/dementia with Parkinsonian features, osteoporosis, autoimmune hepatitis, and history of pneumonia. Neurological examination revealed worsening tremor resulting in difficulty functioning, and increasing memory loss due to dementia. She was also diagnosed with hypokalemia and dehydration while hospitalized. Pain management included morphine and Percocet, and x-rays revealed mild arthritis in addition to acute L1 compression fracture. She was discharged on 12 January 2007. The subject was hospitalized from 06 March 2007 to 14 March 2007 for a femoral neck fracture following a fall, and underwent left hip arthroplasty on 07 March 2007. While hospitalized, medications were discontinued and she was improved by the time of discharge on 14 March 2007. Final diagnosis in addition to femur fracture included Lewy body disease with Parkinsonian features and dementia, and chronic autoimmune hepatitis "quiescent for osteoporosis". Discharge medications included Aricept, Florinef, Seroquel, and Sinemet. According to the subject's husband's report to his physician on 01 October 20007, the subject was "failing at the convalescent home and is pretty much on comfort measures at this point". On 04 January 2002 she complained of decreased energy and lack of appetite, and was assessed to have a probable urinary tract infection. On 04 June 2002, she was evaluated for what appeared to be contact dermatitis with a skin rash. In January 2006 and April 2006 she complained of eye irritation and crustiness that were assessed due to allergic conjunctivitis. The subject also experienced evanescent skin rash with steroid therapy, lower extremity edema, recurrent urinary tract infections, pneumonia with fever and chills, pleural effusion, dehydration, hypokalemia, and orthostatic blood pressure changes with lightheadedness and dizziness, and was diagnosed with obstructive sleep apnea. These were assessed to be incidental findings upon medical records review.