Age: 66.0
Sex: M
Vaccine: UNK
Symptoms: Ataxia, Axonal and demyelinating polyneuropathy, Babinski reflex test, Back pain, Bone marrow disorder
Clinical narrative: CIDP (chronic inflammatory demyelinating polyneuropathy);   This is a study report.  A 66-year-old male patient received blinded study vaccine (PF-06928316; placebo), intramuscular in left arm on 11Jan2022 12:36 as a single dose for prevention of RSV. Relevant medical history included: "hypertension", start date: 2005 (ongoing); "asthma", start date: 2015 (ongoing); "myocardial infarction", start date: 17Jan2022, stop date: 18Jan2022, notes: cardiac catheterization, angioplasty on 17Jan2022. Concomitant medications included: BYSTOLIC oral taken for hypertension, start date: 2008 (ongoing); VALSARTAN oral taken for hypertension, start date: 2007 (ongoing); HYDRALAZINE oral taken for hypertension, start date: Dec2021 (ongoing); ASPIRIN [ACETYLSALICYLIC ACID] oral taken for thrombosis, start date: 18Jan2022 (ongoing); BRILINTA oral taken for anti-platelet antibody, start date: 17Jan2022 (ongoing); COQ-10 oral taken for supplementation therapy, start date: 17Jan2022 (ongoing); TURMERIC [CURCUMA LONGA RHIZOME] oral taken for supplementation therapy, start date: 17Jan2022 (ongoing). There were no concomitant vaccines, or prior vaccinations (within four weeks). Historical Vaccine included a flu vaccine on 27Sep2021 for immunization.  The following information was reported: CHRONIC INFLAMMATORY DEMYELINATING POLYRADICULONEUROPATHY (hospitalization) with onset 18Jan2022, described as "CIDP (chronic inflammatory demyelinating polyneuropathy)". The patient was hospitalized for chronic inflammatory demyelinating polyradiculoneuropathy (start date: 24Feb2022, discharge date: 05Apr2022, hospitalization duration: 40 days). The event "cidp (chronic inflammatory demyelinating polyneuropathy)" required physician office visit and emergency room visit. Clinical course: The patient reported lower back pain beginning from 18Jan2022 and had bilateral lower extremities (BLE) weakness on 24Jan2022. The patient was given atorvastatin from 19Jan2022 to 21Jan2022 via oral route post myocardial infarction (MI) 80mg HS. On 16Feb2022, patient had difficulty walking and fell. Patient was admitted to hospital for lower extremity weakness and ataxia. Per patient, doctors did not determine the cause of his lower extremity weakness and ataxia. Patient was discharged on 19Feb2022 with an updated medications list, walker, and physical therapy. Patient stated he would follow up with principal care physician (PCP), neurology, and rheumatology. The patient reported on 24Feb2022 he was unable to walk. The patient was re-admitted to hospital on 24Feb2022 for worsening lower extremity weakness and worsening ataxia. On 24Feb2022 Neurological exam per Neurologist: Mental Status: Appearance: alert, cooperative, appropriate. Speech: normal. Memory: normal for age. Orientation: O x3. Cognition: able to spell "world" forwards and backwards, able to perform serial 7's, no dysgraphia, no constructional apraxia, no R/L confusion, no finger agnosia. Affect: normal. Mood: normal. Insight: intact. Judgement: intact. Hallucinations/delusions: none. Cranial Nerves: I - not tested. II - visual fields full, fundi benign. III, IV, VI - EOM's full, no pathologic nystagmus, pupils equal, round reactive to light and accommodation. V - Corneas present OU, facial sensation intact to LT and PP. VII - Smile symmetrical. VIII - Hearing intact to finger rub. Tympanic membranes intact. IX, X - Palate elevates in the midline, gag reflex intact. XI - SCM and Trapezius intact bilaterally. XII - Tongue strong without atrophy or fasciculations, protrudes in the midline. Motor: RUE - 5/5 proximally and distally. LUE - 5/5 proximally and distally. RLE - 3+/5 proximally hip flexor/quads, 4+/5 hamstring, and distally 5/5 ankle dorsoflexor and plantar flexor. LLE - 3/5 proximally hip flexor/quads, 4-/5 hamstring, and distally 5/5 ankle dorsoflexor and plantar flexor. Tone: normal without drift, tremor, fasciculations or atrophy. Tremor: none. Bulk: normal. Sensory: Light touch: intact throughout. Pin prick: intact all 4 extremities. Vibration intact all 4 extremities, toe 11 seconds. Position: intact in all 4 extremities. Temperature: intact throughout. Cortical: intact to double simultaneous stimulation. Reflexes: DTR's: 2/4 BUE, absent BLE. Babinski Reflex: toes bilaterally downgoing. Snout: absent. Glabella: absent. Palmomental: absent. Jaw Jerk: absent. Coordination: Finger Nose Finger: normal bilaterally. Heel Knee Shin: not tested due to condition. Rapid Alternating Movements: intact throughout. Fine Finger Dexterity: normal bilaterally. Station and Gait: Gait: unable to stand with support. Romberg: not tested due to condition/steadiness. Nerve conduction study was performed on 25Feb2022 with findings of acute demyelinating polyneuritis of BLE The right median motor study revealed moderately prolonged distal latency, normal amplitude, and mildly decreased conduction velocity. The right ulnar motor study revealed normal distal latency, normal amplitude, and normal distal conduction velocity but mildly decreased conduction velocity across elbow. The left peroneal motor study revealed normal distal latency, normal amplitude, and mildly decreased conduction velocity. The right tibial motor study revealed mildly prolonged distal latency, normal amplitude, and normal conduction velocity. The left sural sensory study revealed moderately prolonged peak latency and mildly decreased amplitude. The right sural and right ulnar sensory studies revealed mildly prolonged peak latencies but normal amplitude. F-waves of BLE showed absent in left peroneal study and moderately severe prolonged in bilateral tibial and right peroneal study. F-waves showed mildly prolonged in both median and ulnar studies. All other nerve study were within normal limits. Concentric needle EMG was performed in selected right upper extremity and bilateral lower extremity and paraspinal muscles innervated by C5-T1 and L2-S1 nerve roots inclusive. Spontaneous activity in the form of low grade fibrillations and positive sharp waves was only seen in right deltoid muscle. Voluntary motor unit morphologies were otherwise normal except signs of electrical instability consistent with a super-acute moderate neurogenic change in BLE proximal muscles. Impressions: The above electrodiagnostic study reveals evidence of acute demyelinating polyneuritis of BLE far more than RUE with severely prolonged or absent F waves and relatively preserved motor nerve conduction velocities and distal latencies along with possible superimposed mild right carpal tunnel syndrome or right C5 radiculopathy. Clinical correlation was highly advised. The patient also had lumbar puncture, cerebrospinal fluid (CSF) protein was 95 mg/dL, CSF color was colorless, CSF clarity was clear, CSF red blood count (RBC) was 2 per mm3, CSF white blood count (WBC) was 3 per mm3, CSF polymorphonuclear neutrophil (SEGS) was 1%, CSF lymph was 45%, CSF monocyte was 51%, CSF macrophage was 3, CSF cells counted was 100, CSF glucose was 67 mg/dL. Per clinical lab scientist in Medical Center, normal range of CSF protein was 15-60 mg/dL. There was no unit for CSF cells counted per clinical lab scientist. The patient began receiving intravenous immunoglobulin (IVIG) therapy. On 03Mar2022 the patient was referred to hospital for acute inpatient rehabilitation unit and had been undergoing physical therapy (PT). The patient also completed 5 sessions of plasmapheresis. The patient was contacted via phone for safety follow-up on 07Mar2022, 16Mar2022, and 29Mar2022. The patient reported he was slowly getting better, however he still needed assistance to stand on his own, even with a walker. Site received Nerve Conduction Study results and Admission history and physical examination (H&P) dated 03Mar2022 including magnetic resonance imaging (MRI) of spine and lower extremities. The patient was conducted via phone on 08Apr2022. The patient was given gabapentin for neuropathy in bilateral hands and feet at 200 mg occlusive as needed from 05Apr2022 and ongoing. The patient was discharged home on 05Apr2022 in the evening. The patient was discharged with home health nurse, PT and occupational therapy (OT). The patient stated he no longer had back pain, but he still had difficulty standing on his own. Site advised the patient to contact site with any changes in health and would follow-up with the patient in 1-2 weeks. Patient presented to clinic on 24May2022 for unscheduled visit and was seen by primary investigator (PI). Per PI's physical exam, patient presented to clinic in a wheelchair. Patient was unable to stand on his own, but he was able to lift his legs and kick. Skin sensation was improving gradually. Patient had an appointment with the neurologist on 10May2022. Per medical records obtained from the neurologist's office, patient was diagnosed with Guillain-Barre syndrome. On 20Jun2022, PI had a conference call with medical monitors with site manager and sub investigator (Sub-I) present. Patient's medical records were discussed along with the possible relationship of investigational product (IP) and the patient's Guillain-Barre syndrome. Medical monitors suggested PI reach out to patient's neurologist regarding symptoms onset, treatment, and assessment of causality. On 14Jul2022, patient was contacted via phone for safety follow-up. Patient reported he was feeling better and was now able to ambulate with 2 canes. Patient had been continuing physical therapy. PI obtained permission from patient to speak to patient's neurologist. PI informed the neurologist that patient was participating in a blinded placebo controlled clinical trial for an RSV vaccine. Per the PT, the neurologist states that the patient started having lower back pain while he was in the hospital status post (s/p) myocardial infarction (MI) and subsequent stent placement. Patient's back pain worsened after he was discharged home for several days. One-week later the patient began having BLE  weakness and hard to get up and down in chair. Patient continued to have worsening weakness and eventually several tests, including spinal tap and nerve conduction study, were done. Guillain-Barre syndrome was then diagnosed. Per the reporting physician, back pain was considered associated to GBS therefore onset date of the SAE GBS was 18Jan2022. Patient presented to clinic for Visit 4 on 30Aug2022. Patient drove himself to the clinic and was able to ambulate without a cane. Patient was able to go from sitting to standing without assistance. Around 01Sep2022, the patient had sudden weakness from the knee down. Patient stated his previous leg weakness was in the hips and thighs, and he regained strength about 80% on the left side and 85% on the right side as of his last site visit. Patient was using the walker to ambulate again. On 06Sep2022, patient went to see his neurologist and was prescribed Methylprednisolone MG Dosepack 4 mg from 06Sep2022 to 11Sep2022. Patient stated he received on 14Sep2022 40mg IVIG, on 15Sep2022 60mg IVIG, and on 16Sep2022 60mg IVIG. Although the patient stated he still used the cane to go up and down stairs, overall, he was feeling much better. Patient was currently admitted at the Hospital for SAE: Diverticulosis (AER PV202200066199). Magnetic resonance imaging (MRI) of spine was performed on 17Feb2022 with procedure: MR L Spine without (WO) + with (W) contrast (CON). Reason for exam: Evaluation (Eval) for cause to lower extremity weakness and pain (worse in left buttock/thigh). Findings: Vertebral body heights were preserved. There were, notes: acute fractures. Bone marrow signal was within normal limits. Alignment was unchanged. The conus terminates at the T12-L1 level. The distal cord was normal in course and caliber. There was no evidence of arachnoiditis. No areas of abnormal enhancement within the conus, central canal, or dural surfaces. The paraspinal muscles and soft tissues were unremarkable. Findings at specific disc levels: T11-T12: Mild loss of disc height with desiccation. NO annular bulge, central canal narrowing, or neural foraminal narrowing. T12-L1: Mild loss of disc height with mild type 1 endplate change. Minimal retrolisthesis. Minimal annular bulge but no central canal or neural foraminal narrowing. L1-L2: Normal disc height and signal. No annular bulge, central canal narrowing, or neural foraminal narrowing. Minimal bilateral facet arthropathy. L2-L3: Normal disc height and signal. Mild 2 mm annular bulge but no central canal narrowing. Minimal bilateral neural foraminal narrowing. Minimal bilateral facet arthropathy. L3-L4: Mild loss of disc height with desiccation. Broad annular bulge measuring up to 3-4 mm extending into the bilateral neural foramen and posterolateral osseous ridging with mild to moderate central canal narrowing and prominence of the epidural fat. Mild bilateral neural foraminal narrowing. Mild bilateral facet arthropathy. L4-L5: Mild loss of disc height with desiccation and 2 mm anterolisthesis. Broad annular bulge measuring up to 3 mm with severe central canal narrowing and narrowing of the bilateral lateral recesses. Mild bilateral neural foraminal narrowing. Severe bilateral facet arthropathy with ligamentum flavum thickening. Slight decrease in size of the 4 mm right synovial cyst medial to the facet joint with right larger than left facet joint effusions. Bone marrow reactive change within the right greater than left facet joints. L5-S1 : Severe loss of disc height with desiccation and vacuum disc, Mild annular bulge and posterolateral osseous ridging without central canal narrowing. Prominence of the epidural fat. Mild bilateral neural foraminal narrowing. Mild bilateral facet arthropathy. RPTAT: ZZ. impression: 1. Severe bilateral facet arthropathy at L4-L5 with inflammation of the right greater than left facet joints with bone marrow reactive change and facet joint effusions. Decreased size of the right synovial cyst at L4-L5 now measuring 4 mm. 2. Severe central canal narrowing at L4-L5 with grade 1 anterolisthesis due to the facet arthropathy with mild degenerative disc disease and a mild annular bulge. 3. Severe degenerative disc disease at L5-S1. 4. Mild to moderate central canal narrowing at L3-L4 with a 3-4 mm annular bulge. 5. Mild epidural lipomatosis within the lower lumbar spine. Patient stated he received a shingles vaccine when he was 55 years old. The treatment received was not completely clear as it mentioned corticosteroid, plasmapheresis and immunoglobulin on medical records. For GBS, either plasmapheresis or immunoglobulin were used but not together. Patient's course of treatment was determined by patient's neurologist. Patient reported he was discharged home on 30Sep2022. Patient stated he was no longer under the care of Neurologist because she was now out of network. Patient was now under the care of another neurologist and had an appointment on 04Oct2022. Patient stated he had regained some strength in his lower extremities, but now he was having some weakness in bilateral hands. Patient was scheduled to do nerve conduction study for upper extremities on 12Oct2022 and for lower extremities on 14Oct2022. Patient was continuing physical therapy (PT) 2x/week. Patient was contacted via phone on 25Oct2022. Patient reported he was admitted to hospital on 15Oct2022 due to increasing bilateral hand and bilateral feet weakness. Patient stated he received another round of IVIG on 16Oct2022, 17Oct2022, 18Oct2022, 20Oct2022, and 21Oct2022. Patient was working with PT 4x/day and could now ambulate w/walker. Patient stated he was slowly regaining strength in bilateral hands and feet. Anticipated discharge date of 26Oct2022 or 30Oct2022. Patient sent copies of Neurology Office Visit Note dated 04Oct2022 and Inpatient Discharge Instructions dated 21Sep2022 (admitted 21Sep2022). Per Neurologist's note, patient was a 67-year-old man with multiple chronic conditions including recently diagnosed GBS with complaints of lower greater than upper extremity weakness for which patient had received plasmapheresis after IVIG failure in Feb2022, that had since been converted to presumed chronic inflammatory demyelinating polyneuropathy (CIPD) with subsequent re-dosing of IVIG in Sep2022. Patient had some slight worsening of his wrist and fingers since last IVIG dose 3 weeks ago. It appeared that he had relapse off IVIG and would need every 3-week IVIG as part of a standard CIDP regimen. Medical records requested were sent on 06Oct2022, 10Oct2022, and 18Oct2022 from hospital for admission dated 13Sep2022 for Diverticulosis. It would submit further requests for nerve conduction study (NCS) of upper and lower extremities results. It would follow-up with patient after discharge from hospital. Site was still making attempts to request medical records from previous Neurologist to confirm the indication of "methylprednisolone" on 06Sep2022 since she had moved her practice. Patient was contacted via phone 23Nov2022 and 02Dec2022. Patient was discharged (d/c) from hospital on 30Oct2022. Patient stated he completed first round of outpatient IVIG on 11Nov2022. Patient stated he received 80mg IVIG at hospital. Patient reported he was feeling better. He was able to ambulate with walker and even take a few steps without it. However, he was unable to stand on his own for long periods of time. He had regained almost all his strength in his hands. Patient was continuing physical therapy (PT). Patient reported he did not have any infections prior to Myocardial infarction (MI). Patient reported he had history of back pain. About 3 years ago, patient tweaked his back while playing with grandson. Patient stated Magnetic resonance imaging (MRI) at that time showed he had stenosis in Lumbar spine. Nerve conduction study (NCS) studies of upper and lower extremities received. BUE NCS Test Date: 12Oct2022 Electromyography (EMG) and Nerve conduction velocity (NCV) Findings: Needle evaluation of the right abductor pollicis brevis, the right first dorsal interosseous, and the left first dorsal interosseous muscles showed increased motor unit amplitude, increased motor unit duration, moderately increased polyphasic potentials, and diminished recruitment. The right flexor carpi radialis, the left flexor carpi radialis, the left flexor carpi ulnaris, and the left extensor digitorum communis muscles showed increased motor unit duration, slightly increased polyphasic potentials, and diminished recruitment. The right flexor carpi ulnaris, the right biceps, the right deltoid, the left biceps, the left deltoid, the left supraspinatus, the left infraspinatus, and the right supraspinatus muscles showed slightly increased polyphasic potentials and diminished recruitment. The right extensor digitorum communis, the right triceps, and the left triceps muscles showed increased motor unit amplitude, slightly increased polyphasic potentials, and diminished recruitment. The left abductor pollicis brevis muscle showed increased motor unit amplitude, increased motor unit duration, very increased polyphasic potentials, and diminished recruitment. All remaining muscles (as indicated in the following table) showed no evidence of electrical instability. Evaluation of the left median motor and the right median motor nerves showed prolonged distal onset latency (L4.5, R5.0 ms), reduced amplitude (L3.8, R2.1 mV), and decreased conduction velocity (Elbow-Wrist, L40, R44 m/s). The left ulnar motor and the right ulnar motor nerves showed decreased conduction velocity (B Elbow-Wrist, L43, R44 m/s) and decreased conduction velocity (A Elbow-B Elbow, L50, R48 m/s). The left median sensory and the right median sensory nerves showed prolonged distal peak latency (L4.3, R4.5 ms) and decreased conduction velocity (Wrist-2nd Digit, L33, R31 m/s). The left ulnar sensory and the right ulnar sensory nerves showed prolonged distal peak latency (L4.0, R6.1 ms) and decreased conduction velocity (Wrist-5th Digit, L35, R23 m/s). The right median/ulnar (palm) comparison nerve showed abnormal peak latency difference (Median Palm-Ulnar Palm, 0.4 ms). All remaining nerves (as indicated in the following tables) were within normal limits. All left vs. right side differences were within normal limits. F Wave studies indicate that the left median F wave had prolonged latency (40.51 ms). Impression: This is an abnormal study. There is electrodiagnostic evidence of a demyelinating sensorimotor polyneuropathy with some axonal feature affecting bilateral upper extremity (UE). In addition, there was electrodiagnostic evidence of a right median neuropathy across the wrist such as seen in Carpal Tunnel Syndrome, mild in degree. BLE NCS Test Date 10Nov2022. EMG & NCV Findings: 1. Bilateral superficial peroneal sensory nerve action potential (SNAPs) were absent. 2. Bilateral sural SNAPs were normal. 3. Bilateral tibial and peroneal compound muscle action potential (CMAPs) showed prolonged distal latency, low amplitude, and slow conduction velocity. 4. Needle examination of the bilateral lower extremity (LE) showed polyphasic motor unit potential (MUAP)s with decreased recruitment in below muscles, 5. Needle examination of the bilateral lumbar paraspinal muscles was normal. Impression: This was an abnormal study. There is electrodiagnostic evidence of a sensorimotor polyneuropathy with axonal and demeylinating feature affecting bilateral LE. The patient was contacted via phone on 10Feb2023. The patient stated he was doing better. The patient was able to ambulate with (w/) cane and he could stand on his own without assistive devices. The patient was able to walk without cane if he was wearing bilateral ankle-foot orthoses (AFOs). The patient had regained strength in bilateral hands. The patient stated he had neuropathy in hands but it was tolerable and had stopped taking gabapentin. The patient received intravenous immunoglobulin (IVIG) 80mg IV on 04Jan2023 and 25Jan2023. The patient's last appointment with neurologist was on 07Feb2023, next appointment would be in 2 months. Would follow-up with the patient in 3-4 weeks. Medical records received from neurologist on 14Feb2023. Per note written on 01Nov2022 under HPI, the patient was a "67-year-old man with history of gout, hypertension, myocardial infarction (MI) had been hospitalized multiple times recently for initially presumed GBS now thought to be CIDP given worsening off immunotherapy". Assessment/plan from same visit notes stated "CIDP" as diagnosis and "IVIG every 3 weeks (q3week), would finish obtaining prior authorization; continued physical therapy; follow up in 3 months" as planned. Patient was contacted via phone for visit 5 on 15May2023. Patient stated he was prescribed pregabalin 50mg three times a day (TID) beginning 02May2023 for continued neuropathy in bilateral hands and feet. Patient received IVIG on 28Apr2023. Patient stated he was still using AFOs or a cane to ambulate. Patient stated on diary entry dated 25Apr2023 he reported symptoms because he had some wheezing due to pollen from a particular tree. Every year around this time, patient would have wheezing episodes. Patient used his albuterol inhaler and symptoms resolved. Per reporter discretion, wheezing was due to medical history of seasonal allergies and asthma; patient did not need to submit nasal swabs. Patient informed that study had ended. Patient verbalized understanding. There was no lack of efficacy. The action taken in response to the event for blinded study vaccine was reported as not applicable. The outcome of the event "CIDP (chronic inflammatory demyelinating polyneuropathy)" was recovering.  The investigator considered there was a reasonable possibility that the event "CIDP (chronic inflammatory demyelinating polyneuropathy)" was related to blinded study vaccine (PF-06928316; placebo), but there was not a reasonable possibility that the event "CIDP (chronic inflammatory demyelinating polyneuropathy)" was related to concomitant drugs, concomitant vaccines, prior vaccination or clinical trial procedure. After discussion with patient's neurologist, both the principal investigator and the neurologist concluded that there was a possibility that the patient's GBS was related to the investigational product (IP). Conclusion of possibility of relatability of IP to GBS was made in part due to BLE weakness onset was about 2 weeks after receiving IP.  The blind was broken by sponsor.  Follow-up (09Mar2022): This is a Study follow-up report. Updated information: event lower extremity weakness onset date updated from 16Feb2022 at 10:00 to 10Feb2022 at 10:00.  Follow-up (06Apr2022 and 11Apr2022): This is a  Study follow-up report. Updated information: weight of the patient, reaction data (additional event AIDP reported), clinical course (updated condition of the patient), lab data.  Follow-up (13Apr2022): This is a Study follow-up report. Updated information: reaction data (updated onset date of SAE AIDP).  Follow-up (19Apr2022): This is a Study follow-up report. Updated information: reaction data (updated SAE from AIDP to acute inflammatory demyelinating polyradiculopathy (AIDP)).  Follow-up (27Jul2022): This is a Study follow-up report. Updated information: reaction data (updated SAE term from acute inflammatory demyelinating polyradiculopathy (AIDP) to Guillan-Barre syndrome).  Follow-up (29Jul2022, 02Aug2022 and 03Aug2022): This is a Study follow-up report. Updated information: lab data, reaction data (For event Guillan-Barre syndrome, onset date update from 10Feb2022 to 18Jan2022, physician office visit checked, investigator causality updated form No to Yes) and clinical course (detail result for lumbar puncture, patient status and investigator causality for Guillan-Barre syndrome).  Follow-up (10Aug2022): This is a Study follow-up report. Updated information: lab data and event data (Guillan-Barre syndrome onset date updated from 18Jan2022 to 24Jan2022).  Follow-up (07Sep2022): This is a Study follow-up report. Updated information: lab data, reaction data (For event Guillan-Barre syndrome, onset date update from 10Feb2022 to 18Jan2022, Events "Lower extremity weakness" and "ataxia" were removed being the symptoms associated with GBS), clinical course (patient's status).  Follow-up (16Sep2022): This is a Study follow-up report. Updated information: clinical course (patient status)  Follow-up (07Oct2022): This is a Study follow-up report. Updated information: additional historical vaccine, additional laboratory tests, and clinical course (patient status, treatments, and neurologist appointments).  Follow-up (31Oct2022): This is a study follow-up report. Updated information included: Clinical course (patient status, treatments, and neurologist appointments).  Follow-up (05Dec2022): This is a study follow-up report. Updated information included: Clinical course (patient status, treatments and test).  Amendment: This follow-up report is being submitted to amend previous reported information: to amend multiple terms (PT, CIDP, SNAP) in narrative.  Follow-up (22Feb2023): This is a study follow-up report. Updated information included: reaction data (SAE term updated to CIDP (chronic inflammatory demyelinating polyneuropathy) and treatment details.  Follow-up (03Mar2023): This is a study follow-up report. Updated information included: treatment details.  Follow-up (09May2023): This is a study follow-up report for the following literature source(s).  The last serious adverse event, also in participant in the vaccine group, was myocardial infarction that developed 6 days after injection. This participant then underwent angioplasty and later received a diagnosis of acute inflammatory demyelination polyradiculoneuropathy, consistent with Guillain-Barre syndrome, that began 7 days after injection. The participant continued to recover and regained most motor function.  Follow-up (08Aug2023): This is a study follow-up report. Updated information: clinical course (treatment details).; Sender's Comments: The event of CIDP (chronic inflammatory demyelinating polyneuropathy) is unlisted in the reference document of the vaccine and unrelated per Company assessment.    Based on the information available, there is not a reasonable possibility that the event CIDP (chronic inflammatory demyelinating polyneuropathy) is related to the blinded therapy (PF-06928316; placebo), concomitant drug or clinical trial procedure. Current data from nonclinical studies and clinical trials do not show immunological and biomolecular evidence attributing the development of CIDP (chronic inflammatory demyelinating polyneuropathy) to the blinded vaccine. Antecedent viral or bacterial infections are the commonly associated triggers. Probing for recent medical conditions prior to the onset of CIDP (chronic inflammatory demyelinating polyneuropathy) such as diarrhea and upper respiratory infection together with detailed lab investigations including pathogens detection are needed to identify an alternative etiology.       The impact of this report on the benefit/risk profile of the Pfizer PF-06928316; PLACEBO on the conduct of the study is evaluated as part of Pfizer procedures for safety evaluation, including the review and analysis of aggregate data for adverse events. Any safety concern identified as part of this review, as well as any appropriate action in response, will be promptly notified to Regulatory Authorities, Ethics Committee and Investigators, as appropriate,Linked Report(s) : JP-PFIZER INC-202101630099 same reporter/article/drug, different patient/AE;AR-PFIZER INC-202101707077 same reporter/article/drug, different patient/AE;