VAERS ID: 1390416

Description

Subarachnoid haemorrhage; Platelets decreased; Hydrocephalus; Intracranial hypertension; Renal function aggravated; Uraemia; This is a spontaneous report from a contactable physician received from the Regulatory Authority. Regulatory authority report number is v21110328. The patient was an 80-year and 12-month-old female. Body temperature before vaccination was 36.2 degrees centigrade. The patient had no family history. Medical history included rheumatoid arthritis diagnosed in Jul2010 (stage 4 class 3. As of 12May2021, activity was only pain of the right hand. Blood test conducted every 3 months showed CRP of 0.21 mg/dL on 17Mar2021 and remission was maintained. Historical drug included BUCILLAMINE 200 mg/day (from Jul2010 to Feb2011, discontinued by the patient), methotrexate (started in Jul2013. Discontinued in Jan2014 due to myelosuppression both for Rheumatoid arthritis. Used between 4 mg/week to 8 mg/week, adjusting by renal function), and iguratimod 50 mg/day for Rheumatoid arthritis (started in May2014 and discontinued in Mar2016 due to lack of effect), ongoing chronic kidney disease (CKD classification of G5A2 (on 17 March, Cr was 2.96 mg/dL, eGFR was 12.4 mL/min, and proteinuria +1), ongoing Hashimoto's disease, ongoing constipation, ongoing mild interstitial pneumonia, ongoing mild bronchiectasis, left ovarian cancer in Jan2003 (postoperative chemotherapy was performed. Recurred in Jun2013, for which surgery was conducted. Not recurred without postoperative chemotherapy), and hypertension (no treatment or oral medication). The patient had no allergies or vaccinations within the last one month. There was no point to be considered in terms of growth status. Concomitant medication included thyroid (THYRADIN) 75 ug/day taken orally for Hashimoto's disease from unknown date and magnesium oxide (MAGNESIUM OXIDE) 990 mg/day taken orally for constipation from unknown date, as well as golimumab (SIMPONI) injection 100 mg received for rheumatoid arthritis from May2014 (dose increased to 100 mg in May2015, dose decreased to 50 mg in Mar2016, and dose increased to 100 mg in Apr2019) and methoxy polyethylene glycol-epoetin beta (MIRCERA) injection 100 ug received for renal failure chronic from 16Aug2017, both of which were received subcutaneously once a month (once every 4 weeks) and last administration was on 12May2021. On 29Apr2021, the patient previously received the first dose of BNT162b2 (COMIRNATY, Lot# and Expiration date were not reported) for COVID-19 immunisation. On 20May2021 at 15:00 (the day of vaccination), the patient received the second dose of BNT162b2 (COMIRNATY, Solution for injection, Lot number EY2173, Expiration date 31Aug2021), at same age, via an unspecified route of administration as a single dose for COVID-19 immunization. On 24May2021 at 14:00 (3 days 23 hours after the vaccination), the patient experienced subarachnoid haemorrhage and platelets decreased. On 24May2021 (4 days after the vaccination), the patient was admitted to the hospital. On 27May2021 (7 days after the vaccination), the outcome of the events was fatal. The course of the event was as follows: The patient received the first dose on 29Apr2021 and the second dose on 20May2021, which were vaccinated by a physician who made a home visit. Between the first and the second dose, the patient visited the reporting hospital; however, blood collection was not conducted because the condition was stable. Previous blood count conducted on 10Jun2020 showed white blood cell of 5900/uL, haemoglobin of 9.0 g/dL, and platelet of 114000/uL. On 02Sep2020, white blood cell was 5900/uL, haemoglobin was 9.4 g/dL, and platelet was 134000/uL. On 28Oct2020, white blood cell was 4400/uL, haemoglobin was 9.2 g/dL, and platelet was 126000/uL. On 20Jan2021, white blood cell was 7100/uL, haemoglobin was 10.3 g/dL, and platelet was 133000/uL. On 17Mar2021, white blood cell was 3200/uL, haemoglobin was 9.2 g/dL, and platelet was 112000/uL, which were relatively low but retained, and bleeding tendency was not observed. Reportedly, the patient had subjective symptoms of headache and queasy on around 20May2021, and the condition was watched. On 24May2021 in the morning, the patient stayed conscious and was able to talk. Until 13:00, the patient was able to wave hands. However, at 14:00, the patient was noticed to have depressed level of consciousness and dark colour vomiting. The reporting department was contacted and the patient was taken to the reporting hospital by ambulance. On arrival, consciousness level was III-100, pupils were 4 mm/4 mm, light reflex was +/+, body temperature was 37.1 degrees centigrade, blood pressure was 120/86 mmHg, pulse rate was 97/minute, 96% (room air), and respiratory rate was 16 breaths/minute. COVID-19 antigen test was negative. Head CT revealed manifestation of subarachnoid haemorrhage. Although there was a high risk of renal function aggravation, consent was obtained from family member and contrast-enhanced CT was performed; however, no apparent aneurysm was noted. A laboratory technician notified us that reexamination was ongoing due to abnormally low levels of platelet count, which was eventually turned out to be 8000/uL. The patient was admitted to GICU and received administration of 10 units of platelet transfusion. On 25May2021, consciousness level improved to 2 digits and the patient could be aroused easily by being spoken to and was able to say name. However, platelet count remained at low level of 16000/uL and treatment such as puncture for the purpose of decompression was difficult. Subsequently, blood transfusion was repeated but no response was obtained. Consciousness level aggravated again to III-200. Renal function aggravation and manifestation of uraemia were observed. On 26May2021, platelet was 3000/uL. On 27May2021, platelet was 4000/uL, which remained at low level. Symptoms of hydrocephalus and intracranial hypertension appeared. On 27May2021 at 13:46, the patient died. Family member did not wish to conduct autopsy. The reporting physician classified the events as serious (death) and assessed that the event was related to BNT162b2. Other possible causes of the event such as any other diseases were reported in reporter's comment. The reporting physician commented as follows: Examinations at the time of hospital admission showed that anti-CCP antibody was positive (142.0 U/mL), RF was positive at high level (871 U/mL), and MMP3 was 111.5 ng/mL, which were manifestations that conformed to rheumatoid arthritis. Although positive conversion of antinuclear antibody and anti-dsDNA antibody due to anti-TNF drugs has been reported, all of these were negative. In addition, anti-RNP antibody was negative, anti-Sm antibody was negative, antiphospholipid antibodies (lupus anticoagulant, anticardiolipin IgG antibody, anticardiolipin beta-2 GP1 antibody) were all negative. C3 was 70 mg/dL, C4 was 18 mg/dL, CH50 was 55.0 U/mL, which were almost within normal ranges; thus, platelets decreased due to complication of SLE was unlikely. IgG was 1547 mg/dL, IgA was 693 mg/dL, and IgM was 70 mg/dL. The patient had no history of heparin use and HIT antibody was negative. PA-IgG was 206.0 ng/10^7 cells (reference value: 46 ng/10^7 cells or lower) and multiple IgGs (antiplatelet antibodies) bound to the surface of platelets were noted. Autoantibodies that showed abnormal values before hospital admission expect for ones associated with rheumatoid arthritis were checked; however, there was no measurement record. In this case, PA-IgG was 206.0 ng/10^7 cells and multiple IgGs (antiplatelet antibodies) bound to the surface of platelets were noted. Causes of a sudden onset of platelets decreased in a patient with rheumatoid arthritis, which was stable for long term, was considered as follows. Positive conversion of antiplatelet antibody in rheumatoid arthritis occasionally occurs; however, polyclonal increase in immunoglobulins were not observed. Also, activity of rheumatoid arthritis was not high. Therefore, positive conversion of antiplatelet antibody in vivo due to rheumatoid arthritis itself was considered unlikely. Next, cases of platelets decreased, although frequencies were unknown, were reported with injections of SIMPONI and MIRCERA, which the patient were receiving. The possibility of these medications having induced platelets decreased could not be denied; however, whether or not the mechanism involved platelet antibodies was unknown. Considering these medications were used safely for a long term, the possibility of them causing platelets decreased was low. Continued accumulation of cases is required and immediate assessment is not possible. However, the events occurred at the timing immediately after the second vaccination and it was surmised that causality between the events and the vaccine could not be denied. At the time of this report, it was most likely that the vaccine administered immediately before the onset (4 days and 25 days before) was the responsible agent that induced lethal platelets decreased and resulted in subarachnoid haemorrhage.; Reported Cause(s) of Death: Renal function aggravated; Uraemia; Hydrocephalus; Intracranial hypertension; Subarachnoid haemorrhage; Platelets decreased

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