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CASE: A 46-year-old African-American female was evaluated for generalized body aches five days after receiving second dose of COVID mRNA-1273 (Moderna) vaccine. Six months prior, she received her first dose of Ad26 (Johnson & Johnson) vaccine without sequelae, Family history includes maternal systemic lupus erythematous. Patient has a history of cystic acne and, most notably, frequent episodes of muscle aches and weakness. In 2006 and 2016, patient was hospitalized for episodes of rhabdomyolysis after receiving influenza vaccine. Autoimmune myositis was ruled out. She has never received statin medication. In late 2017, she was admitted for rhabdomyolysis after upper respiratory tract infection. She reported dark urine but no rash or arthralgia. Patient had elevated CK 107,737 U/L, AST 379 U/L, and ALT 115 U/L. Her renal function, sed rate, TSH, HIV, influenza, direct Coombs, protein electrophoresis, and antinuclear antibodies were negative or within normal limits. She was treated with IV fluids, pain medication, and discharged. In her current admission for rhabdomyolysis, she presented with dark urine, CK 130,702 U/L, AST 692 U/L, ALT 208 U/L, and D-dimer 1,544 ng/mL. No acute renal injury was noted. Patient was treated with intravenous crystalloids and pain medication. CK and transaminases steadily trended down. Patient was discharged as she was asymptomatic and CK had dropped significantly. IMPACT/DISCUSSION: Rhabdomyolysis can be an adverse event to vaccine administration, most commonly influenza vaccination. Detection of SARS-CoV-2 inside skeletal muscle has not been documented. Reports on COVID- 19 vaccine-induced rhabdomyolysis focus on the type of vaccine the patient received, the number of doses that triggered the event, CK level, and presence of risk factors for developing rhabdomyolysis. Although no pathophysiologic mechanism has been established, several hypotheses exist to explain muscle damage including genetic factors, autoimmune reactions to the virus nucleic material, or external adjuvant. This has been described as autoimmune/inflammatory syndrome induced by adjuvants. Our patient had a history of recurrent episodes of rhabdomyolysis after receiving influenza and COVID immunizations, as well as viral infection. CONCLUSION: The mechanism of our patients' reaction is unknown. Reported cases support autoimmunity as the major risk factor for vaccinerelated rhabdomyolysis. This patient had elevated CK level on subsequent episodes of rhabdomyolysis fitting the pattern where a more exaggerated response of the immune system is observed every time patient is re-exposed to known insult. Genetic predisposition may also play a role. AfricanAmericans have higher prevalence of slow acetylation and carnitine palmitoyltransferase II deficiency, a disorder of fatty acid. The myopathic form presents with high CK values. Therefore, patients should be counseled to seek medical attention when symptoms occur and physicians should consider vaccination as a possible cause.
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The COVID19 pandemic has pushed healthcare workers to utilize available therapeutics, often with limited evidence. Theoretically, IL6 inhibitors could help to stop or reverse the damage caused by COVID19 cytokine storm. Published evidence from the United States is conflicting and is largely from academic institutions and nonminority populations. This study assessed the clinical utility of open-label tocilizumab in two multiethnic community hospitals in Queens, NY.Tocilizumab (8mg/kg) was given to 114 patients for treatment of COVID19- related respiratory failure between April 4 and May 19 2020 (96% received 1 dose). A retrospective cohort study was performed to determine 28-day clinical success, defined as achieving a score of 1 using a 6-point scale (1=no O2 requirement or discharged home on 2L/min;2=low-flow O2 in hospital ≤6L/min;3=O2 >6 to ≤15L/min;4=high-flow, CPAP, or BiPAP;5=mechanically ventilated (MV);6=expired). The decision to administer tocilizumab was made by a committee based on unstable or worsening respiratory status. Mean patient age was 60 years (SD=11);77(67%) were male. 25% were Asian, 23% black (31% black Hispanic), 36% white (73% white Hispanic), and 14% other. A majority of patients had at least 1 significant comorbidity, including HTN 56%, DM 40%, HLD 43%, and COPD/asthma 16%. Median days of symptoms at dose was 14(IQR 10-19);SpO2 on RA at admission was 82%(IQR 67-88%). Baseline status by ordinal scale was as follows: 2= 9(8%);3=33(29%);4=38(33%);5=34(30%) (IQR 1-2 days on vent). Median CRP=19.9, d-dimer=1658, ferritin=593, and LDH=1561. 28-day success was achieved in 35(31%) patients;62(55%) patients expired or were MV on day 28. Of patients who were on high-flow, CPAP, BiPAP or MV at baseline, 80% expired or were on MV on day 28. Estimated mortality in all hospitalized patients during the time frame at these hospitals was 36%. No significant differences were seen in labs, comorbidities or age between patients who did and did not have clinical success. Higher baseline ordinal scale score was predictive of mortality.Tocilizumab provided little to no clinical utility, especially in those with high oxygenation needs at time of dosing (success rate <20%). The main limitation is lack of a control group;however mortality was strikingly high. This in part may be due to the demographic and clinical characteristics of our sample.