Since the beginning of COVID-19 vaccination in New Jersey in December 2020, we have observed multiple cases of undetectable adaptive immunity, post-vaccination or post-COVID-19 infection, in patients using immunosuppressants. Here, we present three cases of patients using immunosuppressants: mycophenolate and tacrolimus for renal transplant; ocrelizumab for multiple sclerosis and rituximab for peripheral ulcerative keratitis. All three patients were admitted for acute respiratory distress syndrome (ARDS) from COVID-19 pneumonia; two patients reported having received full COVID-19 vaccination prior to admission and one unvaccinated patient required readmission. Our findings showed that these patients tested negative for SARS-CoV-2 IgM spike and CoV-2 IgG nucleocapsid antibodies. All three patients were treated with standard-of-care remdesivir, dexamethasone and convalescent plasma; two recovered successfully and one patient died from respiratory failure secondary to worsening ARDS from COVID-19 pneumonia. We highlight the challenges of treating immunosuppressed patients with COVID-19 pneumonia, in an era where dissemination of such information is paramount to helping doctors standardise and improve the quality of care for these patients.

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INTRODUCTION: Corona Virus Disease (COVID-19) main presenting feature is hypoxia which coincidentally is a feature of Pulmonary Embolism (PE) that can be life-threatening if not diagnosed early. COVID-19 causes excessive inflammation that can induce expression tissue factors, which is a major coagulation activator1,2. Therefore, PE should also be a consideration for those presenting with COVID-19 with worsening hypoxia. CASE PRESENTATION: 79-year-old a man with non-ischemic cardiomyopathy with Ejection Fraction (EF) 45-50% presented with worsening shortness of breath, dry cough, and bilateral lower limb edema for 2 weeks. On presentation, he was afebrile normotensive with tachypnea, tachycardia, and hypoxia. On physical examination, he was in respiratory distress with faint bilateral crackles and bilateral lower limb edema. Lab Investigations showed elevated Brain Natriuretic Peptide to 1830 pg/ml (normal range 0-100 PG/ml), troponin level to 6.89 ng/ml (normal range 0.00-0.03 ng/ml) and the D-dimer level was >20.00 UG/ ml FEU (normal range 0.00-0.40 UG/ml FEU). Viral PCR confirmed COVID-19. No ischemic changes noted in EKG. Echocardiography (Echo) revealed EF (Ejection Fraction) at 10-15%, dilated right ventricle with reduced function, and left ventricular thrombus. In CT chest with contrast noted to have acute segmental right middle lobe pulmonary arterial embolus. He was therapeutically anti-coagulated with enoxaparin. He received antibiotics, systemic steroids, and diuresis On day 3 of admission, he had worsening hypoxia and dyspnea while on 100% oxygen therapy. The patient opted for no escalation in care with ventilation or resuscitation. As he had no clinical improvement, the family agreed on comfort care. He died on day 5 of admission. No relevant relationships by Fausto Lisung, source¼Web Response No relevant relationships by Rani Sittol, source¼Web Response

INTRODUCTION: Hypertriglyceridemia (HTG) induced recurrent acute pancreatitis (RAP) is a rare entity. Its occurrence with normal pancreatic enzyme levels has not been commonly reported. Herein, we report a case of RAP secondary to hypertriglyceridemia with normal blood lipase level. CASE PRESENTATION:A 48-year old male with a history of hypertriglyceridemia presented with a 72-hour history of right upper quadrant (RUQ) and epigastric abdominal pain. He had hypertriglyceridemic pancreatitis 5 years ago, however was not compliant with treatment. On presentation, he was febrile with RUQ and epigastric tenderness. His laboratory investigations revealed: white cell 10.59 x 10^9/L, sodium 133mmol/L, carbon dioxide 18mmol/L, creatinine 0.7 mg/dL, glucose 138 mg/dL calcium 8.8mg/dL; albumin 4.2g/dL, total bilirubin 1.9mg/dL, alanine transferase 37u/L, aspartate transferase 60u/L, alkaline phosphatase 138 u/L. Triglycerides were significantly elevated at >2,625mg/dL with serum lipase 113 u/L (normal 23-300). CT scan of the abdomen and pelvis revealed extensive inflammatory stranding centered at the head and uncinate process of the pancreas, consistent with acute pancreatitis. He received intravenous crystalloids, opioids and continuous insulin infusion which was discontinued on day 4 once triglyceride level was <500. He was started on gemfibrozil and discharged home.DISCUSSION: With an incidence of 13-45/100,000 acute pancreatitis is one of the most common diagnoses for contacting emergency services and for hospitalization in Europe and the USA. Acute pancreatitis (AP) is defined by two of three criteria: typical belt-like abdominal pain, elevated serum lipase level three times above the normal threshold, or radiological imaging signs of pancreatitis. RAP is defined as 2 or more attacks of AP without any evidence of chronic pancreatitis. HTG is the third-most common, possibly underestimated and missed, cause of AP and it accounts for 1%-7% of cases. Serum amylase can be normal hypertriglyceridemia-induced pancreatitis, but lipase is more sensitive and specific than amylase for diagnosis of AP. Normal lipase levels in HTG induced AP, as in this case, is rare. Several studies have reported a negative predictive value of serum lipase in diagnosing acute pancreatitis to be between 94 and 100 percent.CONCLUSIONS: Though uncommon, HTG induced Acute Pancreatitis can present with normal biomarkers, and if suspicion is high, imaging should be pursued to confirm or exclude the diagnosis.