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INTRODUCTION: Multisystem Inflammatory Syndrome in Adults (MIS-A) is a rare but severe complication associated with COVID-19 infection in which diffuse inflammation involving multiple organ systems ensues. This condition is commonly described as a sequela in patients with moderate to severe COVID-19 pneumonia. Herein, we describe the case of a 74-year-old female patient who was previously fully vaccinated and developed MIS-A after hospitalization for COVID-19 pneumonia. DESCRIPTION: The patient is a 74-year-old female who presented with fever, chills, and shortness of breath. Of note, the patient was discharged four weeks prior, after hospitalization for COVID-19 pneumonia, and treated with dexamethasone and Remdesivir. During that hospitalization, the patient was noted to be hypoxic on 2 liters via nasal cannula. However, the patient's oxygenation status improved during the hospitalization, and she was discharged home two weeks prior on oral dexamethasone. On arrival at ED, the patient was notably hypotensive, tachycardic, tachypneic, febrile, and hypoxic to 88% on room air. Labs showed CRP at 49, IL-6 at 9.51, creatinine level 2.27, and troponin at 1.83. Computed tomography (CT) chest with contrast showed moderate right and multiple basal left pulmonary embolism. The patient was subsequently admitted to medical floors with a diagnosis of post covid inflammatory pneumonitis, pulmonary embolism, and possible myocarditis. The patient's condition worsened during the hospital stay;she was diagnosed with super-added bacterial pneumonia and subsequent sepsis and passed away in the ICU after the family decided to focus on comfort measures. DISCUSSION: The CDC guidelines for diagnosing MIS-A require fever, multi-organ involvement, and elevated inflammatory markers after a recent COVID-19 infection. There have been multiple reported cases, and they have all been in patients with severe COVID-19 pneumonia. After completing her vaccination series, our patient developed COVID-19 infection and subsequent MIS-A. To our knowledge, this is the first reported case of MIS-A in a fully vaccinated patient, adding to the literature that vaccinations, though they prevent severe COVID-19 infection, may not completely prevent the development of rare long-term complications.
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SESSION TITLE: Lung Cancer Imaging Case Report Posters 1 SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: Pulmonary alveolar proteinosis (PAP) is a lung condition that is caused by a build-up of proteins, fats, and other substances (collectively called surfactants) in the alveoli of the lungs. Here we describe a case of a 47-year-old female diagnosed with PAP, with radiologic features conflicting with Coronavirus Disease 19 (COVID-19) pneumonia. CASE PRESENTATION: The patient is a 47-year-old female with no significant medical history who presents to the outpatient pulmonology clinic for shortness of breath evaluation. She reported that for the past 3-4 months she has been having progressively worsening shortness of breath (SOB) associated with dry cough, and nasal congestion. She reports no recent illness, no history of COVID or COVID exposure, no second-hand smoke exposure, no toxin/chemical exposure, no pets/birds at home. Her SOB has been impacting her lifestyle. Pulmonary function tests showed no obstruction, moderate restriction, mildly decreased diffusion capacity. Computed tomography (CT) of the chest showed multiple ground-glass opacities with septal wall thickening (appears crazy paving pattern) - suggestive of infection or inflammatory process. Infectious/inflammatory work up with HIV, COVID-19, hypersensitivity pneumonitis (HP) panel, autoimmune panel, immunoglobulins, QuantiFERON gold, IgM mycoplasma antibodies was negative. Repeat CT chest in 6 weeks as per patient request, was unchanged from prior. A bronchoscopy was done, bronchoalveolar lavage (BAL) negative for infection - fungal, acid-fast bacilli, Mycobacterium tuberculosis;GMS (Grocott's methenamine silver) stain negative for fungus;negative PCP (Pneumocystis pneumonia);left upper lobe and left lung biopsy showed lung parenchyma with scant amorphous eosinophilic material in alveolar sacs, Periodic Acid-Schiff stain (PAS) stain was positive confirming PAP diagnosis. DISCUSSION: PAP is a rare disease, affecting about 1 person in 100,000 people worldwide, with fewer than 10,000 of them in the United States. The "crazy paving pattern" is characteristic of PAP but recently it has appeared in the list of radiologic findings for COVID 19 pneumonia1,2,3. In these COVID times, these kinds of interactions might make the decision tougher, often leading to misdiagnosis. The decision of diagnosis/treatment should be based on symptoms and their duration, medical history, previous tests, response to treatment. Given our patient never had a COVID infection in the past or current infection, CT chest was typical for PAP with a crazy-paving pattern, no significant subjective/radiological improvement lead us to the diagnosis of PAP with eventual work up with bronchoscopy. CONCLUSIONS: A high index of suspicion is needed for the diagnosis of such rare diseases as PAP, which can be misdiagnosed as COVID-19 pneumonia, given radiological similarities. Early diagnosis and treatment can improve morbidity and mortality of PAP. Reference #1: PAP with COVID-19 Radiology - Differential Diagnosis Discussion, PMID: 33646114 Reference #2: Proteinaceous Lung With COVID-19: The Mimicker, PMID: 34703683 Reference #3: COVID-19 pneumonia: the great radiological mimicker - https://insightsimaging.springeropen.com/articles/10.1186/s13244-020-00933-z DISCLOSURES: No relevant relationships by Ahmad Al-Alwan No relevant relationships by Arundhati Chandini Arjun No relevant relationships by Farhan Khalid no disclosure submitted for Boning Li;No relevant relationships by Rana Prathap Padappayil No relevant relationships by Raghu Tiperneni
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Case Report Background COVID-19 infection and COVID-19 mRNA vaccines have been associated with the occurrence of de-novo and relapsing glomerulopathies. Although, Focal Segmental Glomerulosclerosis (FSGS) similar HIV associated Nephropathy (HIVAN) has been reported with COVID-19 infection in African American population with Apolipoprotein L1 gene mutation, amongst the few reported cases post-vaccine, Minimal change disease (MCD), IgA nephropathy (IgAN), Anti-Glomerular basement membrane glomerulonephritis (Anti GBM GN), and membranous glomerulonephritis (MGN) have been reported. Case A 26-year-old Caucasian male with a history of tobacco use complained of Frothy urine and edema for 3 weeks post second dose of Moderna COVID-19 vaccine on 06/01/21. He received the first dose on 5/04/21. On his annual wellness visit on 5/18/21, he had no complaints, normal physical examination with serum albumin 5g/dl, and urinalysis significant for trace proteinuria. A repeat urinalysis post-onset of symptoms on 7/18/21 revealed 3+ proteinuria, no RBCs, 24- hour urine revealed 3.2g proteinuria. Further investigations revealed Hypoalbuminemia (2g/dl), persistent proteinuria, and an unremarkable renal ultrasound, ANA, ANCA, Anti-dsDNA, Anti-PLA2R, anti-streptolysin, RF, HIV, hepatitis panel, and serum complement levels. Renal biopsy revealed Tip lesion variant of FSGS with 100% effacement of podocyte foot process. Therapy with Prednisone 60 mg daily was initiated, following which an improvement in edema and serum albumin levels (2.7 g/dl) were noted. Discussion A few de-novo cases of anti-GBM GN, ANCA positive vasculitis, MCD and IgAN, and relapsing cases of IgAN, MCD, MGN, and Thrombotic microangiopathy have been reported post-COVID 19 mRNA vaccination. Most reported cases of MCD occurred after the first dose whereas IgAN flare-up occurred after the second dose. Our case is unique as our Caucasian patient developed FSGS post-second dose of Moderna vaccine. Although the pathogenesis is unclear, it is thought to be related to an acute T-cell immune response involving cytokine production to COVID 19 spike protein which is responsible for inducing or worsening existing podocytopathies. Interestingly fewer cases have been reported following adenovirus vector or inactivated virus vaccination. Most of the reported cases of IgAN flare-up have been mild and a small number of MCN cases required ICU admission for management of fluid overload. As observed in a few prior case reports our patient had a slow response to steroid therapy. Although guidelines on COVID 19 vaccination in patients with existing glomerulopathies remain unclear and are based on case-by-case scenarios, the benefit of COVID 19 vaccination, may in general, outweighs the risk of glomerular diseases. We encourage further studies on this topic, especially in the era of booster doses with ongoing discussion about mixing two types of vaccines.