Report of the Association Between Multisystem Inflammatory Syndrome and Severe Myocarditis

Introduction: The people worldwide have been affected by severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) infection since its appearance in December, 2019. Kawasaki disease-like hyperinflammatory shock associated with SARS-CoV-2 infection in previously healthy children has been reported in the literature, which is now referred to as a multisystem inflammatory syndrome in children (MIS-C). Some aspects of MIS-C are similar to those of Kawasaki disease, toxic shock syndrome, secondary hemophagocytic syndrome, and macrophage activation syndrome. Case Presentation: This study reported an 11-year-old boy with MIS-C presented with periorbital and peripheral edema, abdominal pain, elevated liver enzymes, severe right pleural effusion, moderate ascites, and severe failure of right and left ventricles. Conclusion(s): Due to the increasing number of reported cases of critically ill patients afflicted with MIS-C and its life-threatening complications, it was recommended that further studies should be carried out in order to provide screening tests for myocardial dysfunction. Adopting a multidisciplinary approach was found inevitable.Copyright © 2023, Author(s). This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/) which permits copy and redistribute the material just in noncommercial usages, provided the original work is properly cited.

Comparative effectiveness and safety of a pharmacist-managed protocol for the transition from intravenous to subcutaneous insulin

Purpose: To evaluate the effectiveness and safety of a pharmacist-managed protocol for transitioning critically ill patients from intravenous (iv) to subcutaneous insulin compared with a provider-managed process. Method(s): This single-center, retrospective, observational study included patients admitted to the medical or surgical/trauma intensive care unit who received a continuous infusion of iv insulin from January 2019 to April 2021. Patients were excluded if they were less than 18 years of age, pregnant, incarcerated, or received iv insulin for the diagnosis of diabetic ketoacidosis, hyperglycemic hyperosmolar state, calcium channel blocker or beta blocker overdose, or hypertriglyceridemia. The primary outcome was the percentage of blood glucose (BG) concentrations within the target range of 70-150 mg/dL from 0 to 48 h following transition to subcutaneous insulin. Secondary outcomes included percentage of BG concentrations within goal range following transition at 0-12 h and 12-24 h, incidence of hypo- and hyperglycemia, and percentage of patients requiring dose adjustments after initial transition. Result(s): A total of 110 unique patients were included with 70 patients in the provider-managed group and 40 patients in the pharmacist-managed group. On average, pharmacists transitioned patients to 63% basal insulin based on their 24-h total day dose of insulin. The pharmacist-managed group achieved glycemic control in 53% of transitions at 12 h, 40% at 24 h, and 47% from 0 to 48 h, while the provider group achieved glycemic control in 25% of transitions at 12 h, 12% at 24 h, and 18% from 0 to 48 h (p < 0.001 for all time points). As for safety end points, the pharmacist-managed group demonstrated lower rates of hypoglycemia (p = 0.001), severe hypoglycemia (p = 0.332), hyperglycemia (p < 0.001), and severe hyperglycemia (p < 0.001) compared with the provider-managed group. Conclusion(s): Pharmacists can effectively and safely transition critically ill patients from iv to subcutaneous insulin utilizing a standardized protocol.Copyright © 2023 Pharmacotherapy Publications, Inc.

Heart Failure With Severely Reduced Ejection Fraction Following Covid-19 Vaccine: A Case Series

Introduction: With the rise of the pandemic, the development of the COVID-19 vaccine has helped alleviate the burden on the healthcare system. However, rare cardiac side effects have been reported, especially within the young healthy population. Herein, we present a case series of four patients who received the Pfizer mRNA COVID-19 vaccine and were noted to have heart failure with severely reduced ejection fraction (<= 25%) a few weeks following the 2nd dose of the Pfizer vaccine. Method(s): This is a retrospective study from January 2021 to August 2021. Patient cases were identified from hospitalizations or clinic visits. Each case was evaluated for underlying predisposing conditions, vaccination type, symptoms onset, diagnostic studies, and outcomes. Result(s): A total of four patients were identified (table). Patients' ages ranged from 22-43 years old. Seventy-five percent of the patient population were male. All patients commonly reported clinical symptoms of heart failure including fatigue, orthopnea, paroxysmal nocturnal dyspnea, and peripheral edema starting within three weeks from receiving the second dose of the Pfizer COVID-19 Vaccine. Patients had no prior known cardiac history or predisposing conditions. Diagnostic workup including a left heart catheterization showed normal coronaries. Echocardiograms showed significantly reduced left ventricular ejection fraction (LVEF) <= 25%. Three patients were confirmed to have non-inflammatory cardiomyopathy via endomyocardial biopsy or cardiac MRI. One patient was unable to get a cardiac MRI due to a concomitant acute renal injury. Patients were started on Guideline-directed medical therapy (GDMT). Two patients were noted to have an improvement in their ejection fraction with one patient achieving full recovery to LVEF of 62%. One patient is currently undergoing evaluation for advanced heart failure therapy while the last patient has relocated. Conclusion(s): s The relationship between the novel mRNA COVID-19 vaccine and cardiomyopathy remains to be an area in need of further investigation. Despite the unclear mechanism, management remains to be with GDMT and advanced therapies as indicated. EF recovery and improved clinical outcomes can be achieved in some.Copyright © 2022

An 81-Year-old Woman With Proximal Weakness

An 81-year-old woman developed progressive proximal weakness and myalgias several months following a COVID-19 infection. She was admitted to her local hospital for progressive weakness, peripheral edema, and exertional dyspnea. Neurology evaluation noted proximal arm and leg weakness. She had creatine kinase 740 U/L, white blood cells 21,000/mL (with abnormal differential), and abnormal antibody serologies. Additional diagnostic testing obtained included a thigh MRI and muscle biopsy. During her COVID-19 admission, a mediastinal mass had been detected, which was increased in size on this current admission. Notably, she had a remote history of an incidentally discovered mediastinal mass, which had been incompletely resected 18 years prior. At neuromuscular follow-up one month later, she reported improvement in peripheral edema and dyspnea but ongoing weakness. Strength exam noted symmetric Medical Research Council grade 4 weakness in neck flexion/extension, shoulder abduction, elbow flexion/extension, wrist extension, hip flexion/abduction/extension, and knee flexion. She had no fatiguability and no facial or bulbar weakness. Remainder of her neuromuscular examination was unremarkable. Her white blood cell count differential remained abnormal but had improved from her initial presentation. Her recent muscle biopsy slides were reviewed again. Bone marrow biopsy and mediastinal mass biopsy were obtained. A unifying diagnosis was made, and she was started on therapy with resolution of her weakness, myalgias, and abnormal cell counts.

Thrombotic Presentation of MIS-C After COVID-19 Infection in a Nine-Year-Old Boy

Introduction: SARS-CoV-2 is the cause of the recent pandemic. Although children are less affected by the virus, they can present with various presentations ranging from asymptomatic or fatigue and fever to multisystem inflammatory syndrome in children (MIS-C). Case Presentation: In this case report, we presented a case of a 9-year-old boy who presented with bilateral deep vein thromboses (DVTs) of the femoral and iliac veins as his main presentation of MIS-C, which occurred following a COVID-19 infection. A complete history was taken from the patient, and then a series of tests, including complete blood counts (CBCs), liver function tests (LFTs), and D-dimer, were performed. Bilateral doppler sonography to confirm the event and its location, as well as a decent follow-up method, were performed. Levels of anti-Xa assays followed the toxic levels of enoxaparin. The child was treated with a regimen of enoxaparin and corticosteroids, with a dosage of 1 mg/kg/12 h for both. The child was in the hospital for two weeks, after which he got better and was managed as an out-patient with a regularly scheduled appointment. Finally, once the radiologic evidence of DVTs was cleared, the patient tapered off his enoxaparin over the course of three weeks. Conclusion(s): Thrombotic events following COVID-19-associated MIS-C are an unlikely yet deadly event, especially in children. Prompt treatment with anticoagulants and corticosteroids alongside monitoring the patients are strongly advised.Copyright © 2022, Author(s).

Purulent Pericardial Effusion with a Swinging Heart Post-Sars-Cov-2 Infection: A Case Report

Background Acute bacterial pericarditis is rare and can decompensate quickly to cardiac tamponade and cardiac arrest. Targeted antibiotic therapy, pericardiocentesis, and pericardiotomy are the cornerstones of management. Case 51-year-old male presented with 2-weeks of progressive chest pain, cough, and fatigue. A month prior he tested positive for COVID-19. On exam he was tachycardiac, tachypneic, and normotensive. JVD and peripheral edema were present. Labs revealed elevated WBC, BNP, HS-troponin, and ESR/CRP. Blood cultures were positive for methicillin susceptible Staphylococcus aureus (MSSA). Echo showed a large pericardial effusion with a swinging heart. ECG showed diffuse ST elevations and PR depression. He was not clinically in tamponade but shortly after became bradycardic and had a PEA arrest. Emergent bedside pericardiocentesis was performed, and after 9-minutes of ACLS, ROSC was attained. Pericardial fluid grew MSSA. Decision-making Vancomycin and cefepime were started and tapered to cefazolin to cover MSSA bacteremia and pericarditis. Repeat blood cultures were negative. A month after discharge he had no cardiac symptoms and echo showed minimal pericardial fluid. Conclusion In patients with COVID-19 and pericardial effusion, bacterial pericarditis can be secondary to contiguous spread from lung parenchyma or myopericarditis with superimposed infection, or due to primary pericarditis. This is the second reported case of spontaneous purulent pericarditis with MSSA. [Formula presented]Copyright © 2023 American College of Cardiology Foundation

Pneumopericardium in COVID-19 Infection

Pneumopericardium is a rare medical condition that occurs following trauma, surgery, or other medical interventions. The presence of pneumopericardium after COVID-19 pneumonia has been reported in some cases, and it has been explained that most cases could be self-limited. Here, we describe a 51-year-old man afflicted by pneumopericardium with COVID-19 infection. The patient had pneumopericardium and massive pericardial effusions, necessitating surgical strategies such as pericardial windows. This case highlights the potential severity of COVID-19. We also suggest that cardiologists pay attention to the possibility of pneumopericardium in cases with COVID-19 infection. © 2023, Iranian Heart Association. All rights reserved.

COVID-19: A CONFOUNDING MIMICKER OF HEMOPHAGOCYTIC LYMPHOHISTIOCYTOSIS

SESSION TITLE: Challenging Cases of Hemophagocytic Lymphohistiocytosis SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Hemophagocytic lymphohistiocytosis (HLH) is a rare syndrome involving pathologic immune activation that is often fatal. The link between the cytokine storm related to COVID-19 and development of HLH has been reported since the onset of the pandemic, but little is known about clinical manifestations of HLH, thereby delaying treatment. CASE PRESENTATION: A 50 year-old male presented with a several day history of progressive weakness in the setting of missed dialysis session. Medical history was significant for ESRD on dialysis and diastolic heart failure (EF 35%). Initial vitals were unremarkable. Physical exam was notable for peripheral edema bilaterally. Laboratory studies were consistent with hyperkalemia, elevated ferritin (28,383) and elevated liver function tests. COVID-19 PCR was positive upon admission. Chest x-ray, CTA chest and a right upper quadrant ultrasound were unremarkable. He was admitted to the medical ICU for emergent dialysis. Soon after arrival to the ICU, he became lethargic and confused with increasing oxygen requirements and a subsequent a code blue was called. Cardiopulmonary resuscitation was immediately initiated, with a first rhythm consistent with ventricular fibrillation. He was shocked and placed on an amiodarone infusion with return of spontaneous circulation. TTE revealed a severely reduced EF <10%. Despite initiation of advanced COVID-19 therapies with Solu-Medrol and tocilizumab he remained ventilator dependent. Due to hemodynamic instability and persistent metabolic acidosis, he was transitioned to continuous renal replacement. Further blood work showed worsening inflammatory markers (ferritin 33,500, LDH 6981). Because of the significantly elevated ferritin, there were concerns for possible HLH. Triglycerides and IL-2 receptor were 395 mg/dL and 9300 pg/mL respectively. Total NK cells were decreased to 1.2%. He remained persistently unstable despite aggressive measures. He suffered a second cardiopulmonary arrest, which was unable to achieve return of spontaneous circulation and he ultimately passed away. DISCUSSION: HLH is characterized by uncontrolled activation and proliferation of benign macrophages in reticuloendothelial organs. This results in histiocytic hemophagocytosis, worsening peripheral blood cytopenia(s), cytokine storm, and cytokine mediated biochemical alteration ultimately culminating in multiorgan dysfunction and disseminated intravascular coagulation. Although a distinctive constellation of features has been described for HLH, diagnosis remains challenging as patients have diverse presentations associated with a variety of triggers. CONCLUSIONS: As HLH is a medical emergency with poor prognosis, prompt recognition and early treatment is crucial for improving clinical outcomes. We hope this case will create increased awareness and timely diagnosis of cytokine storm syndromes in patients with severe COVID-19 infection. Reference #1: Meazza Prina M, Martini F, Bracchi F, Di Mauro D, Fargnoli A, Motta M, Giussani C, Gobbin G, Taverna M, D'Alessio A. Hemophagocytic syndrome secondary to SARS-Cov-2 infection: a case report. BMC Infect Dis. 2021 Aug 13;21(1):811. doi: 10.1186/s12879-021-06532-7. PMID: 34388982;PMCID: PMC8361241. Reference #2: Schnaubelt, Sebastian MDa,*;Tihanyi, Daniel MDb;Strassl, Robert MDc;Schmidt, Ralf MDc;Anders, Sonja MDb;Laggner, Anton N. MDa;Agis, Hermine MDd;Domanovits, Hans MDa Hemophagocytic lymphohistiocytosis in COVID-19, Medicine: March 26, 2021 - Volume 100 - Issue 12 - p e25170 doi: 10.1097/MD.0000000000025170 DISCLOSURES: No relevant relationships by Garrett Fiscus No relevant relationships by Niala Moallem No relevant relationships by Resham Pawar

TIME-LIMITED TREATMENT WITH ACALABRUTINIB PLUS OBINOTUZUMAB IN TREATMENT-NAÏVE CHRONIC LYMPHOCYTIC LEUKEMIA PATIENTS INDUCES DEEP REMISSIONS: EARLY RESULTS OF AN ONGOING PHASE 2 TRIAL

Background: The Bruton's tyrosine kinase (BTK) inhibitor acalabrutinib is approved for treatment of chronic lymphocytic leukemia(CLL). Acalabrutinib induces durable remissions in most CLL patients, which mostly are partial remissions (PR), and therefore treatment typically is given as long-term monotherapy. As a potential alternative we developed a time-limited regimen, combining acalabrutinib with obinutuzumab. Aims: Here, we report early results from 14 treatment-naïve patients with CLL who enrolled in this ongoing phase 2 trial (NCT04505254) since September, 2020 at MD Anderson Cancer Center. Methods: Patients and Study Design: Treatment-naïve CLL patients requiring therapy as per iwCLL criteria receive acalabrutinib 100 mg orally twice a day for 24 cycles, combined with monthly obinotuzumab for 6 doses, starting in cycle 3. The first dose of obinutuzumab is divided into 100 mg on day 1 and 900 mg on day 2 of cycle 3;1000 mg are given during subsequent cycles (cycles 4-8). Patients who do not achieve a complete remission (CR) after cycle 8 can receive an additional 6 monthly doses of obinotuzumab during cycles 9 -14. Treatment is discontinued after 24 cycles, and patients will be monitored. The primary objective is to determine the durability of remissions after treatment discontinuation, secondary objectives are to determine clinical and laboratory characteristics that predict for early versus late relapse after time-limited therapy. Results: The median age of the patients is 70 yrs (range, 40 -83 yrs), 14% had del17p or TP53 mutation, 43% had an unmutated IgHV and 71% advance stage disease (RAI stage III and IV). The median baseline absolute lymphocyte count (ALC) and b2 microglobulin at start of therapy were 39.2x109/L (range: 7.1 - 188.4 x 109/L) and 4.2 mg/L (range: 2.2 - 7.9 mg/L), respectively. After a median follow-up of 7 months (2 - 16 months), 13 (93%) of patients remain on study;one patient died (7%) due from complications from a presumed bacterial (COVID19-negative) pneumonia after 2 months on therapy. The estimated one-year PFS and OS for the cohort is 92.8 %. Seven patients were evaluable for response assessment after 8 months of therapy. No patient has yet discontinued therapy. All patients achieved a PR (one patient with undetectable minimal residual disease/U-MRD in the bone marrow), accounting for an overall responsonse rate of 100%. The median levels of bone marrow infiltration by CLL cells, quantified by flow cytometry, declined from 83.6% (range: 54.3 - 94.0 %) at baseline to 4.1% (range, 0.0 - 63.3%, n=7, p<0.05, see figure) after 6 cycles of combination treatment. Sixty-four percent of patients completed all doses of obinotuzumab, 50% requiered a dose reduction of acalabrutinib to 100 mg per day due to adverse events (AE). Grade 33 AE were observed in 4 patients (29%), which included decreased neutrophil counts (n=2), syncope (n=1), and grade 5 lung infection (COVID19 not detected, n=1). The most frequently reported non-serious related AE (3 2 patients) were anemia (n=5 [36%]), decreased platelets counts (n=3 [21%]), bruising (n=3 [21%]), limbs edema (n=2 [15%]) and headache (n=2 [15%]). All these events were grade 1. Importantly, no bleeding or atrial fibrillation events were observed. 3285 (Figure Presented ) Summary/Conclusion: Our preliminary data indicate that combination therapy of acalabrutinib plus obinotuzumab induces remissions with a major reduction in bone marrow disease after 6 months of combination therapy. Longer treatment and follow-up is warranted to determine the durability of responses after therapy discontinuation.

Acute Onset of Remitting Seronegative Symmetrical Synovitis With Pitting Edema (RS3PE) Two Weeks After COVID-19 Vaccination With mRNA-1273 With Possible Activation of Parvovirus B19: A Case Report With Literature Review.

Remitting seronegative symmetrical synovitis with pitting edema (RS3PE) is a rare clinical entity characterized by "remitting," "seronegative," and "symmetrical" synovitis with pitting edema on the dorsum of the hands and feet. Although rheumatic or malignant diseases are diseases that are known to coexist with RS3PE, other factors such as medication, infection, and vaccination have been reported to be associated with RS3PE. Here, we present a case of RS3PE syndrome that satisfied all four diagnostic criteria of RS3PE (pitting edema in the limbs, acute onset, age ≥ 50 years, and/or rheumatoid factor negativity) after mRNA-1273 SARS-CoV-2 vaccination.

Gentle Giant: An Unusual Cause of Heart Block

Introduction: Inflammatory cardiomyopathies can be a diagnostic dilemma. Early management can lead to reduced morbidity and mortality for patients. We describe a rare presentation of an unusual cardiomyopathy. Case Report: A 58-year-old female presented with a 10-day prodrome of cough, NYHA class III dyspnea, and fatigue with minimal symptoms of orthopnea, paroxysmal nocturnal dyspnea or peripheral edema. She was previously healthy with no cardiac medications. Family history was significant for granulomatosis with polyangiitis. COVID-19 swab was negative. She was symptomatic with transient complete heart block and junctional escape of 20bpm. A temporary transvenous pacemaker was placed. Echocardiogram showed biventricular dysfunction with left ventricular ejection fraction < 30%. Troponin and brain-natriuretic peptide were elevated. Coronary angiogram showed no significant occlusions. CT excluded pulmonary embolism, pneumonia, or adenopathy. She was initiated on heart failure medications but beta blocker was not started given heart block. Six days into admission, her heart failure improved but she developed transient complete heart block without junctional escape. There was no ventricular ectopy. Evaluation for rheumatologic, infectious, and inflammatory causes showed elevated C-reactive protein and antineutrophil cytoplasmic antibodies. The remainder of the workup was negative. Leading diagnoses were idiopathic giant cell myocarditis or cardiac sarcoidosis. An endomyocardial biopsy revealed multinucleated giant cells and myocyte necrosis. She was diagnosed with giant cell myocarditis. Prior to discharge, she had defibrillator insertion and was initiated on prednisone and tacrolimus. Shortly after this time, she returned with critical cardiogenic shock despite intensification of immunosuppressive therapies and was listed for cardiac transplant. Giant cell myocarditis (GCM) is a rare and often fatal autoimmune cause of heart failure. Patients frequently present with congestive heart failure, ventricular arrhythmia and a rapid progression of symptoms. In GCM, it is rare to present with atrioventricular conduction delays. Given the crossover in symptoms with sarcoidosis and GCM, diagnosis may be challenging. In this case of an acute presentation of heart failure and complete heart block, endomyocardial biopsy was central to the diagnosis and management of GCM.

Multisystem inflammatory syndrome in children (MIS-C) in the paediatric intensive care unit

Currently the world is facing a pandemic caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Although most children and adolescents are asymptomatic or only have mild symptoms during the acute stage of infection, a severe post-infectious syndrome may occur several weeks after a SARS-CoV-2 infection, known as multisystem inflammatory syndrome in children (MIS-C). The clinical symptoms of MIS-C mimic Kawasaki disease, with fever, a maculopapular rash, conjunctivitis, peripheral oedema and palmar erythema. However, different to Kawasaki disease, many MIS-C patients primarily present with gastrointestinal symptoms or cardiovascular involvement requiring vasopressor or inotropic support.

Preliminary safety and efficacy of itolizumab, a novel targeted anti-cd6 therapy, in newly diagnosed severe acute graft-versus-host disease: Interim results from the equate study

CD6 is a co-stimulatory receptor predominantly expressed on T cells that acts as a crucial regulator of T-cell activation and is implicated in the pathogenesis of multiple autoimmune diseases. Activated leukocyte cell adhesion molecule (ALCAM), a CD6 ligand, is expressed on antigen-presenting cells, as well as epithelial and endothelial cells of acute GVHD target organs, including the skin and the GI tract.1,2 Previous studies in patients receiving alloHCT showed that ex vivo depletion of donor CD6-positive T cells lowered the incidence of acute GVHD, providing a rationale for therapeutically targeting CD6 in acute GVHD.3 Itolizumab, a humanized immunoglobulin G1 monoclonal antibody undergoing evaluation as treatment for acute GVHD, binds CD6 and blocks interaction with ALCAM to inhibit T-cell activity and trafficking.4 Dr John Koreth presented interim study results from EQUATE, an ongoing phase 1b/2 study of itolizumab in combination with corticosteroids for newly diagnosed severe acute GVHD (grade 3-4) after first alloHCT.5 The phase 1b portion is an open-label, 3+3 dose-escalation study evaluating doses of 0.4, 0.8, 1.6, and 2.4 mg/kg administered intravenously every 2 weeks through day 57. As of November 13, 2020, 10 patients completed treatment: 4 with 0.4 mg/kg, 3 with 0.8 mg/kg, and 3 with 1.6 mg/kg. All patients received corticosteroids at an initial dose of 1 to 2 mg/kg/day. Their mean age was 48 years (standard deviation, 15.7 years), 90% were male, and 90% were white. The graft source was peripheral blood for 80% and bone marrow for 20%, and 80% had an HLA-matched donor. The mean time to onset of GVHD was 43 days, and 100% of patients had GI involvement. At day 57, the ORR was 50% with 0.4 mg/kg, 100% with 0.8 mg/kg, and 100% with 1.6 mg/kg.5 The median percent corticosteroid dose reduction at day 85 was 93%, 87%, and 91% for the 0.4, 0.8, and 1.6 mg/kg groups, respectively (Figure 6). Itolizumab decreased the CD6 levels on T cells in a dose-dependent manner within 24 hours of the first dose, a reduction that was maintained throughout the treatment period. Across the dosing cohorts, all patients developed at least 1 AE. Most AEs were mild to moderate in severity.5 The most common AEs were hypomagnesemia (n=3) and peripheral edema (n=3). One mild infusion reaction was noted. Six patients had serious AEs, including recurrent GVHD (n=1), sepsis (n=2;1 event was considered a dose-limiting toxicity), fever (n=1), COVID-19 (n=1), and disseminated nocardia (n=1).

Challenges in treating new onset systemic lupus erythematosus with lupus nephritis and COVID-19 infection overlap

Case report-IntroductionCOVID-19 infection caused by a novel coronavirus SARS-coV-2 has made the diagnosis and the treatment of inflammatory diseases incredibly challenging. On the one hand, because of its pro-inflammatory state, that may aggravate or trigger flares in autoimmune diseases such as systemic lupus erythematosus (SLE). On the other hand, the risk of an immunosuppressive therapy during the active phase SARS-coV-2 infection that may lead to catastrophic outcomes. We report a case of a 24-year-old female newly diagnosed with SLE during COVID-19 pandemic who developed COVID-19 infection during her induction treatment for lupus nephritis.Case report-Case descriptionA 24-year-old Nepali female, with no past medical history of note, presented to her regional hospital with a history of flu-like symptoms few days ago, peripheral oedema, acute kidney injury with proteinuria and hypertension. Further investigations showed a high titre of double-stranded DNA antibodies, anti-cardiolipin IgM and B2 microglobulin positive and low C3. She also developed a haemolytic anaemia and thrombocytopenia during her admission. She received pulsed steroid therapy and was started on mycophenolate mofetil (MMF) for a probable lupus nephritis awaiting the results of biopsy, which showed later a lupus nephritis Class IV-G with active lesions. She then developed symptoms of COVID-19 infection and had a positive PCR leading to an interruption of her induction therapy. She was recruited to the RECOVERY trial on the lopinavir-ritonavir arm and made a good recovery.Case report-DiscussionIt is well known that viruses can trigger or aggravate auto-immune response in patients predisposed genetically. However, the role of SARS-coV-2 is not elucidated yet. The EULAR COVID-19 registry showed that rheumatoid arthritis and SLE were the most prevalent rheumatic diseases, and there was an increased risk in those who are on moderate to high dose corticosteroids. In patients with SLE and COVID-19 infection, it is agreed by all the national and international rheumatology societies to interrupt their immunosuppressive therapy until the symptoms resolve, especially those with renal involvement or an active disease. Which is the case in our patient. Luckily, she resumed her MMF a month later after a negative PCR and her renal function has continued to improve.Case report-Key learning pointsLupus nephritis is a major risk factor for overall morbidity and mortality in SLE. It requires an early immunosuppressive treatment to induce remission.Randomized clinical trials showed that MMF is at least equally effective as cyclophosphamide in inducing remission and that it has been associated with a reduced risk of infection and amenorrhea. It seems to be a suitable alternative in women of childbearing age. In patients with concomitant COVID-19 disease, immunosuppressive therapy should be paused until the symptoms improve.