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1.
Postgrad Med ; 133(8): 994-1000, 2021 Nov.
Article in English | MEDLINE | ID: covidwho-1450321

ABSTRACT

OBJECTIVES: Multisystem inflammatory syndrome in children (MIS-C) is a rare but severe condition resulting in excessive response of the immune system after SARS-CoV-2 infection. We report a single-center cohort of children with MIS-C, describing the spectrum of presentation, therapies, clinical course, and short-term outcomes. METHODS: This is a prospective observational study from to a tertiary pediatric rheumatology center including patients (aged 1 month to 21 years) diagnosed with MIS-C between April 2020-April 2021. Demographic, clinical, laboratory results and follow-up data were collected through the electronic patient record system and analyzed. RESULTS: A total of 67 patients with MIS-C were included in the study. Fever was detected in all patients; gastrointestinal system symptoms were found in 67.2% of the patients, rash in 38.8%, conjunctivitis in 31.3%, hypotension in 26.9% myocarditis, and/or pericarditis in 22.4%, respectively. Respiratory symptoms were only in five patients (7.5%). Kawasaki Disease like presentation was found 37.3% of the patients. The mean duration of hospitalization was 11.8 7.07 days. Fifty-seven patients (85%) received intravenous immunoglobulin (IVIG), 45 (67%) received corticosteroids, 17 (25.3%) received anakinra, and one (1.5%) received tocilizumab. Seven of the patients (10.4%) underwent therapeutic plasma exchange (TPE). In 21 (31.3%) patients, a pediatric intensive care unit (PICU) was required in a median of 2 days. The first finding to improve was fever, while the first parameter to decrease was ferritin (median 6.5 days (IQR, 4-11.2 days)). Sixty-five patients were discharged home with a median duration of hospital stay of 10 days (IQR, 7-15 days). CONCLUSION: Patients with MIS-C may have severe cardiac findings and intensive care requirements in admission and hospital follow-up. The vast majority of these findings improve with effective treatment without any sequelae until discharge and in a short time in follow-up. Although the pathogenesis and treatment plan of the disease are partially elucidated, follow-up studies are needed in terms of long-term prognosis and relapse probabilities.


Subject(s)
COVID-19/complications , Intensive Care Units, Pediatric/statistics & numerical data , Rheumatology/statistics & numerical data , Systemic Inflammatory Response Syndrome/drug therapy , Systemic Inflammatory Response Syndrome/etiology , Systemic Inflammatory Response Syndrome/physiopathology , Administration, Intravesical , Adolescent , Adrenal Cortex Hormones/administration & dosage , Adrenal Cortex Hormones/therapeutic use , Child , Child, Preschool , Cohort Studies , Female , Humans , Immunoglobulins/administration & dosage , Immunoglobulins/therapeutic use , Infant , Infant, Newborn , Interleukin 1 Receptor Antagonist Protein/administration & dosage , Interleukin 1 Receptor Antagonist Protein/therapeutic use , Male , Oxytocin/administration & dosage , Oxytocin/analogs & derivatives , Oxytocin/therapeutic use , Plasma Exchange , Prospective Studies
3.
Hong Kong Med J ; 26(5): 370-371, 2020 10.
Article in English | MEDLINE | ID: covidwho-903004
4.
Physiol Genomics ; 52(9): 401-407, 2020 09 01.
Article in English | MEDLINE | ID: covidwho-772149

ABSTRACT

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused a worldwide pandemic, infecting over 16 million people worldwide with a significant mortality rate. However, there is no current Food and Drug Administration-approved drug that treats coronavirus disease 2019 (COVID-19). Damage to T lymphocytes along with the cytokine storm are important factors that lead to exacerbation of clinical cases. Here, we are proposing intravenous oxytocin (OXT) as a candidate for adjunctive therapy for COVID-19. OXT has anti-inflammatory and proimmune adaptive functions. Using the Library of Integrated Network-Based Cellular Signatures (LINCS), we used the transcriptomic signature for carbetocin, an OXT agonist, and compared it to gene knockdown signatures of inflammatory (such as interleukin IL-1ß and IL-6) and proimmune markers (including T cell and macrophage cell markers like CD40 and ARG1). We found that carbetocin's transcriptomic signature has a pattern of concordance with inflammation and immune marker knockdown signatures that are consistent with reduction of inflammation and promotion and sustaining of immune response. This suggests that carbetocin may have potent effects in modulating inflammation, attenuating T cell inhibition, and enhancing T cell activation. Our results also suggest that carbetocin is more effective at inducing immune cell responses than either lopinavir or hydroxychloroquine, both of which have been explored for the treatment of COVID-19.


Subject(s)
Adaptive Immunity/drug effects , Anti-Inflammatory Agents/pharmacology , Betacoronavirus/drug effects , Coronavirus Infections/drug therapy , Gene Expression Profiling , Oxytocin/analogs & derivatives , Pneumonia, Viral/drug therapy , T-Lymphocytes/drug effects , Adaptive Immunity/genetics , Betacoronavirus/immunology , COVID-19 , Cell Line , Coronavirus Infections/genetics , Coronavirus Infections/immunology , Coronavirus Infections/virology , Databases, Genetic , Host-Pathogen Interactions , Humans , Oxytocin/pharmacology , Pandemics , Pneumonia, Viral/genetics , Pneumonia, Viral/immunology , Pneumonia, Viral/virology , SARS-CoV-2 , T-Lymphocytes/immunology , T-Lymphocytes/virology , Transcriptome , COVID-19 Drug Treatment
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