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1.
World J Gastroenterol ; 28(37): 5444-5456, 2022 Oct 07.
Article in English | MEDLINE | ID: covidwho-2099932

ABSTRACT

BACKGROUND: Metabolic associated fatty liver disease (MAFLD) is associated with complications and mortality in patients with coronavirus disease 2019 (COVID-19). However, there are no prognostic scores aimed to evaluate the risk of severe disease specifically in patients with MAFLD, despite its high prevalence. Lactate dehydrogenase, aspartate aminotransferase and alanine aminotransferase have been used as markers of liver damage. Therefore, we propose an index based on lactate dehydrogenase, aspartate aminotransferase and alanine aminotransferase for the prediction of complications and mortality in patients with MAFLD and COVID-19. AIM: To evaluate the prognostic performance of an index based on lactate dehydrogenase and transaminases (aspartate aminotransferase/alanine aminotransferase) in patients with COVID-19 and MAFLD [liver fibrosis and nutrition (LNF)-COVID-19 index]. METHODS: In this retrospective cohort study, two cohorts from two different tertiary centers were included. The first was the derivation cohort to obtain the score cutoffs, and the second was the validation cohort. We included hospitalized patients with severe COVID-19 and MAFLD. Liver steatosis was evaluated by computed tomography scan. Area under the receiver operating characteristic (ROC) curve analysis and survival analysis were used. RESULTS: In the derivation cohort, 44.6% had MAFLD; ROC curve analysis yielded a LFN-COVID-19 index > 1.67 as the best cutoff, with a sensitivity of 78%, specificity of 63%, negative predictive value of 91% and an area under the ROC curve of 0.77. In the multivariate analysis, the LFN-COVID-19 index > 1.67 was independently associated with the development of acute kidney injury (odds ratio: 1.8, 95% confidence interval: 1.3-2.5, P < 0.001), orotracheal intubation (odds ratio: 1.9, 95% confidence interval: 1.4-2.4, P < 0.001), and death (odds ratio: 2.86, 95% confidence interval: 1.6-4.5, P < 0.001) in both cohorts. CONCLUSION: LFN-COVID-19 index has a good performance to predict prognosis in patients with MAFLD and COVID-19, which could be useful for the MAFLD population.


Subject(s)
COVID-19 , Fatty Liver , Non-alcoholic Fatty Liver Disease , Humans , COVID-19/complications , Alanine Transaminase , Retrospective Studies , Fatty Liver/complications , Aspartate Aminotransferases , Prognosis , Lactate Dehydrogenases , Oxidoreductases , Non-alcoholic Fatty Liver Disease/complications
2.
J Biomol Struct Dyn ; : 1-9, 2022 Oct 30.
Article in English | MEDLINE | ID: covidwho-2097031

ABSTRACT

The development of resistance to conventional antimalarial therapies, along with the unfavorable impact of the COVID-19 pandemic on the global malaria fight, necessitates a greater focus on the search for more effective antimalarial drugs. Targeting a specific enzyme of the malaria parasite to alter its metabolic pathways is a reliable technique for finding antimalarial drug candidates. In this study, we used an in silico technique to test four novel imidazoles and an oxazole derivative for inhibitory potential against Plasmodium lactate dehydrogenase (pLDH), a unique glycolytic enzyme necessary for parasite survival and energy production. The promising imidazole compounds and the oxazole derivative were then tested for anti-plasmodial efficacy in Plasmodium berghei-infected mice. With a binding energy of -6.593 kcal/mol, IM-3 had the best docking score against pLDH, which is close to that of NADH (-6.758 kcal/mol) and greater than that of chloroquine (-3.917 kcal/mol). The test compounds occupied the enzyme's NADH binding site, with IM-3 forming four hydrogen bonds with Thr-101, Pro-246, His-195 and Asn-140. Infected mice treatment with IM-3, IM-4 and OX-1 exhibited significantly reduced parasitemia over a four-day treatment period when compared to the infected untreated animals. At 5, 10 and 20 mg/kg, IM-3 demonstrated the highest anti-plasmodial activity, suppressing parasitemia by 86.13, 97.71 and 94.11%, respectively. PCV levels were restored by IM-3 and IM-4, and the three selected compounds reduced the lipid peroxidation induced by P. berghei infection in mice. Thus, these compounds may be considered for further development as antimalarial medicines.Communicated by Ramaswamy H. Sarma.

3.
Journal of Acute Disease ; 11(4):140-149, 2022.
Article in English | EMBASE | ID: covidwho-2066825

ABSTRACT

Objective: To identify helpful laboratory paprameters for the diagnosis and prognosis of COVID-19. Methods: An observational retrospective study was conducted to analyze the biological profile of COVID-19 patients hospitalized in the Unit of Pulmonology at Setif hospital between January and December 2021. Patients were divided into two groups: the infection group and the control group with patients admitted for other pathologies. The infected group was further divided according to the course of the disease into non-severe and severe subgroups. Clinical and laboratory parameters and outcomes of admitted patients were collected. Results: The infection group included 293 patients, of whom 237 were in the non-severe subgroup and 56 in the severe subgroup. The control group included 88 patients. The results showed higher white blood cells, neutrophils, blood glucose, urea, creatinine, transaminases, triglycerides, C-reactive protein, lactate dehydrogenase, and lower levels of lymphocyte, monocyte and platelet counts, serum sodium concentration, and albumin. According to ROC curves, urea, alanine aminotransferase, C-reactive protein, and albumin were effective diagnosis indices on admission while neutrophil, lymphocyte, monocyte, glycemia, aspartate aminotransferase, and lactate dehydrogenase were effective during follow-up. Conclusions: Some biological parameters such as neutrophil, lymphocyte, monocyte, glycemia, aspartate aminotransferase, and lactate dehydrogenase are useful for the diagnosis of COVID-19.

4.
Pakistan Journal of Medical and Health Sciences ; 16(8):24-26, 2022.
Article in English | EMBASE | ID: covidwho-2067738

ABSTRACT

Aim: To evaluate the potential use of ivermectin with standard therapy among mild to moderate covid-19 illness. Methods: This is a single-centered, prospective observational, randomized, parallel group (1:1 ratio), standard versus controlled ivermectin study recruited 210 confirmed COVID-19 positive patients who were admitted in COVID treatment center of Dr Ruth Kum Pafu Civil hospital Karachi, Pakistan from 1st November 2020 to 30th May 2021. Data were analyzed using SPSS version Results: Total of 210 patients were enrolled in the study and aged matched patients were divided in two groups 105 patients received ivermectin 6 mg twice a day for five days along with standard therapy while remaining 105 patients received standard therapy as per local and international guidelines. Male were 140(66.7%) and female 70(33.3%);age ranges between 26 to 77 years and majority 140( 66.7%) were more than 50 years of age. Fever, dry cough and dyspnea were the major symptoms seen;112(53.3%) patients had DM as a comorbid illness . Total of 21(20%) of 105 patients of ivermectin group had negative PCR for COVID 19 on day seven while the other group had positive covid test in all of 105 patients . On day 10 total of 49 more patients from ivermectin group found COVID negative along with 21 previously negative had second PCR was found negative in this way total of 70( 66.7%) of ivermectin group had negative PCR for COVID 19 while 21(20%) patients from non ivermectin got negative PCR for COVID 19 on day 10 . Conclusion: Use of ivermectin with standard therapy clear the virus earlier than standard therapy in mild to moderate COVID-19 infected patients admitted in COVID treatment center of Dr Ruth Kum Pafu Civil Hospital Karachi.

5.
Archives of Iranian Medicine ; 25(7):443-449, 2022.
Article in English | EMBASE | ID: covidwho-2067651

ABSTRACT

Background: This study aimed to investigate CURB-65, quick COVID-19 Severity Index (qCSI) and quick Sepsis Related Organ Failure Assessment (qSOFA) scores in predicting mortality and risk factors for death in patients with COVID-19. Method(s): We retrospectively analyzed a total of 1919 cases for whom the rRT-PCR assay for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was positive. For mortality risk factors, univariate and multivariate logistic regression analyses were used. Receiver operator characteristics (ROC) analysis and Kaplan-Meier survival analysis were performed for CURB-65, qCSI and qSOFA scores. Result(s): The patients' average age was 45.7 (21.6) years. Male patients accounted for 51.7% (n = 992). In univariate analysis, some clinical variables including age over 65 years and comorbid diseases such as hypertension, chronic kidney disease, malignancy, lymphopenia, troponin, lactate dehydrogenase (LDH) and fibrinogen elevation were associated with the mortality rate. In multivariate logistic regression analysis: Neutrophil lymphocyte ratio (NLR) 3.3 and above (OR, 9.1;95% CI, 1.9-42), C-reactive protein (CRP)30 mg/L and above (OR, 4.1;95% CI, 1.2-13.6), D-dimer 1000 ng/mL and above (OR, 4;95% CI, 1.5-10.7) and age (OR, 1.11;95% CI, 1.04-1.18-year increase) were identified as risk factors for mortality among COVID-19 patients. The CURB-65 and qCSI scores exhibited a high degree of discrimination in mortality prediction (AUC values were 0.928 and 0.865, respectively). Also, the qSOFA score had a moderate discriminant power (AUC value was 0.754). Conclusion(s): CURB-65 and qSCI scores had a high discriminatory power to predict mortality. Also, this study identified CURB-65, qCSI and qSOFA scores, NLR, CRP, D-dimer level, and annual age increase as important mortality risk factors. Copyright © 2022 Academy of Medical Sciences of I.R. Iran. All rights reserved.

6.
American Journal of Transplantation ; 22(Supplement 3):350-351, 2022.
Article in English | EMBASE | ID: covidwho-2063370

ABSTRACT

Purpose: There is limited data on the outcomes beyond the acute illness among lung transplant (LT) patients with Coronavirus disease 2019 (COVID-19). The current study sought to describe the predictors of 6-month survival among a single center cohort of LT. *Methods: We included all the LT patients diagnosed with COVID-19 during a one-year period (March 2020 to Feb 2021;n=54;median age: 60, 20-73 years;M:F 37:17). All patients completed at least 6-month follow up from COVID-19 diagnosis. We reviewed patient characteristics, presenting features, clinical course, and laboratory abnormalities at presentation and during the acute illness. We reviewed the hospital course and post-discharge outcomes including lung function loss among COVID-19 survivors. Median follow-up duration was 304 days. Six-month survival after COVID-19 was analyzed as the primary outcome variable. Result(s): Restrictive lung disease was the most common LT indication (n=41, 75.9%) and most had undergone bilateral LT (n=43, 79.6%). Patients were a median of 48 months (range <1-139 months) from their transplant. Majority of the patients required hospitalization (n=48) and significant proportion of patients developed respiratory failure (n=26). One month survival was 90.7% (n=49) while the survival dropped to 81.5% (n=44) by 6-month follow-up. On univariate analysis, females (35.3% vs 10.8%) and those with pre-existing chronic lung allograft dysfunction (CLAD, 33.3% vs 11.1%) experienced worse 6-month survival. Peak lactate dehydrogenase (LD) levels had the strongest association with 6-month survival on Mann Whitney U comparisons. On receiver operator characteristic curve analysis, the peak LD levels had an area under the curve of 82.9% (69.1-96.7%, p=0.002) with 400 U/L identified as the best cut-off. A peak LD level >400 U/L during the acute illness from COVID-19 was significantly associated with worse 6-month survival (OR, 95% CI: 4.38, 1.31-14.65, p=0.02).On Cox proportion hazard analysis, female gender (adjusted HR: 5.38, 1.13-25.64;p=0.035), pre-infection CLAD (5.63, 1.24-25.57;p=0.025) and peak LD levels >400 U/L (7.49, 1.72-35.53;p=0.007, see Figure for the Kaplan-Meier survival analysis) were independently associated with survival after COVID-19 among LT patients. Conclusion(s): COVID-19 is associated with significant mortality among LT patients with several patients succumbing beyond the period of acute illness. Female gender, established CLAD prior to COVID-19 and an LD>400 U/L at any time during the acute illness are adverse prognostic markers and may form the basis of customized management strategies. (Table Presented).

7.
Chest ; 162(4):A2478, 2022.
Article in English | EMBASE | ID: covidwho-2060950

ABSTRACT

SESSION TITLE: COVID-19 Case Report Posters 2 SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Pneumomediastinum is the presence of air or other gas in the mediastinum which can be due to trauma related to mechanical ventilation or spontaneous in preexisting lung diseases. Here, we present the case of Covid-19 pneumonia, who developed pneumomediastinum without any trauma or other risk factors. CASE PRESENTATION: A 56-year-old male COVID unvaccinated with a history of essential hypertension presented to the ED with shortness of breath and worsening cough for one week. He was living with his father, who was admitted to the ICU and receiving treatment for COVID pneumonia. The patient appeared to be in respiratory distress. His initial vital signs were temperature of 99.6 F, respiratory rate of 26 breaths per minute, blood pressure 125/71 mm Hg, heart rate 109 beats per minute with a regular rhythm, and oxygen saturation of 50% while he was breathing ambient air. Pulmonary examination revealed use of respiratory accessory muscle and widespread bilateral coarse rhonchi on auscultation. The rest of the physical examination was within normal limits. RT- PCR COVID -19 test was positive. The blood gas analysis reported respiratory alkalosis. Inflammatory markers were elevated: erythrocyte sedimentation rate (35.2 mg/L), C-Reactive Protein (17.70 mg/dL), Ferritin (1108.1 ng/mL), Lactate Dehydrogenase (813 U/L), Lactate (2.4 mg/dL), D-Dimer (35.20 mg/L) and Troponin High Sensitivity-236.6 ng/L. His CBC, electrolytes, and kidney function were normal. Chest X-ray showed Pneumomediastinum with dense basilar predominant consolidation. CT Angio Chest with contrast reported Pneumomediastinum likely from the left central airway source and bilateral dense ground glass consolidation. An echocardiogram showed an ejection fraction of 60-65%, no valvular abnormalities. He was placed on vapotherm(Oxygen 40L/min) with 100% FiO2. He was given Dexamethasone 6mg for ten days, Remdesivir, Barcitinib, and a 7-day course of Azithromycin and Ceftriaxone for community-acquired pneumonia. He was advised to practice prone positioning for 12 hours or more per day. Pulmonology, Infectious Disease, and Cardiology were consulted. Gradually, his oxygen requirement was weaned down and Pneumomediastinum resolved on serial chest x rays. He was discharged on home oxygen in a clinically stable condition. DISCUSSION: Pneumomediastinum in viral pneumonia is rare. The exact mechanism is unknown. Covid-19 pneumonia causes diffuse alveolar wall damage, which might cause air leakage into the mediastinum. The development of pneumomediastinum is an ominous sign in these patients. Fortunately, our patient did not worsen and was weaned off high flow oxygenation requirement. CONCLUSIONS: Few isolated reported cases of pneumomediastinum in a COVID-19 patient have been associated with life-threatening complications. It should be used as a prognostic marker, and close monitoring of these patients is advisable. Reference #1: Damous, S.H.B., dos Santos Junior, J.P., Pezzano, Á.V.A. et al. Pneumomediastinum complicating COVID-19: a case series. Eur J Med Res 26, 114 (2021) DISCLOSURES: No relevant relationships by Saad Ansari No relevant relationships by Akshit Chitkara No relevant relationships by Sudeshna Ghosh No relevant relationships by Femina Patel

8.
Chest ; 162(4):A1810, 2022.
Article in English | EMBASE | ID: covidwho-2060868

ABSTRACT

SESSION TITLE: Diagnosis of Lung Disease through Pathology Case Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Idiopathic pulmonary hemosiderosis (IPH) is a rare pulmonary disease often resulting in diffuse pulmonary fibrosis. The majority of diagnoses present in infanthood with limited studies demonstrating late onset disease in patients older than 30 years. The mainstay of treatment is immunosuppressive therapy including systemic corticosteroids. Here we present a unique case of IPH in an unvaccinated individual with COVID-19 pneumonia. CASE PRESENTATION: Our patient was a 31 year-old male with a history of IPH diagnosed in early childhood with past hospitalizations for DAH and progressive pulmonary fibrosis for which he was treated with corticosteroids and cyclophosphamide years prior to this admission. He presented with six days of progressive shortness of breath and respiratory distress. He tested positive for COVID-19 four days prior to presentation. He was unvaccinated for COVID-19. Initial oxygen saturation was found to be 56% and non-invasive mechanical ventilation was started. CT angiography of the chest revealed diffuse ground glass opacities, bilateral consolidative changes, and redemonstration of pulmonary fibrosis with extensive honeycombing. Lab results were remarkable for elevated inflammatory enzymes including ferritin 1,335 ng/mL, lactate dehydrogenase 1,369 units/L, and C-reactive protein 6.5 ml/dL. Patient was started on intravenous glucocorticoids, IL-6 inhibitor, remdesivir. Work up for bacterial superinfection was unremarkable. His hospitalization was complicated by acute kidney injury, elevated liver enzymes, and anxiety. Despite the immunosuppressive therapy, the patient continued to have refractory hypoxemia. Due to his persistent hypoxemia, the family was contacted regarding the impending need for endotracheal intubation. They ultimately declined and the patient succumbed to his respiratory failure. DISCUSSION: Idiopathic pulmonary hemosiderosis remains to be a largely unstudied and rare disease with catastrophic respiratory sequela. There remains a scarcity of evidence surrounding the most effective treatment of these patients, although limited studies have shown mortality benefit with immunosuppressive therapy. In patients with IPH an insult such as COVID-19 infection could prove fatal. Preventative measures such as vaccination is vital in the protection of these patients. Further research regarding pathogenesis and treatment mechanisms for IPH is an aim of future study. CONCLUSIONS: Idiopathic Pulmonary Hemosiderosis is a rare but deadly disease often complicated by diffuse alveolar hemorrhage and pulmonary fibrosis. Considering the underlying pulmonary compromise in these patients, secondary insult from infection can have catastrophic outcomes. Reference #1: Saha B. K. (2021). Idiopathic pulmonary hemosiderosis: A state of the art review. Respiratory medicine, 176, 106234. https://doi.org/10.1016/j.rmed.2020.106234 Reference #2: Ioachimescu, O. C., Sieber, S., & Kotch, A. (2004). Idiopathic pulmonary haemosiderosis revisited. The European respiratory journal, 24(1), 162–170. https://doi.org/10.1183/09031936.04.00116302 Reference #3: Thornton, G. & Alotaibi, M. (2016). 979: IDIOPATHIC PULMONARY HEMOSIDEROSIS IN ADULT PATIENTS: AN EPIDEMIOLOGIC ANALYSIS. Critical Care Medicine, 44 (12), 321-321. doi: 10.1097/01.ccm.0000509655.03624.6e. DISCLOSURES: No relevant relationships by Allison Kunze No relevant relationships by Mohammed Siddiqui

9.
Chest ; 162(4):A1442-A1443, 2022.
Article in English | EMBASE | ID: covidwho-2060817

ABSTRACT

SESSION TITLE: Management of COVID-19-Induced Complications SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: We discuss a case of successful use of alteplase and dornase per MIST II protocol for the management of a loculated pleural effusion secondary to COVID-19 pneumonia. CASE PRESENTATION: 52 year old male was initially admitted for MRSA bacteremia and began appropriate antibiotic therapy. His chest radiograph on presentation was unremarkable. Seven days into his hospital course he tested positive for COVID-19 pneumonia, and developed increasing shortness of breath and escalating oxygen requirements. At this time he had a large loculated left sided pleural effusion on chest computed tomography. A pigtail catheter was placed with removal of 600ml of cloudy yellowish fluid. Follow-up CXR showed slight interval improvement, however a large loculated effusion remained. Pleural fluid studies was exudative, lymphocytic predominant (78%) with elevated pleural fluid lactate dehydrogenase of 786 U/L, pH 8.0, and glucose 97mg/dl. Additional pleural fluid workup was unremarkable, including negative cultures, AFB staining, and benign cytology. After other known causes of lymphocyte predominant pleural effusion were ruled out, and following review of the current medical literature, the conclusion was made that his effusion was most likely related to COVID-19. The decision was made to attempt lysis of the loculations with alteplase and dornase per MIST II protocol. This resulted in significant chest tube output (totaling 3480ml additional output over the ensuing days) as well as marked improvement in chest imaging. The protocol was continued for 3 days which the patient tolerated well overall. DISCUSSION: COVID-19 related pleural effusions occur with an incidence of about 7.3% of cases with an overall lag time of 11 days from symptom onset. Based on observational studies, these pleural effusions are unilateral in 66.8% of cases with a lymphocyte or neutrophilic predominance and significantly elevated pleural fluid to serum LDH ratio. The differential for exudative lymphocyte predominant pleural effusions with elevated LDH include malignancy, rheumatoid effusion, tuberculosis, and viral infections. The pleural studies workup was unremarkable for these conditions. The MIST-2 protocol was followed per the original study, with instillation of tPA 10mg via pigtail catheter which was clamped for 1 hour, opened to drain for 1 hour, then repeated with dornase 5mg. To the best of our knowledge, this is the first documented case of using MIST 2 protocol for a loculated pleural effusion related to COVID-19. CONCLUSIONS: COVID-19 related loculated pleural effusion is an infrequent occurrence that present as lymphocyte predominant exudative that can loculate with elevated lactate dehydrogenase. This is the first case of using alteplase and dornase for its management and we have demonstrated that it can be both a safe and effective method. Additional prospective studies are needed to further investigate this method. Reference #1: Chong WH, Saha BK, Conuel E, Chopra A. The incidence of pleural effusion in COVID-19 pneumonia: State-of-the-art review. Heart Lung. 2021;50(4):481-490. doi:10.1016/j.hrtlng.2021.02.015 Reference #2: Ahmadinejad Z, Salahshour F, Dadras O, Rezaei H, SeyedAlinaghi S. Pleural Effusion as a Sign of Coronavirus Disease 2019 (COVID-19) Pneumonia: A Case Report. Infect Disord Drug Targets. 2021;21(3):468-472. doi: 10.2174/1871526520666200609125045. PMID: 32516107. Reference #3: Rahman, N, et al. Intrapleural Use of Tissue Plasminogen Activator and DNase in Pleural Infection. N Engl J Med 2011;365:518-526. DOI: 10.1056/NEJMoa1012740 DISCLOSURES: No relevant relationships by Zachary Chandler No relevant relationships by James Cury No relevant relationships by Peter Staiano No relevant relationships by Daniel Weigle

10.
Chest ; 162(4):A1432, 2022.
Article in English | EMBASE | ID: covidwho-2060816

ABSTRACT

SESSION TITLE: Problems in the Pleura Case Posters 1 SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: Severe COVID 19 has now been known to cause devastating damage to the lungs. The manifestations include severe pneumonia, acute respiratory distress syndrome, spontaneous pneumothorax, etc. As we were learning about the pathogenesis of the infection, we were also learning rapidly about the therapeutics targeted against it. A report a case of severe COVID 19 ARDS in a non-vaccinated young male, who later developed empyema during his hospital course. CASE PRESENTATION: A 29-year-old male with no past medical history presented to the emergency department complaining of chest pain and shortness of breath. He was not vaccinated against COVID-19. He was discharged from the hospital on 2 liters of supplemental oxygen two days ago after undergoing treatment for COVID-19 pneumonia with dexamethasone and remdesivir. Physical examination revealed bilateral diminished lung sounds on auscultation. His blood pressure was 112/75 mm Hg, heart rate (HR) 120 per minute, respiratory rate 25 per minute, the temperature of 38.5 Celsius and he was saturating 91% on 15 L of oxygen via a non-rebreather mask. Initial CT scan revealed bilateral ground-glass opacities (figure 1.). Due to high oxygen requirements and CRP of 10.5 MG/DL, the patient was started on Sarilumab. Given his escalating oxygen requirements and worsening respiratory distress, he was intubated and transferred to the intensive care unit. Despite intermittent prone positioning, he became progressively hypoxemic and eventually required Veno-venous Extracorporeal Membrane Oxygenation (VV-ECMO). One week later he developed intermittent fever spikes up to 39.5 C with HR of 120 per minute and leukocytosis of 40.8 K/µL. Bedside point of care ultrasound revealed new bilateral complex pleural effusions. Chest CT-scan showed moderate bilateral pleural effusions with new cystic changes and worsening consolidations (figure 2). Pleural fluid analysis showed lactate dehydrogenase of 2798, pH of 7.11, and cell count of 100 with 98% neutrophils. Despite aggressive therapy with chest tube placements and broad-spectrum antibiotics his condition continued to worsen over the next month with the development of hydropneumothoraxes and traction bronchiectasis (figure 3). Given the clinical deterioration despite aggressive care, his family decided to pursue a comfort-oriented treatment approach and he eventually passed away. DISCUSSION: COVID-19 related pleural effusion is a reported complication of COVID-19 pneumonia in up to 2-11% of the cases [1]. Most cases are associated with comorbid conditions, such as heart failure, superimposed bacterial infections, and pulmonary embolism [2]. CONCLUSIONS: Our case indicates that bacterial empyema may complicate COVID-19 pneumonia later in the disease course even in young immune-competent patients, it is unclear if empyema is directly related to the disease process itself r the therapeutic used to treat the COVID 19 infection. Reference #1: Chong WH, Saha BK, Conuel E, Chopra A. The incidence of pleural effusion in COVID-19 pneumonia: State-of-the-art review. Heart Lung. 2021;50(4):481-490. doi:10.1016/j.hrtlng.2021.02.015 Reference #2: Zhang L, Kong X, Li X, et al. CT imaging features of 34 patients infected with COVID-19. Clin Imaging. 2020;68:226-231. doi:10.1016/j.clinimag.2020.05.016 DISCLOSURES: No relevant relationships by Rimsha Ali No relevant relationships by Konstantin Golubykh No relevant relationships by Iuliia Kovalenko No relevant relationships by Maidah Malik No relevant relationships by Taaha Mirza No relevant relationships by Navitha Ramesh

11.
Chest ; 162(4):A1289-A1290, 2022.
Article in English | EMBASE | ID: covidwho-2060797

ABSTRACT

SESSION TITLE: COVID-19 Case Report Posters 2 SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Much has been learned about the immune dysregulation and release of pro-inflammatory cytokines since the emergence of the COVID-19 pandemic.1 Patients with interstitial lung disease are often on immunosuppressive agents, such as rituximab, which is a B-cell depleting agent. There has been a large retrospective cohort study showing that rituximab therapy was the only immunosuppressive medication with a trend towards in-hospital death.2 We present a case of COVID-19 in a patient on rituximab with ANCA vasculitis. CASE PRESENTATION: A 51-year-old male, never smoker, with ANCA positive vasculitis (positive MPO and PR3) and interstitial lung disease (on 4-5L of oxygen) presented to the hospital with nausea and fever for 2 days and was found to have a positive SARS-CoV-2 PCR. At the time of presentation, he was on rituximab 1000 mg x 2 doses every 6 months with last infusion one month prior to presentation, azathioprine 150 mg daily, prednisone 15 mg daily, nintedanib 100 mg BID, and IVIG monthly. Spirometry showed FVC of 1.60L/37% predicted and an FEV1 1.28L/39% predicted. Patient had 2 COVID vaccinations and one booster (all Pfizer mRNA), the latter 3 months prior to presentation. On admission, he was saturating at 55% on 4L and placed on 15L non-rebreather;he was afebrile, normotensive, and with a pulse of 110 BPM. Exam was notable for a cough, wheezing, and tachypnea. Lab work was notable for positive SARS-COV-2 PCR, a total white blood cell count of 5.3x103 uL, and a normal hemoglobin and platelet count. He had a CO2 of 34, normal creatinine, and no transaminitis. Lactate dehydrogenase (LDH) was elevated at 318 U/L, and lactate was elevated at 3.5 mmol/L. His chest x-ray on admission demonstrated patchy filling opacities and low lung volumes. He received dexamethasone, remdesivir, and the monoclonal antibodies casirivimab and imdevimab (REGEN-COV) on the first day of admission. Patient also received his monthly IVIG dose inpatient. After a week, he was weaned back to his home oxygen and symptomatically back to baseline. Most recent PFTs on the same outpatient immunosuppressive regimen as prior to admission are unchanged. Patient received two doses of preventative monoclonal antibodies (EVUSHELD) 3 months after admission. DISCUSSION: Here we discuss a case of a patient with severe COVID-19 pneumonia requiring inpatient hospitalization despite three COVID mRNA vaccinations, likely secondary to difficulty in mounting an immune response to the vaccinations given his use of immunosuppressive medications. This is also an example of the early use of monoclonal antibodies in an inpatient with long term preservation of his underlying lung function.3 CONCLUSIONS: We recommend counseling and close observation of patients on rituximab due to risk of severe COVID-19 infection as well the use of preventative monoclonal antibodies (EVUSHELD). Reference #1: Jamal M, Bangash HI, Habiba M, Lei Y, Xie T, Sun J, Wei Z, Hong Z, Shao L, Zhang Q. Immune dysregulation and system pathology in COVID-19. Virulence. 2021 Dec;12(1):918-936. doi: 10.1080/21505594.2021.1898790. PMID: 33757410;PMCID: PMC7993139. Reference #2: Andersen, K. M., Bates, B. A., Rashidi, E. S., Olex, A. L., Mannon, R. B., Patel, R. C., Singh, J., Sun, J., Auwaerter, P. G., Ng, D. K., Segal, J. B., Garibaldi, B. T., Mehta, H. B., Alexander, G. C., Haendel, M. A., & Chute, C. G. (2022). Long-term use of immunosuppressive medicines and in-hospital COVID-19 outcomes: A retrospective cohort study using data from the National COVID Cohort Collaborative. The Lancet Rheumatology, 4(1), e33–e41. https://doi.org/10.1016/S2665-9913(21)00325-8 Reference #3: Weinreich, D. M., Sivapalasingam, S., Norton, T., Ali, S., Gao, H., Bhore, R., Xiao, J., Hooper, A. T., Hamilton, J. D., Musser, B. J., Rofail, D., Hussein, M., Im, J., Atmodjo, D. Y., Perry, C., Pan, C., Mahmood, A., Hosain, R., Davis, J. D., Yancopoulos, G. D. (2021). Regen-cov antibody combination and outcomes in outpatients with covid-19. New England Journal of Medicine, 385(23), e81. https://doi.org/10.1056/NEJMoa2108163 DISCLOSURES: Advisory Committee Member relationship with Genentech Please note: 2019-2022 Added 06/06/2022 by Ayodeji Adegunsoye, value=Consulting fee Advisory Committee Member relationship with Boehringer Ingelheim Please note: 2018-2022 Added 06/06/2022 by Ayodeji Adegunsoye, value=Consulting fee Speaker/Speaker's Bureau relationship with Boehringer Ingelheim Please note: 2018-2022 Added 06/06/2022 by Ayodeji Adegunsoye, value=Honoraria Consultant relationship with Genentech Please note: 2018-2020 by Ayodeji Adegunsoye, value=Consulting fee Removed 06/06/2022 by Ayodeji Adegunsoye No relevant relationships by Cathryn Lee No relevant relationships by Kavitha Selvan PI relationship with Boehringer-Ingelheim Please note: >$100000 by Mary Strek, value=Grant/Research Support PI relationship with Galapagos Please note: $70,000-100,00 by Mary Strek, value=Grant/Research Support Endpoint Adjudication Committee Member relationship with Fibrogen Please note: $1-$1000 by Mary Strek, value=Honoraria No relevant relationships by Rachel Strykowski

12.
Chest ; 162(4):A1163-A1164, 2022.
Article in English | EMBASE | ID: covidwho-2060782

ABSTRACT

SESSION TITLE: Studies on COVID-19 Infections Posters SESSION TYPE: Original Investigation Posters PRESENTED ON: 10/18/2022 01:30 pm - 02:30 pm PURPOSE: To evaluate factors associated with early versus late mortality in hospitalized patient with COVID-19. METHODS: This observational study analyzed data of patients who died from COVID-19 at Ben Taub Hospital, a tertiary care County teaching hospital, between from March 2020 to February 2022. Demographic, comorbidities, laboratory values as well as COVID-19 treatments were examined. Patients were divided into two groups: those who had early mortality and those with late mortality (death ≤7 days or >7 days of admission, respectively). RESULTS: 212 patients with COVID-19 died during that period. Of these, 46 patients had early mortality and 166 patients had late mortality. 19/46 (41.3%) of the patients in early mortality group died within 72 hours of presentation. There were no differences between the two groups with regards to age, gender, ethnicity, or body mass index. Both groups were similar with regards to history of tobacco use, hypertension, diabetes mellitus, coronary artery disease, congestive heart failure, cerebrovascular accident, atrial fibrillation, obstructive airway disease, cancer, liver cirrhosis and human immunodeficiency virus infection. There were no differences with regards to COVID vaccination status between the two groups. Peak D dimer, peak C-reactive protein, peak ferritin, peak lactate dehydrogenase and lymphocyte nadir during the hospital course were also similar between the two groups. Patients in the early mortality group had shorter time from symptom onset to admission {3.91 days (SD 5.63) in early vs 6.85 days (SD 8.01) in late}. There were no differences between the two groups regarding use of mechanical ventilation. Patients with late mortality were more likely to have received systemic steroids (90.9% vs 60.9%), anticoagulation (94.6% vs 65.2%), remdesivir (75.3% vs 32.6%), inhaled epoprostenol (50.6% vs 19.6%) compared to early mortality, respectively. In addition to severity of symptoms and clinical condition at the outset of the disease, early death may have been related to not receiving some of these medications.1 CONCLUSIONS: Early mortality in patients with COVID-19 is associated with shorter time to symptoms onset and the lower likelihood to have received systemic steroids, systemic anticoagulation, remdesivir and inhaled epoprostenol. CLINICAL IMPLICATIONS: Early recognition and intervention may prevent early mortality in COVID-19 patients. Reference: Sun, Q., Qiu, H., Huang, M. et al. Lower mortality of COVID-19 by early recognition and intervention: experience from Jiangsu Province. Ann. Intensive Care 10, 33 (2020). https://doi.org/10.1186/s13613-020-00650-2 DISCLOSURES: No relevant relationships by Muhammad Adrish Advisory Committee Member relationship with AstraZeneca, Genentech, GSK, Mylan, Sanofi Please note: 2020-2021 by Nicola Hanania, value=Consulting fee Consultant relationship with AstraZeneca, Genentech, GSK, Mylan, Sanofi Please note: 2020-2021 by Nicola Hanania, value=Consulting fee Advisory Committee Member relationship with Regeneron, Amgen, and Teva Please note: 2020-2021 by Nicola Hanania, value=Consulting fee Consultant relationship with Regeneron, Amgen, and Teva Please note: 2020-2021 by Nicola Hanania, value=Consulting fee Removed 08/02/2022 by Nicola Hanania Research support relationship with Boehringer Ingelheim, GSK, Novartis Please note: 2020-2021 by Nicola Hanania, value=Grant/Research Support Research support relationship with Sanofi Genzyme and Genentech Please note: 2020-2021 by Nicola Hanania, value=Grant/Research Support No relevant relationships by Stephanie Stalcup

13.
Chest ; 162(4):A896, 2022.
Article in English | EMBASE | ID: covidwho-2060720

ABSTRACT

SESSION TITLE: Critical Care Management of COVID-19 SESSION TYPE: Original Investigations PRESENTED ON: 10/17/2022 01:30 pm - 02:30 pm PURPOSE: We hypothesized that supplementation of NIH recommended remdesivir (REM) and dexamethasone (DEX) combination treatment with tocilizumab (TOCI) or baricitinib (BARI) initiated inside 48h of index hospitalization would enhance reduction of inflammatory markers and discharges to home in adults over 18 years old who received intensive care. METHODS: Electronic medical record data were extracted under IRB exemption. Treatment responsiveness was estimated using delta in C-reactive protein (CRP), ferritin, lactate dehydrogenase (LDH) and D-dimer levels from assays respectfully respectively first within 24h and last between 25-72h of initiating REM/DEX with vs without TOCI or BARI. Confounder balanced multigroup contrasts were significant when p<.017. RESULTS: Between March 10, 2020 and January 31, 2022, 891 COVID-19 patients were admitted to the ICU with 459 receiving REM/DEX (n=326) or supplemented with BARI (n=85) or TOCI (n=41). Results are sequenced as REM/DEX, REM/DEX/BARI, REM/DEX/TOCI. Age was 67[57,77] (p<.0001) vs. 61[51,69] and 62[48,68] among statistically similar sex (male, 65%;female, 35%) and race (White, 76%;Black, 8%;Other, 16%) distributions and BMI (32[27,38] kg/m2). Hypertension (70%), obesity (59%), diabetes (38%), deficiency anemia (36%), coagulopathy (29%) chronic pulmonary disease (22%), and renal failure (17%) were similarly distributed. Initial CRP, ferritin, LDH and D-dimer levels -24h to +24h of REM/DEX first dose respectively were 12.1[7.1,18.2], 11.4[7.5,15.7], 14.0[11.2,21.0] mg/dL;811[441,1390], 1178[529,1956], 1110[653,1810] ng/mL (REM/DEX, p=.013);437[321,576], 516[403,695], 518[397,692] U/L (REM/DEX, p=.0001);and 1.02[0.67,2.28], 0.97[0.72,1.88], 1.47[0.86,2.19] ug/mL. Responsiveness quantified using last levels 25h-72h post REM/DEX first dose respectively included -3.4[-7.2,-0.6], -4.3[-7.7,-1.9], -7.2[-10.1,-3.6] mg/dL (REM/DEX/TOCI, p=.014);7[-125,202], -94[-329,69], -29[-181, 535] U/L;-3[-74,80], 85[-58,273], -33[-188,-3] U/L (p=.051);and 0.00[-0.50,1.05], 0.88[-0.45,10.52], -0.01[-0.38,0.50] ug/mL. ICU length of stay (LOS) was 6[3,13], 6[3,12], 8[5,15] days (p<.00001) with hospital LOS of 16[10,24], 20[12,33], 17[11,23] days (REM/DEX/BARI, p<.021). Hospital mortality was 51%, 71%, 43%, with REM/DEX/BARI exhibiting increase (p=.0019), but REM/DEX/TOCI numerically lowest (p>.017). Discharge to home was 24%, 18%, 43%, with REM/DEX/TOCI demonstrating increase (p=.0038). CONCLUSIONS: REM/DEX/TOCI combination therapy provided largest reduction of inflammatory markers and mortality while substantially increasing percentage of discharges to home. REM/DEX treatment responsiveness was adversely impacted by addition of baricitinib, while augmented by tocilizumab. CLINICAL IMPLICATIONS: Our findings highlight need to refine early longitudinal biomarker-tracking to identify patient-centric COVID-19 treatment responsiveness to COVID-19 directed treatments. DISCLOSURES: No relevant relationships by Qassem Abdelal No relevant relationships by Kevin Dawkins No relevant relationships by Karen Hamad No relevant relationships by Natalia Lattanzio No relevant relationships by Richard Walo Jr No relevant relationships by Wilhelmine Wiese-Rometsch No relevant relationships by Stephanie Williams

14.
Chest ; 162(4):A895, 2022.
Article in English | EMBASE | ID: covidwho-2060719

ABSTRACT

SESSION TITLE: Pathologies of the Post-COVID-19 World SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 10:15 am - 11:10 am INTRODUCTION: SARS-CoV-2 related autoimmune and thrombotic complications due to vigorous immune system stimulation and induction of hypercoagulable state are not uncommon. Two hypotheses have been proposed for thrombotic microangiopathy associated with low ADAMTS13 levels in patients with COVID-19 disease. First underscores a significant increase in von Willebrand factor (vWF), likely due to endothelial activation, that overwhelms ADAMTS13. It is observed in the absence of thrombocytopenia or ADAMTS13 inhibitor. The second highlights the formation of autoantibodies against ADAMTS13 because of an immunological trigger (SARS-CoV-2), resulting in the diagnosis of TTP. CASE PRESENTATION: This is a case of a 72-year-old Caucasian man with a history of hypertension, diabetes, chronic obstructive lung disease, and asymptomatic SARS-CoV-2 infection three weeks ago who was transferred to our institution to initiate plasmapheresis for suspected TTP due to new-onset confusion, anemia and worsening renal function. Patient had presented with confusion a day before transfer. Vital signs were remarkable for tachycardia (heart rate of 105 beats/min). Labs were significant for anemia (hemoglobin:6.7 g/dL), thrombocytopenia (platelet count:13 K/µL), acute kidney injury (creatinine:1.8 mg/dL), elevated lactate dehydrogenase (1983 IU/L), high bilirubin (2.3 mg/dL), low haptoglobin (<4 mg/dL), and demonstration of schistocytes on peripheral smear. The coagulation profile was normal. On arrival, he required emergent intubation due to multiple seizures. Computed tomography scan of the head was normal. SARS-CoV-2 molecular testing was negative. Given a PLASMIC score of six, urgent plasmapheresis and high-dose methylprednisolone were started. Screening for human immunodeficiency virus, hepatitis viruses, Epstein-Barr virus, and Cytomegalovirus were negative. Subsequently, his ADAMTS13 activity resulted as being ≤5% with an elevated inhibitor Bethesda titer of 0.9 (normal < 0.4). The patient completed six sessions of plasmapheresis. He was discharged on steroid taper and weekly rituximab. DISCUSSION: COVID-19 associated de-novo TTP has been mostly reported with typical COVID-19 symptoms within a few days of a positive test. One report described presentation with only neurological symptoms 19 days after a positive test with low autoantibody titers, favoring the hypothesis of consumption of ADAMTS13. To the best of our knowledge, this is the first case of new, late-onset immune TTP developing three weeks after asymptomatic COVID-19 infection with a robust positive inhibitor screen and infinitesimal ADATMS13 levels. The temporal sequence of events and lack of other plausible causes aided in the diagnosis of COVID-19 induced TTP. CONCLUSIONS: Our report aims to make clinicians aware of ruling out TTP as a cause of thrombocytopenia and/or altered mental status in patients with past COVID-19 infection, aiding in early management. Reference #1: 1. Mancini I, Baronciani L, Artoni A, Colpani P, Biganzoli M, Cozzi G, Novembrino C, Boscolo Anzoletti M, De Zan V, Pagliari MT, Gualtierotti R, Aliberti S, Panigada M, Grasselli G, Blasi F, Peyvandi F. The ADAMTS13-von Willebrand factor axis in COVID-19 patients. J Thromb Haemost. 2021 Feb;19(2):513-521. doi: 10.1111/jth.15191. Epub 2020 Dec 18. PMID: 33230904;PMCID: PMC7753796. Reference #2: 2. Tehrani HA, Darnahal M, Vaezi M, Haghighi S. COVID-19 associated thrombotic thrombocytopenic purpura (TTP);A case series and mini-review. Int Immunopharmacol. 2021;93:107397. doi:10.1016/j.intimp.2021.107397 Reference #3: 3. Beaulieu, M.-C., Mettelus, D.S., Rioux-Massé, B. and Mahone, M. (2021), Thrombotic thrombocytopenic purpura as the initial presentation of COVID-19. J. Thromb. Haemost., 19: 1132-1134. https://doi-org.libproxy.uams.edu/10.1111/jth.15231 DISCLOSURES: No relevant relationships by Harmeen Goraya No relevant relationships by PRACHI SALUJA

15.
Chest ; 162(4):A863-A864, 2022.
Article in English | EMBASE | ID: covidwho-2060713

ABSTRACT

SESSION TITLE: Biological Markers in Patients with COVID-19 Posters SESSION TYPE: Original Investigation Posters PRESENTED ON: 10/18/2022 01:30 pm - 02:30 pm PURPOSE: Severe COVID19 patients present with low CD8(+) T cell counts. A reduced number of T-cells seems to be correlated with high serum IL-6 and IL-10 levels, and a marked inflammatory state. This study aimed to assess if low CD8(+) counts were associated with inflammation markers, length of stay, and Ichikado CT scores in COVID-19 patients. METHODS: A retrospective study of adult patients admitted to our hospital with COVID-19 infection from June 2021 to September 2021. CD8(+) count was obtained, and patients were divided into less than 150 cells/μl and more than 150 cells/μl. Ferritin, c-reactive protein (CRP), erythrocyte sedimentation rate (ESR), troponin, Lactate dehydrogenase (LDH), and d-Dimer values were also recorded. Primary outcomes were hospital length of stay (LOS), Ichikado CT score, and correlation of CD8(+) count and inflammatory markers. Descriptive statistics, and Mann-Whitney-U methods were utilized. RESULTS: 264 patients were included, median age was 50 years [41-61]. 143 (54.2%) patients were male. There was a statistically significant difference when assessing hospital LOS in patients with CD8(+) counts <150 cells/μl vs > 150 cells/μl (9 days [5-16] vs 5 days [4-9], U=(134, 84)=3742, z=-4.174, p<0.01). The Ichikado CT score was significantly different between groups (190 [150-220] vs [130-190], U=(128,80)=3394, z=-4.094, p<0.01). IL-6 and IL-10 values were higher in those patients with CD8(+) less than 150 μl, when compared to higher CD8(+) counts. IL-10 value was (23.8pg/ml [13.6-43.3] vs (6.6pg/ml [9.4-29.2]), U=(131,78)=3711.5, z=-3.305, p<0.01), and for IL-6 (23.8pg/ml [7.6-88.3] vs (11.9 [4.1-32.1]), U=(125,75)=3473.5, z=-3.064, P<0.01). Ferritin was increased in patients with CD8(+) counts lower than 150 cells/μl compared to more than 150 cells/μl (845.3ng/ml [381.6-1600] vs 480ng/ml [232.6-988.7], U=(133,83)=3939.5, z=-3.550, p=<0.01). Similarly, CRP (83mg/L [46.3-136.7] vs 60.2 mg/L [33.25-100.72], U=(134-82)=4208, z=-2.885, p=<0.01), d-Dimer (1.76mg/L [0.53-7] vs 0.64 mg/L [0.35-1.72], U= (134,84)=3635.5, z=-4.396, p<0.01), and LDH (555IU/L [361-849.2] vs 375.5IU/L [273.2-531.2], U=(122,72)=2740,z=-4.373,p<0.01). Troponin and ESR were not significantly different, median troponin (0.022ng/ml [0.011-0.039] vs 0.012ng/ml [0.007-0.032], U=(111,70)=3218, z=-1.944,P=0.052) and median ESR (78mm/hr [57.2-105] vs 76.5 mm/hr [55-108.7], U=(134,84)=5603, z=-0.055,P=0.95). CONCLUSIONS: CD8(+) counts below 150 cells/μl are associated with increased inflammatory markers, a longer hospital stay, and higher Ichikado CT scores. CLINICAL IMPLICATIONS: CD8(+) count below 150 cells/μl is other indicator of disease severity in COVID-19 DISCLOSURES: No relevant relationships by David Akinwale No relevant relationships by Angelica Almaguer No relevant relationships by Sushen Bhalla No relevant relationships by Ailine Canete Cruz No relevant relationships by Ndiya Emeaba Speaker/Speaker's relationship with johnson and johnson Please note: approx year 2000 Added 03/31/2022 by Joseph Gathe, value=Honoraria clinical research relationship with gilead Please note: since 1990 Added 03/31/2022 by Joseph Gathe, value=Grant/Research clinical research relationship with ansun Please note: 2020 Added 03/31/2022 by Joseph Gathe, value=Grant/Research Support clinical research relationship with regeneron Please note: 2020 Added 03/31/2022 by Joseph Gathe, value=Grant/Research Support No relevant relationships by Jesus Salvador Gonzalez Lopez No relevant relationships by Najia Hussaini No relevant relationships by Claudia Ramirez No relevant relationships by Salim Surani No relevant relationships by Daryelle Varon No relevant relationships by Joseph Varon No relevant relationships by Mohamed Ziad

16.
Chest ; 162(4):A861-A862, 2022.
Article in English | EMBASE | ID: covidwho-2060712

ABSTRACT

SESSION TITLE: Biological Markers in Patients with COVID-19 Posters SESSION TYPE: Original Investigation Posters PRESENTED ON: 10/18/2022 01:30 pm - 02:30 pm PURPOSE: Common markers of inflammation in COVID-19 include erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and ferritin. We aimed to find an association between creatine Phosphokinase (CPK) and other inflammatory markers and enzymes, and their effect on length of hospital stay, and the Ichikado CT scores. METHODS: Retrospective study of the data of 264 adult patients admitted to our hospital between June and September 2021, with COVID-19. Patients were divided into groups with CPK of greater or less than 200mg/dL. Each was assessed for its association with CRP, ESR, ferritin, and lactate dehydrogenase (LDH), length of hospital stay, and Ichikado CT score. Descriptive statistics, Mann Whitney-U were used to address statistical significance. RESULTS: 264 patients were included, median age was 51.95 years [41-63]. 143(53.2%) were male. The median highest CRP value in patients with CPK of <200 mg/dL was (55 mg/L [24-96.4] vs 97.4 mg/L [50.1-139]) in those with CPK of >200 mg/dL, (U=(131,118) =5097, z=-4.638, p<0.01). The median highest ESR with CPK of <200 mg/dL was (72 mm/hr [51.0-102.5] vs 89 mm/hr [60-109]) in those with CPK of >200 mg/dL, (U= (133,119) =6862.5, z=-1.820, p=0.069). The median highest ferritin value in those with CPK of <200 mg/dL was (388.5 ng/mL [187.1-804.4] vs 1046 ng/mL [462.1-1600]) in those with CPK of >200 mg/dL, (U=(132,118) =4156.5, z=6.3985, p<0.01). The median highest phosphate level in patients with CPK of <200 mg/dL was (3.6 mg/dL [3.3-4.2] vs 3.8 mg/dL [3.4-5.2]) in those with CPK of >200 mg/dL,(U=(133,119) =6487.5, z=-2.471, p=0.013). The median highest LDH level in patients with CPK of <200 mg/dL was (352 IU/L [271.5-459] vs 673.5 IU/L[411.7-980.2]) in those with CPK of >200 mg/dL, (U=(113,106) = 2201, z =-8.084, p<0.01). The median highest Ichikado CT score in patients with CPK of <200 mg/dL was (150[130-190] vs 190[140-222.5]) in those with CPK of >200 mg/dL,(U= (142,209) =5188, z=-4.482, p<0.01). The length of hospital stay in patients with CPK of<200 mg/dL was (5 days [3-8] vs 9 days [5-17]) in those with CPK of >200 mg/dL, (U=(144,120) = 5533, z =-5.049, p<0.01). CONCLUSIONS: CPK has a statistically significant association with CRP and ferritin levels but not ESR. Imaging disease severity at presentation (Ichikado CT score) was associated with higher CPK levels. CLINICAL IMPLICATIONS: CPK is another marker of disease severity in COVID-19. DISCLOSURES: No relevant relationships by David Akinwale No relevant relationships by Angelica Almaguer No relevant relationships by Sushen Bhalla No relevant relationships by Ailine Canete Cruz No relevant relationships by Ndiya Emeaba Speaker/Speaker's relationship with johnson and johnson Please note: approx year 2000 Added 03/31/2022 by Joseph Gathe, value=Honoraria clinical research relationship with gilead Please note: since 1990 Added 03/31/2022 by Joseph Gathe, value=Grant/Research clinical research relationship with ansun Please note: 2020 Added 03/31/2022 by Joseph Gathe, value=Grant/Research Support clinical research relationship with regeneron Please note: 2020 Added 03/31/2022 by Joseph Gathe, value=Grant/Research Support No relevant relationships by Jesus Salvador Gonzalez Lopez No relevant relationships by Najia Hussaini No relevant relationships by Claudia Ramirez No relevant relationships by Salim Surani No relevant relationships by Joseph Varon No relevant relationships by Daryelle Varon No relevant relationships by Mohamed Ziad

17.
Chest ; 162(4):A859-A860, 2022.
Article in English | EMBASE | ID: covidwho-2060711

ABSTRACT

SESSION TITLE: Biological Markers in Patients with COVID-19 Posters SESSION TYPE: Original Investigation Posters PRESENTED ON: 10/18/2022 01:30 pm - 02:30 pm PURPOSE: A significant reduction of CD4(+) cells and marked inflammatory activity in moderate and severe COVID-19 cases are seen, both associated with a poor prognosis. This study aimed to assess the association of low CD4(+) counts with inflammatory markers, length of stay, and ICKIKADO scores in COVID-19 patients. METHODS: A retrospective study of adult patients admitted to our hospital with COVID-19 infection from June 2021 to September 2021. CD4(+) count was obtained and patients were divided into two categories: less than 200 cells/μl and more than 200 cells/μl. Ferritin, c-reactive protein (CRP), erythrocyte sedimentation rate (ESR), troponin, Lactate dehydrogenase (LDH), and d-Dimer values were also recorded. Primary outcomes were hospital length of stay (LOS), Ichikado CT scores, and correlation of CD4(+) count and inflammatory markers. Descriptive statistics, and Mann-Whitney-U methods were used. RESULTS: 264 patients were included, median age was 50 years [41-61]. 143(54.2%) were male. There was a statistically significant difference in LOS for patients with CD4(+) counts <200 cells/μl vs > 200 cells/μl CD4(+) (9 days [5-18]vs 6 days [4-9]), U=(111,107)=4330, z=-3.466, p <0.01). The Ichikado CT score was significantly different between groups (190[150-220]vs 160[128.7-192.5], U=(106,102)=3706.5, z=-3.923, p<0.01). IL-10 values and IL-6 values were higher in those patients with CD4(+) less than 200 cells/μl, as compared to higher CD4(+) counts. median IL-10 was (25.2 pg/ml [17-72.45 ] vs 15.7 pg/ml [9.4-26.8 ], U=(109,100)=3463, z=-4.550, p<0.01), and median IL-6 was (23 pg/ml [10.5-99] vs 12 pg/ml [3.77-39], U=(104, 96)=3444.5, z=-3.785, p<0.01). Ferritin was increased in patients with CD4(+) counts lower than 200 cells/μl when compared to counts more than 200 cells/μl (850.2 ng/mL [373.3-1600] vs 541.5 ng/mL [245.1-1034.6], U=(110,106) =4543.5, z=-2.813, p=<0.01). CRP had a similar pattern (82 mg/L[49.5-138.2] vs 60.8 mg/L[30-114.2]), U=(111,105)=4478, z=-2.940, p=<0.01), d-Dimer (2.2 mg/L[0.55-7.14] vs 0.7mg/L[0.37-1.75], U=(111,107)=3992.5, z=-4.180, p<0.01), LDH (630 IU/L[371-888] vs 381 IU/L[276-520.2], U=(102,92)=2631.5,z=-5.227, p<0.01) and troponin (0.024 ng/mL[0.012-0.048] vs 0.012 ng/mL[0.007-0.027], U=(91,90)=2925, z=-3.321,P<0.01). The only inflammatory marker that was not statistically significant different was ESR (86 mm/hr[60-110] vs 72 mm/hr[50-100], U(111-107)=5113, z=-1.773,P=0.076). CONCLUSIONS: CD4(+) counts below 200 cells/μl are associated with increased inflammatory markers, a longer hospital stay, and higher Ichikado CT scores. CLINICAL IMPLICATIONS: CD4(+) count below 200 cells/μl is other indicator of disease severity in COVID-19 DISCLOSURES: No relevant relationships by David Akinwale No relevant relationships by Angelica Almaguer No relevant relationships by Sushen Bhalla No relevant relationships by Ailine Canete Cruz No relevant relationships by Ndiya Emeaba Speaker/Speaker's relationship with johnson and johnson Please note: approx year 2000 Added 03/31/2022 by Joseph Gathe, value=Honoraria clinical research relationship with gilead Please note: since 1990 Added 03/31/2022 by Joseph Gathe, value=Grant/Research clinical research relationship with ansun Please note: 2020 Added 03/31/2022 by Joseph Gathe, value=Grant/Research Support clinical research relationship with regeneron Please note: 2020 Added 03/31/2022 by Joseph Gathe, value=Grant/Research Support No relevant relationships by Jesus Salvador Gonzalez Lopez No relevant relationships by Najia Hussaini No relevant relationships by Claudia Ramirez No relevant relationships by Salim Surani No relevant relationships by Daryelle Varon No relevant relationships by Joseph Varon No relevant relationships by Mohamed Ziad

18.
Chest ; 162(4):A836, 2022.
Article in English | EMBASE | ID: covidwho-2060701

ABSTRACT

SESSION TITLE: Unique Inflammatory and Autoimmune Complications of COVID-19 Infections SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Coronavirus disease 2019 (COVID-19) can manifest as a severe immunologic syndrome known as hemophagocytic lymphohistiocytosis (HLH). HLH is a hyper-inflammatory state with a lethal mortality rate, especially when discovered late in the disease process. The optimal timely approach to diagnosis and treatment of secondary HLH in COVID-19 is unclear, however, risk stratification with Hscore using biomarkers can be useful to increase confidence in an HLH diagnosis. CASE PRESENTATION: A 36-year-old morbidly obese male with a history of well controlled mild intermittent asthma presented to the hospital complaining of a one week history of dyspnea and cough after failing outpatient COVID-19 treatment. Upon arrival, he was hypoxic on room air and was placed on non-invasive ventilation. He unfortunately decompensated further and was transferred to the intensive care unit where he was intubated for severe hypoxia and increased work of breathing. His course was complicated by superimposed bacterial pneumonia, vasopressor dependent septic shock, and anuric acute kidney injury requiring continuous renal replacement therapy. He remained profoundly hypoxic despite rescue therapy with multiple sessions of prone ventilation. On hospital day seventeen his platelets declined acutely and a serotonin release assay confirmed heparin-induced thrombocytopenia. His clinical status remained tenuous into the third week of admission. Notably, he developed persistent fever with associated bicytopenia and elevated lactate dehydrogenase, D-dimer, fibrinogen, triglycerides, and aspartate aminotransferase. His calculated Hscore was 189. Hematology recommended initiating HLH therapy with daily dexamethasone and etoposide, however the latter was held due to the patient's rapid hemodynamic decline. The patient succumbed to illness after a twenty-day hospitalization. His HLH was confirmed with a positive postmortem soluble-IL-2-receptor test. DISCUSSION: Proposals of routine HLH screening in critically ill patients are endorsed to promote early detection of this morbid condition. Calculating Hscore using vital signs, imaging, laboratory tests, and patient history can guide suspicion of diagnosis, since HLH-specific markers are often not feasible. Hscores more than 169 correspond to 93% sensitivity and 86% specificity in HLH diagnosis. Immunosuppression is standard therapy with hematology guidance due to the complex pathophysiology and limited research. CONCLUSIONS: This case emphasizes the importance of understanding the relationship between COVID-19 and secondary HLH. A timely diagnosis is vital in order to attempt to effectively treat a syndrome that carries a 65% mortality rate. Reference #1: Dimopoulos G, Mast Q. de, Markou N, et al. Favorable Anakinra responses in severe COVID-19 patients with secondary hemophagocytic lymphohistiocytosis. Cell Host Microbe 2020;doi: 10.1016/j.chom.2020.05.007. PubMed PMID: 32411313. Reference #2: Bauchmuller K, Manson JJ, Tattersall R, et al. Haemophagocytic lymphohistiocytosis in adult critical care. J Intensive Care Soc 2020;21:256–68. Reference #3: 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 Kristina Catania No relevant relationships by Katie Kennedy No relevant relationships by Josef Kinderwater No relevant relationships by MaryKate Kratzer no disclosure submitted for Ogugua Obi;

19.
Chest ; 162(4):A678, 2022.
Article in English | EMBASE | ID: covidwho-2060666

ABSTRACT

SESSION TITLE: COVID-19 Case Report Posters 3 SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Pneumocystis Pneumonia (PCP) is an opportunistic infection caused by a yeast-like fungus pneumocystis jirovecii. It is characterized by hypoxemia and increased inflammatory markers with elevated lactate dehydrogenase (LDH) often used as a clinical indicator of possible infection. COVID-19 is a viral infection caused by severe acute respiratory syndrome coronavirus and presents with a variety of symptoms, pneumonia being the most frequent and serious manifestation. Common laboratory markers include lymphopenia, elevated LDH and inflammatory markers. CASE PRESENTATION: Our patient is a 54 yo African American male with an unremarkable history who presented to our facility from an outside hospital (OH) for worsening respiratory failure in the setting of a large left pulmonary artery thrombosis. He was infected with COVID-19, four months prior and had experienced worsening weakness, SOB and anorexia two months before admission. Work up at OH revealed the large pulmonary emboli as well as extensive multifocal opacities consistent with prior COVID infection and described as post- COVID fibrosis. His sputum also tested positive for pseudomonas aeruginosa and mycoplasma pneumoniae for which he was treated. Unfortunately his hypoxemia worsened and he required intubation;prompting transfer to our facility for hopes of thrombectomy. He continued with hypoxemic, hypercarbic respiratory failure and underwent a bronchoscopy which was grossly normal. As serology indicated lymphopenia and paraprotein gap > 4, we decided to order HIV RNA PCR, which came back positive (CD4 count 11cells/ mm3). One week later, pneumocystis jirovecii was identified from an immunohistochemical stain from bronchial alveolar lavage (BAL). DISCUSSION: PCP is a common opportunistic infection in patients with human immunodeficiency virus, generally presenting when CD4 counts decrease below 200 cells/ mm3. Along with similar symptoms and elevated inflammatory markers, COVID-19 and PCP share common radiographic findings of ground glass opacities. In addition to his compromised lung (from COVID-19) and prolonged hospitalization, the positive cultures of m. pneumoniae and p.aeruginosa were originally misleading. Although cases of co-infection of PJP and COVID-19 exist, our case demonstrates that having a broad differential after recovery from COVID-19 continues to be necessary. CONCLUSIONS: PCP and COVID-19 pneumonia share similarities in radiographic and laboratory findings proving difficult to differentiate from each other. This case highlights the importance of assessing the immunological status of patients with unknown HIV history especially in a time where considering different etiologies of pneumonia have taken the backseat in the height of the COVID-19 pandemic Reference #1: Anggraeni AT, Soedarsono S, Soeprijanto B. Concurrent COVID-19 and Pneumocystis jirovecii pneumonia: The importance of radiological diagnostic and HIV testing. Radiol Case Rep. 2021;16(12):3685-3689. Published 2021 Oct 2. doi:10.1016/j.radcr.2021.09.002 Reference #2: Analysis of underlying diseases and prognosis factors associated with Pneumocystis carinii pneumonia in immunocompromised HIV-negative patients. Roblot F, Godet C, Le Moal G, Garo B, Faouzi Souala M, Dary M, De Gentile L, Gandji JA, Guimard Y, Lacroix C, Roblot P, Becq-Giraudon B. Eur J Clin Microbiol Infect Dis. 2002;21(7):523. DISCLOSURES: No relevant relationships by Cynthia Espinosa No relevant relationships by Jason Kovacevic No relevant relationships by Laura Mendez Morente No relevant relationships by Zuleikha Muzaffarr

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Chest ; 162(4):A625, 2022.
Article in English | EMBASE | ID: covidwho-2060650

ABSTRACT

SESSION TITLE: Unusual Pneumonias SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Cytomegalovirus (CMV) is an important infectious organism in the morbidity and mortality of immunocompromised patients. CMV is a known cause of pneumoina in transplant patients, such as lung transplant recepients. Pneumocytis Jiroveci Pneumonia (PCP) is also a known risk factor for potentially life-threatening infections in immunocompromised patients. In this , we are presenting a rare case of an immunocompromised patient who had penumonia caused by a concurrent CMV and PCP infections. CASE PRESENTATION: A 53 year-old female patient with history of Rheumatoid Arthritis treated with immunomodulating medications admitted for Shortness of breath, fatigue and tiredness but no fever. COVID-19 and influenza infections (PCR) tests were both negative. At presentation, her WBC was 9900. CT with contrast of her chest showed no embolism, but multi-focal widespread groundglass opacities. Blood culture was negative, MRSA screen was negativetoo, but Fungitell test was positive (with a value of more than 500) and serum LDH test was elevated to 382. CMV quantitaive PCR was elevated to 10,000 copies. A bronchoscopy was done and CMV PCR Bronchoalveolar lavage (BAL) is detected at 650 copies/ ml. A BAL EBV PCR tests was negative. Pneumocystis Jiroveci pneumonia was detected on BAL Direct fluorescent antibody test (DFA). CMV retinitis has been ruled out by an ophthalmology exam. Patient was diagnosed with concurrent CMV and PCP pneumonia infection and her respiratory status worsened mandating a brief ICU stay. Treatment was started with Bactrim, Valganciclovir and Ganciclovir with progressive improvement. In a follow up appointment at the infectious diease clinic two months later, the patient condition improved but was still in need for supplemental oxygen through nasal canula. DISCUSSION: A concurrent CMV and PCP microorganisms lung infection is rare, but patient with underlying immunocompromise constitue a major risk factor for that. CONCLUSIONS: Patients with underlying immuncompromise conditions are at risk of many infections with grave morbidity and mortality risks. Though it is a rare to have a concurrent CMV and PCP lung infection, a patient treated with immunomodulating medications including methotrexate, prednisone and rituximab was a culprit for severe infection. Reference #1: Peghin, M., Hirsch, H. H., Len, Ó., Codina, G., Berastegui, C., Sáez, B., Solé, J., Cabral, E., Solé, A., Zurbano, F., López-Medrano, F., Román, A., & Gavaldá, J. (2016). Epidemiology and immediate indirect effects of respiratory viruses in lung transplant recipients: A 5-year prospective study. American Journal of Transplantation, 17(5), 1304–1312. https://doi.org/10.1111/ajt.14042 DISCLOSURES: No relevant relationships by MohD Ibrahim

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