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Inflammation was described as early as 4000 BC in an Egyptian papyrus and is still a common problem despite continuous advancements in prevention and treatment methods. Over the years new strains of microorganisms causing infections appear such as the recently discovered new Covid-19 infection. The proper diagnosis and delineation of the site and extent of inflammation are crucial to the clinical management of infection and for monitoring the response to therapy. The strategy to reach diagnosis by imaging depends on understanding the pathophysiologic basis of different types of infection and the mechanisms of accumulation of the radiotracers for scintigraphic diagnosis. © The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland AG 2015, 2022.
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The course of a new coronavirus infection is associated with immune system disorders during the acute stage of the desease. Administration of effective etiotropic drugs contributes to early elimination of the virus. At the same time, risks of post-COVID immune system disorders are minimized. The aim of the study was to investigate features of the immune response formation against the background of etiotropic therapy in patients who underwent COVID-19. Material and methods. An observational retrospective comparative study was conducted. The study involved patients with COVID-19 3 months after treatment with etiotropic drugs (riamilovir or umifenovir). The study involved 87 patients (52 women and 35 men) with varying degrees of COVID-19 severity. In accordance with the study design, participants were divided into 2 groups: the first group - 41 patients (received riamilovir during the acute period of the disease);the second group - 46 patients (received umifenovir in the acute period of the disease). Statistical processing of the results was carried out using the Statistica 8.0 software package. Extensive indicators, median (Me) and interquarter range Q25-Q75 were calculated. Statistical significance between the indicators of independent samples was assessed by Mann-Whitney nonparametric test and Chi-square test. P-values below 0.05 were considered statistically significant. Results and discussion. Analysis of clinical and laboratory data showed that after suffering COVID-19, not all indicators of the immune system in patients who had had COVID-19 recovered to control values. However, it is noted that in patients of the main group, which using riamilovir, compared to the comparison group was less likely to be diagnosed with chronic systemic syndrome, inflammation, dysregulation of the cellular link of immunity in the early post-COVID period.Copyright © Eco-Vector, 2022.
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Background: People with HIV (PWH) on antiretroviral therapy (ART) appear to be at higher risk for worse COVID-19 outcomes, but the underlying mechanisms-including effects of COVID-19 and host factors on the broader humoral immune repertoire-are poorly understood. Method(s): REPRIEVE enrolled a global cohort of ART-treated PWH ages 40-75. COVID+ was defined by positive receptor binding domain IgG or IgA from annual visits 5/2020-2/2021. Antibody isotype, subclass, and Fc receptor Luminex arrays to SARS-CoV-2, CMV, EBV, HSV, HIV, influenza, pneumococcus, and RSV were assessed. Report of COVID diagnosis (collected every 4 months) was defined as mild, moderate, or severe (asymptomatic if no clinical diagnosis but IgG/ IgA+). FDR-corrected regression was used to assess effects of 1) COVID+ on non- SARS-CoV-2 repertoire in full cohort and 2) host factors on non-SARS-CoV-2 and SARS-CoV-2 repertoire in COVID- and COVID+ cohorts, respectively, adjusted for age, sex, region, nadir CD4, and HIV VL at entry. Result(s): Of 2,464 unvaccinated participants, 283 (11%) were COVID+;260 (92%) were asymptomatic. Median age was 53, 35% were women, 50% had nadir CD4 < 200, median current CD4 was 649, and 97% had HIV VL < 400. In the full cohort, COVID+ was associated with higher CMV PP65 IgG3 and FcgammaRIIA (P< 0.05);COVID severity was not associated with the non-SARS-CoV-2 repertoire. Among COVID-, older age, female sex, and lower nadir CD4 were associated with higher EBV and CMV responses;IgG1 levels were higher in women for all non-SARS-CoV-2 antigens assessed (P< 0.05). Among COVID+, higher BMI was associated with amplified SARS-CoV-2 IgG, IgA, IgM, and FcgammaRIIA responses (P< 0.05). Lower nadir CD4 was associated with a SARSCoV- 2 repertoire shift toward IgM and FcgammaRIIB (P< 0.05). Age and sex were not associated with SARS-CoV-2-related repertoire changes in COVID+. Conclusion(s): Our analysis presents a comprehensive view of host factors associated with the humoral immune repertoire among a global cohort of ART-treated PWH. COVID's association with higher CMV responses may suggest increased susceptibility to or a consequence of persistent inflammation after infection. The striking amplification of SARS-CoV-2 responses with higher BMI suggests an excessive inflammatory response. Lower nadir CD4 was related to uncontrolled extra-follicular and inhibitory SARS-CoV-2 responses, which are unlikely to be protective. These findings may suggest mechanisms underlying factors associated with worse COVID-19 outcomes among PWH. (Figure Presented).
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To date, the severe acute respiratory syndrome coronavirus 2 that causes the disease Coronavirus 2019, has infected 601 million people, claiming the lives of 6.4 million people worldwide. Of the patients who survive, 60% suffer from inflammatory problems leading to post-acute sequelae of COVID-19 (PASC). Inflammation in these patients is marked by an increase in pro-inflammatory cytokines which ultimately damage the body's organs, contributing to PASC. Understanding the main mechanism by which this cytokine storm occurs is of utmost importance in order to develop therapeutic strategies for counteracting inflammation in people suffering from COVID-19 and PASC. This project seeks to find out if an innate anti-inflammatory mechanism, the cholinergic anti-inflammatory response (CAR), works properly in patients suffering from COVID-19 and PASC by interrogating its functioning in its cellular substrate, macrophages.We hypothesized that disruption of the CAR in primary human monocytederived macrophages (MDMs) exposed to the SARS-CoV-2 spike protein trimer contributes to the chronic inflammation/ cytokine storm exhibited in these patients. To this end, we exposed MDMs to the SARS-CoV-2 spike protein in order to assess levels of the anti-inflammatory alpha-7 nicotinic acetylcholine receptor (alpha7-nAChR) by means of confocal imaging. Our results demonstrate a statistically significant reduction (P <= 0.01) of alpha7-nAChR expression in MDMs, in a time-dependent manner, after the addition of SARS-CoV-2 spike protein concentrations (30 nM and 100 nM), at different time points. Interestingly, when the receptor employed by the virus to infect, Angiotensin-converting enzyme 2 (ACE-2), was blocked, we detected a significant reduction in the levels of alpha7- nAChRs (P <= 0.001). Collectively, our results support the hypothesis of this work given that the SARS-CoV-2 spike protein is capable of compromising the functioning of the CAR by reducing the levels of alpha7-nAChRs available in macrophages to suppress inflammation. These results could position the alpha7- nAChR as a key target for the development of novel anti-inflammatory therapeutic strategies to counteract the inflammatory problem found in patients suffering from COVID-19 and PASC. We would like to acknowledge Dr. Negin Martin & Dr. Jerrel Yakel, for providing the Purified Spike Protein expressed by SARS-CoV-2 and Pseudotyped Virions in this collaborative study. Also, these experiments are being supported by the University of Puerto Rico - Rio Piedras NIH-RISE program. RISE Grant Number: 5R25GM061151-20.Copyright © 2023 The American Society for Biochemistry and Molecular Biology, Inc.
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The family of cytokines that comprises IL-3, IL-5, and GM-CSF was discovered over 30 years ago, and their biological activities and resulting impact in clinical medicine has continued to expand ever since. Originally identified as bone marrow growth factors capable of acting on hemopoietic progenitor cells to induce their proliferation and differentiation into mature blood cells, these cytokines are also recognized as key mediators of inflammation and the pathobiology of diverse immunologic diseases. This increased understanding of the functional repertoire of IL-3, IL-5, and GM-CSF has led to an explosion of interest in modulating their functions for clinical management. Key to the successful clinical translation of this knowledge is the recognition that these cytokines act by engaging distinct dimeric receptors and that they share a common signaling subunit called ß-common or ßc. The structural determination of how IL-3, IL-5, and GM-CSF interact with their receptors and linking this to their differential biological functions on effector cells has unveiled new paradigms of cell signaling. This knowledge has paved the way for novel mAbs and other molecules as selective or pan inhibitors for use in different clinical settings.
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Introduction: Severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) exhibits 25-30% mortality in hospitalized patients with heart failure (HF). Cardiovascular disease is the most significant comorbidity associated with increased mortality in COVID-19 patients with data suggesting local and systemic inflammation play a critical role in cardiac functional abnormalities. SARS-CoV-2 vaccination reportedly reduces severity of infection. We sought to characterize if vaccination had any protective effect on patients with HF hospitalized for acute COVID-19. Hypothesis: Baseline cardiac biomarkers including CRP, ferritin, high sensitivity cardiac troponin I (hs-cTnI), and pro-brain natriuretic peptide (pBNP) may be lower in vaccinated COVID-19 HF patients revealing the impact of vaccination on reducing inflammation by SARS-CoV-2 infection. Method(s): Electronic health records underwent IRB exempted extraction of demographics, anthropometrics, vital signs, laboratory tests, and ICD-10-CM-based Elixhauser comorbidity categories. Continuous data summarized with median [IQR] were compared using Kruskal-Wallis test and discrete data with chi-squared test. Result(s): Among HF patients with a recorded vaccine status admitted between July 3, 2021 and March 17, 2022, 206 underwent acute COVID-19 hospitalization. Vaccinated (n=91, 44%) and unvaccinated (115, 56%) patients exhibited statistically similar distribution of males (56%), aged 78[69-86] years with comorbidities 5[4-7] distributed across Whites (88%), Blacks (8%), and other races (4%). There were no intergroup differences with most prevalent comorbidities at admission including hypertension (99%), diabetes (41%), chronic pulmonary disease (37%), obesity (36%), deficiency anemia (31%), and renal failure (25%). There were no intergroup differences in initiation of COVID-19 directed treatments. Baseline biomarkers in vaccinated versus unvaccinated were CRP 6.0[1.3-9.5] vs. 6.9[2.7-11.3] mg/dL (p=.25), ferritin 171[76-552] vs. 432[79-876] ng/mL (p=.13), LDH 245[192-317] vs. 338[260-439] U/L (p=.003), D-dimer 0.89[0.53-1.73] vs. 1.36[0.95-2.80] mg/L FEU (p=.06), hs-cTnI 27[14-67] vs. 28[16-81] ng/L (p=.39), and pro-BNP 3487[1516-7162] vs. 3278[1549 vs. 9001] pg/mL (p=.90). Clinical visit criteria respectively were hospital LOS 4.9[2.9-10.3] vs. 5.4[3.4-10.3] days (p=.27), ICU admission 10% vs. 17% (p=.15), and discharge disposition expired or Hospice 15% vs. 16% (p=.48). Rehospitalization occurred similarly between groups and was not significant. Conclusion(s): Acute and chronic inflammation are pathogenic drivers of HF. Inflammatory biomarkers lower among vaccinated patients with HF included CRP, ferritin, D-dimer, and hs-cTnI, although not significant. LDH, however, was significantly lower suggesting improved host widespread tissue perfusion as one mechanism of reduced severity in patients with HF undergoing SARS-CoV-2 vaccine breakthrough infection. One study caveat is that despite inclusion of all patients, these preliminary findings are likely not sufficiently powered to validate our hypothesis.Copyright © 2022
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INTRODUCTION: Ulcerative colitis (UC) is a chronic inflammatory condition characterized by diarrhea, abdominal pain, rectal bleeding, and weight loss. Upadacitinib is an oral, selective, small molecule Janus Kinase (JAK) inhibitor that was recently approved in the United States for moderate to severe UC. Clinical trials evaluating the efficacy of upadacitinib excluded patients with a previous exposure to tofacitinib, a nonselective JAK inhibitor;therefore, the efficacy of upadacitinib in patients with previous exposure to tofacitinib remains largely unknown. METHOD(S): We present a small retrospective case series of all patients with a diagnosis of ulcerative colitis seen at our institution between with a prior exposure to tofacitinib who were initiated on upadacitinib between May and August of 2022. Demographic data was collected as well as outcome data on clinical improvement, steroid-free remission, biochemical improvement, colectomy status, and adverse events. RESULT(S): Eleven tofacitinib-refractory patients with ulcerative colitis were initiated on upadacitinib. Mean age was 38.1 years, five (45.5%) patients were female, nine (81.8%) patients were white, seven (63.6%) patients had pancolitis, and mean duration of UC was 7.4 years (Table 1). In this group, there were high rates of prior targeted therapy failures. These patients were followed for a mean of 121 days. The clinical course of each patient is presented in Table 2. Of the 11 patients included in our study, nine (81.8%) patients reported symptomatic improvement, six (54.5%) patients were able to successfully taper corticosteroids, and two (18.2%) patients underwent colectomy, one of which was elective and planned prior to initiating upadacitinib. The mean fecal calprotectin improvement was 1430mg/kg of patients with both baseline and follow-up testing. Three (27.3%) patients experienced an adverse event;two (18.2%) patients with mild COVID-19 not requiring hospitalization and one (9.1%) patient with Enteropathogenic E. Coli. DISCUSSION: This real-world single-center case series of 11 patients, suggests that upadacitinib may be an effective option for patients with a previous tofacitinib exposure. Larger prospective studies are needed to confirm these findings. [Formula presented] [Formula presented]Copyright © 2023
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COVID-19 has affected several aspects of health care systems worldwide. While our understanding of the impact of cancer and its treatment on COVID-19 mortality is improving, there is still little known regarding the possible mechanisms by which COVID-19 might affect cancer cells, especially breast cancer. Several factors activated during COVID-19 have been implicated in tumorigenesis and the development of metastasis. Inflammation, hypoxia, reduced levels of angiotensin-converting enzyme 2, and elevated levels of interleukin 6 and some other cytokines that are hallmarks of COVID-19 are capable of inducing tumor relapse and metastasis. Understanding the interaction between COVID-19 and breast cancer cells is essential for evaluating the potential long-term risks of COVID-19 in patients and for scheduling necessary preventive, screening, and therapeutic interventions.Copyright © 2022 Elsevier Masson SAS. All rights reserved.
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Background Graft versus host disease (GVHD) most often occurs 100-365 days after hematopoietic stem cell transplant (HSCT). Manifestations most often are dermatologic, hepatic or pulmonic, and are rarely cardiac. We present a unique case of GVHD inducing cardiogenic shock necessitating advanced heart failure therapies. Case This is a 34 year-old male with a history of acute lymphoblastic leukemia who completed chemoradiation and HSCT from an HLA perfect sibling in 1992. In May 2020, he presented with dyspnea for 6 weeks. An echocardiogram at that time showed an EF of 10% and severe biventricular dilatation. He was originally hospitalized at an outside institution for hypoxia where a left heart catheterization showed normal coronaries and goal directed therapy was initiated. After 2 negative COVID tests, he was discharged with a LifeVest. One month later, despite medication compliance, he returned in cardiogenic shock after his LifeVest was activated for ventricular tachycardia (VT). Decision-making He was started on inotropic therapy and an intra-aortic balloon pump (IABP) was placed 1:1 prior to transfer to our tertiary center. After support was started, a right heart catheterization showed a right atrial pressure of 13 mmHg, a wedge of 17, and a cardiac index of 2.6. His course was complicated by VT storm. Differentials for his non-ischemic cardiomyopathy (NICMO) included myocarditis (viral vs. giant cell) with a possible component of chemotherapy/radiation induced NICMO. Immediate AHFT work-up was started. He was unable to be weaned off his IABP or inotropic support. The decision was made to pursue emergent left ventricular assist device placement (LVAD) and achieve a definitive diagnosis with a core biopsy. Pathology resulted with myocyte hypertrophy, chronic inflammation with eosinophils concerning for chronic GVHD. Conclusion There have only been a handful of case reports describing cardiac manifestations of GVHD, and none with NICMO and cardiogenic shock requiring an LVAD. Despite this, suspicion should remain present for GVHD in HSCT patients regardless of time frame from oncologic therapies or specificity of HLA match when presenting in cardiogenic shock.Copyright © 2023 American College of Cardiology Foundation
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Patients with hidradenitis suppurativa (HS) often present to our tertiary service with severe perianal disease that is extremely debilitating. We are able to provide a holistic service for our patients through our perianal virtual clinic (PVC), a weekly service comprising dermatologists, colorectal surgeons, gastroenterologists and a gastroenterology clinical nurse specialist. Virtually, we discuss and optimize the management of patients who have a diagnosis of either HS or gastrointestinal/ cutaneous Crohn disease (CD), or both. Through discussion of the medical management, review of pelvic magnetic resonance imaging scans and the discussion of surgical treatment in detail with our colleagues, we are able to streamline treatment for these complex patients. We provide a review of the activity in this service over the last 2 years, from January 2019 to December 2020. As part of the clinical work in our tertiary hidradenitis clinic, we routinely treat patients with significant perianal HS. These patients have discharging sinus tracts and fistulating disease in apocrine gland-bearing areas. A proportion have gastrointestinal or cutaneous CD. From a medical perspective, these patients have often failed multiple therapeutic interventions, and surgery can provide a useful adjunct to treatment. Surgical intervention involves extensive laying open and debridement of disease, including biopsy, and seton control of anal fistulae. Perianal skin cancer can be identified at the time ofsurgery, a complication known to affect those with chronic inflammation and those on immunosuppressive drugs. In the last 2 years, following surgery, one patient has been diagnosed with cutaneous squamous cell carcinoma (SCC), one with SCC in situ and one with extramammary Paget disease. In reviewing the activity of the PVC, we discussed 26 patients with HS and severe perianal disease in 2019 and 42 patients in 2020, despite interruption to the service due to the COVID-19 pandemic in 2020. This increase in activity reflects our expanded service and the severity and complexity of the patients referred. We identify those that may benefit from early surgery and also take referrals of patients with both HS and CD that may need optimization of medical therapy. In total, eight patients were admitted under the joint care of the colorectal and dermatology teams for surgery in 2019 and seven in 2020. The PVC has become an important one-stop service in the optimization of complex treatment for patients with perianal HS and/or CD referred to our tertiary service.
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INTRODUCTION: Ulcerative colitis (UC) is a chronic inflammatory condition characterized by diarrhea, abdominal pain, rectal bleeding, and weight loss. Upadacitinib is an oral, selective, small molecule Janus Kinase (JAK) inhibitor that was recently approved in the United States for moderate to severe UC. Clinical trials evaluating the efficacy of upadacitinib excluded patients with a previous exposure to tofacitinib, a nonselective JAK inhibitor;therefore, the efficacy of upadacitinib in patients with previous exposure to tofacitinib remains largely unknown. METHOD(S): We present a small retrospective case series of all patients with a diagnosis of ulcerative colitis seen at our institution between with a prior exposure to tofacitinib who were initiated on upadacitinib between May and August of 2022. Demographic data was collected as well as outcome data on clinical improvement, steroid-free remission, biochemical improvement, colectomy status, and adverse events. RESULT(S): Eleven tofacitinib-refractory patients with ulcerative colitis were initiated on upadacitinib. Mean age was 38.1 years, five (45.5%) patients were female, nine (81.8%) patients were white, seven (63.6%) patients had pancolitis, and mean duration of UC was 7.4 years (Table 1). In this group, there were high rates of prior targeted therapy failures. These patients were followed for a mean of 121 days. The clinical course of each patient is presented in Table 2. Of the 11 patients included in our study, nine (81.8%) patients reported symptomatic improvement, six (54.5%) patients were able to successfully taper corticosteroids, and two (18.2%) patients underwent colectomy, one of which was elective and planned prior to initiating upadacitinib. The mean fecal calprotectin improvement was 1430mg/kg of patients with both baseline and follow-up testing. Three (27.3%) patients experienced an adverse event;two (18.2%) patients with mild COVID-19 not requiring hospitalization and one (9.1%) patient with Enteropathogenic E. Coli. DISCUSSION: This real-world single-center case series of 11 patients, suggests that upadacitinib may be an effective option for patients with a previous tofacitinib exposure. Larger prospective studies are needed to confirm these findings. (Table Presented).
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This review article discusses the pathophysiological mechanisms of the development of coronavirus infection in obese patients. It has been shown that obesity is considered as the most important risk factor for the development of many comorbid diseases, including severe forms and deaths as a result of a new coronavirus infection. The higher incidence and severity of a new coronavirus infection in obese patients is based on a complex of factors, the main of which are an increase in cardiovascular risk, including a tendency to thrombosis, a decrease in the efficiency of the respiratory system, impaired immune response, and the presence of chronic inflammatory state. The article discusses non-drug approaches and issues of pharmacological therapy in patients with obesity in the context of a pandemic of a new coronavirus infection. It is shown that the implementation of national quarantine measures has led to an increase in physical inactivity, the level of stress and a change in the eating behavior of the population, closing a vicious circle and contributing to an increase in body weight. For this reason, the efforts of physicians of therapeutic specialties should be directed primarily to increasing resistance to infection among obese patients and combating physical inactivity. The main groups of drugs that can be used to combat lipotoxicity are listed. It was noted that infectious disease doctors and endocrinologists can use those groups of drugs that affect the most vulnerable pathogenetic triggers for the development of obesity and comorbidities: hunger and satiety processes, decreased insulin sensitivity, development of lipotoxicity and chronic inflammation. It has been proven that the range of positive effects of new antihyperglycemic drugs from the groups of type 1 glucagon-like peptide agonists and type 2 sodium-glucose transporter inhibitors, combined with a well-studied efficacy and safety profile, represents a new opportunity for the treatment of obesity in the context of a coronavirus infection pandemic.Copyright © 2022 Authors. All rights reserved.
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This review article discusses the pathophysiological mechanisms of the development of coronavirus infection in obese patients. It has been shown that obesity is considered as the most important risk factor for the development of many comorbid diseases, including severe forms and deaths as a result of a new coronavirus infection. The higher incidence and severity of a new coronavirus infection in obese patients is based on a complex of factors, the main of which are an increase in cardiovascular risk, including a tendency to thrombosis, a decrease in the efficiency of the respiratory system, impaired immune response, and the presence of chronic inflammatory state. The article discusses non-drug approaches and issues of pharmacological therapy in patients with obesity in the context of a pandemic of a new coronavirus infection. It is shown that the implementation of national quarantine measures has led to an increase in physical inactivity, the level of stress and a change in the eating behavior of the population, closing a vicious circle and contributing to an increase in body weight. For this reason, the efforts of physicians of therapeutic specialties should be directed primarily to increasing resistance to infection among obese patients and combating physical inactivity. The main groups of drugs that can be used to combat lipotoxicity are listed. It was noted that infectious disease doctors and endocrinologists can use those groups of drugs that affect the most vulnerable pathogenetic triggers for the development of obesity and comorbidities: hunger and satiety processes, decreased insulin sensitivity, development of lipotoxicity and chronic inflammation. It has been proven that the range of positive effects of new antihyperglycemic drugs from the groups of type 1 glucagon-like peptide agonists and type 2 sodium-glucose transporter inhibitors, combined with a well-studied efficacy and safety profile, represents a new opportunity for the treatment of obesity in the context of a coronavirus infection pandemic.Copyright © 2022 Authors. All rights reserved.
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Background Understanding the underlying mechanisms of post-COVID sequelae (Long COVID) is urgently needed to guide interventions. Aim To compare the inflammation profiles of four recovery clusters post-hospitalisation. Methods Post-Hospitalisation COVID-19 (PHOSP-COVID) is a prospective, multi-centre study across UK. Four recovery clusters previously identified using clinical data (symptoms, mental health, cognitive impairment, and physical function) at 5 months post-discharge were used based on severity of on-going health impairments: very severe, severe, moderate (cognitive), and mild. Inflammatory profiling performed from plasma samples using the Olink Explore 384 inflammation panel. Multinomial logistic regression for each protein was undertaken comparing the mild cluster with each of the remaining clusters with FDR of 0.1 to adjust p values. Results 626 participants (clusters: very severe n=111, severe n=173, moderate/cognitive n=73 and mild n=269). Proteomic results from 296 proteins were included. After adjustment for age, BMI, and comorbidity count, 13 proteins were significantly elevated in the very severe cluster, and 2 proteins in the moderate/cognitive cluster, compared to the mild cluster (Figure 1). Conclusion Inflammatory mediators consistent with persistent lung and systemic inflammation were associated with the severity of ongoing health impairments highlighting potential therapeutic pathways to be tested.
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Introduction: The effective control of coronavirus disease 2019 (COVID-19) can be achieved by implementing a global vaccination strategy. After millions of mRNA vaccines targeting severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) have been administered worldwide, several reports have shown the cases with gross hematuria (GH) following the mRNA vaccine against SARS-CoV2 in patients with glomerulonephritis, especially immunoglobulin A nephropathy (IgAN). A total of 22 articles including 36 cases of GH after COVID-19 vaccination as on July 31, 2022, were found in PubMed and Google Scholar databases. The most cases which had performed kidney biopsy were IgAN or IgA vasculitis. So, it suggested that GH after COVID-19 vaccination is rerated IgAN. Although there are many reported cases of IgAN after COVID-19 vaccination, the detailed clinical characteristics and outcome have not determined in these patients. Moreover, it remains unclear whether COVID-19 vaccination causes the new onset of nephritis or exacerbates pre-existing nephritis. To address this, herein, we conducted a prospective cohort study over a six-month period. Method(s): We analyzed 82 patients who presented with GH after COVID-19 vaccination and conducted a 6-month observational study. Patients, 18 years or older, who presented to the hospital with GH after COVID-19 vaccination were recruited. All the patients visited either Juntendo University Hospital or Juntendo University Urayasu Hospital between May 11, 2021, and July 31, 2022. Result(s): During the study period, a total of 82 individuals who presented with GH after COVID-19 vaccination were enrolled. The median age of the patients was 38 years;58 cases (70.7%) were females. All the patients received an mRNA COVID-19 vaccine. Most patients showed GH within three days after the second or third dose. Among the 82 patients, 22 had been already diagnosed with IgAN or IgA vasculitis (IgAV) before vaccination, and 45 of the 60 undiagnosed patients had a history of abnormal urinary findings. We performed kidney biopsies on 42 of the 60 undiagnosed patients, who were then diagnosed with IgAN (N=41) or IgAV (N=1). Pathological findings demonstrated that chronic inflammation of glomeruli, such as the expansion of mesangial matrix and glomerular sclerosis, is similarly observed in these newly diagnosed patients compared to patients with IgAN unrelated to vaccination. Finally, we evaluated the levels of biomarkers known to be elevated in IgAN at diagnosis during the course of the study and found that they did not increase. Notably, only few cases showed a slight increase in the level of serum creatinine, and no patients progressed to severe renal dysfunction. Conclusion(s): Present prospective study with 82 cases with GH after COVID-19 vaccination have identified their clinical characteristics and outcome. Furthermore, the acute manifestation of vaccine-induced GH may have highlighted the high prevalence of undiagnosed or preclinical IgAN in Japan. No conflict of interestCopyright © 2023
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Introduction: Acute respiratory distress syndrome develops in up to 30% of COVID-19 pneumonia patients. Characterizations of cytologic criteria in bronchoalveolar lavage (BAL) specimens are not well-established. This study evaluates the value of applying several cytologic criteria for the diagnosis of COVID-19 infection in BAL samples. Material(s) and Method(s): We performed a retrospective review of 64 BAL samples collected 6/2020 - 8/2021, divided into two groups: COVID-19 positive group (n=30) and negative group (n=34). Median time from COVID-19 diagnosis to BAL collection was 23 days (range;9-208). The type of inflammation and the cytologic features of alveolar macrophages and respiratory epithelial cells were enumerated. The most common features in COVID-19 positive patients were defined as major diagnostic criteria. Blinded review by a second cytopathologist was performed to predict COVID-19 diagnosis using the defined criteria. Result(s): COVID-19 positive group showed more mixedtype (acute and chronic) inflammation (67% vs 21%;P=0.002), fewer pigment-laden macrophages (22% vs 62%;P=0.001), more enlarged macrophages (85% vs 32%;P<0.001), multi-nucleated macrophages (67% vs 21%;P=0.002) and multi-vacuolated cytoplasm of the macrophages (78% vs 29%;P=0.003) [Figures 1&2]. There was insignificant difference for reactive respiratory epithelial Acta Cytologica 2022;66(suppl 1):1-150 DOI: 10.1159/000527858 12 Exfoliative - Fluids (CSF, Pleural, Peritoneal, etc.) cells (37% vs 24%;P=0.4) and macrophages abundance (63% vs 44%;P=0.5). Identification of diagnostic criteria by a second cytopathologist in COVID-19 positive group, predicted COVID- 19 disease in 27% (>3 major criteria present). After exclusion of cases with remote COVID-19 infection (n=4), the mean interval in days between COVID-19 infection and BAL collection was significantly higher in cases with positive disease prediction (30.5 vs 20.7, P=0.04). Conclusion(s): Features associated with macrophage activation (enlarged and multinucleated macrophages with multi-vacuolated cytoplasm) are prominent in COVID-19 BAL samples. These features may become more recognizable with longer time intervals after infection. Observation of these findings suggest consideration of COVID-19 as the etiology of an individual's pneumonia. (Figure Presented).
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Background We present a unique case of a female who developed a large pericardial effusion (PEff) from a rare cause. Case A 36-year-old female with recent COVID-19 infection presented with acute dyspnea. She had undergone liposuction, rectus plication and breast augmentation two months ago. Heart rate was 90/min and blood pressure 86/57mmHg. CT angiogram of the chest revealed a massive PEff with tamponade. She had large right-sided pleural effusion also. She underwent ultrasound-guided pericardiocentesis with the removal of 950 milliliters of serosanguineous fluid. Follow-up echocardiogram showed re-accumulation of fluid. Due to the rapid onset of PEff, she underwent a pericardial window and bilateral chest tube placement. Decision-making Pleural and pericardial fluid analysis showed silicone-gel particles (Figure. 1). Pericardial biopsy showed nonspecific chronic inflammation. Autoimmune workup was unremarkable. Elevated ESR and CRP in the presence of embolized gel particles indicated foreign body reaction from silicone embolism. Plastic surgery advised implant removal. Silicone embolism is known to cause silicone thorax, pleural effusions, and anaplastic large cell lymphoma. To our knowledge, this is the first reported case of PEff due to silicone embolism from breast implants. Conclusion Cardiologists should be aware of this rare but serious complication. Silicone embolism should be considered in the differential of PEff in patients with breast implants. [Formula presented]Copyright © 2023 American College of Cardiology Foundation