The COVID-19 pandemic has raised concerns about potential links between SARS-CoV-2 infection and autoimmune diseases. This study investigated changes in the incidence rate (IR) of autoimmune diseases among children following the pandemic's onset.

A retrospective cross-sectional study analyzed data from Clalit Health Services, Israel's largest healthcare provider, examining the IR of different autoimmune diseases in children aged 0-18. The study compared pre-pandemic (2019) with pandemic/post-pandemic periods (2020-2023), encompassing a cohort of over 1.5 million children.

Significant IR increases were observed across multiple autoimmune diseases. Rheumatic diseases (Juvenile Idiopathic Arthritis, Systemic Lupus Erythematosus, Henoch Schoenlein Purpura (HSP)) showed consistent increases, with HSP demonstrating the most pronounced trend. Endocrine disorders exhibited diverse patterns, with autoimmune thyroid diseases and Type 1 diabetes showing overall increases, while diabetic ketoacidosis exhibited an initial spike followed by a decline. Gastrointestinal diseases displayed heterogeneous patterns; Celiac disease and Ulcerative colitis showed general increases, Crohn's disease showed a downward trend, and autoimmune hepatitis exhibited an initial significant decrease followed by a significant increase. Dermatological conditions, including Psoriasis and Vitiligo, demonstrated consistent elevations throughout 2020-2023. Immune Thrombocytopenia Purpura showed initial decreases followed by significant increases in 2022-2023.

This comprehensive analysis reveals significant changes in pediatric autoimmune disease incidence following the COVID-19 pandemic, suggesting potential associations between SARS-CoV-2 infection and autoimmune dysregulation. The diverse patterns observed across different conditions highlight the complex interplay between viral infection and autoimmunity, emphasizing the need for continued surveillance and investigation of long-term immunological consequences of COVID-19 in pediatric populations.

To assess the impact of severe COVID-19 in patients with immune-mediated rheumatic diseases (im-RD) and compare their morbidity, mortality, hospitalization issues, post-COVID-19 sequelae, and the financial burden of COVID-19 with those of patients without im-RD.

We conducted a retrospective case-control study that included 132 consecutive patients with im-RD who visited the Rheumatology Department of a public hospital in the Emirate of Dubai and were hospitalized for COVID-19 infection between March 1st, 2020, and December 31st, 2021, (cases). We included 264 and 132 age- and sex-matched patients without im-RD in matched-I and matched-II control groups, respectively. The median age of patients and controls was 48.5 years, and 74.2% were female. Patients with im-RD were paired with an unforced nearest neighbor match using a caliper width of 0.2 standard deviations of the matched-II control group's propensity score. We compared the relative risk of death, disease progress, use of medical resources, and financial impact of COVID-19 between patients and controls.

Patients with im-RD had higher mortality rates than the matched-I (odds ratio, OR: 11.2, p < 0.000) and matched-II (OR: 16.8, p < 0.006) control groups. The overall complication rate was also significantly higher in patients with im-RD than in matched-I (OR = 2.9, p < 0.000) and matched-II (OR = 2.8, P < 0.0001) control groups. Lastly, patients with im-RD required more frequent visits to the clinic, a longer recovery time following hospital discharge, and increased healthcare costs compared to the control groups.

COVID-19 infection in patients with im-RD is associated with increased morbidity and mortality, exerting a significant burden on the healthcare system.

This investigation aims to identify and evaluate the most common and critical drugs associated with the risk of noninfectious myocarditis utilizing the US Food and Drug Administration Adverse Event Reporting System (FAERS) database.

Data pertaining to noninfectious myocarditis from 2004 Q1 to 2024 Q2 were extracted. Following data standardization, multiple signal quantification techniques, including Reporting Odds Ratio (ROR) and Proportional Reporting Ratio, were employed for analysis.

The study identified a total of 10,763 adverse event reports associated with noninfectious myocarditis. Disproportionality analysis revealed that the top 5 drugs by ROR were phendimetrazine tartrate (ROR 104.64), trimethoprim + sulfamethoxazole (ROR 67.65), aldesleukin (ROR 52.67), mesalazine (ROR 49.73), and balsalazide disodium (ROR 45.26). Notably, among the 30 drugs with the strongest ROR signals, 8 drugs lacked myocarditis risk information in their package inserts.

Through comprehensive analysis of the FAERS database, our study identified drugs with a strong signal for myocarditis that are not currently indicated on their labels. The findings suggest that the potential risk of myocarditis associated with these medications is significant and warrants close monitoring in clinical practice.

COVID-19 disease has been associated with flares or new onsets of various autoinflammatory diseases such as psoriasis and atopic dermatitis. Our aim is to investigate the occurrence and risk factors of flares or new onsets of Hidradenitis Suppurativa (HS) following COVID-19 disease.

A retrospective cohort study was performed including 310 patients with HS following COVID-19 disease. Data on the rate of HS flares, new lesions, time of flare onset, and flare duration were recorded. Demographics, clinical characteristics, and treatment parameters were compared between patients with and without HS flares.

HS flares developed in 69 (22.2%) patients, with 14 experiencing their first episode. The median period between COVID-19 and flare onset was 17 days, with a median flare duration of 14 days. For new HS onset, the median period was 9.5 days, and the median duration was 13 days. Biologic treatment was less common in patients with flares (7.2% vs. 23.2%, p = 0.003), and fewer patients with flares were vaccinated (81.1% vs. 99.1%, p < 0.001). Multivariable analysis showed lower risk for flares in those receiving biologics (aOR = 0.14, p = 0.002) and those who were vaccinated (aOR = 0.02, p < 0.001).

COVID-19 may trigger HS flares and new onset, with biologic treatment and vaccination offering protection.

We herein summarize currently available and clinically relevant information regarding the human immune responses to SARS-CoV-2 infection and vaccination, in relation to COVID-19 outcomes with a focus on acute respiratory distress syndrome (ARDS) and myocarditis.

COVID-19 vaccines reduced mortality, hospitalizations and ICUs admissions. Conversely, the impact of vaccination on Long COVID-19 syndrome is still unclear. This study compared the prevalence of post-acute sequelae at short and long-term follow-up among hospitalized unvaccinated and vaccinated COVID-19 survivors through a multidisciplinary approach.

After 2 months from discharge, unvaccinated and vaccinated COVID-19 survivors underwent a follow-up visit at a dedicated "post-COVID-19 Outpatient Clinic". The follow-up visit included a cardiovascular evaluation, blood tests, chest computed tomography, 6-min walking test (6MWT), spirometry. A one-year telephone follow-up was performed to assess re-hospitalizations, death and long-lasting symptoms. An additional 1:1 case-control matching analysis adjusted for baseline characteristics was performed.

Between June 2020 and June 2022, a total of 458 unvaccinated and vaccinated patients (229 per group) underwent the follow-up visit. Vaccinated patients had lower rates of ICU admissions (1.7 % vs 9.6 %, p= <0.001) and severe respiratory complications requiring intubation (1.3 % vs 7 %, p = 0.002) or non-invasive ventilation such as high-flow nasal oxygen therapy (1.7 % vs 7.9 %, p = 0.02), CPAP (1.3 % vs 20.1 %, p= < 0.001), and low-flow oxygen therapy (3.5 % vs 63.3 %, p= <0.001) compared to unvaccinated ones. At 2-month follow-up, vaccinated patients had fewer persistent ground-glass opacities (2.6 % vs 52.8 %, p= <0.001) or consolidations (0.9 % vs 8.3 %, p= <0.001). Additionally, unvaccinated patients experienced more frequent myocarditis (4.8 % vs 0.9 %, p = 0.013) and pulmonary embolism (1.8 % vs 0 %, p = 0.042) and exhibited more significant respiratory impairment as evidenced by desaturation during the 6MWT(10.2 % vs 3.5 %, p = 0.005) and altered spirometry (14 % vs 8.7 %, p = 0.043) compared to vaccinated ones. At one-year, unvaccinated patients reported more symptoms such as dyspnea (20.5 % vs 10 %, p = 0.002), psychological symptoms (10 % vs 3.5 %, p = 0.005) and chronic rhinosinusitis/cough (6,6 % vs 2,6 %, p = 0.04) as compared to vaccinated ones. The 1:1 case-control matching analysis also confirmed these results.

COVID-19 vaccines improve short-term outcomes and may reduce Long COVID-19 prevalence.

By extracting early chest CT radiomic features of COVID-19 patients, we explored their correlation with laboratory indicators and oxygenation index (PaO2/FiO2), thereby developed an Artificial Intelligence (AI) model based on radiomic features to predict the deterioration of oxygenation function in COVID-19 patients.

This retrospective study included 384 patients with COVID-19, whose baseline information, laboratory indicators, oxygenation-related parameters, and non-enhanced chest CT images were collected. Utilizing the PaO2/FiO2 stratification proposed by the Berlin criteria, patients were divided into 4 groups, and differences in laboratory indicators among these groups were compared. Radiomic features were extracted, and their correlations with laboratory indicators and the PaO2/FiO2 were analyzed, respectively. Finally, an AI model was developed using the PaO2/FiO2 threshold of less than 200 mmHg as the label, and the model's performance was assessed using the area under the receiver operating characteristic curve (AUC), sensitivity and specificity. Group datas comparison was analyzed using SPSS software, and radiomic features were extracted using Python-based Pyradiomics.

There were no statistically significant differences in baseline characteristics among the groups. Radiomic features showed differences in all 4 groups, while the differences in laboratory indicators were inconsistent, with some PaO2/FiO2 groups showed differences and others not. Regardless of whether laboratory indicators demonstrated differences across different PaO2/FiO2 groups, they could all be captured by radiomic features. Consequently, we chose radiomic features as variables to establish an AI model based on chest CT radiomic features. On the training set, the model achieved an AUC of 0.8137 (95% CI [0.7631-0.8612]), accuracy of 0.7249, sensitivity of 0.6626 and specificity of 0.8208. On the validation set, the model achieved an AUC of 0.8273 (95% CI [0.7475-0.9005]), accuracy of 0.7739, sensitivity of 0.7429 and specificity of 0.8222.

This study found that the early chest CT radiomic features of COVID-19 patients are strongly associated not only with early laboratory indicators but also with the lowest PaO2/FiO2. Consequently, we developed an AI model based on CT radiomic features to predict deterioration in oxygenation function, which can provide a reliable basis for further clinical management and treatment.

This review examines the pathophysiological interactions between COVID-19 and heart failure, highlighting the exacerbation of heart failure in COVID-19 patients. It focuses on the complex mechanisms driving worse outcomes in these patients.

Patients with pre-existing heart failure experience more severe symptoms and higher mortality rates due to mechanisms such as cytokine storms, myocardial infarction, myocarditis, microvascular dysfunction, thrombosis, and stress cardiomyopathy. Elevated biomarkers like troponin and natriuretic peptides correlate with severe disease. Long-term cardiovascular risks for COVID-19 survivors include increased incidence of heart failure, non-ischemic cardiomyopathy, cardiac arrest, and cardiogenic shock. COVID-19 significantly impacts patients with pre-existing heart failure, leading to severe symptoms and higher mortality. Elevated cardiac biomarkers are indicators of severe disease. Acute and long-term cardiovascular complications are common, calling for ongoing research into targeted therapies and improved management strategies to better prevent, diagnose, and treat heart failure in the context of COVID-19.

Morphea, is a chronic inflammatory disease of the dermis and subcutaneous tissue. Research has indicated a connection between morphea and Type I Diabetes (T1D). COVID-19 can cause autoimmune diseases like scleroderma, T1D, systemic lupus erythematosus, and others. A 12-year-old girl with type 1 diabetes who was on insulin therapy was brought into the clinic for a metabolic evaluation. The patient had induration, skin hardness, and cutaneous erythema upon inspection. The onset of T1D was following a mild COVID-19 infection. Signs of morphea merged 3 months after the onset of T1D. Known as "long-term COVID," this sickness phase that follows the acute stage of COVID-19 is most likely the result of autoimmune activation. As this patient under evaluation reveals, COVID-19 has been demonstrated in the literature to cause the production of autoantibodies and to either cause or worsen autoimmune disorders in people who have a genetic susceptibility.

Viral infections caused by exposure to viruses such as Epstein-Barr, cytomegalovirus, or Parvovirus B19 have always been considered predisposing environmental factors for the onset of autoimmune diseases. More recently, autoimmune mechanisms such as molecular mimicry, T-cell activation, transient immunosuppression and inflammation have also been observed in cases of SARS-CoV-2 infection. Several newly diagnosed autoimmune disorders have been reported post-COVID-19, such as COVID-19-associated multisystemic inflammatory syndrome in children (MIS-C), type 1 diabetes mellitus, systemic lupus erythematosus, or rheumatoid arthritis. In this article, we present a new case of paediatric systemic lupus erythematosus (SLE) with haematological (macrophage activation syndrome), renal (stage 2), cutaneous (urticarial vasculitis) and digestive involvement, onset three and a half months post-COVID-19. In the dynamics, de novo infection generated by Epstein-Barr exposure was associated. The diagnosis was confirmed based on EULAR/ACR 2019 criteria. The aim of the article is to present a possible correlation between SARS-CoV-2 and Epstein-Barr as extrinsic factors in triggering or activating paediatric systemic lupus erythematosus. Keywords: paediatric systemic lupus erythematosus; post-COVID-19; Epstein-Barr; SARS- CoV-2; case report; paediatric patient.

Myeloperoxidase antineutrophil cytoplasmic antibody (MPO-ANCA) microscopic polyangiitis is a rare but life-threatening small vessel vasculitis in childhood that affects multiple systems. Emerging clinical evidence suggests a possible association between SARS-CoV-2 infection or multisystem inflammatory syndrome in children (MIS-C) as well as the futuredevelopment of autoimmune diseases. A 14-year-old boy with a diagnosis of MIS-C two years prior to presentation was admitted to our hospital due to edema and left lower limb joint pain along with concomitant upper surface petechia. The patient had a positive higher SARS-CoV-2 IgG than MIS-C diagnosis titers and MPO-ANCA-positive antibody titers. Kidney biopsy favored a pauci-immune crescentic glomerulonephritis. Restrictive lung disease with concomitant diffusion abnormalities was also observed. Pancreatitis and gastrointestinal wall edema were additional clinical manifestations. SARS-CoV-2 breakthrough infection and MIS-C could contribute to the onset of autoimmune vasculitis through various immunological mechanisms. Further research is still needed to elucidate the role of SARS-CoV-2 in the pathophysiology of newly diagnosed autoimmune vasculitis.

Evidence supporting the possible causal association of myopericarditis with the coronavirus disease (COVID-19) vaccine has mainly come from case reports. Epidemiological evidence indicating an increased relative risk for myopericarditis after COVID-19 vaccination is lacking. Therefore, this study aimed to identify and assess all confirmed COVID-19 vaccine- related cases of myopericarditis presenting to major cardiac centers in the Eastern Region of Saudi Arabia, before and after the introduction of the COVID-19 vaccine.

According to case definition, the hospital's information system database detected all confirmed cases at two main cardiac centers.

Of the 18 confirmed myocarditis and myopericarditis cases detected after the administration of COVID-19 vaccines, three were possibly related to COVID-19 immunization. The first case was of myopericarditis following a third dose of mRNA-1273. The second case was myocarditis, which occurred seven days after the first dose of AstraZeneca. The third case was myocarditis, which occurred 12 days after the third dose of BNT162b2. A cardiologist carefully evaluated the cases using recognized protocols and case definitions to demonstrate a direct relationship with vaccination consequences rather than coincidence.

We found no difference in the occurrence of myocarditis and myopericarditis after the COVID-19 vaccine compared with the background rate during a similar period (P = 0.9783). The incidences of myocarditis and myopericarditis following immunization were low. The advantages of the COVID-19 vaccination outweigh the risk of myopericarditis.

This study reports the prevalence and characteristics related to the development of thyroid autoimmunity among children newly diagnosed with type I diabetes (T1D) during the COVID-19 pandemic in Kuwait.

This is a prospective observational study of all children under age 14 years newly diagnosed with T1D in Kuwait. We define the duration of the COVID-19 pandemic from the official declaration of the first identified positive COVID-19 case on 24 February 2020 until 31 December 2022. For comparison, we use the time period directly before the COVID-19 pandemic, 1 January 2017 to 23 February 2020.

One thousand twenty-four (1024) children newly diagnosed with T1D in Kuwait during the study period were included. Among newly diagnosed children, 20.3% tested positive for thyroid antibodies during the COVID-19 pandemic, compared with 14.5% during the pre-pandemic period (p = 0.015). Children with positive COVID-19 status were more likely to present with thyroid antibodies (p = 0.035). After adjusting for other characteristics, patients diagnosed with T1D during the COVID-19 pandemic had double the odds of testing positive for thyroid antibodies (Adjusted odds ratio = 2.173, 95%CI: 1.108, 4.261, p = 0.024).

Incident cases of T1D during the COVID-19 pandemic may be different in aetiology or contextual factors leading to a higher risk of thyroid autoimmunity. Longitudinal studies are needed to understand the role of COVID-19 in the onset and progression of T1D and on thyroid autoimmunity and disease.

Bivalent COVID-19 mRNA vaccines, which contain two different components, were authorized to provide protection against both the original strain of SARS-CoV-2 and the Omicron variant as a measure to address the COVID-19 pandemic. Concerns regarding the risk of myocarditis/pericarditis associated with bivalent vaccination have been raised due to the observed superior neutralizing antibody responses. This study aimed to investigate the risk of myocarditis/pericarditis following bivalent COVID-19 mRNA vaccination compared to monovalent vaccination.

The CDC COVID Data Tracker and the Vaccines Adverse Event Reporting System (VAERS) were analyzed between December 13, 2020 to March 8, 2023. Reporting rates were determined by dividing the number of myocarditis/pericarditis cases by the total number of vaccine doses administered. Disproportionality patterns regarding myocarditis/pericarditis were evaluated for various COVID-19 mRNA vaccinations using reporting odds ratios (RORs).

The reporting rate for myocarditis/pericarditis following original monovalent COVID-19 mRNA vaccination was 6.91 (95 % confidence interval [95 %CI] 6.71-7.12) per million doses, while the reporting rate for bivalent vaccination was significantly lower (1.24, 95%CI 0.96-1.58). Disproportionality analysis revealed a higher reporting of myocarditis/pericarditis following original vaccination with a ROR of 2.21 (95 %CI 2.00-2.43), while bivalent COVID-19 mRNA vaccination was associated with fewer reports of myocarditis/pericarditis (ROR 0.57, 95 %CI 0.45-0.72). Sub-analyses based on symptoms, sex, age and manufacturer further supported these findings.

This population-based study provides evidence that bivalent COVID-19 mRNA vaccination is not associated with risk of myocarditis/pericarditis. These findings provide important insights into the safety profile of bivalent COVID-19 mRNA vaccines and support their continued use as updated boosters.

Following mass vaccinations for the control of the COVID-19 epidemic, a spectrum of cardiac and neurological disorders was reported among vaccinated individuals. This study examined the range of complications documented and factors related to their occurrence. Three electronic databases were searched for case reports and case series with descriptions of cardiac and/or neurological complications in COVID-19 vaccine recipients. A total of 698 vaccinees were included in this review, of which 259 (37.1%) had cardiac and 439 (62.9%) had neurological complications. Inflammatory conditions were the commonest among the cardiac complications; while polyneuropathy, demyelinating diseases and cerebrovascular disorders were the more common neurological complications. The mean age of those with cardiac complications (33.8 years) was much younger than those with neurological complications (49.7 years). There was no notable difference in the gender distribution between these two groups of vaccine recipients. mRNA vaccines (all brands) were associated with almost 90.0% of the cardiac complications, whereas viral vector vaccines were associated with slightly over half (52.6%) of the neurological complications. With regard to the dose, cardiac complications were more common after the second (69.1%), whereas neurological complications were more common after the first dose (63.6%). The majority of the cases had an uncomplicated clinical course. Nevertheless, 5.9% of cases with neurological complications and 2.5% of those with cardiac complications were fatal, underscoring the significance of the consistent surveillance and vigilant monitoring of vaccinated individuals to mitigate these occurrences.

Cronkhite-Canada syndrome is a rare gastrointestinal polyposis syndrome with distinctive clinical features and endoscopic findings. Diagnosis can be challenging without suspicion, and the disease carries high mortality due to complications such as infection, gastrointestinal bleeding, and malignancies. This paper presents two cases of Cronkhite-Canada syndrome occurring after coronavirus disease 2019 (COVID-19) mRNA vaccination. Both cases exhibited typical clinical findings, including hypogeusia, onychodystrophy, alopecia, and weight loss. Typical polyposis in the gastrointestinal tract was confirmed through endoscopies. As symptomatic treatment did not improve the symptoms, corticosteroids were administered, and symptoms and laboratory test results improved immediately. The patients improved upon corticosteroids tapering. These cases illustrate typical presentations of Cronkhite-Canada syndrome and the course of the disease following corticosteroid treatment. Additionally, they suggest the possibility that Cronkhite-Canada syndrome may be triggered by COVID-19 mRNA vaccination.

Coronavirus disease 2019 (COVID-19) is associated with coagulation abnormalities and increased risk for venous and arterial thrombi. This study aimed to evaluate D-dimer levels and lupus anticoagulant (LAC) positivity in pregnant individuals with and without Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.

This was a prospective cohort study of pregnant individuals delivering at a single academic institution from April 2020 to March 2022. Individuals with a positive SARS-CoV-2 result during pregnancy were compared with a convenience sample of those without a positive SARS-CoV-2 result. For individuals with SARS-CoV-2 infection, severity was assessed based on the National Institutes of Health classification system. The primary outcome was D-dimer level measured during delivery admission. The secondary outcomes were LAC positivity and thromboembolic events. Outcomes were compared between individuals with and without a positive SARS-CoV-2 result, and further by disease severity.

Of 98 participants, 77 (78.6%) were SARS-CoV-2 positive during pregnancy. Among individuals with SARS-CoV-2 infection, severity was asymptomatic in 20 (26.0%), mild in 13 (16.9%), moderate in 4 (5.2%), severe in 38 (49.4%), and critical in 2 (2.6%). The D-dimer concentration at delivery did not significantly differ between those with a SARS-CoV-2 positive result compared with those without (mean 2.03 µg/mL [95% confidence interval {CI} 1.72-2.40] vs. 2.37 µg/mL [95% CI 1.65-3.40]; p = 0.43). Three individuals (4%) with SARS-CoV-2 infection and none (0%) without infection were LAC positive (p = 0.59). There were no clinically apparent thromboses in either group. D-dimer concentrations and LAC positive results did not differ by COVID-19 severity.

Thrombotic markers did not differ in pregnant individuals by SARS-CoV-2 infection; however, high rates of LAC positivity were detected.

· Thrombotic markers did not differ in pregnant individuals by SARS-CoV-2 infection.. · Higher than expected rates of LAC positivity were detected.. · There were no clinically apparent thromboses..

In December 2019, the emergence of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) led to the COVID-19 pandemic, with millions of deaths worldwide. Vaccine breakthroughs in late 2020 resulted in the authorization of COVID-19 vaccines. While these vaccines have demonstrated efficacy, evidence from vaccine safety monitoring systems around the globe supported a causal association between COVID-19 vaccines, in particular those using mRNA technology, i.e., Moderna's mRNA-1273 and Pfizer-BioNTech's BNT162b2, and myocarditis.

This paper aims to investigate the epidemiology of mRNA COVID-19 vaccine-induced myocarditis, including age, ethnicity, and gender associations with these vaccines. It also discusses the immunopathophysiological mechanisms of mRNA COVID-19 vaccine-associated myocarditis and outlines principles of diagnosis, clinical presentation, and management.

A literature review was conducted using PubMed, Embase, and Queen Mary University of London Library Services databases. Search terms included "myocarditis," "coronavirus disease 2019," "SARS-CoV-2," "mRNA Covid-19 vaccines," "Covid vaccine-associated myocarditis," "epidemiology," "potential mechanisms," "myocarditis diagnosis," and "myocarditis management."

While the definite mechanism of mRNA COVID-19 vaccine-associated myocarditis remains ambiguous, potential mechanisms include molecular mimicry of spike proteins and activation of the adaptive immune response with dysregulated cytokine expression. Male predominance in COVID-19 vaccine-induced myocarditis may be attributed to sex hormones, variations in inflammatory reactions, coagulation states based on gender, and female-specific protective factors. Moreover, an analysis of diagnostic and management strategies reveals a lack of consensus on acute patient presentation management.

In contrast to viral infections that stand as the predominant etiological factor for myocarditis with more severe consequences, the mRNA COVID-19 vaccination elicits a mild and self-limiting manifestation of the condition. There is currently insufficient evidence to confirm the definite underlying mechanism of COVID-19 vaccine-associated myocarditis. Further research is needed to develop preventive and therapeutic solutions in this context.

Since the beginning of the pandemic, many skin manifestations associated with COVID-19 have been reported. New reports show that COVID-19 can lead to autoimmune diseases (AIDs) and autoinflammatory diseases, especially dermatological.

A prospective study was conducted by the dermatology department of the Centre Hospitalier Universitaire Ibn Rochd (CHU Ibn Rochd) of Casablanca in Morocco since the beginning of the pandemic including 18 patients with COVID-19-related skin manifestations.

Eighteen cases were collected with confirmed SARS-CoV-2 infection. The mean COVID score was 0.7. A percentage (94.44%) of the cases had general symptoms. Skin involvement was variable, mainly maculopapular rash (44.44%), purpura (27.77%), urticaria, varicelliform rash, necrotic lesions of the face, and pityriasis rosea Gibert (PRG)-like lesions. Mucosal involvement was found in 50%. Viral reactivation was found in 5.55%. Telogen effluvium was found in 22.22%. Moreover, AID was triggered by COVID-19: lupus (11.11%), associated with antiphospholipid syndrome (APL Sd) (5.55%), psoriasis (11.11%), alopecia, and pemphigus. Severe toxidermia was potentiated by SARS-CoV-2 infection (22.22%): Stevens-Johnson syndrome (Sd), acute generalized exanthematous pustulosis (APEG), and drug reaction with eosinophilia and systemic symptoms (DRESS).

 The interest of this work is to report our experience during the COVID-19 pandemic to understand some pathophysiological mechanisms of its dermatological manifestations and to draw the attention of clinicians to the link of this infection with autoimmune and autoinflammatory diseases and toxidermia.

SARS-CoV-2 infection has been linked to hyperinflammation in multiple organs with a potential mechanistic link with resulting autoimmunity. There have been reports of many inflammatory complications following COVID-19, including sarcoidosis. A literature review on new-onset sarcoidosis following COVID-19 is lacking. We evaluated potential associations between COVID-19 and development of new-onset sarcoidosis.

Articles discussing biopsy-proven sarcoidosis after confirmed COVID-19 infection, published 1956 until April 2023, were included. All article types were deemed eligible except opinion and review articles.

A pooled total of 15 patients with new-onset diagnosis of sarcoidosis after COVID-19 infection were included, 45.5% female, mean age 46.1 years (standard deviation 14.7) at onset of sarcoidosis. Patients were from: Europe (n=11); North America (n=2); South America (n=1); Asia (n=1). The mean time between COVID-19 infection and diagnosis of sarcoidosis was 56.3 days, although this ranged from 10 to 140 days. Organ systems predominantly affected by sarcoidosis were: pulmonary (n=11); cutaneous (n=3); cardiac (n=2); ocular (n=1); systemic (n=1) (with overlapping features in certain patients). Sarcoidosis was treated as follows: glucocorticoids (n=8); azathioprine (n=1); cardiac re-synchronisation therapy (n=1); heart transplant (n=1). All patients were reported to have survived, with one requiring intensive care admission.

Our result suggests there is a potential link between COVID-19 and new-onset sarcoidosis. The potential mechanism for this is through cytokine mediated immune modulation in COVID-19 infection. Obtaining a tissue sample remains key in confirming the diagnosis of sarcoidosis and this may be delayed during active COVID-19 infection.

This report introduces a Brighton Collaboration (BC) case definition for autoimmune hepatitis (AIH), which has been classified as a priority adverse event of special interest (AESI), as there were possible cases seen following COVID-19 vaccination. The case definition was developed by a group of subject matter and BC process experts to facilitate safety data comparability across pre- and post-licensure clinical trials, as well as pharmacovigilance activities in multiple settings with diverse resources and healthcare access. The usual BC case definition development process was followed in an expedited manner, and took two months to complete, including finalising the manuscript for publication, instead of the usual 1 year development time. It includes a systematic review of the literature and an expert consensus to define levels of diagnostic certainty for AIH, and provides specific guidelines for data collection and analysis. Histology, serological and biochemical tests and exclusion of alternate diagnosis were considered necessary to define the levels of certainty (definitive, probable and possible). AEFI reports of suspected AIH were independently classified by the WG members to test its useability and these classifications were used to finalise the case definition. The document underwent peer review by external AIH experts and a Reference Group of vaccine safety stakeholders in high-, low- and middle-income countries to ensure case definition useability, applicability, and scientific integrity. The expedited process can be replicated for development of other standardised case definitions for priority AESIs for endemics and epidemics. While applicable to cases reported following immunisation, the case definition is independent of lapsed time following vaccination and, as such, can also be used to determine background incidence for vaccinated and unvaccinated control groups in studies of causal association. While use of this case definition is also appropriate for the study of safety of other products including drugs, it is not meant to guide clinical case management.

Guillain-Barré syndrome associated with Coronavirus-2-related severe acute respiratory syndrome (COV-GBS) occurs as para- or post-infectious forms, depending on the timing of disease onset. In these two forms, we aimed to compare the cerebrospinal fluid (CSF) and serum proinflammatory cytokine profiles to evaluate differences that could possibly have co-pathogenic relevance.

We studied a retrospective cohort of 26 patients with either post-COV-GBS (n = 15), with disease onset occurring > 7 days after SARS-CoV-2 infection, or para-COV-GBS (n = 11), with disease onset 7 days or less. TNF-α, IL-6, and IL-8 were measured in the serum with SimplePlex™ Ella™ immunoassay. In addition to the para-/post-COV-GBS patients, serum levels of these cytokines were determined in those with non-COVID-associated-GBS (NC-GBS; n = 43), paucisymptomatic SARS-CoV-2 infection without GBS (COVID, n = 20), and in healthy volunteers (HV; n = 12). CSF cytokine levels were measured in patients with para-/post-COV-GBS, in those with NC-GBS (n = 29), or with Alzheimer's disease (AD; n = 24).

Serum/CSF cytokine levels did not differ in para- vs post-COV-GBS. We found that SARS-CoV-2 infection raises the serum levels of TNF-α, IL-6, and IL-8, as well as an increase of IL-6 (in serum and CSF) and IL-8 (in CSF) in either NC-GBS or COV-GBS than controls. CSF and serum cytokine levels resulted independent one with another.

The change of cytokines linked to SARS-CoV-2 in COV-GBS appears to be driven by viral infection, although it has unique characteristics in GBS as such and does not account for cases with para- or post-infectious onset.

A few months after the beginning of the coronavirus disease of 2019 (COVID-19) vaccination, several reports of myocarditis secondary to the vaccines were published, sometimes with fulminant cases, but until today there is no proven causal link between these 2 events, but with many hypotheses proposed.

A systematic review of current evidence regarding myocarditis after COVID-19 vaccination was performed by searching several databases including PubMed/Medline and Web of Science. The quality of Meta-analysis was assessed using the AMSTAR-2 tool as well as other qualitative criteria.

Our umbrella review appraised 4 Meta-analysis of retrospective studies (range: 5-12), The number of vaccine doses included ranged from 12 to 179 million, with the number of myocarditis cases observed ranging from 343 to 1489. All types of vaccines were evaluated, with no exclusions. The overall incidence ranged from 0.89 to 2.36 cases of myocarditis per 100 000 doses of vaccine received. Heterogeny was assessed in 3 of the Meta-analysis, and was highly significant (>75%) in all included studies, and with a significant P-value (P < .05). Regarding publication bias, 3 of the Meta-analysis conducted the egger and begg regression, with a significant result in only 1. Regarding the assessment of the methodology by the AMSTAR-2 scale indicating that the quality was very critical in 1, low in 2, and moderate in 1 Meta-analysis.

The quality of current non-randomized evidence on real causality and incidence of myocarditis after COVID-19 vaccine is still low.

Nowadays, data concerning the risk of autoimmune disease after SARS-CoV-2 (COVID-19) vaccination is controversial. The aim of this single centre prospective follow-up study was to evaluate whether healthcare workers (HCWs) vaccinated with BNT162b2 mRNA and mRNA-1273 will show a development and/or a persistence of autoantibodies, focussing on the detection of antibodies against nuclear antigens (antinuclear antibodies, ANA). We enrolled 155 HCWs, however only 108 of them received the third dose and were considered for further analysis. Blood samples were collected before vaccine inoculation (T0), at 3 (T1) and 12 months (T2) after the first dose. All samples were analysed for the presence of a) ANA using indirect Immunofluorescence [IIF] (dilutions of 1:80, 1:160. 1:320 and 1:640), and anti-smooth muscle antibodies (ASMA); b) anti-myeloperoxidase (anti-MPO), anti-proteinase 3 (anti-PR3) and anti-citrullinated peptide antibodies (aCCP) [FEIA]; c) anti-phospholipid antibodies (anticardiolipin [aCL], anti-beta-2- glycoprotein I [anti-ß-2GPI] (Chemiluminescence). Line-blot technology was performed using the following kit: EUROLINE ANA profile 3 plus DFS70 (IgG). Our research suggests that mRNA based anti-SARSCoV-2 vaccines can induce the production of de novo ANA in 22/77(28,57%) of subjects and that the percentage of positivity seems to be directly correlated to the number of vaccine expositions: 6/77 (7,79%) after 2 doses; 16/77 (20,78%) after 3 doses. Since it is known that hyperstimulation of the immune system could lead to autoimmunity, these preliminary results seem to further sustain the idea that the hyperstimulation of the immune system might lead to an autoinflammatory mechanism and eventually to autoimmune disorders. However, the link between SARS-CoV-2 vaccination and the development of autoimmune diseases needs to be further investigated.

This review examines the immunological and autoimmune adverse events associated with COVID-19 vaccines, highlighting their frequencies, reported cases, and associations with specific vaccine classes. The concept of vaccine-induced immune thrombotic thrombocytopenia is crucial in addressing vaccine skepticism. Understanding this concept helps healthcare professionals identify and manage potential adverse events after vaccination. Despite their rarity, immunological and autoimmune adverse events cause concern and anxiety among the public. To maintain public trust in vaccination programs, healthcare professionals and public health agencies must actively monitor and address these adverse events, promptly disclose suspicious incidents, take measures to mitigate dangers, and inform the public with transparency and accurate information. Continuing research and surveillance are essential for understanding the underlying mechanisms of these adverse events and developing strategies to minimize their occurrence.

Data regarding the risk of incident pericarditis in coronavirus disease 2019 (COVID-19) recovered patients are lacking. We determined the risk of incident pericarditis after COVID-19 infection by performing a systematic review and meta-analysis of available data.

Following the PRISMA guidelines, we searched MEDLINE and Scopus to locate all articles published up to 11 February 2023 reporting the risk of incident pericarditis in patients who had recovered from COVID-19 infection compared to noninfected patients (controls) defined as those who did not experience the disease over the same follow-up period. Pericarditis risk was evaluated using the Mantel-Haenszel random effects models with hazard ratio (HR) as the effect measure with 95% confidence interval (CI) while heterogeneity was assessed using Higgins I2 statistic.

Overall, 16 412 495 patients (mean age 55.1 years, 76.8% males), of whom 1 225 715 had COVID-19 infection, were included. Over a mean follow-up of 9.6 months, pericarditis occurred in 3.40 (95% CI: 3.39-3.41) out of 1000 patients who survived COVID-19 infection compared with 0.82 (95% CI: 0.80-0.83) out of 1000 control patients. Recovered COVID-19 patients presented a higher risk of incident pericarditis (HR: 1.95, 95% CI: 1.56-2.43, I2 : 71.1%) compared with controls. Meta-regression analysis showed a significant direct relationship for the risk of incident pericarditis using HT ( P  = 0.02) and male sex ( P  = 0.02) as moderators, while an indirect association was observed when age ( P  = 0.01) and the follow-up length ( P  = 0.02) were adopted as moderating variables.

Recovered COVID-19 patients have a higher risk of pericarditis compared with patients from the general population.

Coronavirus disease 2019 (COVID-19) is an infectious disease affecting multiple systems and organs, including the reproductive system. SARS-CoV-2, the virus that causes COVID-19, can damage reproductive organs through direct (angiotensin converting enzyme-2, ACE-2) and indirect mechanisms. The immune system plays an essential role in the homeostasis and function of the male and female reproductive systems. Therefore, an altered immune response related to infectious and inflammatory diseases can affect reproductive function and fertility in both males and females. This narrative review discussed the dysregulation of innate and adaptive systems induced by SARS-CoV-2 infection. We reviewed the evidence showing that this altered immune response in COVID-19 patients is the major indirect mechanism leading to adverse reproduction outcomes in these patients. We summarized studies reporting the long-term effect of SARS-CoV-2 infection on women's reproductive function and proposed the chronic inflammation and chronic autoimmunity characterizing long COVID as potential underlying mechanisms. Further studies are needed to clarify the role of autoimmunity and chronic inflammation (long COVID) in altered female reproduction function in COVID-19.

Immunologic and inflammatory adverse effects following vaccination against COVID-19 are being reported. While some reactions may develop denovo others concern its immunogenic effect in patients with pre-existing inflammatory conditions.

Retrospective consecutive patients diagnosed with ocular inflammatory manifestations within 8 weeks of receiving COVID-19 vaccination who presented to a tertiary eye care centre in South India.

Ninety-eight eyes of 67 patients presenting with ocular inflammatory manifestations within 8 weeks following COVID-19 vaccination were studied. The mean age was 43 years (+/- 14.82; range 19-80 years). The most common presentations were anterior uveitis (n = 31, 31.7%), followed by panuveitis (n = 24, 24.5%). The mean time to onset of symptoms was 25 days (+/- 15.48; range 2-55 days) following a dose of vaccine. Among all patients, 39 (58.2%) had a previous history of ocular inflammation. Mean presenting visual acuity was 0.4 (0-4) logMAR units and mean final visual acuity was 0.2 (0-4) logMAR units. The causes for reduced vision included of cystoid macular edema (n=2, 2%), chorioretinal atrophy (n=2.2%), optic atrophy (n=1.1%), retinal vascular occlusion (n=1.1%) and acute retinal necrosis (n=1.1%).

Infective and immunogenic adverse events should be watched out for after COVID-19 vaccination. It is difficult to establish causality for such manifestations, nevertheless, most of them were mild and had good final visual outcomes.

There has been much interest in the possible adverse events associated with available anti-coronavirus disease of 2019 (COVID-19) vaccines, given the rapid pace at which they had to be developed during the pandemic. One such adverse event is myocarditis post-COVID-19 vaccination. Several pathophysiological mechanisms have been proposed that might help us understand the relationship between the messenger ribonucleic acid (mRNA) vaccine and the occurrence of myocarditis, though we are yet to ascertain the causal link between them. Although the actual absolute incidence of myocarditis post-COVID-19 vaccination remains low among the large, general population that has been vaccinated, there has been a high relative incidence of this adverse event. We aim to review the existing literature and bring to light what we have so far understood with respect to the association between COVID-19 vaccination and myocarditis. This will help in better understanding the burden of the pathology along with alleviating apprehensions associated with it.

To report three cases of ocular myositis and scleritis, bilateral scleritis and unilateral single muscle myositis after mRNA COVID-19 vaccination.

Case series of three patients who presented to the Orbit Outpatient Service of Fondazione Policlinico Universitario A. Gemelli with a history of unilateral proptosis, diplopia and pain, bilateral red eye and pain during eye movements and unilateral proptosis and inconstant diplopia respectively with onset 5-10 days after m-RNA COVID-19 vaccine. A thorough hematologic work up and orbital contrast enhanced magnetic resonance imaging (MRI) in patients with proptosis was performed.

Patients were females, 64, 58 and 45 years old respectively. MRI showed enlargement of all right rectus muscles, with both muscle belly and insertion involvement in the first case associated to right scleritis. A bilateral scleritis was diagnosed in the second patient and a single muscle myositis in the third patient. Serological tests excluded thyroid diseases. The first and second patient were treated respectively with oral and topical glucorticoids with a complete clinical response. Two 2 cycles of oral non-steroidal anti-inflammatory drugs were administered to the third patient with a partial response.

As far as we know these are the first report of orbital myositis and scleritis presenting after mRNA BNT162b2 vaccine (Pfizer/BioNTech) and mRNA-1273-(Moderna) vaccine, an uncommon effect of a likely autoimmune reaction triggered by the virus antigen.

Despite the reports on glomerulonephritis associated with COVID-19 mRNA vaccines, no study has reported about the dense deposit disease (DDD). Here, we present a case of hilar lymphadenopathy after the COVID-19 mRNA vaccination, following which the patient developed tubulointerstitial nephritis (TIN) and DDD. A 74-year-old man received his second dose of mRNA vaccine, and on the next day, he developed fever, urticaria, and dyspnea. On further examination, he had pleural effusion and right hilar lymphadenopathies, which were improved with conservative therapy. After 48 days of the second vaccination, he developed renal dysfunction and new-onset hematuria. Light microscopy findings by renal biopsy revealed apparent mesangial cell proliferation, increased mesangial matrix in the glomeruli, and diffuse inflammatory cell infiltration in the interstitium. Immunofluorescence analysis revealed 1 + positive results for IgG and IgM, negative results for IgA, and 2 + positive results for C3 with a garland pattern on the capillary walls. Electron microscopy revealed that severe cell proliferation in the capillary rumen, and continuous, thickened, and highly dark-stained spotty dense deposits in the glomerular basement membrane; and noncontinuous spotty dense deposits in the tubular basement membrane. Based on the decrease in C3 and pathological findings, TIN accompanied with DDD was diagnosed. The mRNA vaccine might have contributed to the development of lymphadenopathies, TIN, and DDD in this case. Moreover, TIN and DDD might be associated with the activated alternative pathway induced by the mRNA vaccine.

COVID-19 infection not only profoundly impacts the detection of tuberculosis infection (Tbc) but also affects modality in tuberculosis patient immune response. It is important to determine immune response alterations in latent tuberculosis infection as well as in SARS-CoV-2-infected tuberculosis patients. Such changes may have underlying effects on the development and course of further tuberculosis. Here, we aimed to review the characteristics of immune response in TB patients or convalescent COVID-19 patients with latent TB infection (LTBI).

We analyzed the features of immune response in tuberculosis and COVID-19 patients. For this, we analyzed publications released from December 2019 to March 2023; those which were published in accessible international databases ("Medline", "PubMed", "Scopus") and with keywords such as "COVID-19", "SARS-CoV-2", "tuberculosis", "pulmonary tuberculosis", "latent tuberculosis infection", "Treg", "follicular Treg", and "Treg subsets", we considered.

Through our analysis, we found that tuberculosis patients who had been infected with COVID-19 previously and elevated Th1 and Th2 cell levels. High levels of Th1 and Th2 cells may serve as a positive marker, characterizing activated immune response during TB infection. COVID-19 or post-COVID-19 subjects showed decreased Th17 levels, indicating a lack of tuberculosis development. Moreover, the typical course of tuberculosis is associated with an increase in Treg level, but COVID-19 contributes to a hyperinflammatory response.

According to the data obtained, the course of tuberculosis proceeds in a dissimilar way due to the distinct immune response, elicited by SARS-CoV-2. Importantly, the development of active tuberculosis with a severe course is associated with a decline in Treg levels. Both pathogens lead to disturbed immune responses, increasing the risk of developing severe TB. The insights and findings of this paper may be used to improve the future management of individuals with latent and active tuberculosis.

A literature review on new-onset autoimmune connective tissue diseases (ACTDs) following COVID-19 is lacking. We evaluated potential associations between COVID-19 and the development of new-onset ACTDs. The "population" was adults with disease terms for ACTDs, including systemic lupus erythematosus (SLE), Sjogren's syndrome, systemic sclerosis (SSc), idiopathic inflammatory myositis (IIM), anti-synthetase syndrome, mixed CTD and undifferentiated CTD, and "intervention" as COVID-19 and related terms. Databases were searched for English-language articles published until September 2022. We identified 2236 articles with 28 ultimately included. Of the 28 included patients, 64.3% were female, with a mean age was 51.1 years. The USA reported the most cases (9/28). ACTD diagnoses comprised: 11 (39.3%) IIM (including four dermatomyositis); 7 (25%) SLE; four (14.3%) anti-synthetase syndrome; four (14.3%) SSc; two (7.1%) other ACTD (one lupus/MCTD overlap). Of eight, four (14.3%) patients (including that with lupus/MCTD) had lupus nephritis. The average time from COVID-19 to ACTD diagnosis was 23.7 days. A third of patients were admitted to critical care, one for treatment of haemophagocytic lymphohistiocytosis in SLE (14 sessions of plasmapheresis, rituximab and intravenous corticosteroids) and nine due to COVID-19. 80% of patients went into remission of ACTD following treatment, while three (10%) patients died-one due to macrophage activation syndrome with anti-synthetase syndrome and two from unreported causes. Our results suggest a potential association between COVID-19 and new-onset ACTDs, notably in young females, reflecting more comprehensive CTD epidemiology. The most common diagnosis in our cohort was IIM. The aetiology and mechanisms by which ACTDs emerge following COVID-19 remain unknown and require further research.

A 14-year-old Japanese girl died unexpectedly 2 days after receiving the third dose of the BNT1262b2 mRNA COVID-19 vaccine. Autopsy findings showed congestive edema of the lungs, T-cell lymphocytic and macrophage infiltration in the lungs, pericardium, and myocardium of the left atria and left ventricle, liver, kidneys, stomach, duodenum, bladder, and diaphragm. Since there was no preceding infection, allergy, or drug toxicity exposure, the patient was diagnosed with post-vaccination pneumonia, myopericarditis, hepatitis, nephritis, gastroenteritis, cystitis, and myositis. Although neither type of inflammation is fatal by itself, arrhythmia is reported to be the most common cause of death in patients with atrial myopericarditis. In the present case, arrhythmia of atrial origin was assumed as the cause of cardiac failure and death. In sudden post-vaccination deaths, aggressive autopsy systemic search and histological examination involving extensive sectioning of the heart, including the atrium, are indispensable.

For over three years, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in children and adolescents has generated repercussions, especially a few weeks after infection, for symptomatic patients who tested positive, for asymptomatic ones, or even just the contacts of an infected person, and evolved from severe forms such as multisystem inflammatory syndrome in children (MIS-C) to multifarious clinical manifestations in long COVID (LC). Referred to under the umbrella term LC, the onset of persistent and highly heterogeneous symptoms such as fatigue, post-exertion malaise, cognitive dysfunction, and others have a major impact on the child's daily quality of life for months. The first aim of this review was to highlight the circumstances of the pathophysiological changes produced by COVID-19 in children and to better understand the hyperinflammation in COVID-19 and how MIS-C, as a life-threatening condition, could have been avoided in some patients. Another goal was to better identify the interplay between infection, dysbiosis, and inflammation at a molecular and cellular level, to better guide scientists, physicians, and pediatricians to advance new lines of medical action to avoid the post-acute sequelae of SARS-CoV-2 infection. The third objective was to identify symptoms and their connection to molecular pathways to recognize LC more easily. The fourth purpose was to connect the triggering factors of LC with related sequelae following acute SARS-CoV-2 injuries to systems and organs, the persistence of the virus, and some of its components in hidden reservoirs, including the gut and the central nervous system. The reactivation of other latent infectious agents in the host's immune environments, the interaction of this virus with the microbiome, immune hyperactivation, and autoimmunity generated by molecular mimicry between viral agents and host proteins, could initiate a targeted and individualized management. New high-tech solutions, molecules, probiotics, and others should be discovered to innovatively solve the interplay between RNA persistent viruses, microbiota, and our immune system.

It is assumed that SARS-CoV-2- and COVID-19-associated autoimmune processes may affect the outcomes of assisted reproductive technology (ART) cycles. This observational prospective study included 240 infertile patients: 105 patients had no history of COVID-19 (group 1) and 135 patients had experienced COVID-19 (group 2) in a mild (n = 85) or moderate (n = 50) form less than 12 months prior to oocyte retrieval. Using ELISAs, the profiles of their serum autoantibodies were determined, including antiphospholipid antibodies and antibodies to nuclear and thyroid antigens. The parameters of oogenesis and embryogenesis, as well as the pregnancy and childbirth rates, did not differ between groups 1 and 2, and also between the subgroups with different severities of COVID-19. However, when oocyte retrieval was performed less than 180 days after COVID-19, a higher proportion of poor-quality blastocysts was obtained (p = 0.006). A high risk of early miscarriage was found in the patients with moderate COVID-19. In group 2, IgG antibodies to annexin V, phosphatidylethanolamine (PE), and TSHr were detected more often than in group 1 (p = 0.035; p = 0.028; and p = 0.033, respectively), and a weak inverse correlation was revealed between anti-PE IgG and the number of oocytes and zygotes obtained. The results of the study suggest a possible adverse effect of COVID-19 and its associated autoantibodies on the outcomes of fresh oocyte ART cycles and early pregnancy, which depends on the severity of COVID-19 and the time interval after the disease.

Evidences show that there may be a link between SLE and COVID-19. The purpose of this study is to screen out the diagnostic biomarkers of systemic lupus erythematosus (SLE) with COVID-19 and explore the possible related mechanisms by the bioinformatics approach.

SLE and COVID-19 datasets were extracted separately from the NCBI Gene Expression Omnibus (GEO) database. The limma package in R was used to obtain the differential genes (DEGs). The protein interaction network information (PPI) and core functional modules were constructed in the STRING database using Cytoscape software. The hub genes were identified by the Cytohubba plugin, and TF-gene together with TF-miRNA regulatory networks were constructed via utilizing the Networkanalyst platform. Subsequently, we generated subject operating characteristic curves (ROC) to verify the diagnostic capabilities of these hub genes to predict the risk of SLE with COVID-19 infection. Finally, a single-sample gene set enrichment (ssGSEA) algorithm was used to analyze immune cell infiltration.

A total of 6 common hub genes (CDC6, PLCG1, KIF15, LCK, CDC25C, and RASGRP1) were identified with high diagnostic validity. These gene functional enrichments were mainly involved in cell cycle, and inflammation-related pathways. Compared to the healthy controls, abnormal infiltration of immune cells was found in SLE and COVID-19, and the proportion of immune cells linked to the 6 hub genes.

Our research logically identified 6 candidate hub genes that could predict SLE complicated with COVID-19. This work provides a foothold for further study of potential pathogenesis in SLE and COVID-19.

This study aims to reevaluate and compare the data from the Brazilian Unified Health System (SUS) on the number of diagnoses of systemic lupus erythematosus (SLE) in the pre-pandemic period with those in the pandemic period, as well as to compare the first year (2020) of the COVID-19 pandemic in Brazil with the last year (2021), to update the data, and to verify whether SLE disease control measures were effective in 2021. There was a consistent and significant increase in the incidence of SLE cases all over Brazil between the first and second pandemic years and between the pre-pandemic triennium and the second pandemic year. Therefore, it is inescapable to have larger clinical studies with different populations to better understand the relationship between these two conditions and find measures to improve the control of this disease.

Anti N-Methyl-D-Aspartate (NMDA) receptor antibody associated ADEM is a diagnosis that was first described relatively recently in 2007 by Dalmau et al. The recent COVID-19 pandemic has resulted in multiple neurological complications being reported. However, there is limited data on Anti-NMDA receptor antibody associated ADEM in COVID-19 patients. Furthermore, the MRI findings in these patients have not been fully elucidated. This case report adds to the growing body of knowledge of neurological complications in COVID-19 patients.

A 50 year old Caucasian female with no previous medical co-morbidities presented with symptoms of COVID-19 and subsequently developed neurological symptoms which included confusion, limb weakness and seizures. The patient developed marked behavioural abnormalities which required attention. She was found to have anti NMDA receptor antibodies present in a significant titres, an elevated total protein on lumbar puncture and cytotoxic magnetic resonance imaging (MRI) changes in the brain and spinal cord and was subsequently diagnosed with an anti-NMDA Receptor Antibody associated ADEM. The bilateral symmetric involvement of the corticospinal tract on MRI was considered unusual in our case. She was treated with a combination of corticosteroids and plasmapheresis which halted disease progression. Thereafter she was commenced on intravenous immunoglobulin as maintenance therapy and she has shown continuous improvement with ongoing physiotherapy.

The recognition of COVID 19 neurological complications may be difficult in the initial disease as early symptoms of lethargy, weakness and confusion may be very nondescript. However, it is imperative that these complications are sought for as they are imminently treatable. Early institution of therapy is imperative in decreasing long term neurological consequences.

Acute myocarditis has been described as a relatively rare cardiovascular complication of COVID-19 infection. However, data regarding the risk of myocarditis during the post-acute phase of COVID-19 are scant. We assess the risk of incident myocarditis in COVID-19 survivors within 1 year from the index infection by a systematic review and meta-analysis of the available data.

Data were obtained by searching Medline and Scopus for all studies published at any time up to September 1, 2022, and reporting the long-term risk of incident myocarditis in COVID-19 survivors. Myocarditis risk data were pooled using the Mantel-Haenszel random-effects models with hazard ratio (HR) as the effect measure with 95% confidence interval (CI). Heterogeneity among studies was assessed using the Higgins-Thompson I2 statistic.

Overall, 20,875,843 patients (mean age 56.1 years, 59.1% male) were included in this analysis. Of them, 1,245,167 experienced (and survived) COVID-19 infection. Over a mean follow-up of 9.5 months, myocarditis occurred to 0.21 (95% CI 0.13-0.42) out of 1000 patients survived to COVID-19 infection compared with 0.09 [95% CI 0.07-0.12) out of 1000 control subjects. Pooled analysis revealed that recovered COVID-19 patients presented an increased risk of incident myocarditis (HR 5.16, 95% CI 3.87-6.89; P < 0.0001; I2 = 7.9%) within 1 year from the index infection. The sensitivity analysis confirmed yielded results.

Our findings suggest that myocarditis represents a relatively rare but important post-acute COVID-19 sequelae.