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Objectives: To assess the immunological [Lymphocyte populations (LP) and Autoantibodies (Ab)] and clinical profile of rheumatoid arthritis (RA) patients who suffered from COVID-19 compared with non-COVID-19 RA patients. Method(s): A nested case-control study of RA patients treated under a strict follow-up model. RA patients and confirmed COVID-19 infection (last 24 months) and RA patients without the infection were included. Subgroups of cases: Long COVID (LC): symptoms after infection for >=4 weeks;Post COVID syndrome (PCS): symptoms for >=12 weeks;and patients with symptoms alpha4 weeks. Sociodemographic, clinical, and paraclinical variables of RA and COVID-19 infection (in cases) were captured. Antinuclear antibodies (ANA), anticardiolipin antibodies, lymphocyte populations (BD FACSDuetTM-BDFACSLyricTMmultiparameter flow cytometry) T cells, B cells, and NK were evaluated. Univariate and bivariate analyzes (STATA 17) were done. Result(s): 300 patients were included (148 cases/152 controls;87.3% women). Median age 59 years (IQR 11). 71.86% were in low disease activity. There were no significant differences in sociodemographic and clinical characteristics between cases and controls. Cases had a time since infection of 18.5 months (IQR 7). Of the total cases, 69%presented LC and 63%PCS.No significant differences were found between cases and controls in the lymphocyte population nor in the antibodies evaluated. There were no differences in the immune profile when comparing patients with LC and PCS with those with symptoms alpha4 weeks after COVID-19 infection. Conclusion(s): No differences were found in the behavior of the immunological profile (independent of symptoms of LC and PCS) in RA patients under strict follow up, evaluated long-term after infection with those who did not have COVID-19. This suggest that patients returned to their baseline homeostatic state, something that has not yet been reported up to now. These results should be replicated in populations with different RA characteristics.
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OBJECTIVES: In this study, we investigated whether SARS-CoV-2 stimulates autoantibody production. METHODS: The study included 91 patients hospitalized due to COVID 19, with no previous history of immunological diseases. Immunofluorescence assays were performed to detect antinuclear antibodies (ANAs) and antineutrophil cytoplasmic antibodies (ANCAs), along with tests for specific autoantibodies. RESULTS: The median age (57% male) was 74 years (range 38-95 years). Autoantibodies were positive in 67 (74%), ANA in 65 (71%), and ANCA in 11 (12%) patients. Female gender (p = 0.01), age (p = 0.005), and Charlson comorbidity index (p = 0.004) were significant predictors for the development of ANA/ANCA antibodies (p = 0.004). Nuclear mitotic apparatus (NuMA)-like, positivity was the strongest predictor of acute kidney injury (AKI), together with noninvasive ventilation and eGFR (χ2 = 49.01, P < 0.001). CONCLUSION: Positive autoantibodies in a large proportion of patients suggest a role of autoimmunity in the pathophysiology of acute COVID-19 disease. NuMA was the strongest predictor of AKI.
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Hepatitis A is a common viral infection worldwide that is transmitted via the fecal-oral route. Since the introduction of an efficient vaccine, the incidence of infection has decreased but the number of cases has risen due to widespread community outbreaks among unimmunized individuals. Classic symptoms include fever, malaise, dark urine, and jaundice, and are more common in older children and adults. People are often most infectious 14 days prior to and 7 days following the onset of jaundice. We will discuss the case of a young male patient, diagnosed with acute hepatitis A, leading to fulminant hepatitis refractory to conventional therapy and the development of subsequent kidney injury. The medical treatment through the course of hospitalization was challenging and included the use of L-ornithine-L-aspartate and prolonged intermittent hemodialysis, leading to a remarkable outcome. Hepatitis A is usually self-limited and vaccine-preventable;supportive care is often sufficient for treatment, and chronic infection or chronic liver disease rarely develops. However, fulminant hepatitis, although rare, can be very challenging to manage as in the case of our patient.Copyright © 2023 The Author(s).
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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induces an overreaction of the immune system, resulting in the production of auto-antibodies. Several studies have reported that autoantibodies are prevalent in COVID-19 patients. In our study, antinuclear antibodies were evaluated in patients with COVID-19. We examined 131 sera from patients (>17-year-old) with confirmed COVID-19. Samples were collected prior to receiving any medication and antinuclear antibodies (ANA) levels were measured by the indirect immunofluorescence (IIF) method. Furthermore, the immunoblotting test was used to determine the presence of anti-nuclear antigen antibodies. The IIF-ANA test was positive in 36.4% (48/131) of patients. Overall, non-ICU patients had higher IIF-ANA titers than ICU patients. In particular, ICU patients had fewer nuclear, cytoplasmic, and mitotic IIF-ANA antibodies than non-ICU patients. In conclusion, COVID-19 patients frequently have ANA possibly reflecting the immune dysregulation due to several damaged cells by SARS-CoV-2 virus.
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Antibodies, Antinuclear , COVID-19 , Humans , Adolescent , SARS-CoV-2 , Autoantibodies , Fluorescent Antibody Technique, Indirect/methodsABSTRACT
Objective: The effect of severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection on autoimmunity in both disease and post-disease stages has not been fully explained. There is not enough information about the evaluation of autoimmune antibodies in convalescent SARS-CoV-2 patients. This study aimed to investigate the presence and types of autoantibodies in post-illness coronavirus disease-2019 (COVID-19) patients and to compare them with indirect immunofluorescence assay (IIF)-antinuclear antibody (ANA) results before SARS-CoV-2 infection. Material(s) and Method(s): Twenty-four COVID-19 patients with known and reported ANA test results prior to SARS-CoV-2 infection were included in this study. Patients' IIF-ANA, extractable nuclear antigen blot and anti-dsDNA tests were studied three and nine months after SARS-CoV-2 infection. Result(s): Three months after SARS-CoV-2 infection, 41.66% of patients had a positive IIF-ANA test. When we compared these results with pre-infection ANA results, 3 patients (12.5%) were variable. The first case was chromosomal granular positive before infection and was found to be homogeneous, and cytoplasm was speckled positive after infection. Additionally, Scl-70, DFS70, and anti-dsDNA were found to be positive. We think that lupus symptoms were triggered after COVID-19. The second case had negative ANA before infection, while the ANA was antinuclear membrane positive (2+) three months after infection. Also, anti-RNP/Sm was detected as positive. The third case had negative ANA before infection, and was detected to have speckled weakly positive ANA three months after infection. However, autoantibody positivity was not detected. Conclusion(s): As a result, these data support the idea that SARS-CoV-2 infection may trigger autoimmunity and be associated with the development of autoantibodies.Copyright © 2022 by the Turkish Society of Immunology. Turkish Journal of Immunology published by Galenos Publishing House.
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Protein S is a multifunctional plasma protein, whose deficiency, results in a rare congenital thrombophilia, inherited in an autosomal dominant pattern. It can aggravate the hypercoagulable state of pregnancy, when it presents in parallel with the condition, leading to adverse maternal outcomes and foetal loss. A 35-year-old female third gravida having previous 2 deliveries by Lower Segment Caesarean Section (LSCS) presented to emergency at 10 weeks pregnancy with chief complaints of pain and swelling in left thigh since 4-5 days. After thorough investigations and work-up, the patient was diagnosed with Protein S deficiency. She was managed conservatively and was delivered by elective LSCS with bilateral tubal ligation at 38 weeks of gestation with good foetal and maternal outcomes.The rarity of Protein S deficiency along with the successful outcome of the pregnancy makes this a unique case.Copyright © 2023 Journal of Clinical and Diagnostic Research. All rights reserved.
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Background: Chronic spontaneous urticaria (CSU) is a common chronic inflammatory disease. There have been small case series of new onset CSU post COVID-19 infection as well as reports of new onset CSU or worsening of existing CSU post COVID-19 vaccination. Dermatological side effects post COVID-19 vaccine are typically delayed, self-limiting urticaria. We have described the characteristics of patients who have developed new onset CSU post COVID-19 vaccination. Method(s): All patients referred to the UCT Lung Institute Allergy clinic from the initiation of the COVID-19 vaccine roll out (February 2021) were reviewed to identify patients that developed new onset CSU within 12 weeks of receiving a COVID-19 vaccine. Medical history, response to therapy, and available laboratory investigations were reviewed by clinic physicians. Result(s): We identified seven patients that developed CSU post COVID-19 vaccine. The median age of the cohort is 39 (IQR 32-45) and the majority are female (n = 5). The most common vaccine was the Pfizer-BioNTech BNT162b2 mRNA COVID-19 vaccine (n = 6, 85.7%), and one patient received the Jansen Ad26.COV2.S vaccine. No patients had COVID-19 infection prior to vaccination and only one patient contracted COVID-19 post vaccination. The median time to the development of symptoms post vaccination was 14 days (IQR 2;44) and the median time to diagnosis was 90 days (IQR 45;120). Most patients (n = 4) reported angioedema and urticaria, one patient reported isolated angioedema, and two isolated urticaria. The median initial UAS7 score was 37.5 (IQR 24.5;46) and the initial CU-Q2oL score was 72 (IQR 56;76) indicating severe disease activity. All but one patient had a history of atopy with the most common diagnoses being allergic rhinitis (n = 5) and atopic dermatitis (n = 3). All patients had normal eosinophil counts and over half of the patients (n = 4) had an elevated total IgE level (median 26.4 [IQR 9.8;194]). All patients were HIV negative and one patient had positive Helicobacter pylori serology. All had normal serum protein electrophoresis, thyroid function (with negative thyroid autoantibodies), and negative antinuclear antibodies. All patients started on high dose antihistamine therapy with 71.1% having partial or no response to therapy. Conclusion(s): New onset CSU is a rare side effect of COVID-19 vaccination with poor response to high dose antihistamine therapy. It is important that allergists and physicians are aware of the possibility of new onset CSU post COVID-19 vaccine and further research is needed to identify risk factors.
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Introduction and Objectives: Acute autoimmune-like liver injury has been increasingly reported after vaccination against SARS-CoV-2. Pathogenesis, steroid requirement and long-term prognosis are unknown. This study aimed to evaluate clinical, serological and histological features, response to treatment and prognosis in patients with post-vaccination acute hepatitis. Material(s) and Method(s): We included patients without known pre-existing liver diseases with transaminase levels >= 2.5 upper limits of normal within 90 days after the SARS-CoV-2 vaccine with an available liver biopsy. Clinical data and outcomes after a six months follow-up were collected. Result(s): 17 patients were included,12 females, median age 60 (51,5/66) exposed to vectorial (Sputnik V n=7, AstraZeneca n=6), inactivated (Sinopharm n=3) or ARNm Vaccines (Moderna=1). In 8 patients, liver injury developed after the first dose and in 7 after the second dose and in 2 after the third dose. The median time to the development of injury was 33(23,50/53,50) days. Eight patients had a history of extrahepatic autoimmune disease and five patients had metabolic syndrome and used statins. Immune serology showed anti-antinuclear antibody in 10 (58,8%), anti-smooth muscle antibody in 5(29,4%). 14/17 patients presented with elevated IgG levels. Liver histology showed lobular hepatitis in 13/17, portal hepatitis in 17/17 with plasmocytic lymphocytic infiltrate and 4/17 had eosinophils, 6/17 with severe interface hepatitis, and one patient had fibrosis Ishak stage >=3. 12/17 (70,5%) were treated with steroids. Transaminases improved in 17 cases and normalized in 6/12 by month 6. Only 1/17 developed liver function deterioration, yet no patient required liver transplantation. Most patients tolerated the tapering of steroids and in 6 azathioprine was started before month 3. Conclusion(s): Long-term follow-up might help to differentiate between induced classical autoimmune hepatitis, autoinflammatory self-limited events, or drug-induced liver injury in these patients.Copyright © 2023
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Livedoid vasculopathy (LV) is a noninflammatory thrombotic disease caused by occlusion of dermal small vessels associated with systemic autoimmune disorders and coagulopathies. However, LV is often reported as being 'idiopathic', despite extensive investigation. We report a case of severe LV in an otherwise healthy 27-year-old woman, associated with parvovirus infection. The patient presented with a short history of a livedoid rash initially covering her torso, which spread to acral sites. Burning pains in the lower limb caused reduced mobility;systemically, she remained well and stable throughout. Examination revealed generalized acral skin pallor, livedoid patches of violet erythema and purpura with deep serpiginous ulcerations over extensor aspects of upper and lower limbs with a more broken/racemosa nonulcerated livedoid appearance on the trunk. On admission a transaminitisareas continued to ulcerate. Codeine was present with a creatine kinase of 1569 U L.1, but other blood test results were unremarkable including erythrocyte sedimentation rate, complement, cryoglobulins, antinuclear antibodies, antineutrophil cytoplasmic antibodies, extractable nuclear antigen, rheumatoid factor, myositis screen, antiphospholipid screen and thrombophilia screen. Parvovirus IgG and IgM were both positive and tested for, as the patient's young daughter had recently been diagnosed with 'slapped cheek disease'. Magnetic resonance imaging of the thighs showed a diffuse mild myositis;electromyography, nerve-conduction studies, barium swallow and computed tomography of the chest, abdomen and pelvis were all normal. An incisional skin biopsy was performed, which revealed a blood vessel with organizing (Solimani F, Mansour Y, Didona D et al. Development of severe pemphigus vulgaris following SARS-CoV-2 vaccination with BNT162b2. J Eur Acad Dermatol Venereol 2021;35: e649- 51) have been reported. The main proposed mechanisms for AstraZeneca vaccine-induced pemphigus could be a hyperimmune reaction in genetically predisposed individuals, with eventual formation of anti-desmoglein antibodies. An alternative hypothesis is that vaccine components could act as foreign antigens resulting in a cross-reaction with pemphigus antigens. The close association of COVID-19 vaccination with the acute onset of pemphigus in our patient, as well as exacerbations after subsequent vaccine administration, is more than coincidental. Considering the recent pandemic with COVID-19 and the widespread administration of the COVID-19 vaccine, continued observation and documentation of true adverse events is essential.
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Autoantibodies against melanoma differentiation-associated protein 5 (MDA5) associated with dermatomyositis have recently been described in Asians with rapidly progressive respiratory disease. Here we report the case of a middle-aged white woman with anti-MDA5 antibody-associated amyopathic dermatomyositis with interstitial lung disease (ILD), which is stable with minimal immune suppression. A 55-year-old woman was referred to a virtual dermatology clinic during the COVID-19 pandemic suspected of having widespread eczema involving the chest, face, arm and hands on the background of atopy. On direct questioning, she admitted to having constitutional symptoms, exertional dyspnoea, joint pain and symptoms of proximal muscle weakness. On clinical suspicion of possible connective tissue disorder, she was urgently reviewed in the hospital, where she was found to have a photodistributed rash involving cutaneous ulceration and violaceous plaques. Hand examination showed mechanic's hand mimicking hand eczema, ragged nail cuticles and acute tenosynovitis in the left index finger. Her upper and lower limb muscle power was normal and respiratory examination revealed bi-basal fine end-expiratory crepitation. Her repeated biochemical, haematological and muscle enzymes remained normal. Skin biopsy taken from photosensitive rash over the wrist showed hypergranulosis, Civatte body formation, colloid bodies and dyskeratotic keratinocytes, in keeping with severe lichenoid eruption. Superficial dermis showed patchy red-cell extravasation, perivascular chronic infiltration, dermal oedema and serum on the surface, in keeping with ulceration secondary to severe inflammatory processes. There were no eosinophils and eccrine coils were free of inflammation, raising the suspicion of a drug eruption. Her antinuclear antibody and double-stranded DNA were repeatedly negative. Myositisspecific antibody panel was performed owing to a high clinical suspicion of photosensitive dermatoses, both clinically and histologically. Histology revealed positive anti-MDA5 antibodies;repeated positive testing confirmed this. Although lung function was normal, computed tomography revealed evidence of ILD. We made a diagnosis of anti-MDA5 antibodyassociated amyopathic dermatomyositis with ILD. Her malignancy screening was negative. The patient was started on lowdose prednisolone and hydroxychloroquine 200 mg twice daily, with topical steroid applications, which resulted in remarkable clinical improvement. Anti-MDA5 associated dermatomyositis has characteristic cutaneous lesions consisting of skin ulceration and tender palmar papules, mechanic's hands, inflammatory arthritis and rapidly progressive ILD, which is frequently fatal. Although our patient had ILD, she was relatively stable on minimal immunosuppression. It is important for clinicians to have an increased awareness of this disease as it could have a highly variable clinical presentation in the white population.
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An 86-year-old woman presented to the emergency department with acute shortness of breath. She was treated with intravenous furosemide for acute-on-chronic heart failure. Her past medical history included atrial fibrillation, hypertension, diverticulosis and hypothyroidism. Rivaroxaban and levothyroxine were her only long-term medications. On day 5 of hospital admission, she developed painful haemorrhagic and purulent bullae on her dorsal hands, head and neck. These evolved to large suppurative, vegetative plaques over a 72 h period and she developed additional lesions on her trunk, upper back and thighs. The patient had routine blood tests, which showed a raised C-reactive protein at 260 mg L-1, and an acute kidney injury with a glomerular filtration rate of 54 mL-1 min-1. She had a negative COVID-19 swab, and swabs from the lesions for bacterial culture and viral polymerase chain reaction were negative. She had a normal serum protein electrophoresis, immunoglobulin, antinuclear antibody and antineutrophil cytoplasmic antibody. She had computed tomography of her chest 24 h prior to the onset of her lesions, which showed mild bilateral pleural effusions in keeping with fluid overload secondary to heart failure. A biopsy taken from her hand showed orthokeratosis and parakeratosis, and there was bulla formation subepidermally. There was a dense neutrophilic infiltrate with microabscess formation with scattered eosinophils and lymphocytes. There was no evidence of vasculitis. Direct immunofluorescence was negative and a tissue culture for atypical mycobacteria was negative. The patient was commenced on high-dose intravenous methylprednisolone at 500 mg for 3 days followed by 40 mg prednisolone orally for 1 week, but there was a limited response. Our initial differential was Sweet syndrome or pyoderma vegetans;however, the patient had no fevers and no risk factors (malignancy, inflammatory disease, infection, etc.). She also had no response to high-dose oral prednisolone. Given the timing of her CT examination in relation to her acute dermatosis and the use of radioiodine for contrast, we assessed the patient's serum iodine and urine iodine. These were both high at 1.02 mmol L-1 (reference interval 0.32- 0.63) and 3.46 mmol L-1 (reference interval 0.0-2.43), respectively. A diagnosis of iododerma was made. The patient's eruption slowly resolved and at 12 weeks there was evidence of postinflammatory skin changes only. Her urine and serum iodine were rechecked, and both had normalized. In the last 20 years there have been approximately 20 case reports of iododerma. Most have been following iodine contrast use in patients with abnormal kidney function, like our patient. Most describe an acneiform eruption that subsequently evolves to vegetative plaques (Chalela JG, Aguilar L. Iododerma from contrast material. N Engl J Med 2016;374: 2477). Iododerma is largely a diagnosis of exclusion, but histopathology and urine and serum iodine levels can help support diagnosis.
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A 59-year-old man presented with a widespread morbilliform rash after receiving the second dose of the Pfizer-BioNTech COVID-19 mRNA vaccine. He had no significant medical history and no known allergies. He did not take any regular medication. He developed pruritus without rash 4 h after his first vaccine. This resolved after 10 days without intervention. One day after his second dose, he developed an extensive pruritic morbilliform eruption on his trunk and limbs, affecting 35% of his body surface area. with no mucous membrane involvement. The rash persisted for 4 weeks after his second vaccination and he was referred to dermatology. Eosinophils were raised at 0.54 and liver function tests were normal. Antinuclear antibodies and extractable nuclear antigen were negative. Complement levels were normal. Histology showed mild epidermal acanthosis, spongiosis and subcorneal vesicles. Within the superficial to mid-dermis, there was a mixed chronic inflammatory infiltrate comprising lymphocytes, plasma cells, neutrophils and numerous eosinophils. Direct immunofluorescence was negative. He received a tapering dose of oral prednisolone with mometasone topically. Despite substantial improvement with this regimen, his rash began to worsen 2 days following discontinuation of oral prednisolone. He was still using daily mometasone on cessation of oral steroids. He was trialled on oral doxycycline for 1 month, which led to a marked improvement in the morbilliform rash. Despite improvement in the rash, the patient reported ongoing intense daily pruritus which was having a marked impact on his quality of life. He has commenced on narrowband ultraviolet B (UVB) phototherapy to treat his persistent pruritis, with good effect to date. Morbilliform eruptions have been reported as a cutaneous manifestation of COVID-19 and as a side-effect of mRNA vaccines. Proposed mechanisms for the development of skin rashes post-mRNA vaccines include viral protein expression following vaccination, prior infection with COVID-19 causing cross-reaction with the mRNA vaccine encoded antigen and vaccine components acting as haptens inducing a T helper 2 inflammatory reaction characterized by interleukin (IL)-4 and IL-13 expression. Drug-induced maculopapular eruptions typically resolve within 7-14 days on withdrawal of the culprit medication. The persistent nature in our patient may imply a complex immune response. The use of phototherapy to treat inflammatory dermatoses and pruritic conditions such as nodular prurigo is well described. The antipruritic effect of phototherapy is thought to work via modulation of both the neural pathways involved in itch and local immune cells in the skin. Our case highlights that phototherapy can be used in the treatment of cutaneous side-effects that arise after COVID-19 vaccines. To the best of our knowledge, this case is one of the first to use narrowband UVB phototherapy to treat a cutaneous side-effect of an mRNA vaccine.
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INTRODUCTION Chronic spontaneous urticaria (CSU) is a common chronic inflammatory disease. There have been small case series of new onset CSU post-COVID-19 infection and reports of new onset or worsening of existing CSU post COVID-19 vaccination. A dermatological side-effect post COVID-19 vaccine is typically delayed, self-limiting urticaria. We have described the characteristics of patients who have developed new-onset CSU post COVID-19 vaccination. METHOD All patients referred to the Allergy Clinic since the initiation of the COVID-19 vaccine roll-out in South Africa were reviewed to identify patients who had developed new-onset CSU within 12 weeks of receiving a COVID-19 vaccine. Medical history, response to therapy and available laboratory investigations were reviewed by clinic physicians. RESULTS We identified seven patients who developed CSU post COVID-19 vaccination. The median age of the cohort is 39 (IQR 32-45) and the majority are female (n = 5). The most common vaccine was the Pfizer-BioNTech BNT162b2 mRNA COVID-19 vaccine (n = 6;85). The median time to the development of symptoms post-vaccination was 14 days (IQR 2;44) and the median time to diagnosis was 90 days (IQR 45;120). The median initial UAS7 score was 37.5 (IQR 24.5;46) and the initial CU-Q2oL score was 72 (IQR 56;76), which indicated severe disease activity. All but one patient had a history of atopy, with the most common diagnoses being allergic rhinitis (AR) (n = 5) and atopic dermatitis (AD) (n = 3). All the patients had normal eosinophil counts and more than half of the patients (n = 4) had an elevated total IgE level (median 26.4 [IQR 9.8;194]). All of the patients were HIV-negative. All of them had normal serum protein electrophoresis, thyroid function (with negative thyroid autoantibodies) and negative antinuclear antibodies. All of them started on high-dose antihistamine therapy, with 71.1% having partial or no response to the therapy. CONCLUSION New-onset CSU is a rare side-effect of COVID-19 vaccination, with poor response to high-dose antihistamine therapy. It is important that allergists and physicians are aware of the possibility of new-onset CSU post COVID-19 vaccination and further research is needed to identify any risk factors.
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AIM: Coronavirus disease 2019 (COVID-19) has been proposed as triggering autoimmunity. The aim of this study was to evaluate the presence and clinical significance of autoantibodies in patients with COVID-19. METHODS: We retrospectively collected data from 245 patients who were hospitalized for COVID-19. All patients were tested for the presence of antinuclear antibody (ANA), rheumatoid factor (RF), anti-citrullinated peptide antibody (ACPA), and anti-cytoplasmic neutrophil antibody (ANCA). Risk factors for death and critical COVID-19, defined as the need for invasive mechanical ventilation or extracorporeal membrane oxygenation, were analyzed. RESULTS: Ninety (36.7%) patients tested positive for ANA, and 51 (20.8%) patients tested positive for RF. Three patients each (1.2%) tested positive for ACPA and ANCA. RF-positive patients had higher rates of invasive mechanical ventilation and death than RF-negative patients (70.6% vs 28.4%, P < 0.001 and 45.1% vs 18.6%, P < 0.001, respectively). Underlying lung disease, kidney disease, heart disease, quick COVID severity index (qCSI), and lactate dehydrogenase (LDH) were associated with in-hospital death. RF (odds ratio [OR] 7.31, 95% CI 2.50-21.37, P < 0.001), qCSI (OR 1.42, 95% CI 1.19-1.69, P < 0.001), and LDH (OR 1.004, 95% CI 1.002-1.005, P < 0.001) were associated with critical COVID-19. Combination of RF, qCSI, and LDH showed good prognostic value (area under the curve = 0.903, P < 0.001) for critical COVID-19. CONCLUSIONS: ANA and RF were frequently detected in COVID-19 patients. RF could be a risk factor for critical COVID-19. The results of this study suggest immune dysfunction contributes to the complications of COVID-19.
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Arthritis, Rheumatoid , COVID-19 , Humans , Rheumatoid Factor , Retrospective Studies , Antibodies, Antineutrophil Cytoplasmic , Hospital Mortality , Autoantibodies , Antibodies, AntinuclearABSTRACT
Background & Aims: Liver injury with autoimmune features after vaccination against severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) is increasingly reported. We investigated a large international cohort of individuals with acute hepatitis arising after SARS-CoV-2 vaccination, focusing on histological and serological features. Methods: Individuals without known pre-existing liver diseases and transaminase levels ≥5x the upper limit of normal within 3 months after any anti-SARS-CoV-2 vaccine, and available liver biopsy were included. Fifty-nine patients were recruited;35 females;median age 54 years. They were exposed to various combinations of mRNA, vectorial, inactivated and protein-based vaccines. Results: Liver histology showed predominantly lobular hepatitis in 45 (76%), predominantly portal hepatitis in 10 (17%), and other patterns in four (7%) cases;seven had fibrosis Ishak stage ≥3, associated with more severe interface hepatitis. Autoimmune serology, centrally tested in 31 cases, showed anti-antinuclear antibody in 23 (74%), anti-smooth muscle antibody in 19 (61%), anti-gastric parietal cells in eight (26%), anti-liver kidney microsomal antibody in four (13%), and anti-mitochondrial antibody in four (13%) cases. Ninety-one percent were treated with steroids ± azathioprine. Serum transaminase levels improved in all cases and were normal in 24/58 (41%) after 3 months, and in 30/46 (65%) after 6 months. One patient required liver transplantation. Of 15 patients re-exposed to SARS-CoV-2 vaccines, three relapsed. Conclusion: Acute liver injury arising after SARS-CoV-2 vaccination is frequently associated with lobular hepatitis and positive autoantibodies. Whether there is a causal relationship between liver damage and SARS-CoV-2 vaccines remains to be established. A close follow-up is warranted to assess the long-term outcomes of this condition. Impact and implications: Cases of liver injury after vaccination against severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) have been published. We investigated a large international cohort of individuals with acute hepatitis after SARS-CoV-2 vaccination, focusing on liver biopsy findings and autoantibodies: liver biopsy frequently shows inflammation of the lobule, which is typical of recent injury, and autoantibodies are frequently positive. Whether there is a causal relationship between liver damage and SARS-CoV-2 vaccines remains to be established. Close follow-up is warranted to assess the long-term outcome of this condition. © 2022 The Author(s)
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Background: Disseminated infections such as tuberculosis are known to result in a systemic inflammatory response leading to thrombosis, with increasing reported cases of thrombotic event being observed in patients infected with covid-19. This is the first reported case on co-infection with COVID-19 pneumonia and disseminated tuberculosis causing catastrophic antiphospholipid syndrome (CAPS). Method(s): The report highlighted the challenges in the diagnosis and management which include the use of corticosteroid in setting of systemic infections. Another diagnostic dilemma was to explain the cause of myositis by tuberculous or autoimmune. Case Presentation: We report a 26-year- old man with HbE trait thalassemia who reported unintentional weight loss, night sweats for 1 month prior to the diagnosis of covid-19 infection on 10th March 2022. Seven days later, he was hospitalized for suspected perforated appendix. Computed tomography (CT) abdomen revealed hepatosplenomegaly, prostatitis, seminal vesiculitis. Multiple matted abdominal lymph nodes were not amenable for biopsy. Soon, he appeared toxic, dyspneic required non-invasive ventilation with bilateral parotitis. He had raised erythrocyte sedimentation (ESR) 52 mm/hour, C-reactive protein (CRP) 221 mg/dl, lactate dehydrogenase (LDH) 730U/L. Direct Coomb's antibody was positive but did not have any form of haemolysis. Complement 3 (0.45 g/L) and complement 4 (0.1 g/L) levels were low. Serum IgG4, procalcitonin, anti-nuclear antibody, cultures and virology were negative. Sputum for acid fast bacilli (AFB) was positive on Auramine O stain but the Ziehl-Nelson (ZN) stain and tuberculous PCR (GeneXpert) were negative. Diagnosis of disseminated tuberculosis was made but his abdominal pain persisted despite being on anti-tuberculous therapy (ATT), and he had new evidence of splenic infarct. CT angiogram also revealed celiac trunk and superior mesenteric artery thrombosis. Antiphospholipid (aPL) test was positive for lupus anticoagulant, beta 2 glycoprotein 1 and anti-cardiolipin antibodies. Therapeutic anticoagulation and plasma exchange were initiated for probable CAPS followed by intravenous immunoglobulin and corticosteroid. Thereafter, the patient developed severe bilateral pelvic girdle pain with evidence of myositis on the MRI (Figure 2). Serum creatine kinase was never elevated. Anti-PL- 7 and anti Ro-52 were borderline elevated. He recovered well and ambulant before discharged home. Conclusion(s): Our case highlight the complexicity of presentation of CAPS who manifested as multiple arterial thrombosis. The diagnosis of disseminated tuberculosis relied strongly on microbiological, imaging and clinical presentation as histopathological evidence was not feasible. Management challenges were deciding on corticosteroid in disseminated infection and the need for confirmation of persistent positive aPL test and to monitor myositis symptom to help guide decision making. (Figure Presented).
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Background/Purpose: Concomitant systemic lupus erythematosus (SLE) and human immunodeficiency virus (HIV) infection cases are rare worldwide. It is established that SLE patients have an increased risk of opportunistic infection due to immune dysregulation, as well as in HIV. Method(s): A case of a 25-year- old Filipino man with systemic lupus erythematosus admitted due to a 1-week intermittent fever associated with headache, loss of appetite, and generalized body weakness was reviewed in a tertiary hospital in the Philippines. Result(s): An initial diagnosis was made from the clinical presentation of Raynaud's phenomenon, an elevated antinuclear antibody (1:320;nuclear, speckled), 2+ proteinuria, thrombocytopenia, and nail fold capillaroscopy findings consistent with mixed connective tissue disease. Patient was started on hydroxychloroquine and prednisone. He was admitted as a case of Streptococcus bacteremia with COVID-19 pneumonia after initial diagnosis, presenting as fever, and thrombocytopenia as low as 23.000/mul. Patient presented with a scaly erythematous annular lesion at his left wrist since December 2021 where a skin punch biopsy showed findings consistent with dermatophytosis. Direct immunofluorescence staining showed deposition of granular IgM (+3), C3 (+1), Fibrinogen (+3), and C1q (+1) in the basement membrane zone consistent with Lupus Erythematosus. Additional findings were oral thrush, dermatophytosis, and Pneumocystis pneumonia. Patient was started on antibiotics, remdesivir, and antifungal medications. Being severely immunocompromised, work up for HIV was initiated. Rapid HIV screening was positive, CD4 count revealed 7 (3.14%), and subsequent confirmatory western blot was positive. Additional treatment included hydroxychloroquine, methylprednisolone pulse therapy, and platelet concentrate transfusion. He was referred for CD4 monitoring, and ARV treatment enrollment, however, the patient expired a month after his discharge. Conclusion(s): This case is thereby reported to document a rare case of systemic lupus erythematosus (SLE) male patient with concomitant HIV, SARS-CoV- 2, and opportunistic infections secondary to AIDS. Diagnosis becomes challenging in patients with autoimmune diseases and multiple infectious diseases as clinical presentations tend to overlap and may show similar manifestations. In this setting, skin biopsy utilizing direct immunofluorescence can help establish an accurate diagnosis especially when clinical features and histopathology are overlapping.