Toxic Epidermal Necrolysis Post COVID-19 Vaccination – First Reported Case

Authors: Mohamad BakirHanan AlmeshalRifah AlturkiSulaiman ObaidAreej Almazroo

Published: August 16, 2021


Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) is a spectrum of acute, delayed-type hypersensitivity reactions that affect the skin and the mucous membranes. Medications are the culprit cause of these disorders in addition to infections and in very rare instances vaccinations. We report a case of TEN in a 49-year-old woman with no previous medical history. The disorder developed one week after receiving the first dose of COVID-19 vaccine with no other identifiable causes. The patient received two doses of tumor necrosis factor-alpha inhibitor (etanercept) and she stopped developing new lesions after two days of the initial dose; complete healing was observed after 22 days and no side effects were observed in our patient. This case demonstrates an extremely rare complication to the COVID-19 vaccine. The benefits of receiving the COVID-19 outweigh the potential risk. 


Toxic epidermal necrolysis (TEN) is a rare immune-mediated, life-threatening skin reaction characterized by blistering and extensive epidermal detachment of more than 30% of body surface area. The incidence is estimated to be 0.4 to 1.9 cases per million population per year worldwide and an estimated mortality rate of 25% to 35% [1, 2]. Medication is usually the cause of TEN (e.g., certain antibiotics and antiepileptics) [3]. Vaccination-induced Stevens-Johnson syndrome (SJS)/TEN is rare, with less than twenty reported cases in the published literature, with the measles vaccine being reported to cause both SJS and TEN, varicella, smallpox, anthrax, tetanus, and influenza vaccines were reported to cause SJS alone, and MMR (measles, mumps, rubella), hantavirus and meningococcal B vaccines were reported to cause TEN [4, 5, 6]. The patient usually develops a fever and other flu-like symptoms one to three weeks after being exposed to medication followed by painful erythematous to purpuric skin lesions that tend to coalescence. Next erosions and vesiculobullous lesions and epidermal detachment over wide body surface area develop. Mucous membranes are also involved, and the patient develops oral ulcers, vaginal ulcers, and possible acute conjunctivitis [7]. In this paper, we report a case of TEN following the administration of the Pfizer COVID-19 vaccine (Pfizer, Inc., New York, USA).

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SARS-CoV-2 infection: The role of cytokines in COVID-19 disease

Authors: Víctor J Costela-Ruiz 1Rebeca Illescas-Montes 1Jose M Puerta-Puerta 2Concepción Ruiz 3Lucia Melguizo-Rodríguez 1

COVID-19 disease, caused by infection with SARS-CoV-2, is related to a series of physiopathological mechanisms that mobilize a wide variety of biomolecules, mainly immunological in nature. In the most severe cases, the prognosis can be markedly worsened by the hyperproduction of mainly proinflammatory cytokines, such as IL-1, IL-6, IL-12, IFN-γ, and TNF-α, preferentially targeting lung tissue. This study reviews published data on alterations in the expression of different cytokines in patients with COVID-19 who require admission to an intensive care unit. Data on the implication of cytokines in this disease and their effect on outcomes will support the design of more effective approaches to the management of COVID-19.

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Cytokine storm in COVID-19: pathogenesis and overview of anti-inflammatory agents used in treatment

Authors: Mehmet Soy 1Gökhan Keser 2Pamir Atagündüz 3Fehmi Tabak 4Işık Atagündüz 5Servet Kayhan

COVID-19 infection has a heterogenous disease course; it may be asymptomatic or causes only mild symptoms in the majority of the cases, while immunologic complications such as macrophage activation syndrome also known as secondary hemophagocytic lymphohistiocytosis, resulting in cytokine storm syndrome and acute respiratory distress syndrome, may also occur in some patients. According to current literature, impairment of SARS-CoV-2 clearance due to genetic and viral features, lower levels of interferons, increased neutrophil extracellular traps, and increased pyroptosis and probable other unknown mechanisms create a background for severe disease course complicated by macrophage activation syndrome and cytokine storm. Various genetic mutations may also constitute a risk factor for severe disease course and occurrence of cytokine storm in COVID-19. Once, immunologic complications like cytokine storm occur, anti-viral treatment alone is not enough and should be combined with appropriate anti-inflammatory treatment. Anti-rheumatic drugs, which are tried for managing immunologic complications of COVID-19 infection, will also be discussed including chloroquine, hydroxychloroquine, JAK inhibitors, IL-6 inhibitors, IL-1 inhibitors, anti-TNF-α agents, corticosteroids, intravenous immunoglobulin (IVIG), and colchicine. Early recognition and appropriate treatment of immunologic complications will decrease the morbidity and mortality in COVID-19 infection, which requires the collaboration of infectious disease, lung, and intensive care unit specialists with other experts such as immunologists, rheumatologists, and hematologists.

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Accumulating evidence suggests anti-TNF therapy needs to be given trial priority in COVID-19 treatment

Authors: Philip C Robinson, Duncan Richards, Helen L Tanner, Marc Feldmann

The COVID-19 pandemic continues to wreak havoc on global health-care systems and to claim an increasing number of lives. Although some treatments have shown promise, including dexamethasone and remdesivir, problems remain with access to medication and high mortality despite treatment. Patient selection also appears to be critical, with some patient groups benefitting from treatment, but not others. One potential treatment that deserves higher priority in COVID-19 trials, based on the documented evidence of its effects, is the biological agent anti-TNF.Feldmann and colleagues1 described the rationale for trialling anti-TNF therapies in COVID-19. These therapies neutralise TNF, a major component of the cytokine response that is part of the damaging excess inflammatory phase of COVID-19, which is termed hyperinflammation or cytokine release syndrome. This hyperinflammatory response in COVID-19 is characterised by elevated concentrations of serum TNF, interleukin (IL)-6, and IL-8, but relatively little IL-1.2 However, IL-1 has a short serum half-life, and mononuclear transcriptome data show that genes and pathways upregulated by TNF, IL-1β, and type I interferon predominate.3 A major component of deteriorating lung function in patients with COVID-19 is capillary leak, a result of inflammation driven by key inflammatory cytokines: TNF, IL-1, IL-6, and vascular endothelial growth factor. Administration of anti-TNF to patients for treatment of autoimmune disease leads to reductions in all of these key inflammatory cytokines.45 It is therefore conceivable that anti-TNF therapy could reduce inflammation-driven capillary leak in COVID-19 and have a major impact on the need for ventilation and mortality.

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TNF Biologics and COVID-19: What Autoimmune Patients Need to Know


If you’re taking a type of medication known as tumor necrosis factor inhibitors, also called anti-TNF or TNFis, you may be wondering how these drugs could impact your chances of contracting COVID-19, or having more severe complications from it. After all, the common cold or other upper respiratory tract infections can be more common in people taking anti-TNF inhibitors.

On the other hand, some rheumatologists are pointing out that TNF biologics may actually be protective against COVID-19 inflammation — and they are calling for more clinical trials to study these drugs as a potential COVID treatment.

No wonder there is confusion and anxiety among the people who take these medications to manage conditions like rheumatoid arthritis, psoriasis, and Crohn’s disease.

While more research is needed to fully understand the impact of these medications on COVID-19, at least there is some preliminary data from the first few months of the pandemic, which is helping doctors and researchers make decisions help keep you healthy and safe.

We talked with top rheumatologist to help quell your fears and answer your questions. Read on to learn about how anti-TNF biologics work in the body, what the latest coronavirus research says, and how to best manage your inflammatory condition and minimize your risk of COVID-19.

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Pathways in the Pathophysiology of Coronavirus 19 Lung Disease Accessible to Prevention and Treatment

Authors: Michael Eisenhut 1Jae Il Shin 2

Background: In COVID 19 related lung disease, which is a leading cause of death from this disease, cytokines like tumor necrosis factor-alpha (TNF alpha) may be pivotal in the pathogenesis. TNF alpha reduces fluid absorption due to impairment of sodium and chloride transport required for building an osmotic gradient across epithelial cells, which in the airways maintains airway surface liquid helping to keep airways open and enabling bacterial clearance and aids water absorption from the alveolar spaces. TNF alpha can, through Rho-kinase, disintegrate the endothelial and epithelial cytoskeleton, and thus break up intercellular tight junctional proteins, breaching the intercellular barrier, which prevents flooding of the interstitial and alveolar spaces with fluid. Hypotheses: (1) Preservation and restoration of airway and alveolar epithelial sodium and chloride transport and the cytoskeleton dependent integrity of the cell barriers within the lung can prevent and treat COVID 19 lung disease. (2) TNF alpha is the key mediator of pulmonary edema in COVID 19 lung disease. Confirmation of hypothesis and implications: The role of a reduction in the function of epithelial sodium and chloride transport could with regards to chloride transport be tested by analysis of chloride levels in exhaled breath condensate and levels correlated with TNF alpha concentrations. Reduced levels would indicate a reduction of the function of the cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel and a correlation with TNF alpha levels indicative of its involvement. Anti-TNF alpha treatment with antibodies is already available and needs to be tested in randomized controlled trials of COVID 19 lung disease. TNF alpha levels could also be reduced by statins, aspirin, and curcumin. Chloride transport could be facilitated by CFTR activators, including curcumin and phosphodiesterase-5 inhibitors. Sodium and chloride transport could be further regulated to prevent accumulation of alveolar fluid by use of Na(+)/K(+)/2Cl(-) cotransporter type 1 inhibitors, which have been associated with improved outcome in adults ventilated for acute respiratory distress syndrome (ARDS) in randomized controlled trials. Primary prevention of coronavirus infection and TNF alpha release in response to it could be improved by induction of antimicrobial peptides LL-37 and human beta defensin-2 and reduction of TNF alpha production by vitamin D prophylaxis for the population as a whole.

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