Anti-TNF alpha-induced immune-mediated skin adverse reactions resolved by switching to ustekinumab

2019 ◽  
Vol 73 (6) ◽  
pp. 496-500 ◽  
Author(s):  
Karolína Vorčáková ◽  
Marta Horáková ◽  
Juraj Péč
Keyword(s):  
Adverse Reactions ◽  
Tnf Alpha ◽  
Immune Mediated

scholarly journals T cell mediated hypersensitivity to previously tolerated iodinated contrast media precipitated by introduction of atezolizumab

2021 ◽  
Vol 9 (5) ◽  
pp. e002521
Author(s):  
Sean Hammond ◽  
Anna Olsson-Brown ◽  
Joshua Gardner ◽  
Paul Thomson ◽  
Serat-E Ali ◽  
...  
Keyword(s):  
Contrast Media ◽  
Adverse Reactions ◽  
Stevens Johnson Syndrome ◽  
Iodinated Contrast ◽  
Immune Mediated ◽  
Johnson Syndrome ◽  
Healthy Donors ◽  
Concomitant Medications

Many adverse reactions associated with immune checkpoint inhibitor (ICI) treatments are immunologically driven and may necessitate discontinuation of the ICI. Herein, we present a patient who had been administered the radio contrast media amidotrizoate multiple times without issue but who then developed a Stevens-Johnson syndrome reaction after coadministration of atezolizumab. Causality was confirmed by a positive re-challenge with amidotrizoate and laboratory investigations that implicated T cells. Importantly, the introduction of atezolizumab appears to have altered the immunologic response to amidotrizoate in terms of the tolerance–elicitation continuum. Proof of concept studies demonstrated enhancement of recall responses to a surrogate antigen panel following in-vitro (healthy donors) and in-vivo (ICI patients) administrations of ICIs. Our findings highlight the importance of considering all concomitant medications in patients on ICIs who develop immune-mediated adverse reactions. In the event of some immune-related adverse reactions, it may be critical to identify the culprit antigen-forming entity that the ICIs have altered the perception of rather than simply attribute causality to the ICI itself in order to optimize both patient safety and treatment of malignancies.

Hypoallergenic Infant Formulas

PEDIATRICS ◽  
1989 ◽  
Vol 83 (6) ◽  
pp. 1068-1069
Author(s):  
Keyword(s):  
Adverse Reactions ◽  
Villous Atrophy ◽  
Young Infant ◽  
Specific Antigen ◽  
Double Blind ◽  
Parental History ◽  
Pulmonary Hemosiderosis ◽  
Immune Mediated ◽  
Dietary Antigens

Antigenic constituents of human milk or of alternative feedings for infants may be responsible for adverse reactions in a subset of infants with milk protein intolerance. These reactions include those commonly associated with atopy, such as angioedema, urticaria, wheezing, vomiting, and eczema. Pulmonary hemosiderosis, malabsorption with villous atrophy, and eosinophilic enterocolitis, perhaps mediated by immune complexes or T cells, have also been associated with the ingestion of cow's milk proteins and/or soy proteins in infant feedings. Colic, sleeplessness, and irritability are symptoms seen in almost all infants at some time during infancy, including those few infants with immune-mediated reactions to dietary antigens. Determining that adverse reactions are, in fact, immune mediated is often difficult and is accomplished by an in vivo challenge with the potential offending antigen, together with in vitro confirmation of immunoreactivity to the challenge antigen. Double-blind challenge with purified dietary antigens is useful in relating symptoms to a specific antigen, but the results may be difficult to interpret if the appearance of symptoms is delayed beyond several hours in a young infant. In vitro testing is compromised by the presence of some form of immunoreactivity, such as hemagglutinating antibodies, to dietary antigens in a large percentage of infants without symptoms and by lack of standardization of clinical tests for cell-mediated reactions to dietary antigens. Much effort also has been devoted to predicting in which infants immune-mediated reactions to dietary proteins will develop in advance of their introduction into the diet. Increased cord blood IgE concentrations and parental history of atopy place an infant at highest risk for atopic disease during infancy and early childhood.

Serious hepatitis B vaccine adverse reactions, are they immune-mediated?

Vaccine ◽  
1993 ◽  
Vol 11 (13) ◽  
pp. 1358-1359 ◽  
Author(s):  
Yehuda Carmeli ◽  
Tali De-Medina
Keyword(s):  
Hepatitis B ◽  
Adverse Reactions ◽  
Hepatitis B Vaccine ◽  
Immune Mediated

scholarly journals Release of endogenous chondroitin sulfate and heparin as consequence of dysregulated proteolysis in COVID-19

2021 ◽  
Author(s):  
Marco Ruggiero
Keyword(s):  
Adverse Effect ◽  
Platelet Aggregation ◽  
Chondroitin Sulfate ◽  
Plasma Proteins ◽  
Adverse Reactions ◽  
Proteolytic Enzymes ◽  
Protective Role ◽  
Platelet Factor ◽  
Sequential Release ◽  
Immune Mediated

Abstract Infection by severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2), the pathogen responsible for COVID-19, is associated with immune-mediated responses that lead to dysregulated activation of proteolytic enzymes; these contribute to damage to the endothelium, thrombosis, hypercoagulability, and other hematologic complications that include thrombotic thrombocytopenia, a complication of severe COVID-19 as well as a potentially fatal adverse effect of COVID-19 vaccination. Here, it is demonstrated that proteolysis of plasma proteins leads to sequential release of endogenous glycosaminoglycans (GAGs), first chondroitin sulfate (CS), followed by heparin (HP). The extension and degree of what is called "proteolytic storm" determines whether only one endogenous type of GAGs (CS), or both (CS and HP), are released. Sulfated GAGs such as CS and HP exert a protective role against SARS-CoV-2 infection. However, sustained and excessive release of endogenous HP may be responsible for thrombotic thrombocytopenia just as it happens in HP-induced thrombocytopenia (HIT) a well-known side effect of HP administration that results in thromboembolisms in atypical sites, thrombocytopenia, and synthesis of autoantibodies directed against platelet factor 4 (PF4) that contribute to platelet aggregation. It is concluded that release of endogenous HP as consequence of dysregulated proteolysis occurring during COVID-19 or COVID-19 vaccination may play a fundamental role in the pathophysiology of the disease as well as in adverse reactions to vaccination.

Abstract 17062: Reversible Golimumab Induced Cardiomyopathy - First Reported Case Report

Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Mian Tanveer Ud Din ◽  
Michael Nestasie ◽  
John Balacko ◽  
Craig Alpert
Keyword(s):  
Lower Extremity ◽  
Troponin T ◽  
Inflammatory Diseases ◽  
Systolic Function ◽  
Left Ventricular ◽  
Tnf Alpha ◽  
Lower Extremity Edema ◽  
Ventricular Systolic Function ◽  
Immune Mediated ◽  
Biventricular Systolic Function

Case Presentation: An 80 year old female with medical history of hypertension, diabetes mellitus, chronic atrial fibrillation presented with four weeks of lower extremity edema and dyspnea. Notably, she had also been taking Golimumab for 6 months for Rheumatoid Arthritis (RA). Vital signs on presentations were: Temp:99 F, HR: 140bpm, BP: 105/64, oxygen saturation of 88% on room air. Physical exam revealed crackles at the mid lower lung fields bilaterally and 2+ lower extremity edema. EKG showed new ST inversions in lead 1, avF and V2. Troponin T was elevated to 0.11 ng/ml and proBNP was 21,246 pg/ml. Chest X Ray showed cardiomegaly with diffuse alveolar opacities. Transthoracic echocardiogram (TTE) revealed severely reduced left ventricular systolic function with LVEF of 25-29%, left ventricular regional wall hypokinesis and mildly reduced right ventricular systolic function. All findings were new compared to her last TTE 3 months prior, which showed preserved biventricular systolic function. Coronary angiography revealed no coronary artery disease. The patient was started on intravenous furosemide, and her home beta blocker and ARB were resumed. The patient’s Golimumab was discontinued given prior reports of TNF alpha inhibitor induced cardiomyopathy. Over the ensuing days, she was aggressively diuresed with improvement in oxygenation and ultimately discharged home. Three months after discontinuation of Golimumab, repeat TTE showed normalization of biventricular systolic function. Discussion: TNF alpha inhibitors have revolutionized the treatment of chronic immune mediated inflammatory diseases. Several TNF alpha inhibitors have been associated with cardiomyopathy, however there remains a paucity of evidence regarding cardiotoxicity with Golimumab. We now present, to our knowledge, the first reported case of reversible heart failure due to Golimumab in an 80 year old woman with RA. Golimumab, like other TNF alpha inhibitors, represents a historic advancement in the treatment of immune mediated inflammatory diseases. However, our case implicates this innovative drug in cardiotoxicity similar to other TNF alpha inhibitors. Further prospective studies are needed to establish a stronger correlation between Golimumab and cardiotoxicity.

Increased risk of late‐onset, immune‐mediated, adverse reactions related to dermal fillers in patients bearing HLA‐B *08 and DRB1 *03 haplotypes

2020 ◽  
Author(s):  
Tom S. Decates ◽  
Peter J. Velthuis ◽  
Leonie W. Schelke ◽  
Neubury Lardy ◽  
Eduard Palou ◽  
...  
Keyword(s):  
Adverse Reactions ◽  
Late Onset ◽  
Dermal Fillers ◽  
Immune Mediated ◽  
Increased Risk

scholarly journals Challenge of immune-mediated adverse reactions in the emergency department

2019 ◽  
Vol 36 (6) ◽  
pp. 369-377 ◽  
Author(s):  
Gregory A Daniels ◽  
Angela D Guerrera ◽  
Donna Katz ◽  
Jayne Viets-Upchurch
Keyword(s):  
Immune System ◽  
Immune Checkpoint ◽  
Immune Checkpoint Inhibitors ◽  
Adverse Reactions ◽  
Checkpoint Inhibitors ◽  
Immune Checkpoints ◽  
High Dose ◽  
Clear Understanding ◽  
Immune Mediated ◽  
Multiple Drugs

Multiple drugs of a new class of cancer treatments called immune checkpoint inhibitors, which work by enabling the immune system to attack tumour cells, have been approved for a variety of indications in recent years. Immune checkpoints, such as cytotoxic T-lymphocyte antigen-4 and programmed death-1, are part of the normal immune system and regulate immune activation. Treatment with inhibitors of these checkpoints can significantly improve response rates, progression-free survival and overall survival of patients with cancer; it can also result in adverse reactions that present similarly to other conditions. These immune-mediated adverse reactions (IMARs) are most commonly gastrointestinal, respiratory, endocrine or dermatologic. Although patients’ presentations may appear similar to other types of cancer therapy, the underlying causes, and consequently their management, may differ. Prompt recognition is critical because, with appropriate management, most IMARs resolve and patients can continue receiving immune checkpoint inhibitor treatment. Rarely, these IMARs may be life-threatening and escape detection from the usual evaluations in the emergency environment. Given the unusual spectrum and mechanism of IMARs arising from immune checkpoint inhibitors, emergency departmentED staff require a clear understanding of the evaluation of IMARs to enable them to appropriately assess and treat these patients. Treatment of IMARs, most often with high-dose steroids, differs from chemotherapy-related adverse events and when possible should be coordinated with the treating oncologist. This review summarises the ED presentation and management of IMARs arising from immune checkpoint inhibitors and includes recommendations for tools and resources for ED healthcare professionals.

scholarly journals Pathological findings in central nervous system demyelination associated with infliximab

2019 ◽  
Vol 26 (9) ◽  
pp. 1124-1129 ◽  
Author(s):  
Alicja Kalinowska-Lyszczarz ◽  
Mahboobeh Fereidan-Esfahani ◽  
Yong Guo ◽  
Claudia F Lucchinetti ◽  
W Oliver Tobin
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Tnf Alpha ◽  
Infliximab Treatment ◽  
Necrosis Factor Alpha ◽  
Immune Mediated ◽  
Central Nervous System Demyelination ◽  
Factor Alpha ◽  
Cns Demyelination ◽  
Necrosis Factor

Background: Tumor necrosis factor alpha (TNF-alpha) inhibitors, such as infliximab, are commonly used to treat rheumatoid arthritis (RA) and other immune-mediated disorders. Objective: To determine whether infliximab-associated central nervous system (CNS) demyelination can be differentiated from multiple sclerosis (MS). Methods: We present a case of pathologically proven CNS demyelination in a patient treated with infliximab and describe clinical–radiographic–neuropathological findings. Putative mechanisms of TNF-alpha inhibitor-associated CNS demyelination are described. Results and conclusion: Infliximab treatment is associated with CNS inflammatory demyelinating activity, which is histopathologically indistinguishable from MS.

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