scholarly journals When the Red Tide Rolls In: A Red Tide Associated Angioedema Case Report

2021 ◽  
Vol 2 (5) ◽  
pp. 222-225
Author(s):  
Sarah Rabinowitz ◽  
Joshua Solano
Keyword(s):  
Case Report ◽  
Cell Activation ◽  
Red Tide ◽  
Mast Cell Activation ◽  
Red Tides ◽  
Respiratory Compromise ◽  
Laboratory Findings ◽  
Voice Changes ◽  
Low Concentrations ◽  
Life Threatening

Introduction: Histamine-mediated angioedema is a potentially life-threatening reaction following exposures that incite mast cell activation. In Florida, red tides are a frequent phenomenon caused by overgrowth of the harmful algae species Karenia brevis, which contain environmentally detrimental brevetoxins. Even in low concentrations, brevetoxins can cause disease in humans through inducing histamine release. We report the first documented case of angioedema associated with red tide exposure. Case Report: A 52-year-old-male presented with severe angioedema encompassing both lips within a few hours after exposure to red tide algae. Other symptoms included voice changes and difficulty swallowing. Laboratory findings revealed complement factors that were within reference range, which ruled out a bradykinin-mediated pathology and supported the diagnosis of histaminergic angioedema. Symptoms resolved after 24 hours in the intensive care unit under management with epinephrine, diphenhydramine, methylprednisolone, and famotidine. Conclusion: In coastal regions, red tide algae should be recognized as a rare cause of acute angioedema. Emergency management of histamine-mediated angioedema should focus on preventing respiratory compromise with frequent airway monitoring and treatment with steroids, antihistamines, and epinephrine.

scholarly journals Diagnosis, Classification and Management of Mast Cell Activation Syndromes (MCAS) in the Era of Personalized Medicine

2020 ◽  
Vol 21 (23) ◽  
pp. 9030
Author(s):  
Peter Valent ◽  
Cem Akin ◽  
Boguslaw Nedoszytko ◽  
Patrizia Bonadonna ◽  
Karin Hartmann ◽  
...  
Keyword(s):  
Mast Cell ◽  
Personalized Medicine ◽  
Cell Activation ◽  
Combined Treatment ◽  
Allergic Inflammation ◽  
Mast Cell Activation ◽  
Detailed Knowledge ◽  
Inflammatory Reactions ◽  
Targeting Therapy ◽  
Life Threatening

Mast cell activation (MCA) is seen in a variety of clinical contexts and pathologies, including IgE-dependent allergic inflammation, other immunologic and inflammatory reactions, primary mast cell (MC) disorders, and hereditary alpha tryptasemia (HAT). MCA-related symptoms range from mild to severe to life-threatening. The severity of MCA-related symptoms depends on a number of factors, including genetic predisposition, the number and releasability of MCs, organs affected, and the type and consequences of comorbid conditions. In severe systemic reactions, MCA is demonstrable by a substantial increase of basal serum tryptase levels above the individual’s baseline. When, in addition, the symptoms are recurrent, involve more than one organ system, and are responsive to therapy with MC-stabilizing or mediator-targeting drugs, the consensus criteria for the diagnosis of MCA syndrome (MCAS) are met. Based on the etiology of MCA, patients can further be classified as having i) primary MCAS where KIT-mutated, clonal, MCs are detected; ii) secondary MCAS where an underlying IgE-dependent allergy or other reactive MCA-triggering pathology is found; or iii) idiopathic MCAS, where neither a triggering reactive state nor KIT-mutated MCs are identified. Most severe MCA events occur in combined forms of MCAS, where KIT-mutated MCs, IgE-dependent allergies and sometimes HAT are detected. These patients may suffer from life-threatening anaphylaxis and are candidates for combined treatment with various types of drugs, including IgE-blocking antibodies, anti-mediator-type drugs and MC-targeting therapy. In conclusion, detailed knowledge about the etiology, underlying pathologies and co-morbidities is important to establish the diagnosis and develop an optimal management plan for MCAS, following the principles of personalized medicine.

scholarly journals Rhabdomyolysis and influenza a (H3N2) infection: A case report

2017 ◽  
Vol 70 (5-6) ◽  
pp. 173-175
Author(s):  
Anja Stojsin ◽  
Vedrana Petric ◽  
Grozdana Canak ◽  
Vesna Turkulov ◽  
Sinisa Sevic ◽  
...  
Keyword(s):  
Case Report ◽  
General Condition ◽  
Influenza A ◽  
Polymerase Chain Reaction Analysis ◽  
Reference Ranges ◽  
Laboratory Findings ◽  
Progressive Muscle Weakness ◽  
Good General Condition ◽  
Life Threatening ◽  
Acute Polyneuropathy

Introduction. Extrapulmonary complications of influenza infections are often unrecognized. The aim of this paper is to point to rhabdomyolysis as a potentially life threatening complication of influenza. Case Report. A month after the onset of influenza complicated by bronchopneumonia, the general condition of a nineteen year old female deteriorated with development of progressive muscle weakness and dark-colored urine. Despite intensive hydration and antibiotic therapy, her condition got worse, laboratory findings showed pancytopenia, hypoalbuminemia and creatine phosphokinase about 1000 times higher than normal. Influenza A H3N2 was confirmed by polymerase chain reaction analysis of the throat swab sample. Electromyoneurography showed severe acute polyneuropathy of muscles innervated by perineal nerve and signs of polymyositis; pathohistological examination of gastrocnemius muscle biopsy sample confirmed chronic myositis with necrotic neurogenic atrophy. In spite of intense hydration, the patient?s status continued deteriorating, so methylprednisolone was administered. Six weeks later, the patient was discharged in a good general condition, with blood test results within reference ranges, with weakness of foot dorsiflexors and tilting of the pelvis to the left during verticalization. Conclusion. Rhabdomyolysis caused by influenza-A is on the increase, and given the degree of morbidity and mortality, thorough assessment of patients is necessary.

scholarly journals Case Report: Treatment of systemic mastocytosis with sunitinib

F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 2182 ◽  
Author(s):  
Gerhard J. Molderings ◽  
Lawrence B. Afrin ◽  
Hans-Jörg Hertfelder ◽  
Stefan Brettner
Keyword(s):  
Mast Cell ◽  
Case Report ◽  
Cell Activation ◽  
Kinase Inhibitors ◽  
Systemic Mastocytosis ◽  
Mast Cell Activation ◽  
Oral Allergy Syndrome ◽  
Inhibition Of Proliferation ◽  
Imatinib Resistant ◽  
Activation Syndrome

Mast cell activation disease typically presents as chronic multisystem polymorbidity of generally inflammatory ± allergic theme.  Presently, treatment of the rare, cytoproliferative variant systemic mastocytosis employs empirically selected therapies to impede mast cell mediator production and action and, when necessary, inhibition of proliferation. Some tyrosine kinase inhibitors (TKIs) have been used successfully in uncommon cases of systemic mastocytosis not bearing that disease’s usual imatinib-resistant KITD816V mutation. Recently, sunitinib, a multi-targeted TKI, had been successful in a case of systemic mast cell activation syndrome. In addition, most allergy is principally a mast cell activation phenomenon, and sunitinib has been shown helpful in controlling a murine model of oral allergy syndrome. Here, we present the first use of sunitinib in systemic mastocytosis.

Mast Cell Activation Syndrome Mimicking Breast Cancer: Case Report With Pathophysiologic Considerations

2018 ◽  
Vol 18 (3) ◽  
pp. e271-e276 ◽  
Author(s):  
Gerhard J. Molderings ◽  
Ruth Knüchel-Clarke ◽  
Hans-Jörg Hertfelder ◽  
Christiane Kuhl
Keyword(s):  
Breast Cancer ◽  
Mast Cell ◽  
Case Report ◽  
Cell Activation ◽  
Breast Cancer Case ◽  
Mast Cell Activation ◽  
Cancer Case ◽  
Mast Cell Activation Syndrome ◽  
Activation Syndrome

scholarly journals Mast cell activation disorder masquerading as a nervous breakdown

2017 ◽  
Vol 4 (3) ◽  
pp. 51
Author(s):  
Anh P. Nguyen ◽  
Suzanne S. Teuber
Keyword(s):  
Mast Cell ◽  
Cell Activation ◽  
Mast Cell Activation ◽  
Health Clinic ◽  
Emotional Lability ◽  
Allergy Clinic ◽  
Gastrointestinal Discomfort ◽  
Life Threatening ◽  
Nervous Breakdown ◽  
Severe Anxiety

While mast cells have been implicated in human disease since the early 1900s, mast cell activation syndrome (MCAS) was only recently discovered and recognized as a disorder caused by aberrant release of mast cell mediator enzymes. These mediators trigger a wide variety of symptoms ranging from headache, pruritis and gastrointestinal discomfort to life-threatening anaphylaxis. MCAS is frequently unrecognized and misdiagnosed because symptoms associated with MCAS are often present in other medical conditions and are highly variable among patients. We describe a case of a 62-year-old male who presented to the emergency department (ED) with three days of recurrent flushing, diarrhea, mild edema of his hands bilaterally, and severe emotional lability with recurrent crying. In the ED, he was misdiagnosed with severe anxiety and directly sent to a mental health clinic for assistance. However, he was previously seen in allergy clinic for suspected MCAS. Fortuitously standing labs including plasma histamine, tryptase, and urine studies that were ordered in allergy clinic were drawn concurrently with the initial ED workup. He was found to have elevated histamine level during his ED episode and treatment for MCAS was initiated. In subsequent visits, his symptoms, except for episodes of “brain fog” and emotional lability, improved significantly on a combination of antihistamines, oral cromolyn sodium, and montelukast. Additionally every other day prednisone has substantially cleared the neurocognitive symptoms. This case highlights the difficulty of MCAS diagnosis and the importance of assessing for MCAS, especially in patients who have multisystem complaints.

scholarly journals Tuning IgE: IgE-Associating Molecules and Their Effects on IgE-Dependent Mast Cell Reactions

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1697
Author(s):  
Tomoaki Ando ◽  
Jiro Kitaura
Keyword(s):  
Mast Cell ◽  
Cell Activation ◽  
Immunoglobulin E ◽  
Allergic Diseases ◽  
Mast Cell Activation ◽  
Effector Cells ◽  
Recent Emergence ◽  
Life Threatening ◽  
Mechanistic Basis ◽  
High Affinity Ige Receptor

The recent emergence of anti-immunoglobulin E (IgE) drugs and their candidates for humans has endorsed the significance of IgE-dependent pathways in allergic disorders. IgE is distributed locally in the tissues or systemically to confer a sensory mechanism in a domain of adaptive immunity to the otherwise innate type of effector cells, namely, mast cells and basophils. Bound on the high-affinity IgE receptor FcεRI, IgE enables fast memory responses against revisiting threats of venoms, parasites, and bacteria. However, the dysregulation of IgE-dependent reactions leads to potentially life-threatening allergic diseases, such as asthma and anaphylaxis. Therefore, reactivity of the IgE sensor is fine-tuned by various IgE-associating molecules. In this review, we discuss the mechanistic basis for how IgE-dependent mast cell activation is regulated by the IgE-associating molecules, including the newly developed therapeutic candidates.

scholarly journals Pathogenic Mechanisms of Vaccine-Induced Immune Thrombotic Thrombocytopenia in People Receiving Anti-COVID-19 Adenoviral-Based Vaccines: A Proposal

2021 ◽  
Vol 12 ◽  
Author(s):  
Bruno Azzarone ◽  
Irene Veneziani ◽  
Lorenzo Moretta ◽  
Enrico Maggi
Keyword(s):  
Mast Cells ◽  
Platelet Activation ◽  
Cell Activation ◽  
Blood Stream ◽  
Extracellular Dna ◽  
Spike Protein ◽  
Mast Cell Activation ◽  
Pathophysiological Mechanism ◽  
Heparin Complexes ◽  
Life Threatening

VITT is a rare, life-threatening syndrome characterized by thrombotic symptoms in combination with thrombocytopenia, which may occur in individuals receiving the first administration of adenoviral non replicating vectors (AVV) anti Covid19 vaccines. Vaccine-induced immune thrombotic thrombocytopenia (VITT) is characterized by high levels of serum IgG that bind PF4/polyanion complexes, thus triggering platelet activation. Therefore, identification of the fine pathophysiological mechanism by which vaccine components trigger platelet activation is mandatory. Herein, we propose a multistep mechanism involving both the AVV and the neo-synthetized Spike protein. The former can: i) spread rapidly into blood stream, ii), promote the early production of high levels of IL-6, iii) interact with erythrocytes, platelets, mast cells and endothelia, iv) favor the presence of extracellular DNA at the site of injection, v) activate platelets and mast cells to release PF4 and heparin. Moreover, AVV infection of mast cells may trigger aberrant inflammatory and immune responses in people affected by the mast cell activation syndrome (MCAS). The pre-existence of natural antibodies binding PF4/heparin complexes may amplify platelet activation and thrombotic events. Finally, neosynthesized Covid 19 Spike protein interacting with its ACE2 receptor on endothelia, platelets and leucocyte may trigger further thrombotic events unleashing the WITT syndrome.

scholarly journals Hypotension, Syncope, and Fever in Systemic Mastocytosis without Skin Infiltration and Rapid Response to Corticosteroid and Cyclosporin: A Case Report

2010 ◽  
Vol 2010 ◽  
pp. 1-4 ◽  
Author(s):  
Didem Ozdemir ◽  
Selcuk Dagdelen ◽  
Tomris Erbas ◽  
Kemal Agbaht ◽  
Songul Serefhanoglu ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mast Cell ◽  
Case Report ◽  
Cell Activation ◽  
Systemic Mastocytosis ◽  
Mast Cell Activation ◽  
Organ Systems ◽  
Abnormal Accumulation ◽  
Skin Infiltration ◽  
Principles Of Treatment

Mast cell disorders are defined by an abnormal accumulation of tissue mast cells in one or more organ systems. In systemic mastocytosis, at least one extracutaneous organ is involved by definition. Although, systemic mastocytosis usually represents with skin lesion called urticaria pigmentosa, in a small proportion, there is extracutaneous involvement without skin infiltration. Other manifestations are flushing, tachycardia, dyspepsia, diarrhea, hypotension, syncope, and rarely fever. Various medications have been used but there is not a definite cure for systemic mastocytosis. The principles of treatment include control of symptoms with measures aimed to decrease mast cell activation. We describe a case of systemic mastocytosis presenting with hypotension, syncope attacks, fever, and local flushing. In bone marrow biopsy, increased mast cell infiltration was demonstrated. She had no skin infiltration. A good clinicopathological response was obtained acutely with combination therapy of glucocorticoid and cyclosporine.

Sign in / Sign up

Export Citation Format

Share Document