Adult-onset mast cell activation syndrome following scombroid poisoning: a case report and review of the literature

Abstract

Background Mast cells are closely associated with epithelium, serving as sentinels responsible for the recognition of tissue injury and coordination of the initial inflammatory response. Upon detection of the injured cell content, mast cells then tailor the release of preformed and newly produced chemical mediators to the detected challenge, via an array of pathogen receptors. In addition to immunoglobulin E receptor-triggered mast cell activation, commonly referred to as allergic or atopic disorders, non-immunoglobulin E receptor mediated mast cell activation follows engagement of toll-like receptors, immunoglobulin G receptors, and complement receptors. Upon containment of the extrinsic challenge, acute inflammation is downregulated, and repair of the injured tissue ensues. The mast cell compartments must return to a baseline steady state to remain tolerant towards self-antigens and harmless entities, including environmental conditions, to prevent unnecessary immune activation and chronic hypersensitivity disorders. Over the past 50 years, an increasing number of patients are experiencing episodes of aberrant mast cell activation, not associated with allergen-specific mast cell disease or systemic mastocytosis. This led to proposed diagnostic criteria of mast cell activation syndrome. Mast cell activation syndrome is a heterogeneous disorder, defined by a combination of (1) recurrent symptoms typical of mast cell activation, (2) an increase of validated mast cell derived mediators, and (3) response to treatment with mast cell stabilizing or mast cell mediator-targeted therapies. Onset of mast cell activation syndrome ostensibly reflects the loss of tolerance in the mast cell compartment to nonthreatening entities and nonhazardous environmental conditions. The etiology of chronic mast cell dysregulation and associated intolerance to self-antigens or harmless entities is not well understood, but a growing number of studies point to exposure of the epithelial borders, which leads to inappropriate or excessive mast cell activation or impaired resolution of acute inflammation following neutralization of the identified pathogen. Case presentation Here we present a case of adult onset mast cell activation syndrome following scombroid poisoning. Scombroid toxicity is usually a self-limited illness, but there are individuals who have been shown to have severe symptoms or persistent illness following histamine fish poisoning. We describe a 74-year-old Caucasian woman, with a history of drug-induced urticaria, who developed a constellation of hypersensitivity illnesses consistent with the diagnosis of mast cell activation syndrome after ingestion of tainted fish. Conclusion Mast cell activation disease causes problems of increased complexity in children and adults. The increased prevalence and severity of mast cell activation disease has been attributed to dramatic changes in our lifestyles and modern living environments. These changes likely impact the integrity of the epithelial barriers, leading to loss of tolerance in the mast cell compartment. Here, we present a case of a nonatopic, 74-year-old female who developed mast cell activation disease after exposure to a potent environmental toxin. Mast cell activation disease commonly involves several organ systems, with patients often referred to a succession of different specialists. This results in delayed diagnosis and suboptimal care. Instead, early recognition of mast cell activation disease would lead to better outcomes. We review the literature, describing the diagnostic criteria for mast cell activation disorders that can improve recognition of this multiorgan system syndrome. Further research is needed into the interaction of epithelial barrier disruption and the dysregulation of the immune system.

Mast Cell Activation Syndromes: Collegium Internationale Allergologicum Update 2022

“…MCA may occur in a number of different physiologic and pathologic conditions. Acute MCA is commonly seen in various allergic reactions, other hypersensitivity reactions (e.g., intolerance) and toxic reactions against exogenous elicitors, such as venoms [ 4 , 8 , 9 , 19 , 20 , 21 , 22 , 23 , 29 ]. The most common underlying condition is an overt IgE-dependent allergic disorder.…”

Development of Histamine in Fresh and Canned Tuna Steaks Stored under Different Experimental Temperature Conditions

“…In general, the onset of symptoms is rapid, ranging from immediate to 30 min after eating the implicated food [ 47 , 49 ]. However, in some cases, they can occur up to 60 min after food ingestion [ 50 , 51 ] or even up to 90 min after food ingestion [ 52 , 53 ]. Symptoms are generally fleeting and do not require treatment, resolving on their own within a few hours or at most within 24 h, but feelings of malaise may last for several days [ 45 , 47 ].…”

Scombroid Poisoning

“…The initial presentation of scombroid poisoning can mimic an IgE-mediated response with symptoms such as, hives, rash, nausea, facial swelling, diarrhea, and flushing, unlike an IgE-mediated response anxiety is less frequently observed (Brock, Eng, & Maitland, 2021). Typically, the symptoms of scombroid poisoning will present within 10 min to 1 hr following the consumption of toxic fish (Brock et al, 2021). Symptoms unique to scombroid poisoning following consumption of infected fish are peppery or metallic taste in the mouth, oral numbness, headache, dizziness, and possibly a rapid and weak pulse (Brock et al, 2021).…”

“…Fish allergy typically involves an IgE-mediated response, whereas scombroid is due to the release of histamine from the flesh of the fish (Feng et al, 2015; Gonzalez et al, 2021). The initial presentation of scombroid poisoning can mimic an IgE-mediated response with symptoms such as, hives, rash, nausea, facial swelling, diarrhea, and flushing, unlike an IgE-mediated response anxiety is less frequently observed (Brock, Eng, & Maitland, 2021). Typically, the symptoms of scombroid poisoning will present within 10 min to 1 hr following the consumption of toxic fish (Brock et al, 2021).…”

“…Typically, the symptoms of scombroid poisoning will present within 10 min to 1 hr following the consumption of toxic fish (Brock et al, 2021). Symptoms unique to scombroid poisoning following consumption of infected fish are peppery or metallic taste in the mouth, oral numbness, headache, dizziness, and possibly a rapid and weak pulse (Brock et al, 2021). Scombroid differs entirely from other fish-borne illnesses as it is entirely preventable with proper storage and preparation.…”