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Fish Allergy
Published in Andreas L. Lopata, Food Allergy, 2017
Annette Kuehn, Karthik Arumugam
Fish allergy-like symptoms can occur as pharmacological reactions to histamine, a biogenic amine. These reactions have been described especially for members of the family Scombridae (e.g., mackerels, tunas, bonitos) (McLauchlin et al. 2006). Scombroid fishes have a naturally high content of the amino acid histidine while the normal concentration is below 0.1 mg/100 g of fresh muscle tissue (Rehbein and Oehlenschläger 2009). The US Food and Drug Administration (FDA) have considered a histamine content of more than 50 mg/100 g of fish toxic (http://www.fda.gov). Inadequate storage accompanied by bacterial contamination causes enzymatic decarboxylation of histidine to histamine (Attaran and Probst 2002). Binding of histamine to H1/H2-receptors in the cell membrane triggers the clinical manifestations of fish poisoning. Symptoms occur minutes to hours after ingestion, mostly as allergy-like reactions such as skin rash, nausea, abdominal pain and diarrhea. Histamine intolerance imitated a fish allergy (Thewes et al. 1999). Scombroid poisoning is a global health problem representing up to 40% of all seafood-related adverse reactions in the United States and Europe (Gould et al. 2013).
Scombrotoxin
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Histamine poisoning can occur in all individuals as a result of ingesting food containing high amounts of histamine. Histamine intolerance is caused by ingestion of food containing small amounts of histamine by individuals with a genetic predisposition, gastrointestinal disease, or medication with monoamine oxidase inhibitors (26). In humans, ingested histamine is metabolized in two different ways. It can be oxidatively deaminated by diamine oxidase (DAO) to imidazole acetaldehyde or imidazole acetic acid, or methylated by histamine methyl transferase (HMT) to form methyl histamine. In addition, histamine is converted to acetylhistamine in the intestine by bacterial enzymes (3). Histamine exerts its physiologic action in humans by binding to receptors belonging to a family of seven transmembrane G-protein coupled receptors. Four different histamine receptors exist: H1R, H2R, H3R, and H4R (27,28). In humans, histamine is naturally distributed throughout the body and is present in high concentration in the lungs, skin, and gastrointestinal tract. It acts as a neurotransmitter in the nervous system and as a local mediator in the gut, skin, and immune system. In SFP, when a high amount of histamine is ingested, activation of the H1 receptor results in an immediate allergic response, while activation of the H3 receptor modulates neurotransmitter release in the central nervous system, resulting in nausea, vomiting, and headaches (29). SFP can occur in healthy individuals, when at least 50 mg histamine is consumed in fish and fishery products. Considering an average serving size of 250 g, a level of 200 ppm in fish has been suggested (24). However, the illness cannot be replicated when histamine is ingested by itself.
Symptoms of mast cell activation syndrome in functional gastrointestinal disorders
Published in Scandinavian Journal of Gastroenterology, 2019
Clive H. Wilder-Smith, Asbjørn M. Drewes, Andrea Materna, Søren S. Olesen
Patients with functional gastrointestinal disorders (FGID), including irritable bowel syndrome (IBS) or functional dyspepsia (FD), have a wide range of gastrointestinal (GI) and extra-GI symptoms. Extra-GI symptoms are not included in the diagnostic Rome criteria for FGID and are generally attributed to separate functional or somatisation syndromes [1]. Recent mechanistic studies have shown increased numbers and activation of mast cells and abnormal release of biogenic amines and pro-inflammatory mediators in FGID, which may contribute to the commonly reported multi-organ symptoms [2–6]. Mast cell activation syndrome (MCAS) shares substantial similar symptoms with FGID, but there is little data regarding an overlap of the syndromes. MCAS is defined by ‘chronic, inappropriate, non-neoplastic mast cell activation resulting in multisystem inflammatory and allergic phenomena not fitting other defined allergic or inflammatory diseases’, distinguishing the condition from mastocytosis with pathologic clonal markers [7]. Currently proposed diagnostic criteria include a symptomatic response to histamine receptor blockers or mast cell-targeting agents and potential biochemical markers, besides typical symptoms [7,8]. MCAS shows considerable overlap with the ambiguous entity of histamine intolerance [9,10]. This large exploratory study investigated the prevalence of symptoms associated with MCAS in FGID.
Mast cell activation: beyond histamine and tryptase
Published in Expert Review of Clinical Immunology, 2023
Theoharis C. Theoharides, Adam I. Perlman, Assma Twahir, Duraisamy Kempuraj
Minimizing exposure to potential triggers (e.g. allergens, foods, heat, stress) is clearly important. If there allergy to food antigens [302,303] or histamine intolerance is present [304], supplementation with the main histamine metabolizing enzyme, diamine oxidase (DAO) [305] shortly before meals could be beneficial especially if its activity is low or there is the presence of gene polymorphisms. The initial treatment approach is the use of second-generation, H-1 antihistamines up to 4 times the recommended doses as tolerated [306–310]. Unique among these, is the histamine-1 receptor antagonist rupatadine, which was specifically developed to have potent anti-PAF activity [311]. Rupatadine is not available in the US although it has been available in Europe for over 20 years and in Canada since about 2000 (Canadian online pharmacies will send it with a US prescription). Rupatadine at 40 mg/day is well tolerated and inhibits histamine- and PAF-induced flares and ex vivo platelet aggregation in normal male subjects [312]. When compared to other second second-generation H-1 antihistamines in chronic urticaria, 20 mg/day of rupatadine showed the greatest efficacy in the treatment of CSU (71.6%) as compared to 20 mg/day of desloratadine (50%), and 20 mg/day of levocetirizine (21.7%) Notably, rupatadine also inhibited histamine and TNF release from human mast cells in response to PAF [256], and the release of histamine and IL-6 from human mast cells was stimulated by different triggers [313]. Rupatadine, unlike desloratadine and levocetirizine, also inhibited the PAF-induced release of histamine from human mast cells [314].
Cow milk protein allergy and other common food allergies and intolerances
Published in Paediatrics and International Child Health, 2019
Wiparat Manuyakorn, Pornthep Tanpowpong
There is a high histamine content in ripened or fermented foods such as aged cheese or yeast products [65,66]. It has been proposed that reduced diamine oxidase activity causes symptoms such as urticaria, flushing, rhinorrhoea and diarrhoea. Histamine intolerance has been described in children [67], but the true prevalence is unknown. An observational study in Austria reported 31 children (mean age 8 years) who presented with chronic abdominal pain, a history of ingesting histamine-rich foods and low serum diamine oxidase related to a presumed diagnosis of histamine intolerance, but it was later found that most of the children failed to show a positive response in DBPCFC. Patients with IBS also report gastrointestinal symptoms related to histamine-rich foods [42].