Sesame seed

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Code: f10
Latin name: Sesamum indicum
Source material: Unpolished seeds
Family: Pedaliaceae
Common names: Sesame seed, Sesame, Benne seed
Other species of Sesame include S. indicum, S. radiatum, S. schum, and S. thoron.

Allergen Exposure

Geographical distribution
The Pedaliaceae family contains 18 or more species, most of them indigenous to Africa and Asia. Sesamum indicum, originally from India, is now grown very widely: in India, the Middle East, the United States, Latin America, China, and elsewhere. It is a perennial herbaceous plant that grows up to 1 metre high. Its flowers are pink or light blue (1).

Sesame may be the first seasoning ever used. The Chinese burned Sesame oil for light and to make soot for their ink blocks. African slaves brought Sesame seeds to America. The Japanese use Sesame seed as a health food and lead the world in Sesame seed imports, followed by Europe and the US.

The fruit is a small capsule containing many seeds, which are black, white, yellow or red. They are used in food either unprocessed or after hulling. Sesame seeds are used crushed, for their oil, and as cakes (the solid residue left after processing of the oil). About 70% of the world's Sesame seed is processed into oil and meal.

Environment
The seed is available packaged in supermarkets and can be found in bulk in Middle Eastern markets and health food stores. Sesame seeds often feature in candies and baked goods, and are a common ingredient in savoury dishes of ethnic cuisines. A special process produces a clear white seed that is common on hamburger buns.

The seed can also be ground and used as flour, or as butter, known as "tahini". It can also be fermented into "tempeh", or ground into a powder and mixed with a sweetener to make “halva”. The seeds can also be sprouted and used in salads. Edible oil is obtained from the seed. It is used for cooking, in margarines, and so on.
Sesame seed is rich in unsaturated fatty acids, calcium, protein, and vitamins A, B and E.

Sesame has bactericidal activities, and it also acts as an antioxidant that can inhibit the production and absorption of cholesterol. It is believed to help prevent and/or combat cancer and heart disease and to have anti-diabetic, anti-ulcer and laxative properties. The lecithin in Sesame is a treatment for dermatitis and dry skin. Other uses include the treatment of blurred vision, dizziness, headaches, and nasal mucosa dryness. In addition, Sesame features in a huge variety of folk remedies, with purposes ranging from burn treatment to increasing milk production in nursing mothers.
 
Unexpected exposure
Sesame is used in the production of perfumes, cosmetics, toiletries (especially UV-barrier creams), lubricants, insecticides and fungicides. The oil is sometimes burned for lighting. Sesame oil is a solvent for intramuscular injections and has been used in plasters, liniments, ointments, capsules, and emulsions, and in the formulation of medicinal suspensions and ophthalmic preparations. Liniment that contains Sesame oil has been used in the treatment of eczema and leg ulcers (2).

Sesame oil is often a "hidden allergen" in food. For example, pastries containing Sesame that are not sold may be “recycled” and thereby become a hidden allergen (3). Sesame meal is a feed for poultry and livestock.
 

Allergens

A wide range of IgE-binding proteins of Sesame seed has been identified: 78, 52, 45, 34, 32, 29, 25, 20, 9, and 7 kDa proteins (4). The proteins of white, brown and black Sesame extracts have been shown to have major quantitative differences (e.g., white seeds have more protein than black seeds, 182 vs. 28 mg/g). The white extract contained 15 proteins of 12-79 kDa in size. Ten of the 15 proteins (12-57.5 kDa) bound to serum-specific IgE from Sesame seed-allergic individuals. The 12-13 kDa and 22-33 kDa proteins were thought to constitute the main allergens. Similar studies have reported that 2 proteins in this size range appear to be major allergens (5).

Similarly, in a study of the allergens of Sesame seed, serum of 12 Sesame-sensitised patients (7 with food allergy, 5 with food sensitisation) were utilised. Sesame protein extracts were prepared from black, white and brown Sesame seeds. Analysis showed similar protein patterns in the 3 extracts, and 19 protein bands were isolated. Two proteins, of 14 kDa and 25 kDa, were identified and shown to be the major allergens involved in Sesame IgE-dependent hypersensitivity, the 25 kDa band displaying several characteristics of a major allergen (6).

Insoluble 11S globulin and soluble 2S albumin, conventionally termed alpha-globulin and beta-globulin, are the 2 major storage proteins and constitute 60-70 and 15-25% of total Sesame proteins, respectively (7-9).

The following allergens have been characterised in Sesame seed:
  • Ses i 1, a 9 kDa protein, a 2S albumin (7,10-12).
  • Ses i 2, a 7 kDa protein, a 2S albumin (4,7,10).
  • Ses i 3, a 45 kDa, 7S vicilin-type globulin (4,10,13).
  • Ses i 4, a 17 kDa protein, an oleosin (10,14).
  • Ses i 5, a 15 kDa protein, an oleosin (10,14).
  • Ses i 6, a 11S globulin (7,10,15-16).
  • Ses i 7, a 11S globulin (7-8,10,15).
  • Ses i Profilin (17).

Ses i 1, a major protein and a 2S albumin, has been shown to be thermo-stable up to 90°C and also highly resistant to digestion. After 2 hours of gastric digestion, the allergen remained completely intact, and only the small subunit was cloven during 2 hours of subsequent duodenal digestion, leaving a major IgE epitope region of this protein intact (12). Ses i 1 has been shown to be a potent allergen. Researchers have questioned whether the 9 kDa protein corresponds to a 2S albumin or a lipid transfer protein (18).

The 45 kDa protein, Ses i 3, a 7S vicilin-type globulin, a seed storage protein, binds to allergen-specific IgE in 75% of sera of Sesame-allergic patients. Ses i 2, a 7 kDa protein, is a 2S albumin, another seed storage protein of Sesame (4).

In some cases of severe allergy to Sesame seed, skin and serum tests do not produce any evidence of IgE reactivity. A study was done of the serum of 10 patients out of 32 who had displayed severe immediate symptoms and whose Sesame allergy was diagnosed by double-blind placebo-controlled food challenge or convincing clinical history, and in whom no specific skin reactivity or serum IgE antibodies could be detected. In reducing conditions, 2 protein bands (15-17 kDa) could be separated from 2S albumin proteins and shown to be oleosins, which are present in oil body fractions. These proteins were recognised by IgE from all 10 patients' sera. The authors suggest that oleosins are major allergens of Sesame seed and may in particular be relevant to severe anaphylaxis. Falsely negative prick tests could be due to the lack of oleosins in presently available extracts, or to the epitopes being buried in the inner molecule. The oleosins were named Ses i 4 and Ses i 5 (14).

The 11S globulins, Ses i 6 and Ses i 7, have only 36% identity. In 24 patients with Sesame seed allergy, 13 showed strong IgE binding to recombinant Ses i 6, whereas 10 of the patients show clear binding to recombinant Ses i 7 (15).

Sesame seed has recently been shown to contain a lipid transfer protein. This protein appears to be most abundantly expressed in developing seeds but is also detected in flower tissues. The abundant LTPs in developing Sesame seed are involved in lipid transfer into the extracellular matrix (19). The allergenic potential of this LTP was not evaluated.

Potential cross-reactivity

Cross-reactivity between allergens in Sesame and allergens in other foods, including Hazel nut, Rye, Kiwi, Poppy seed, Black walnut, Cashew, Macadamia, Pistachio, and Peanuts, has been reported (2,20-21). One author attributed these cross-reactions to 2 broad causes: the first being multiple allergens, Sesame proteins or glycoproteins, present in Sesame seed and linked mainly to immediate hypersensitivity reactions mediated by IgE antibodies; and the second being lignin-like molecules in Sesame oil (sesamol, sesamin, and sesamolin, which are all reported to be unsaponifiable fractions of Sesame oil) (2).

Allergy to Kiwi, Poppy seeds, and/or Sesame seeds has been reported to often occur in patients with a simultaneous sensitisation to nuts and flour. These cross-reactions were verified by RAST inhibition studies reporting that the degree of cross-reactivity among Kiwi, Sesame seeds, Poppy seeds, Hazel nuts, and Rye was found to be very high in the patients studied. The existence of both cross-reacting and unique components was seen, but the authors reported that the cross-reacting and unique components could be different for different patients (20).

A study described 3 patients with severe immediate-type allergic reactions to Poppy seed, all of whom showed serologic positivity to Sesame seed. The authors suggested that this may have been due to cross-reactivity to similar allergens (22). The clinical relevance was not investigated further.

A known IgE-binding epitope of the Peanut allergen Ara h 1 has been shown to have an 80% homology with the corresponding area of the Ses i 3 allergen of Sesame seed. (But the amino acids concerned had been previously shown not to be critical for IgE binding in Ara h 1 of Peanut) (4). Furthermore, tree nut and Sesame allergy have been reported to occur more often in patients with Peanut allergy. Although this may be a coincidence, simply due to a predisposition to food allergy in these individuals, cross-reactivity has been demonstrated between Peanut and Sesame seed. A study described 3 patients, previously sensitised to but now tolerant of Peanut, who were diagnosed as having either tree nut or Sesame allergy. The study concluded that demonstration of tolerance to Peanut may give false assurance that patients no longer need to avoid tree nuts or Sesame; on the contrary, tree nut and Sesame allergy can exist or develop in patients despite the development of tolerance to Peanut (23).

The 19 kDa protein of Buckwheat has weak homology with the vicilin-like allergen of Cashew (Ana o 1), English walnut (Jug r 2) and 7 S globulin from Sesamum indicum (24).

The clinical relevance of Sesame profilin and its cross-reactivity have not been investigated (17).

Clinical Experience

IgE-mediated reactions
Sesame seed has become a significant and common inducer of food allergy symptoms in sensitised individuals; earlier reports of this allergy were quite infrequent (2,25-27). The prevalence of Sesame seed hypersensitivity is increasing due to the increasing popularity of vegetarian dishes, to Sesame's use in international fast-food and bakery products, and to the spread of Middle Eastern and Asian cuisines. Sesame seed is regarded as an “emerging” food allergen (9,28-33).

In an evaluation of the results of 4.5 million allergen-specific IgE antibody tests performed on Japanese individuals, Apple was found to have the highest number of positive tests, followed by Sesame seed (34). Similarly, Sesame was reported to be a major cause of IgE-mediated food allergy in Israel, and second only to Cow's milk as a cause of anaphylaxis. In 9,070 children, the food allergy prevalence was found to be 1.7%, with Sesame the third most common food causing sensitisation (0.18%), following Hen's egg (0.5%) and Cow's milk (0.3%), and exceeding Peanut sensitisation (0.04%). Sesame was second only to Cow's milk as a cause of anaphylaxis (35). In a French study, the prevalence of Sesame seed allergy was reported to be 2.14% in children and 5.81% in adults (36). A prevalence study of immediate hypersensitivity to foods among Australian children found that Sesame was in fourth place (0.42%), following Hen's egg (3.2%), Milk (2%), and Peanut (1.9%). Sensitivity to Sesame was more common than sensitivity to any single tree nut studied (32). In the report of a government research project in the United Kingdom in 1996, the estimated overall prevalence of severe allergic reactions to Sesame in the general population was 1 in 2,000 (0.05%) (37).

An early report describes 2 individuals who experienced severe allergic reactions with pruritus, generalised erythema, angioedema of the uvula, clinical shock and wheezing. The author suggested that Sesame seed should be considered an extremely potent allergen (38). Since then, numerous types of allergic reaction have been reported, including nausea, vomiting, diarrhoea, angioedema, angioedema of the tongue, burning of the mouth and lips, itching of the pharynx, symptoms of Oral Allergy Syndrome, wheezing, respiratory distress asthma, contact dermatitis and urticaria.

In a study of 14 children recruited from 3 allergy clinics in France, all of whom had a diagnosis of Sesame seed allergy based on a convincing clinical history and positive SPT or allergen-specific IgE, the median age for the onset of Sesame seed allergy was found to be 5 years (the range being from 5 months to 16 years). All patients reacted immediately after Sesame seed consumption, and they presented the following as a first manifestation: oedema (9 cases, 48%), and urticaria (5 cases, 27%), and 1 case of each of the following symptoms: vomiting, rhinitis, conjunctivitis, asthma and anaphylactic shock. One patient had recurrent anaphylactic shocks, and another an anaphylactic shock after a further Sesame seed exposure; these 2 patients were asthmatic. SPT with a commercial Sesame seed extract was less sensitive than with the native seed. The median of Sesame seed-specific IgE was 5.58 kUA/l (range 0.35 to 100 kUA/l). Three patients outgrew their food allergy. The authors reported that a spontaneous outgrowing of Sesame seed allergy can occur, but that predictive criteria could not be established (39).

In an Israeli study of 32 children with Sesame seed allergy, 3 subgroups were identified. Group I (n = 23) manifested IgE-mediated Sesame allergy. The mean age of the first allergic reaction was 11.7 months. The main clinical manifestation was urticaria/angioedema in 14 (60%), but anaphylaxis was the presenting symptom in 7 (30%) patients; all of these were younger than 1 year. Sixteen (70%) were found to be allergic to other foods, and other atopic diseases were identified in 18 (78%). Three patients "outgrew" their allergy within 1-2 years. In Group II (n = 2), Sesame allergy was ruled out based on the lack of positive SPT and a negative open oral challenge. Group III (n = 7) consisted of patients who were found to have skin reactivity for Sesame as part of a screening for other food allergies (40).

A study evaluating Ses i 6 and Ses i 7 described 24 patients with Sesame seed allergy. Clinical reactions involved the skin in 19 patients, and these reactions were mainly urticaria and angioedema; reactions involved the gastrointestinal tract in 11 patients, and the respiratory system in 6 patients. One patient had a decrease in blood pressure. Twelve patients had more than one organ system involved. Sesame seed-specific IgE levels ranged from 0.73 to greater than 100 kUA/l (15).

Severe food-induced anaphylaxis has also been reported by many authors (6,10,41-43). Anaphylaxis to Sesame in a vegetable burger has been described (1,44). Sesame seeds were responsible for 3% of life-threatening allergic reactions to foods in France in 2002 (45). In Israel, Sesame was second only to Cow's milk as a cause of anaphylaxis (35,41). This may result from the high levels of exposure to Sesame in the Israeli diet, but although the use of Sesame in food is common in India, no published reports exist of Sesame allergy from this country (2). In a British study of Sesame allergy, 17% of respondents claimed to have suffered potentially life-threatening allergic symptoms, with 65% of severe reactions happening on first known exposure (46). A 6-year-old child who developed an anaphylactic reaction after eating bread and Sesame paste has been described (47). Significantly, not all Sesame-allergic individuals will have IgE antibodies directed at Sesame seed (9).

Sesame seeds are often present in gluten-free foods in therapeutic diets of coeliac patients; an instance of anaphylaxis in a coeliac patient following Sesame ingestion has been reported (48-49). Sesame seed can be regarded as a "hidden" allergen. Significantly, cases of severe allergy to Sesame seed may lack corroboration through SPT and IgE antibody determinations. The reasons for this are unknown. In a study of 32 patients who had displayed immediate symptoms such as anaphylactic shock, asthma, urticaria, and angioedema, Sesame allergy was diagnosed by double-blind placebo-controlled food challenge or a convincing clinical history. Ten patients had negative SPT and in vitro tests for Sesame. The authors were able to demonstrate that the allergens involved were oleosins (named Ses i 4 and Ses i 5), which appear to be major allergens of Sesame seeds and may be relevant to severe anaphylaxis (14).

Anaphylaxis has been described both to Sesame seed and Sesame oil (50-51). A study reports on 9 cases of IgE-dependent allergy to Sesame seed and/or Sesame seed oil. Commercial SPT were not very sensitive, whereas the sensitivity of SPT with a freshly prepared Sesame seed flour extract was greater. The diagnosis of this allergy was established by double-blind oral provocation tests, with doses of Sesame seed flour ranging from 100 mg to 10 g. Allergy to Sesame seed oil was also demonstrated in some of these cases (52). A previous report described generalised urticaria as a result of Sesame seed, but this could not be confirmed using SPT or allergen-specific IgE; instead, oral challenges confirmed it (53).

Immediate hypersensitivity reactions to Sesame in cosmetics have been reported (54).

An anaphylactic reaction to Cashew nut occurred in a non-atopic 60-year-old man 25 days after receiving a liver allograft from a 15-year-old atopic boy who died of anaphylaxis after Peanut ingestion. The liver recipient had no history of nut allergy. Post-transplantation skin prick test results were positive for Peanut, Cashew nut, and Sesame seed, and the donor had allergen-specific IgE antibodies to the same 3 allergens. This illustrates that transfer of IgE-mediated hypersensitivity can occur after liver transplantation and have serious consequences (55).

Occupational exposure to Sesame seed can occur though animal husbandry, bakery, mill and other work. Occupational asthma, rhinitis and urticaria due to Sesame seed contact have been reported (56-58). Systemic urticaria, facial erythema, dizziness and loss of consciousness were reported in a 36-year-old baker following exposure to Sesame. Commercial SPT and IgE antibody tests were negative, but SPT to crushed Sesame seeds in sodium chloride solution was detected (3).

 

Other reactions
Non-IgE-mediated reactions have been reported. A 45-year-old woman experienced facial erythema, flushing, generalised pruritus, and conjunctivitis after she had eaten crackers. Similar symptoms occurred several times after ingestion of Sesame oil in various preparations. Within minutes after ingestion of Sesame-dressed chicken, she had flushing, generalised itching, nausea, vomiting, and dizziness. Skin tests, including intra-cutaneous testing, were negative for common allergens. Skin testing using prick and scratch methods with native Sesame oil (cold-pressed and heat-extracted) and raw, peeled, crushed, and unpeeled Sesame seeds was negative. No IgE antibodies for Sesame seed or for common allergens was detected. In an oral challenge, 10 minutes after 2 bites of bread masking 10 g crushed Sesame seed and 10 g Sesame oil, the patient developed generalised flushing, itching, and conjunctival symptoms. Serum tryptase remained normal but urinary histamine increased (59).

If the extraction process for Sesame oil is not of a high standard, Sesame protein may be present in the oil, which can result in allergic reactions, including anaphylaxis, in sensitised individuals (60-62). Sesame seed oil may be used in cosmetics and pharmaceuticals, resulting in contact dermatitis, as described in 13 patients. The contact allergens sesamol, sesamin and sesamolin were identified in crude and purified (pharmaceutical) Sesame oil. Patch tests showed 8 of 13 patients to be positive to sesamol and 12 to sesamolin and sesamin (63). Cheilitis due to Sesame oil in a lipstick has been reported in a female patient. She reacted to sesamolin and sesamin, but not to sesamol. In this instance, sesamolin and sesamin were detected in the Sesame seed oil, but sesamol was not (52). Contact sensitivity to an ointment composed of 60% Sesame oil, used for the treatment of a burn on the forearm, has also been described. Contact dermatitis developed 10 days after application (64).

Salmonella outbreaks have been reported as a result of contaminated Sesame seed products, including halvah and tahini. An international outbreak of multiresistant Salmonella typhimurium that was correlated to the consumption of halvah resulted in an investigation of Sesame seed products. Out of 117 ready-to-eat food items containing Sesame, salmonella was isolated from 11 (9.4%). The products included Sesame paste (tahini) and Sesame seed sold for raw consumption in cereals (65). Similarly, in a report of 3 outbreaks of Salmonella montevideo infection in Australia and New Zealand, imported tahini was identified as the source of infection. Of a total of 66 cases of S. montevideo infections, 54 (82%) reportedly involved consumption of Sesame seed-based foods (66).

Compiled by Dr Harris Steinman, harris@zingsolutions.com

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As in all diagnostic testing, the diagnosis is made by the physican based on both test results and the patient history.