GI tract allergy is a type of FA. However, the symptoms of vomiting, bloody stool, and diarrhea are caused by IgE-independent mechanisms. Cow’s milk was the most prevalent cause.

Many affected patients will naturally outgrow this disease.

The onset of this type of FA is most commonly observed in infants and is preceded by AD. Avoidance of the causative food generally leads to improvements in skin symptoms [19]. Additionally, FA symptoms tend to decrease naturally with age [16–18, 20]. Hen’s egg, cow’s milk, and soybean are the main causative agents of FA-related AD in Japan [1, 2]. Comorbid FA and AD occur at a high frequency. Generally, AD is considered the first step in the “allergic march” [1–3] and is followed by asthma, allergic rhinitis (AR), and FA in approximately 50% of cases. Furthermore, up to 80% of children with AD will reportedly develop AR or asthma later in childhood [1, 2, 16, 20].

Tupker et al. suggested [21] that inhalation of house dust mites (i.e., respiratory route) could induce dermatitis episodes in patients with AD. The authors concluded that a causal relationship might link bronchial and skin reactions.

We have experienced the same situation in clinical practice.

Pollen-food syndrome (PFS) is a type I IgE-dependent FA that is generally localized to the oral mucosal membrane. The main causative agent is fresh vegetables or fruit. Patients with PFS often have complicating pollinosis; accordingly, PFS is also called pollen-associated syndrome [36, 37].

Patients with birch pollinosis in Hokkaido manifest a type I FA reaction after eating fruits from the rose family, which exhibit cross-reactivity with birch pollen antigen. Mild oral symptoms are common, although life-threatening anaphylaxis may occur, especially during the pollination season. Approximately one third of patients with PFS have concomitant AD. Therefore, asymptomatic individuals with AD may experience an exacerbation of AD even after eating cooked antigens [38, 39]. In Japan, rose family fruits are the most common cause of PFS [40].

FDEIA is induced in response to a combination of intake of a particular food and exercise; either alone will not induce anaphylaxis. IgE-mediated anaphylactic symptoms are induced within 2 h after eating the causative food and performing exercise. FDEIA is not common; it occurs in some adolescent and young adult patients in response to exercise and the intake of mainly wheat flour and shellfish, or occasionally fruit. More intense exercise and/or a larger quantity of causative food correlate with more severe symptoms [41–44]. Moreover, the use of nonsteroidal anti-inflammatory drugs (NSAIDs) exacerbates the severity of anaphylaxis [45, 46]. In Japan, many researchers have reported on FDEIA but not FDEIA-related AD [47]. Measurement-specific IgE antibodies to ω − 5 gliadin are useful for the diagnosis of wheat-dependent exercise-induced anaphylaxis [48, 49].

In Japan, the presence of hydrolyzed wheat protein in facial soap and consequent induction of wheat allergy responses, including wheat-dependent exercise-induced anaphylaxis (WDEIA), has become a social issue. People who used the affected soaps experience wheat anaphylaxis caused by transdermal or transmucosal sensitization to the hydrolyzed wheat proteins. Some reports suggest that surfactants might aggravate skin permeability. This case suggested that we should understand the risk of skin sensitization to non-dietary food antigens [50–54]. Oatmeal for skin product for AD has occurred anaphylaxis accidentally, too [55].

Approximately 30–50% of patients with latex allergy will exhibit concomitant type I FA symptoms after the intake of fresh and/or processed fruits with cross-reactivity to latex, such as chestnuts, bananas, and kiwifruit. Anaphylaxis, asthma attack, urticaria, and oral allergy syndrome may be induced. This allergic reaction is known as LFS. Medical workers with individual atopic reactions, patients with spina bifida who undergo recurrent procedures involving latex, and workers who use latex gloves occupationally are at a high risk of LFS [56–58]. Although patients with AD are considered high-risk, a recent report suggests that these patients are less likely to be sensitized to latex and consequently develop LFS [59]. On the other hand, a case report described a patient with AD and concomitant FDEIA who quickly became sensitized to latex and developed a delayed-type latex allergy [60]. Medical advice regarding the use of latex leads to improved AD symptoms in affected patients. Generally, AD patients could potentially develop various allergic symptoms. LFS is a frequent type of FA and an important risk factor for occupational allergy [61].

Some patients with “bakery asthma” develop secondary WDEIA and/or wheat flour FA, similar to workers who develop an occupational latex allergy. Workers with atopic factors are at a high risk of developing allergic disease following sensitization to even low concentrations of occupational food antigens [62]. In particular, AD may cause patients to change their occupation [63]. We must understand the social and individual burdens of AD and consider the quality of life related to health.