Clinical and Translational Allergy最新文献

To the Editor

Cashew nut allergy (CNA) is increasing worldwide and is responsible for severe anaphylaxis, particularly in young children.¹ Symptoms range from mild reactions to severe anaphylaxis. The three main allergens are storage proteins: Ana o 1, Ana o 2 (cupin superfamily) and Ana o 3 (prolamin superfamily).² Lifetime avoidance of cashew nut is currently recommended for those with CNA. However, little is known about the natural history of CNA.

We report a cohort of five children with severe anaphylaxis to cashew nut who recovered and were able to eat cashew nut after a successful oral food challenge (Table 1). They all presented severe anaphylaxis according to the ordinal food allergy severity score (oFAAS-5)³ (grade 3 to grade 5) at diagnosis at a mean age of 3 years [1.5–4]. Two patients had no atopy, one had a personal and familial atopic history and two others had only personal atopy. They all had no allergies or sensitizations to peanuts or tree nuts. Three patients consumed native cashew (between one and three cashew units) during the first reaction and two patients consumed cashew in cooked meals (unknown quantity). Allergology explorations were performed a mean 1.1 years [0.15–5] after the first reaction. All patients were sensitized to pistachio, but only two had a confirmed food allergy to pistachio. Skin prick tests (SPTs) were performed with commercial extract (ALK-Abello) and were deemed positive when wheal size was ≥ 3 mm. Cashew SPTs were positive for four children (mean 6 mm, range [3–20]). Cashew-specific IgEs (ImmunoCap® by Phadia 1000 System, Thermo Fisher Scientific) were positive for all patients, with a mean of 1 KU/L [0.36–2.49]. The recombinant Ana o 3 was not tested for at diagnosis for three patients and was positive for two of them (0.63 and 1.97 KU/L). After the reaction, they all observed strict avoidance of cashew and pistachio in their diet, without any recurrence. During a mean follow-up of 2.4 years (range [1–4]), the SPT and the cashew-specific IgEs became negative (Figure 1) and all patients tested negative for recombinant Ana o 3. An oral food challenge in four patients was successful at a cashew nut cumulated dose of 7800 mg. One patient refused the challenge, but after a successful pistachio challenge, he ate one cashew unit at home without any reaction.

We reported the cases of five children who presented severe anaphylaxis to cashew nut and who spontaneously recovered after a mean follow-up of 2.4 years [1–4]. As for peanut, ingestion of cashew is associated with a high rate of severe anaphylactic reactions,⁴ but in our cohort it seemed not to be correlated with persistence of the allergy. Oral immunotherapy (OIT) may help develop tolerance to cashew, as reported by Elizur et al.⁵ in a cohort of 50 children aged >4 years, who presented severe clinical reactio

Cow's milk protein allergy (CMPA) significantly decreases the quality of life of infants and their families, necessitating effective management. Avoidance of cow's milk protein (CMP) has been the primary approach, awaiting the development of a natural tolerance.¹

Oral immunotherapy (OIT) for CMPA gradually increases the use of pure CMP, such as milk, to enhance tolerance. A previous study demonstrated the efficacy and safety of early OIT (E-OIT) for infants with CMPA.² The Milk Ladder (ML) method modifies the OIT strategy and enhances CMP tolerance through stepwise exposure to milk-containing foods.^{1, 3-5} Despite growing adoption, ML lacks extensive validation and requires further research.⁴ To the best of our knowledge, there have been no comparative studies of E-OIT and ML in infants with CMPA. This study aimed to compare the efficacy and safety of ML and E-OIT in infants with CMPA.

We retrospectively analyzed infants younger than 2 years who started intervention for CMPA at the Department of Allergy at Kanagawa Children's Medical Center from April 2016 to March 2022, with a treatment protocol shift in April 2018 from E-OIT to ML. Inclusion criteria included a CMPA diagnosis based on parent-reported immediate allergic reaction to CMP ingestion or a serum milk-specific IgE level greater than 5 kU_A/L.³ Patients with only gastrointestinal symptoms were excluded due to different CMPA types. The ML protocol started with baked milk (BM), advancing toward less processed forms, while E-OIT began with controlled doses of milk or yogurt. For detailed protocols, see the Supplementary materials in Supporting Information S1.

CMP tolerance was defined as the ability to consume 100 mL of milk or an equivalent amount of approximately 3300 mg of CMP daily without experiencing symptoms. Low dairy tolerance for processed foods was defined as the ability to consume processed foods. Products high in dairy ingredients, such as cheese, yogurt, and pizza were excluded. These were confirmed through repeated intake at home. All patients underwent treatment review and assessment through interviews approximately every 3 months to assess progress and adjust care, as necessary.

This study conformed to the guidelines established by the Declaration of Helsinki and was approved by the Kanagawa Children's Medical Center Research Ethics Committee (approval no. 2105-4). Informed consent was obtained from the parents of all patients.

The analyses were performed according to the intention-to-treat principle (ITT) 2 years post intervention. The Mann–Whitney U test was used to compare continuous variables, while the Chi-squared test or Fisher's exact test was used for categorical variables. To evaluate the progression of CMP tolerance over time, Kaplan–Meier analysis with a log-rank test was performed. Statistical s

To the Editor,

Mastocytosis is a heterogeneous group of diseases characterized by a numerical increase and accumulation of clonal mast cells in various organ systems. In systemic mastocytosis, the severity varies from indolent to aggressive mastocytosis, the latter being associated with a worse prognosis.¹ Although the lungs are known to be rich in mast cells, comorbid respiratory diseases have only been sporadically suggested as associated with SM in case reports.^2-4 To our knowledge, no data are available on chest CT scans in patients with SM.

The aim of our study is to determine clinical and biological characteristics associated with bronchial or pulmonary abnormalities on chest CT scans in patients with SM.

A retrospective observational study was carried out at Toulouse University Hospital Center from 2003 to 2022 using our mastocytosis registry. All patients with (1) a diagnosis of SM based on bone marrow biopsy according to criteria published elsewhere¹ and (2) a CT scan image available in their medical record were included. This study was conducted in accordance with French ethics requirements (RC31/17/0095) and the guidelines of the National Commission for Data Protection and Liberties (CNIL number: 2206723 v 0).

Chest CT scans were evaluated by two physicians blinded to the patients' clinical and functional details. The two observers easily established a consensus about the predominant chest CT scan pattern according to the definitions of the Fleischner Society.⁵

Continuous data were expressed as median and interquartile range and categorical data as number of patients and percentages. An increased risk of a predominant pattern on chest CT scan was assessed for aggressive versus indolent SM and serum tryptase ≥20 μg/L versus <20 μg/L. For this analysis, we used a multivariable logistic regression with a calculation of adjusted odds ratios (aORs) with a 95% confidence interval. aORs were adjusted on the following covariates: age, sex and smoking status. We were not able to determine aOR if the CT scan abnormality was absent in the control group.

A total of 103 patients with SM were included in the study (Table 1). Of them, 60.2% were females and the median age was 54 [40–60]. Mastocytosis was indolent in 70 (73%) patients, cKit mutation was found in 91 (85%) patients and median serum tryptase was 15 [30–51] µg/l. A predominant chest CT scan pattern was observed in 36 (35.0%) patients. The lung lesions were as follows: nodules (n = 11), emphysema (n = 9), bronchiectasis (n = 6), bronchial wall thickening (n = 6) and interstitial lung diseases (n = 4).

According to the multivariable analysis, an increased risk of emphysema was observed for aggressive mastocytosis compared to indolent mastocytosis (aOR 5.0 [95% CI: 1.1–27.6]) (Figure 1). An increased risk of bronchi