Case report Background: Buckwheat (Fagopyrum esculentum) is a member of the Polygona- ceae family, original from Central Asia. It is a popular traditional food in Asian countries (bread, pancakes, pasta, noodles) and common cause of food-induced anaphylaxis in Japan and Korea. Buckwheat is becoming increasingly popular in many western countries as a health and gluten-free food, but it is not included in the EU allergen labelling list. It is of concern the presence of buckwheat as an un- declared allergen in foods. Case report: We report the case of a 42 years-old female patient with rhinocon- junctivitis to grass pollen, who was referred for study of two systemic reactions with foods. The first one in 2011 appeared after the ingestion of a sesame and pasta salad at a Japanese restaurant and consisted on OAS, conjunctivitis, eme- sis and dyspnea. The second reaction in 2018 started immediately after the first bite of a crépe at a Thai restaurant and consisted on OAS, conjunctivitis, abdomi- nai pain and generalized urticaria. Both reactions needed emergency room treatment. She also referred OAS with the ingestion of hazelnut and gastric complains with peanut, almonds and sunflower seed. No other symptoms with foods were referred. Skin prick tests (SPT) were positive to walnut and hazelnut and negative to other tree nuts, cereals, mustard, soy, peanut, celery, tomato, lettuce and lentil. Tryptase 2.5 mg/l. Serum specific IgE (sIgE) was positive to hazelnut (1.78 kUa/I) and walnut (9.64 kUa/I). ImmunoCAP ISAC showed sIgE to Fel d 1 and to Fage 1 (2S albumin of buckwheat). Sesame SPT, sIgE to sesame and Ses i 1 and and open food challenge with sesame were negative. An SDS-PAGE IgE immunoblotting showed several IgE-binding bands detected in buckwheat between 16 and 55kDa, and between 11 and 35 kDa in hazelnut and walnut extracts. Cross reactivity between buckwheat, hazelnut and walnut was shown by Igé immunoblotting inhibition.Case report Keywords: Andean Maca; anaphylaxis; Brassicaceae; superfood. Background: The consumption of organic foods known as “superfoods” has been increasing in recent years. The Andean Maca (Lepidium meyenii) is an original plant of the Central Andes of Peru, belonging to the family of the Brassicaceae. Maca is considered a “superfood”, and its consumption is increasing in our area due to its high nutritional value, antioxidant action and presumed health benefits, supposedly increasing fertility and energy levels. Case report: We report the case of a 44 years-old female with rhinoconjunctivitis due to pollens (cypress, olive, plane tree and grasses) and rhinoconjunctivitis and asthma due to cat dander. In 2011 she presented 3 hours after the second intake of Andean Maca rhinoconjunctivitis, palpebral edema, bronchospasm, dysphagia and general discomfort. She tolerates other brassicaceae such as mustard, turnip, cabbage, brussel sprouts, cauliflower, broccoli and radish, and prick-prick tests were negative to all of them. Total IgE was 165 U/I, and tryptase determination was normal. ImmunoCAP ISAC was positive to Phl p 4, Cryj 1, Cup a 1, Ole e1, Pla a 1, Plaa 2, Feld 1 and nega- tive to all PR-10 proteins, profilins, nsLTPs and storage proteins (2S, 7S, 11S) present in the microarray. A PBS extract of Andean Maca at a concentration of 1 tg protein/ml tested in prick test yielded a positive result with a wheal of 5 mm. Negative SPT were found in 5 exposed and unexposed controls. The Andean Maca extract was resolved with sodium dodecyl sulfate polyacryla- mide gel electrophoresis (SDS-PAGE) and an IgE immunoblotting was performed. IgE-binding bands were detected at around 23, 38, 48,60 and 76 KDa. Conclusion: To the best of our knowledge this is the first case of allergy to An- dean Maca. Due to the increasing consumption of Maca, it can become an impor- tant allergen in the future.Case report Background: Drug reaction with eosinophilia and systemic symptoms (DRESS) is a severe drug reaction. Clinical presentation resembles infectious and rheumato- logic diseases making the diagnosis a challenge. Treatment strategies are based in immune suppression. We present a case of an adolescent with autoimmune encephalitis that developed DRESS syndrome whilst on high-dose corticosteroids (HCS) and intravenous immunoglobulin (IVIG). Case report: A 10 year-old male, ethnicity Han Chinese, was admitted with acute onset of altered mental status and seizures. Inicial empiric treatment included ceftriaxone, ciprofloxacin, acyclovir, benzodiazepines and sodium valproate. After the initial approach, he was diagnosed with an autoimmune encephalitis. Targeted-therapy included high-dose of metilprednisolone (1g/day-8 days) follo- wed by IVIG. Steroids were then tapered to 2 mg/Kg/day. He maintained clinical and EEG features compatible with a non-convulsive status epilepticus. Phenobarbital and phenytoin were introduced, parallel to rituximab and a new infusion of HCS. Three weeks later, he started with spiking fever, nonspecific rash in the knees, arthralgias, cervical adenophaties and sore throat. No relevant laboratory findings were found. A week later, it was observed a sudden facial edema, widespread skin eruption and mucositis. Laboratory findings revealed anemia, leukopenia, monocitosis, elevated levels of transaminases and gamma-GT. Probable diagno- sis of DRESS was made (RegiSCAR criteria-score 5). Phenytoin was discontinued and antihistaminic was started. The rash disappeared in a week and the blood changes began to normalize. Months later, He had a clinical relapse and the immune therapy included IVIG, cy- clophosphamide and HCS. Patch tests were not possible due to clinical instability and need of maintained immunosuppressive drugs. Instead Lymphocyte transformation test was perfor- med with phenobarbital and phenytoin. The result was negative. HLA typing using PCR-SSO revealed HiA allele groups: A*02, A*11, B*50 and B*51. Conclusion: The clinical history and the presence of HLA-B*51 favours phenytoinConclusion: The clinical history and the presence of HLA-B*51 favours phenytoin as the culprit drug. It remains unclear what effect the immunosuppressive drugs may have on in-vivo and in-vitro tests. The key treatment is withdrawal of the suspected drug, while the role of corticos- teroids and IVIg remains controversial in certain cases like this, since the patient developed DRESS syndrome whilst on corticosteroids and IVIG.Case report Cold urticaria (ColdU) is defined by the appearance of itchy wheals or angioedema, typically within minutes after contact cooling and rewarming of the skin. ColdU is usually considered benign and self-limiting. However, severe cases may include anaphylaxis. Causes of ColdU are currently unknown. Some infec- tious diseases have been associated with ColdU. The authors describe the case of a 47-year-old female that at the age of 43 began to experience episodes of itchy wheals developed within minutes after contact with cold air or water. On one episode, after swimming in the sea she had urticaria, dyspnea, dizziness, fatigue, and lipothymia. Assymptomatic sponta- neously within 1h after. She was referred to our consultation. She had asthma controlled with inhaled budesonide/fosmoterol; no family history of allergic, immunologic diseases and/or chronic urticaria. Diagnostic workup included: Full blood count; ESR; biochemistry; CRP; serum Igs; protein electrophoresis; complement; cryoglobulins; basal serum tryptase; thyroid hormones; antithyroid and other autoantibodies; serologies for Toxoplasma, Tre- ponema pallidum, Helicobacter pylori (Hp), EBV, HSV, HBV, HCV, HIV; skin prick tests (SPT) for aeroallergens; lung function test; chest x-ray; autologous serum skin test; ice cube test (ICT). Diagnostic workup revealed: Raised total IgE (949UI/ml); positive serology for Kp; SPT positive for grasses, mites, cat and dog; positive ICT with a stimulation time threshold (STT) of 1min [wheal diameter (WD)=38mmn]. An urea breath test (UBT) was positive. She began eradication therapy of Hp with triple therapy: Proton pump inhibitor, clarithromycin and amoxicillin, 14 days. She was advised to avoid exposure to cold air, liquids or objects, swimming in the sea and was medicated with Bilastine 20mg od, Montelukast 10mg od, and epine- phrine (0.3mg) autoinjector. Symptomatic control was obtained. Testing to prove eradication was performed using an UBT that was negative. ICT was repeated: positive with a STT of 1min but with a WD of 8mm which sug- aests an improvement in response. {~Diagnosis of ColdU relies on a thorough history and cold provocation testing. Laboratory workup must be performed to exclude any associated severe disease which requires a different approach. Patients need to be counseled to avoid a prolonged skin contact with cold. The first-line symptomatic treatment is a nonsedating H1 antihistamine and an epinephrine autoinjector should be prescribed for severe reactions.Case report Background: Wheeze is one of the main symptoms of asthma in addition to short- ness of breath, chest tightness and cough. However, wheeze is not specific to this disease and can be present in other lung conditions. Case Report: A 27-year-old woman with allergic rhinitis to house dust mites, tree pollen and grass pollen was observed in an emergency appointment in our Allergy Department complaining of productive cough, occasional wheezing and fever. She underwent a chest x-ray and it came out clean. Diagnosis of lower respiratory infection was made and she was treated with antibiotics, a mucolytic and once- daily inhaled fluticasone furoate/vilanterol 92/221g. Maintaining occasional wheezing, she was observed again in another emergency appointment after a month. A 5-day course of oral corticosteroids was prescribed and her usual inhaler therapy was changed to budesonide/formoterol 160/4.5 zg three times a day with partial improvement of the symptoms. Due to the lack of personal past pulmonary disease, she performed lung function tests and a computed tomography of the chest. The lung function tests revealed air trapping and the computed tomogra- phy demonstrated an endoluminal lesion of the left lower lobe bronchus (LLLB). The patient was subsequently referred to the Pneumology Department and the bronchoscopy performed identified a lesion from the left lower lobe with partial obstruction of the LLLB. A biopsy taken from the mass revealed bronchial carci- noid tumor. The patient underwent a left lower sleeve lobectomy. Currently, the patient has neither respiratory symptoms nor need for daily inhaled medication. Conclusion: With this case, we aim to highlight the importance of careful interpre- tation of wheezing. Bronchial carcinoid like other obstructive endobronchial le- sions may cause wheezing and should be recognized as early as possible so that patients can be optimally treated.Case report Background: Food allergy affects more than 200 million people worldwide with an increase in prevalence. Several edible seeds such as sunflower seed (Hellianthus annus) are introduced globally into diet with a consequent risk of hypersensitivity reactions (HSR), since urticaria to anaphylaxis. Although exposure is mainly by ingestion, inhalation and skin contact have also been implicated particularly in oc- cupational environments. As they are considered potential allergens they should appear on food labels. Sunflower is known to be cross-reactive with othes foods (cereals, seeds, nuts) and pollen (mugwort, wall pellitory) through albumin 2s or lipid transfer protein (LTP). Case report: Female, 50 years old, without previous food allergy. She went to the emergency department with generalized skin pruritus and facial edema (mainly in the lips), abdominal pain and vomit one hour after ingesting sunflower seeds for the first time, controlled with antihistaminic and corticosteroid drugs. During the investigation at the consultation she performed: skin prick tests (SPT) with com- mercial extract-positive for sunflower, grass and house dust mites; SPT with natu- ral foods-negative for other seeds; and specific IgE (ImmunoCAP ISAC®-Thermo- Fisher Scientific, Sweden)-positive for Phl p 1/4, Der p 1/2, Der f 1/2 and Lep d 2. She was advised to avoid sunflower seeds and other products related. Months la- ter she had episodes of edema and facial erythema in the mornings upon waking up and later she recognized that it was associated with a sunflower seed facial cream she applied at night. She had no complaints with other products. At the moment she avoids sunflower seeds and oil. Discussion: With the increasingly inclusion of edible seeds globally it is expected that this allergy will increase exponentially. A strong index of suspicion is required and a detailed clinical history together with SPT and oral provocation help perfor- ming the diagnosis, since sunflower seed HSR is not common. Cross-reactivity (CR) through LTP is expected mainly with mugwort pollen. The gold-standard treatment is the avoidance of this allergen and others with potential for CR which is not easy due to the easy food contamination. The patient also carries an adre- naline auto-injector. The most interesting in this case is that the patient doesn't have any CR with possible allergens described. Despite the few studies on sunflo-Background Phenylephrine is a sympathomimetic agent wich mainly produce effect on adre- nergic receptors. It is usually used to dilate the pupil and increase blood pressure. On the other hand, cyclopentolate hydrochloride is a muscarinic cholinergic anta- gonist that also induce mydriasis and cycloplegia. Both drugs are often used in Ophthalmology like eye drops. Cases of contact dermatitis, urticaria, pustulosis and even anaphylaxis have been describe after topical administration. Method A 67 years old woman with a history of bilateral cataracts that required phaquectomy. Presented itchy erythema that evolved to eyelid angioedema imme- diately after using phenylephrine and cyclopentolate hydrochloride eye drops prior to performing right eye phaquectomy. The symptoms disappeared 24 hours later, with any residual skin lesion. Two months later, an allergological study was car- tied out with patch testing, intraepidermal and intradermal tests. Seven months after the first reaction, the left eye phaquectomy was performed. And she was treated with phenylephrine, vancomycin, povidone iodine, and dexamethasone. Twenty four hours later, she presented itchy erythema affecting the ipsilateral eye- lid and malar region that evolved to papulodescamative rash. On this ocassion the cutaneous reaction lasted approximately 4 weeks despite the treatment with oral antihistamine and topical steroids. A second allergological study was performed with patch testing. Results During the first tests it was objectified a positive result for cyclopentolate hydro- chloride at the intradermal test (0.01mg/ml): 6mm, with a negative result for phenylephrine. Patch testing with both were negative. The other drugs involved and excipients were discarted. In the second study, a positive result for phenyle- phrine was obtained at the patch testing. Allergy to other medications involved was excluded. “zaResults During the first tests it was objectified a positive result for cyclopentolate hydro- chloride at the intradermal test (0.01mg/ml): 6mm, with a negative result for phenylephrine. Patch testing with both were negative. The other drugs involved and excipients were discarted. In the second study, a positive result for phenyle- phrine was obtained at the patch testing. Allergy to other medications involved was excluded. Conclusion We describe the first case of a patient with two distinct allergic clinical presenta- tions using eye drops, suggesting different immunological mechanisms: An eyelid angioedema due to cyclopentolate hydrochloride, which confirmed a type | allergy reaction, and an allergic contact dermatitis due to phenylephrine, that corrobora- ted a type IV allergy reaction. With this case we affirm that the same patient can present several types of reactions, reinforcing the importance of repeating the study whenever the patient needs it.Case report A 35-year-old female presented with severe chronic spontaneous urticaria (CSU) and angioedema for the last 10 months in 2019. The patient did not respond to any dosage of antihistamines but responded well to oral and injection corticosteroids. At the start, UCT test was 0 point and USA7 was 42 points. For the past 2 months, she was taking daily dexamethasone 8 mg/day. Laboratory investigation revealed highly positive IgG to thyroperoxidase (anti-TPO 230.7 (<60). All other analyses, including total IgE (16.2 KU/I), TSH (2.37), H. pylori (Negative), CRP (12 mg/l), ECR (22 mm/h), creatinine (0.76 mg/dl), urea (28mg/dl), total cho- lesterol (179mg/dl), were normal. We started by bilastine 20 mg 2 tabs. 2 times per day for 14 days. After 2 weeks UAS7 - 36. Thereafter, a dose of 16 mg methylprednisolone was added and a re- commendation for injecting omalizumab 300 mg was given. In June, 300 mg omalizumab was administered every two weeks, a total of 600 mg per month. 4 weeks after the last injection, UCT - 4, UAS7 - 36. After this cyclosporine (CsA) treatment was started at dose of 2 mg/kg/day (100 mg 2 time day), 1 month, then reduced to 1 mg/kg/day, after 1 month we gave 0.5 mg/kg/day for 1 month. Even 2 days after the start of CsA, the condition has been fully stabilized and currently remains in complete remission. The main indi- cators are UCT 16, UAS7 - 0. Discussion: This case evaluates the effectiveness and safety of CsA in the treat- ment of patients who fail to respond to omalizumab therapy and requiring long- term systemic steroid treatment. Our case shows that cyclosporine is better in the presence of an autoimmune component. Conclusion: A low dose of CsA is a good option for patients who suffer from es- pecially severe refractory CSU. In most cases, this therapy regimen is considered effective and safe. The result of our case makes obvious the necessity of perso- nalized management of CSU.Case report Background: Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome is an uncommon and not universally known disease. It is particularly difficult to recognize in the paediatric population. Materials and methods: Case report of a paediatric patient with suspected DRESS syndrome. Assessment of clinical manifestations, timing of onset of disease and diagnostic work-up. Results: We described a 12-year-old girl, hospitalized due to a pansinusitis com- plicated by extradural empyema which needed surgical drainage, posterior and anterior ethmoidectomy and bilateral myringotomy. She started treatment with endovenous ceftriaxone (100mg/kg/day 2 times per day) and vancomycin (70mg/kg/day 4 times per day). Previously to admission she had already under- gone 1 day of amoxicillin-clavulanic acid. Her postoperative period had no compli- cations and she was apyretic since day 4 of antibiotics. On the ninth day of anti- biotics there was a recrudescence of the fever (>38.5°C). The next day, a pruritic full-body and infiltrative maculopapular exanthema developed with discrete facial oedema. Analytical exams showed an eosinophil peak count of 840cells/pL (9.9%) 4 days after the start of exanthema and no other target organ damage. Lymphadenopathy was not found. Allergists were called, antibiotics were swit- ched and topical corticosteroids were started. Exanthema and facial oedema gra- dually resolved over a course of 7 days, with no need for systemic corticosteroids. Nine months after discharge she performed drug allergy diagnostic work-up at the Allergy and Clinical Immunology department. Intradermal skin tests were ne- gative to ceftriaxone, cefazolin and vancomycin, however, lymphocyte transforma- tion test results were 161.7 (stimulation index [Si]>2) to ceftriaxone, 118.3 SI to vancomycin, 3.0 SI to cefazolin and 4.1 S? to amoxicillin-clavulanic acid. Conclusion: Dress syndrome typically manifests 2-6 weeks after the beginning of the administration of the offending drug. However, recent studies have shown an earlier onset, particularly in children treated with antibiotics. In this case report we presented a paediatric patient with typical and atypical characteristics of DRESS, with a conflicting diagnostic work-up. The existence of an intermediary form ofvase repure Background: Gadolinium-based contrast agents (GBCAs) are the most commonly used contrast media in the performance of magnetic resonance imaging (MRI), a type of radiological imaging test increasingly used today for the diagnosis of dif- ferent medical conditions. Although GBCAs are considered safe and effective drugs, there are unwanted health effects with their use that need to be accounted for, such as hypersensiti- vity reactions. Materials and Methods: In this report we describe two patients who developed allergic reactions to GBCAs documented through positive skin test results: A 74-year-old woman, with no allergic history of interest and a medical history of Crohn's disease and gastroesophageal reflux disease. Two years ago, an MRI scan with GBCA was performed in another hospital to study the extension of her digestive pathology. The patient reports that it was the first time that the drug was administered, and after the test was carried out, she reported loss of consciousness, without other accompanying symptoms. Since then, the patient has been considered allergic to GBCAs and no other imaging tests have been performed to date. A 42-year-old male with no allergic history of interest. He was diagnosed HIV posi- tive in 2009. When detecting a brain injury a few months ago, an MRI (previously tolerated) was performed. Within minutes of administrating the drug, he develo- ped non-itching macular rash in his abdomen. He didn’t receive any treatment at the time and skin lesions disappeared in less than one hour. No other imaging studies have been performed since then. Results: Skin tests were conducted in both our patients within months to deter- mine whether or not they were allergic to the MRI contrast agents gadobutrol and gadoterate. In both patients we obtained negative prick tests. Nevertheless, our first patient had positive intradermal tests (IDT) to Gadobutrol (6x5mm) and our second patient had positive IDT to both GBCAs (7x7 mm each IDT). An intravenous provocation test with gadoterate was performed in our first pa- ‘tient with negative result and its use was authorized. Our second patient was diagnosed with hypersensitivity to GB( ~ and was recommended to avoid these contrast media agents.Case report Severe anaphylaxis induced by bee or wasp sting is a clinical event highly asso- ciated with the diagnosis of systemic mastocytosis, representing an important risk and prognostic factor. Mastocytosis is a heterogeneous group of rare disor- ders characterized by abnormal proliferation and tissue infiltration with activated mast cells, frequently associated with the characteristic gain- of-function c-KIT mutation D816V. Due to generally limited knowledge, confirmation of diagnosis of mastocytosis is generally delayed for years, mostly in cases without skin involvement. We report two cases of young adults who presented to allergist evaluation for re- current severe anaphylaxis after hymenoptera sting. The first case is a 31 years old female with mild form of urticaria pigmentosa since 2014, who had one epi- sode of severe anaphylaxis after bee sting in 2016, preceded by two extended lo- cal reactions in the past years. Allergist evaluation after 4 months revealed signifi¢ cantly increased serum tryptase and specific Ig-E for bee venom and negative c- KIT mutation. Venom immunotherapy was started but three other severe anaphy- laxis occurred during the initiation phase, therefore she remained on a low main- tenance dose, anti-mast cell activation therapy and close monitoring. The second case is a 38 years old man with no history of allergy and no skin lesions, who presented for allergist evaluation, after two episodes of anaphylaxis happened three and two years ago, both occurred after bee and wasp sting. Initial evaluation showed significantly increased serum tryptase, high specific Ig-E for bee and wasp venom and positive c-KIT mutation. We recommended initiation of venom specific immunotherapy, anti-mast cell activation therapy and close monitoring. The reported cases confirm that severe anaphylaxis induced by hymenoptera ve- nom is highly suggestive for mastocytosis diagnosis and should be investigated as soon as possible. We concluded that the awareness of mast cell disorders wi- thin medical staff is still limited despite possible severe outcome and the need for personalized and complex medical approach.Case report Background: The alpha-gal syndrome is IgE-dependent allergy to galactose-alpha- 1,3-galactose (alpha-gal) resulting in delayed anaphylaxis after consumption of ‘red meat. It was first described in the Southeastern United States and causally lin- ked to bites from ticks. Later on some cases have been also described in a few European countries. Here, we report a clinical case of a Polish patient with alpha- gal syndrome. To our knowledge, it is the first such case observed and confirmed in our country. Methods: We collected a detailed medical history supported by follow up observation. The patient underwent a routine allergological diagnostic work-up, including measurement of specific IgE to alpha-gal and panel of food allergens. Results: A 32-years old male patient reported having five anaphylactic reactions during the past 3 months. The typical reaction included abdominal pain and pruri- tic urticarial rush involving the torso, forearms and lower limbs. One episode led also to shortness of breath and throat tightness. Symptoms occurred 3-6 hours after ingestion of red meat (pork, beef and mutton) and 2-3 hours after meal with ‘ed meat and alcohol or after a meal followed by physical exercises. The patient had no symptoms after consumption of chicken. He acquired two tick bites (most probably from Ixodes ricinus). The first one took place two week before the onset of anaphylactic symptoms. Laboratory testing revealed significantly high level of IgE against alpha-gal (72.6 KAU/L). The reference range of IgE titers for this aller- gen was <0.35 kAU/L. Other food specific IgE levels were within the nosmal refe- sence ranges. The patient was prescribed an emergency treatment and was advi- sed to avoid mammalian meat and other products containing alpha-gal. No fur- ther episodes have been observed under this diet to date. Conclusions: This case aims to improve awareness of the alpha-gal syndrome and to highlight a possibility of its occurrence in new geographical areas. Due to the atypical delay in onset of symptoms many cases remain still undiagnosed or are recognized as idiopathic anaphylaxis, whereas potentially life-threatening complications claim for early diagnosis. —Case report Background: Cow’s milk allergy (CMA) is one of the most common food allergies in children. Management includes avoidance, substitutes or alternative drinks, and tolerance induction protocols. These are helpful for reintroducing milk in the diet of those who do not outgrow CMA. Case report: The case of an 8-year-old boy is described. Consent for the publica- tion of clinical data was obtained from the parents. He was referred to our allergy department when he was 3 years old with the diagnosis of CMA. Only trace amounts of milk were tolerated and he was drinking soy beverages. The diagnos- tic workup revealed a skin prick to prick test with raw milk of 15 mm, total IgE le- vels of 54.5 kU/L and specific IgE levels as follow: cow's milk 6.58; casein 2.36; lactalbumin 7.44; lactoglobulin 1.00. During the initial follow-up he had an episode of anaphylaxis after eating milk bread at home that was managed in the emer- gency department. Oral food challenges (OFC) with baked milk were negative and increasing amounts of baked milk were successfully introduced in the diet, inclu- ding the milk bread. An OFC with raw milk at age 5 was positive (127 mL) and with boiled milk at age 6 was also positive (40 mL). Oral immunotherapy with boi- led milk was undertaken at age 7. The starting dose was 5 ml. followed by a dose duplication every two weeks until the target dose of 200 mL was achieved. Since the past summer, raw milk has been progressively introduced with 5 mL incre- ments every few weeks without any reactions. He now tolerates a daily dose of 75 mL of raw milk and he is able to eat cheese and ice-cream. Conclusion: There are no established clinical guidelines for oral tolerance induc- tion in patients with CMA and the role of boiled milk is even less defined. We re- port a successful case of progression to raw milk after oral immunotherapy initia- ted with boiled milk in a child who previously only tolerated trace amounts of milk.Case report Background: Metronidazole is a nitroimidazole antibiotic commonly used for gas- trointestinal infections due to its antimicrobial activity for anaerobe bacterial in- fections and amebiasis. Hypersensitivity reactions (HR) to metronidazole are ra- rely reported being considering the drug provocation test the gold standard for es- tablishing the diagnosis. It seems that less than 2% of the patients with confirmed hypersensitivity reactions to drugs are allergic to metronidazole. We present the case of a child patient with suspected HR to metronidazole that was attendant in our Allergy Department. Patient: A 11-years-old female with medical background of ileocecal resection for necrotizing enterocolitis during the neonatal period and non-IgE mediated cow's milk allergy°. From the age of 9 she had suffered intermittent abdominal pain and disturbed bowel habit and was diagnosed of bacterial overgrowth syndrome. She started a therapeutic trial with rifaximin, but due to its lacked efficacy it was swit- ched to cycles of metronidazole (Flagyl®) 250 mg every 12 hours for 1 week every month. The first cycle was well tolerated, however, she referred that since the second cycle, during the sixth or seventh day, she presented itchy hives throu- ghout the body that lasted about 15 to 20 days. After three cycles she suspended this treatment and no new reactions were reported. Methods: SPT was carried out with metronidazole at a concentration of 2.5mg/ml, 1mg/ml for intradermal test and 30% (in petrolatum) for epicutaneous test (readings at 48 and 96 hours). We also performed an oral provocation test with metronidazole 250mg every 12 hours for 7 days. Results: SPT, ID, EPIT showed a negative result. Oral provocation showed a posi- tive result after 7 days. She presented generalized itching and a micropapular exanthema on thorax and back that improved after oral H1-antihistamines. She was diagnosed of delayed hypersensitivity reaction to metronidazole and it was prohibited. Treatment with rifaximin and cholectvramine racin wae etahlichad withCase report Introduction: Paracetamol is one of the most commonly used analgesic and anti- pyretic agents worldwide, attributable in part to its excellent safety profile when administered at recommended doses. The majority of paracetamol reactions are related to the pharmacological action of cyclooxygenase 1 inhibition. Selective IgE-mediated hypersensitivity reactions, are rare. Case Reports: The first case is a 30-yeas-old woman experienced 3 episodes of generalized urticaria 10 to 20 minutes after an oral administration of 1000 mg of paracetamol (Ben-u-ron /Antigrippine®). The patient had no reactions with acetyl- salicylic acid (AAS), ibuprofen or nimesulide. Skin prick tests (SPT) with injectable paracetamol solution (10 mg/ml) were positive. In the “in vitro” study, we highlight the positive basophil activation test (BAT), showing an activation of 24.61% anda stimulation index of 35, in a concentration of mg/mL of the paracetamol. A healthy control was also performed and are negative in this concentration thus excluding a false positive. The second case is a 26-year-old female, who had her first episode of generalized urticaria after oral intake of 1000mg of paracetamol (Doliprane®), and second episode characterized by generalized urticaria and eye- lid angioedema 10 minutes after oral administration of of 500 mg of paracetamol (Ben-u-ron®). She also suffered a third episode of palmar and plantar itching, ur- ticarial and conjunctivitis that started within 10 minutes of oral administration of paracetamol and caffeine (Ben-u-ron Caff®). After this episode, she tolerated ibuprofen, metamizole and AAS. We performed SPT and intradermal tests with injectable paracetamol solution (10mg/ml), with positivity in the intradermal test at the concentration of 1/100 (0.1 mg/dL). BAT was performed in the following concentrations: 1.25, 1.0, 0.5 and 0.31 mg/ml of paracetamol, with an activation of 18.41, 18.36, 13.40, 8.50% and a stimulation index of 17.2, 17.16, 12.5, 7.94, respectively. Conclusion: Paracetamol allergy is not common. Clinical presentation of these reactions may not differ from those associated with cyclooxygenase 1 inhibition, being relevant to differentiate the two mechanisms. Patients with IgE-mediated paracetamol allergy will be able to tolerate the remaining non-steroidal anti-in- flammatory drugs. The authors describe two cases in which the mechanism ofCase report Background: In patients with chronic urticaria, the use of non-steroidal anti-in- flammatory drugs (NSAIDs) can be an aggravating factor in approximately 10-30% of cases. The therapeutic measure is avoidance. The indication for desensitiza- tion is controversial due to poor experience. There is only one case reported about the use of Omalizumab as a therapeutic aid in these cases. Methodology and results: We present the case of a 52-year-old male patient with a history of bilateral nephrolithiasis, chronic hepatitis B and secondary Cushing's syndrome. He was admitted to the emergency department due to acute myocar- dial infarction (AMI) with indication of using dual antiplatelet therapy (Aspirin plus Clopidogrel). The patient reported that 20 years ago he was treated with aspirin due to pharyn- gitis and then developed an outbreak of generalized urticaria. Since then, he pre- sents episodes of urticaria daily, without clear trigger or cofactors. He has been treated with oral antihistamines and corticosteroids for 10-15 years with poor control and developing secondary Cushing syndrome. Six years ago, after taking ibuprofen, he presented generalized urticaria, so he currently avoids all NSAIDs. At the time of the assessment during hospitalization for AMI, the patient presen- ted with generalized urticaria that was treated with methylprednisolone to control the outbreak. Among the complementary tests performed, the only positive fin- dings were sensitization to Anisakis and the presence of Dientamoeba fragilis in the stool exam that was treated with Paramomycin. The oral aspirin challenge test was positive, and then all NSAIDs were avoided. Since the indication for dual antiplatelet therapy persisted, we decided to start treatment with Omalizumab 300 mg every 4 weeks, obtaining remission of urticaria; subsequently we performed a new oral aspirin challenge test (cumulative dose of 175 mg) that was tolerated, continuing with a dose of 100 mg daily. The patient is currently being treated with Omalizumab 300 mg every 4 weeks be- cause the attempts of its withdrawal elicited the urticaria.Case report Background: Chronic spontaneous urticaria (CSU) is often associated with au- toimmune disorders, including autoimmune thyroiditis (AIT). 2nd generation H1- antihistamines are the main therapy of CSU in children. However, even updosing of H1-antihistamines in some cases don't lead to disease control. In case of se- vere CSU, resistant to standard therapy, adding of anti-IgE (omalizumab) is indicated. But there are not enough studies about the use of omalizumab in the- rapy of CSU with AIT in pediatrics. Report: A 17 y. 10 m. old girl appealed to the department with complaints of wheals and pruritus, urticaria activity score over 7 days (UAS7) was 25. Girl's heredity was not burdened by allergy; she didn't suffer from any atopic diseases. At the age of 11 the girl was diagnosed with AIT and hypothyroidism, her treatment was levothyroxine irregularly. The first urticaria symptoms occurred at the age of 16 after acute respiratory infection. Symptoms reduced after prolon- ged betamethazone IM injection, but have returned after 7 days. The girl was trea- ted with cetirizine in the standard dose, then with levocetirizine in an increased up to 3 times dose and montelucast for 3 months without an effect. Then methyl- prednisolone 8 mg daily was added to therapy for 2.5 months. The control was achieved, but after the drug cancelation the exacerbation was noted. Then cyclo- sporine therapy 200 mg daily was added, the attempts of dose reducing leaded to sever exacerbations. During the examination in the department increased levels of IgG anti-TG 581,4 1U/ml, anti-TPO 370 IU/ml, TSH 37 mIU/I and reduced level of T4 8,03 pmole/I were revealed; total IgE (10 kIU/ml) - at normal level, sigE (ImmunoCAP) were not detected. On the next step omalizumab 300 mg SC monthly was started, the cyclosporine 200 mg daily was continued, levocetirizine was changed to ebastin 40 mg/day, le- vothyroxine dosage was corrected. After the second injection of omalizumab the significant improvement was noted. After 3 months from the beginning of therapy UAS7 reduced to 0, cyclosporine was canceled. After 6 injections of omali, A ab antihistamines were canceled. The natient received amaliziimah theranv far 12 months Durina 18 months afterAfter 3 months from the beginning of therapy UAS7 reduced to 0, cyclosporine was canceled. After 6 injections of omalizumab antihistamines were canceled. The patient received omalizumab therapy for 12 months. During 18 months after omalizumab discontinuation the remission remains (UAS7=0). Conclusions: The multidisciplinary approach to diagnostics and management of this patient, omalizumab administration allowed us to achieve total disease control and, finally, its remission.Case report Meat allergy is becoming an increasingly recognized condition and a higher preva- lence is seen in pediatric age compared to adults. Allergy to bovine serum albu- min (bosd6) is the main predictor of allergy to cow's milk proteins (CMP) and cow's meat proteins. We present a case of a 3-year-old child with CMP who, since the age of 6 months, after some ingestions of cow's meat, developed episodes of irritability, urticaria, angioedema and syncope. Skin prick tests were performed which were positive for milk and all milk proteins. Specific IgE's were requested with positive results to milk, nBos d 4 a-lactalbumin; nBos d 5 B-lactoblobulin, nBos d 8 casein, cow’s and pork’s meat. An ImmunoCap® and ISAC® were requested and the main results are showed in table 1. Specific IgE to cow's meat was positive (40,5 KUA/L) and the ImmunoCap identi- fied Bosd6 (3.54 kUA/L) as the responsible for the clinical picture. Meat allergy is not usually associated with severe reactions once bosd6 is a heat labile protein, however, the process of cooking meat may be, in some cases, in- sufficient to have an effect on the complex matrix of meat and the associated se- rum albumins. The irregular pattern of the episodes and the previous diagnosis of CMP allergy may act as confounding factors leading to a delayed diagnosis. Besides the severity of its presentation in some cases, this condition usually re- solves within years, and so the follow-up of these children with subsequent tes- ting for evaluation of tolerance acquisition is recommended.Case report Some patients with food protein-induced enterocolitis syndrome (FPIES) who have positive serum-specific IgE (slgE) to cow’s milk (CM) develop into an IgE-me- diated CM allergy. Contrarily, only a few cases of conversion from IgE-mediated food allergy to FPIES have been reported. A female infant, exclusively breastfed from birth, experienced several episodes of urticaria within one hour of ingesting CM. Because her sIgE to CM was positive, she was diagnosed as having IgE-me- diated CM allergy. Dairy products were eliminated from her complementary diet. At two years and ten months of age, a follow-up examination revealed decreases in slgE. Dairy products were re-introduced without elicitation of any symptoms. At four years and seven months of age, when viral enterocolitis was epidemic in the child's kindergarten, she presented with vomiting and diarrhea. Four weeks later, she was referred to our hospital due to weight loss, persistent diarrhea, hemato- chezia and a remarkable eosinophilia (WBC 25,000 /UL, eosinophils 40%). Duode- num biopsy specimens obtained by endoscopy revealed infiltration of eosinophils in the mucosa. Allergen specific lympho-proliferation index against lactoferrin was positive. Her symptoms and eosinophilia disappeared after elimination of dairy products but recurred by their commencement. Since her oral food chal- lenge test was negative after one year of elimination of dairy products, she be- came able to ingest dairy products without any symptoms. Eosinophilic esophagi- tis has been shown to occur in patients who underwent oral immunotherapy for IgE-mediated food allergy. Given that intestinal inflammation caused by viral in- fection might make inducible regulatory T cells lose their regulatory function, and that dairy products were introduced into the patient's diet despite the presence of sIgE against CM. The conversion from IgE-mediated food allergy to FPIES might be triggered by epidemic gastroenteritis and similar mechanisms involved in the development of eosinophilic esophagitis during oral immunotherapy in this case. In cases with gastrointestinal symptoms associated with eosinophilia in children who recovered from IgE-mediated food allergy, food elimination and elicitation tests against the previous sensitized food antigens should be performed.