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Vernal keratoconjunctivitis (VKC) is a persistent, severe allergic eye disease, mainly occurring in children, that can lead to severe ocular complications including visual loss. The underlying etiology and pathophysiology of VKC remain unclear. Common therapies include topical antihistamines and mast cell stabilizers that are effective in mild-to-moderate forms of VKC but are often ineffective in severe forms that require topical or systemic corticosteroids. Dependence on steroids is common with potential adverse effects both local, as increased intraocular pressure, glaucoma, infection and cataract, as well as systemic ones, as reduction in child growth velocity. Alternative therapies are immunosuppressive drugs, like cyclosporine A and tacrolimus, that usually are effective but may also cause adverse effects. A promising therapeutic option is omalizumab, a recombinant anti-IgE humanized monoclonal antibody, currently used as add-on therapy for moderate to severe uncontrolled allergic asthma and chronic spontaneous urticaria. Here, we report the short-time duration of effective relief of symptoms after the prolonged use of omalizumab in a patient affected by refractory VKC. However, in our case any apparent beneficial effect was short lasting, and we propose that the duration of the disease and the concomitant long-term use of steroids leads to iatrogenic damage; thus, the disease becomes refractory to anti-IgE treatment.

Mast cells are abundant in the heart, among myocardial fibers, around coronary arteries, within arterial intima and intramural vessels, and in atherosclerotic plaques. Their mediators can be released during anaphylaxis and be responsible for acute coronary syndrome. This condition has been described as Kounis syndrome (KS). We report three cases of acute myocardial ischemia, which fulfill the definition for KS. In Cases 1 and 2, the association of intense chest pain with acute urticaria after an allergenic contact (wasp sting and betalactam antibiotic administration, respectively) was suspected to be an attack of angina related to an allergic reaction. No signs of an allergic reaction were observed in Case 3, but only the history of a wasp sting suggested its relationship to loss of consciousness and heart ischemia when hypersensitivity to venom was ascertained. These cases strongly recommend measurement of anaphylactic biomarkers, such as tryptase, during acute coronary syndromes to detect the possible involvement of an allergic reaction. Conversely, measurement of cardiac biomarkers during anaphylaxis, even without obvious signs of myocardial ischemia, might identify patients at risk of myocardial injury.

Omalizumab has been recognized to be effective in the treatment of chronic spontaneous urticaria (CSU). The Italian Medicines Agency authorizes two omalizumab courses, only for patients with CSU unresponsive to antihistamines, and this schedule may limit omalizumab use. Unfortunately, in the majority of CSU, the schedule is unsatisfactory because symptoms usually recur shortly after discontinuation of treatment. A case of a patient needing more than two treatment courses with omalizumab is reported, in order to discuss the rationale for its long-term use. Patient had needed systemic steroids almost continuously for 4 years. Two severe glucocorticoid-associated adverse events (GAEs) occurred during long-term treatment. Omalizumab 300 mg monthly was started with immediate disappearance of the urticarial lesions. Beneficial effects waned shortly after discontinuation of treatment, and further steroid use was needed. A second omalizumab course showed the same clinical pattern, with prompt response and recurrence of symptoms after suspension. Therefore, we decided to repeat the 6 months omalizumab treatment as soon as symptoms recurred, to avoid further emergency steroid treatments and GAEs. This experience suggests that long-term use of omalizumab could be useful. Evidences show that omalizumab is effective and safe for re-treatment and long-term use of responding patients after recurrence.

For several years now, medicine has been benefiting from the contribution of nanoparticles (NPs) technology for both diagnosis and therapy. They can be used as adjuvants, being capableThe review focuses on experimental use of NPs as adjuvants/carriers for allergen immunotherapy (AIT). Human clinical trials conducted so far are discussed.Results of experimental studies and recent clinical trials support the use of NPs as carrier/adjuvant in AIT. Comparisons between NP-based and classical AIT are needed, to show the usefulness of the NP-based approach. However, there are still unsolved problems: the persistence of non-degradable NPs with possible toxicological consequences, and the formation of the protein corona around the NPs, which could alter their activity and fate. Virus-like particles seem the most promising NPs for allergy treatment, as for other vaccines. Over the next decade, NP-based AIT will be largely used to treat allergic disorders.

Nickel is one of the most common skin sensitizers, usually responsible for allergic contact dermatitis (ACD). The ingestion of nickel-rich foods is also able to elicit cutaneous (in the absence of physical contact with nickel) and gastrointestinal symptoms in some subjects with nickel ACD, a condition referred to as systemic nickel allergy syndrome (SNAS). The pathogenesis of this disease involves both Th1 and Th2 cells and cytokines, with involvement of both CD8- and CD4-positive T lymphocytes. Clinical aspects include flares of previous ACD lesions and/or positive nickel patch test reactions, widespread eczema, and gastrointestinal disturbance essentially characterized by meteorism and colic. This diagnosis may be suspected in patients with nickel ACD whose gut and skin symptoms disappear or improve after a low nickel diet. Essential for the diagnosis is to confirm that symptoms reappear after a double-blind placebo-controlled oral nickel challenge. In such cases, the low nickel diet can be used as treatment. Of note, to maintain a nickel-free diet for a long time may strongly impact a patient’s quality of life. Therefore, a desensitization treatment should be considered in these patients. Nickel hyposensitization is effective in patients suffering from SNAS. The majority of such patients can safely ingest nickel-containing foods after 1 year of treatment. Clinical experience in patients with ACD alone, although positive and encouraging, is scarce in terms of the number of patients treated and length of the hyposensitization course, which is usually followed, after a relatively short period of time, by a relapse of cutaneous symptoms. In any case, nickel hyposensitization is able to modulate immune responses to nickel by restoring a state of tolerance that seems to be mediated by T regulatory lymphocytes.

This article reviews the main aspects for the prevention and management of occupational asthma due to allergic sensitization in the workplace. An accurate allergen identification and characterization is the essential aspect of the primary prevention. Both high and low molecular weight molecules (the first acting as complete antigens the second as haptens) can induce asthma. Sensitization is a dose-related phenomenon, therefore the lower the exposure the lower the risk of sensitization. Health surveillance is the key action of the secondary prevention; it aims at the early identification of workers with occupational exposure to asthma-causing agents by means of respiratory questionnaires; preplacement and periodic visits, with spirometry; immunologic tests; and further investigations to confirm diagnosis and then remove the person from further exposure. Asthma management may be identified with the tertiary prevention. In this phase other than the pharmacological treatment, the occupational doctor should remove the worker from the exposure, as the reduction of allergens is a negative prognostic factor for a severe decline of lung function. In any case, workers should be informed on the risk they encounter at work for a better outcome of the preventive measures.