Omalizumab. An option in vernal keratoconjunctivitis?

Vernal keratoconjunctivitis (VKC) is a severe ocular disease with immediate and delayed hypersensitivity reactions which can produce loss of visual acuity and blindness. In its physiopathology a Th1 and Th2 response is present and the therapeutic approach is very difficult because the use of local immunosuppressive therapy such as topical corticosteroids for a long time could produce severe adverse effects. As with other allergy conditions, allergens can induce an immune response mediated through expression of IgE antibodies. Omalizumab is a monoclonal anti-IgE antibody indicated in severe asthma, but in recent years has demonstrated its usefulness in other allergic diseases as atopic dermatitis. We present a 16-year-old male patient with VKC with no response to conventional therapy but with important improvement in clinical symptoms after beginning omalizumab. The patient began at two years of age with moderate atopic dermatitis and at four years of age with rhinitis and asthma. At the age of eight he presented severe ocular bilateral symptoms with red eyes, marked burning and itchy sensations, moderate photophobia, pseudogerontoxon, lacrimation, stringy discharge, papillae arranged in cobble stone and heaviness of eyelids. He received topical cyclosporine and corticosteroids in cycles for a long time without control. At the age of 13 he presented keratoconus in both eyes and required bilateral cornea transplant and permanent topical cyclosporine as immunosuppressive therapy for the transplant. At the moment it is his first visit to our allergy service. The patient had moderate atopic dermatitis with regular control with topical corticosteroids, lubricants and tacrolimus 0.1%; persistent moderate/severe rhinitis controlled with nasal corticosteroids and non-controlled asthma. We began tacrolimus 0.03% ointment for VKC and a combination of inhaled corticosteroids/B2 agonist for severe asthma with regular response for both therapies. The patient had total IgE 340 UI/L and sensitisation to house dust mites (Der f, Der p) and we began immunotherapy but this was suspended after six months because of poor treatment adherence (Fig. 1). At age of 15 we decided to start omalizumab 300 mg each two weeks for non-controlled asthma and VKC, ophthalmic and systemic immunosuppressive therapy was completely suspended and we only left tacrolimus 0.03%. After six weeks the patient presented an important improvement in ocular symptoms. After nine months he had a reduction of papillae. Other allergic conditions had an important improvement such as complete asthma control after six doses and atopic dermatitis after six months (Table 1). Ocular allergies are categorised in seasonal or perennial conjunctivitis and vernal or atopic keratoconjunctivitis. Ocular symptoms normally run with asthma and rhinitis. Some articles describe ocular symptomatic changes in these patients following omalizumab treatment. Sotohi et al. observed a significant improvement in a group of seasonal rhinoconjunctivitis patients after a four-month period and one year after re-treatment. The same investigation group observed in a controlled study that the omalizumab patients group had less symptoms compared with suplast tosilate group. Additionally to conjunctivitis typical symptoms, atopic keratoconjunctivitis (AKC) and vernal keratoconjunctivitis (VKC) make conjunctiva and corneal damage which can lead to blindness. These diseases management is usually complicated and their pathophysiology is not totally clear but a Th2 and Th1 immunological response seems to be