Olopatadine hydrochloride ophthalmic solution for the treatment of allergic conjunctivitis

Introduction: Olopatadine hydrochloride is an antihistamine and mast cell stabilizer available as oral, intranasal and ocular preparations. Most of the practical applications of olopatadine therapy focus on the treatment of allergic rhinoconjunctivitis via intranasal and ocular routes.

Areas covered: This article was created from a comprehensive literature search with information taken from meta-analyses, systematic reviews, and clinical trials of children and adults. The articles that have been selected, evaluate the use of intranasal and ocular antihistamines and their role in allergic rhinoconjunctivitis.

Expert opinion: Olopatadine is significantly more effective than placebos in relieving the symptoms of allergic rhinoconjunctivitis. It can function both as a viable alternative or addition to first line therapies such as intranasal steroids and oral antihistamines.     

Advances in pharmacotherapy for allergic conjunctivitis

Introduction: Allergy is the fifth leading group of chronic diseases, affecting as much as 40% of the first-world population. Its pathophysiology has a genetic component, and is driven by the immune system’s sensitized response to antigens and environmental factors. As research continues to uncover the mediators responsible for ocular allergy, the development of novel drugs should progress.

Areas covered: A literature review of allergic conjunctivitis, ocular allergy and their treatment was performed using PubMed and Medline. Additional information is also included from clinicaltrials.gov and associated web sites for drugs currently in clinical trials.

Expert opinion: The initial step of therapy remains identification and avoidance of allergic triggers. The mainstay of treatment is the new generation of dual-acting antihistamines. Drugs that improve the magnitude and duration of relief, with greater subject responder rates, are gradually making their way into the clinic. Allergic conjunctivitis is a relatively easy disease to study because of the availability of models such as the conjunctival allergen challenge. New classes of drugs that target inflammatory pathways or mediators involved in the early and late-phase allergic response are being screened in these models and we are making progress in identifying the next generation of anti-allergic therapy.     

A review of olopatadine for the treatment of ocular allergy

Ocular allergy affects > 20% of the general population and many therapeutic preparations are available to individuals experiencing the most common forms – seasonal and perennial allergic conjunctivitis. 0.1% Olopatadine topical ophthalmic solution is currently approved for the treatment of allergic signs and symptoms in patients ≥ 3 years of age. Olopatadine is available in Europe as Opatanol^® and in > 30 other countries as Patanol^®. It inhibits mast cell degranulation and antagonises histamine receptors to manage the itching, redness, chemosis, tearing and lid swelling of the ocular allergic reaction, and its mast cell stabilising ability has been demonstrated both in vitro (using human conjunctival mast cells) and in vivo (human clinical experience). This article reviews both the laboratory and clinical information available on olopatadine, prefaced by a discussion of the current understanding of the ocular allergic reaction and followed by the future implications for this compound. Both laboratory and clinical studies have established the efficacy, safety and comfort of olopatadine in several study design models and comparisons to other antiallergy medications. The application of olopatadine, specifically in the management of lid swelling, an allergic sign recalcitrant to therapy and nasal allergic symptoms has also been established. In the future, a new formulation containing 0.2% olopatadine exhibits a duration of action up to 24 h, supporting once-daily dosing.     

Emerging drugs for allergic conjunctivitis

Introduction: Allergic conjunctivitis (AC) is a very common disease, especially in association with allergic rhinitis but may also occur in isolated presentation. The treatment of AC has long been based on antihistamines, cromones and topical corticosteroids, but none of these drugs completely abolishes the clinical expression of AC.

Areas covered: The development of new drugs for AC is analyzed highlighting the recent insights into the pathophysiological mechanisms of the disease. The major aim of development of drugs for AC is to have agents able to prevent the inflammatory effects of the interaction between the allergen and the specific IgE antibodies on mast cell surface. This may be obtained by blocking the effects of histamine (the main mediator of early allergic response) by H1-receptor antagonists, inhibiting the release of soluble factors able to recruit inflammatory cells (that sustain prolonged inflammation) by mast-cell stabilizers, inhibiting the effects of single mediators, inducing tolerance to the allergen by specific immunotherapy or even acting on factors related to activation and differentiation of T lymphocytes such as the toll-like receptors.

Expert opinion: AC is an underestimated disease for which there is a search of more effective treatments. The availability of the drugs under current evaluation will allow more refined therapeutic strategies to apply according to the characteristics and the clinical severity of AC.     

Olopatadine nasal spray for the treatment of seasonal allergic rhinitis in patients aged 6 years and older

Importance of the field: Allergic rhinitis is an IgE-mediated condition that produces inflammation of the mucosa of the nose, paranasal sinuses and, frequently, of the ocular conjunctiva. Allergic rhinitis causes a significant disease burden in terms of quality of life, lost productivity and medical treatment costs. One of the newest treatments approved by the FDA is Patanase^® (olopatadine hydrochloride) Nasal Spray, 665 μg/spray (OLO). Olopatadine is an antihistamine with selective H₁-receptor antagonist activity.

Areas covered in this review: This review details the basic and clinical research on the olopatadine molecule and OLO nasal spray from 1996 to the present day.

What the reader will gain: The reader will gain a better understanding of the pharmacology of OLO nasal spray, the clinical trial data that have established the efficacy of OLO nasal spray and the overall role of OLO nasal spray in the management of allergic rhinitis.

Take home message: Olopatadine nasal spray is one of the newest treatments approved by the FDA for the management of allergic rhinitis. OLO has a rapid onset of action, efficacy comparable to intranasal steroid sprays and is approved for seasonal allergic rhinitis in patients aged ≥ 6 years.     

Long-term cultures of mast cells: a new model for studying the allergic response

Mast cells are the key cells of allergic reactions and probably play also a role in chronic inflammatory reactions resulting in fibrosis. Although their biochemical and functional properties have been extensively investigated, several studies have been hampered by the absence of a tissue culture system to keep these cells alive and functionally active for long periods of time. Recently we have developed an in vitro system in which rat peritoneal mast cells are cocultured with 3T3 mouse skin derived fibroblasts (MC/3T3). Under these tissue culture conditions, mast cells do not proliferate and maintain their viability and functional activity for more than a month. This system allowed us to carry out long-term studies on the functional properties of mast cells. We have found that mast cells activated both by IgE-dependent and IgE-independent stimuli survive, and slowly replenish their histamine content. After a non-immunological challenge mast cells retain their full potential to release histamine upon a repeated similar challenge. In contrast, immunologically challenged mast cells become partially unresponsive to a similar activation event for up to 3 weeks. By exploiting this long-term culture system we described a novel type of mast cell activation induced by cytokines. The onset of this activation is slow and its course appears to be chronic-continuous, very different from the classical anaphylactic type activation that is completed within few minutes. Since MC/3T3 release higher amounts of histamine, this system is a sensitive tool to investigate the antiallergic properties of various drugs. By employing MC/3T3 cultures we were able to show that the gold salt auranofin inhibits histamine release from mast cells stimulated by different secretagogues. In addition, salbutamol inhibited histamine release from repeatedly challenged mast cells; and nedocromil sodium was effective in preventing mast cell activation when incubated for a week with MC/3T3.     

Association between perfluorooctanoic acid exposure and degranulation of mast cells in allergic inflammation

Perfluorooctanoic acid (PFOA) has wide applications, including as a raw material for converted paper and packaging products. With the widespread use of PFOA, concerns regarding its potential environmental and health impacts have increased. In spite of the known hepatotoxicity and genotoxicity of PFOA, correlation with PFOA and allergic inflammation is not well known. In this study, the effect of PFOA on the degranulation of mast cells and mast cell‐mediated allergic inflammation in the presence of FcεRI cross‐linking was evaluated. In immunoglobulin (Ig) E‐stimulated mast cells, PFOA increased the release of histamine and β‐hexosaminidase by the up‐regulation of intracellular calcium levels. PFOA enhanced gene expression of several pro‐inflammatory cytokines, including tumor necrosis factor (TNF)‐α, interleukin (IL)‐1β, IL‐6, and IL‐8 by the activation of nuclear factor (NF)‐κB in IgE‐stimulated mast cells. Also, PFOA exacerbated allergic symptoms via hypothermia, and an increase of serum histamine, TNF‐α, IgE and IgG₁ in the ovalbumin‐induced systemic anaphylaxis. The present data indicate that PFOA aggravated FcɛRI‐mediated mast cell degranulation and allergic symptoms. Copyright © 2016 John Wiley & Sons, Ltd.     

The protective effect of Tinospora cordifolia on various mast cell mediated allergic reactions

This study investigated the effect of an aqueous extract of Tinospora cordifolia (Willd.) Miers (Menispermaceae) stem on mast cell mediated allergic reactions in vivo and in vitro and studied its possible mechanism. T. cordifolia (125 to 1000?mg/kg) dose-dependently inhibited compound 48/80 induced lethality in rats, histamine induced paw edema in mice and histamine induced bronchial asthma in guinea pigs. T. cordifolia significantly (p?<?0.001) inhibited the cutaneous anaphylaxis reaction activated by histamine in a rat model and compound 48/80 induced ear swelling response in mice. T. cordifolia (2.5-160?μg/mL) also showed significant (p?<?0.001) inhibition of histamine induced contraction of guinea-pig ileum in vitro implying the H₁ antihistamine activity. T. cordifolia (0.01 to 10?mg/mL) significantly (p?<?0.001) inhibited the histamine release from rat peritoneal mast cells activated by compound 48/80. In addition, T. cordifolia (0.01 to 10?mg/mL) significantly (p?<?0.001) inhibited the secretion of tumor necrosis factor-α (TNF-α) in antidinitrophenyl (DNP) IgE-stimulated rat peritoneal mast cells. The level of cAMP in RPMC transiently and significantly increased compared with that of control cells when T. cordifolia was incubated with mast cells. T. cordifolia (0.01 to 10?mg/mL) showed concentration-dependent inhibition in compound 48/80 induced reactive oxygen species (ROS) generation. In addition, T. cordifolia decreased intracellular calcium levels of activated mast cells. These results show that T. cordifolia may be beneficial in the treatment of acute and chronic allergic disorders.     

Pharmacological targeting of the KIT growth factor receptor: a therapeutic consideration for mast cell disorders

KIT is a member of the tyrosine kinase family of growth factor receptors which is expressed on a variety of haematopoietic cells including mast cells. Stem cell factor (SCF)-dependent activation of KIT is critical for mast cell homeostasis and function. However, when KIT is inappropriately activated, accumulation of mast cells in tissues results in mastocytosis. Such dysregulated KIT activation is a manifestation of specific activating point mutations within KIT, with the human D816V mutation considered as a hallmark of human systemic mastocytosis. A number of other activating mutations in KIT have recently been identified and these mutations may also contribute to aberrant mast cell growth. In addition to its role in mast cell growth, differentiation and survival, localized concentration gradients of SCF may control the targeting of mast cells to specific tissues and, once resident within these tissues, mast cell activation by antigen may also be amplified by SCF. Thus, KIT inhibitors may have potential application in multiple conditions linked to mast cells including systemic mastocytosis, anaphylaxis, and asthma. In this review, we discuss the role of KIT in the context of mast cells in these disease states and how recent advances in the development of inhibitors of KIT activity and function may offer novel therapies for the treatment of these disorders.     

花青素对IgE介导的肥大细胞活化的影响

观察花青素 (anthocyanidin) 对肥大细胞活化脱颗粒的影响。通过大鼠被动皮肤过敏反应 (PCA) 实验, 采用比色测定法检测花青素在体内对肥大细胞的影响; 体外观察花青素对肥大细胞脱颗粒, 细胞内钙摄入, 肿瘤坏死因子-α (TNF-α) 及白细胞介素6 (IL-6) 释放以及p38MAPK、Akt、NF-κB磷酸化的影响。动物实验显示, 花青素 (50和100 mg·kg⁻¹) 明显抑制大鼠PCA。细胞实验显示, 花青素 (50和100 µmol·L⁻¹) 抑制肥大细胞释放组胺、TNF-α及IL-6, 并可抑制 p38MAPK、Akt和NF-κB的磷酸化。结果提示, 花青素的抗过敏作用与其抑制肥大细胞的脱颗粒, 抑制组胺、TNF-α、IL-6等炎症介质释放以及抑制细胞内钙摄入有关; 花青素抑制肥大细胞的活化可能与其抑制NF-κB、p38MAPK和Akt的活性相关。     

Doxycycline exerts multiple anti-allergy effects to attenuate murine allergic conjunctivitis and systemic anaphylaxis

Allergic diseases, which affect up to 20–30% of the world population, are still therapeutic challenge for allergists. Tetracyclines, which belong to an antibiotic drug family that possesses a striking variety of non-antibiotic properties, have been successfully applied to a wide range of diseases. However, their roles in allergic conjunctivitis and anaphylaxis and their underlying anti-allergy mechanisms remain elusive. Here, we reported that treatment with doxycycline significantly reduced IgE release from mouse B cells and the degranulation and inflammatory cytokines production of mouse mast cells (MCs) activated by IgE-dependent way. Furthermore, doxycycline treatment significantly inhibited histamine-induced vascular hyperpermeability in vitro. Mechanistically, the doxycycline-mediated inhibition of B cells, MCs and histamine may occur via modulation of the PI3K/Akt pathway. In vivo, our results demonstrated that treatment with doxycycline significantly attenuated clinical symptoms of mouse models of experimental allergic conjunctivitis (EAC) with a significant decrease in inflammatory cell frequency, IgE production, histamine release, and a decrease in TNF-α and IL-4 production. Using mouse models of MCs-dependent passive systemic anaphylaxis (PSA), we further confirmed anti-allergy effects of doxycycline and doxycycline-mediated inhibitory effects on MCs. Furthermore, our results showed that doxycycline significantly attenuate histamine-induced systemic anaphylaxis-like reaction (HISA) with a significantly downregulation of PI3K/Akt/eNOS/VE-cadherin pathway. The doxycycline-mediated anti-allergy effects during EAC, PSA and HISA were abrogated when an Akt activator, SC79, was administered. These findings suggest that doxycycline inhibits B cell, MC and histamine function and attenuates experimental allergic conjunctivitis and systemic anaphylaxis by possible modulating the PI3K/Akt pathway.     

Clinical efficacy of olopatadine vs epinastine ophthalmic solution in the conjunctival allergen challenge model

SUMMARY

Background: Olopatadine hydrochloride 0.1% ophthalmic solution (Patanol*) and epinastine hydrochloride 0.05% ophthalmic solution (Elestat?) are two topical antiallergic agents. Olopatadine is indicated for the treatment of the signs and symptoms of allergic conjunctivitis that include itching, redness, tearing, lid swelling, and chemosis. Epinastine is indicated for the prevention of itching associated with allergic conjunctivitis.

Objective: This study compared the clinical efficacy of olopatadine and epinastine in the prevention of itching and conjunctival redness in the conjunctival allergen challenge (CAC) model.

Research design and methods: This was a prospective, randomized, double-masked, contralaterally-controlled, single center allergen challenge study. Ninety-six subjects with a history of allergic conjunctivitis were screened, and the 66 who responded to conjunctival allergen challenge at visits 1 and 2 were randomized into 1 of 3 treatment groups at visit 3 to receive one drop of study medication in each eye: (1) olopatadine in one eye and epinastine in the fellow eye, (2) olopatadine in one eye and placebo in the fellow eye, and (3) epinastine in one eye and placebo in the fellow eye. Five minutes after study drop instillation, subjects were bilaterally challenged with the allergen concentration that had elicited a positive conjunctival allergic response at Visits 1 and 2. Subjective itching assessments were given at 3?min, 5?min, and 7?min post challenge. Objective redness and chemosis assessments were made at 10?min, 15?min, and 20?min post challenge. Paired sample two-tailed t-tests were performed on the mean scores at each time point to assess statistical significance in the differences between treatments.

Main outcome measures; results: Fifty-three subjects were randomized into the olopatadine/epinastine treatment group, the primary analysis group. Olopatadine treated eyes exhibited significantly lower mean itching and conjunctival redness scores than the contralateral epinastine treated eyes, –0.19 (?p = 0.003) and –0.52 (?p < 0.001), respectively. Olopatadine treated eyes also exhibited significantly less chemosis –0.24 (?p < 0.001), ciliary redness –0.55 (?p < 0.001), and episcleral redness –0.58 (?p < 0.001) than epinastine treated eyes.

Conclusion: Olopatadine is significantly more effective than epinastine in controlling itching, redness and chemosis associated with allergic conjunctivitis in the CAC model.

* Patanol is a registered tradename of Alcon Laboratories Inc, Forth Worth, TX, USA     

Gallic acid inhibits histamine release and pro-inflammatory cytokine production in mast cells.

The discovery of drugs for the treatment of inflammatory allergic diseases such as, asthma, allergic rhinitis, and sinusitis is a very important subject in human health. Gallic acid (3,4,5-trihydroxybenzoic acid), a polyphenyl natural products from gallnut and green tea, is known to have anti-oxidant, anti-inflammatory, anti-microbial, and radical scavenging activities. The aim of the present study was to elucidate whether gallic acid modulates the inflammatory allergic reaction and to study its possible mechanisms of action. Gallic acid attenuated compound 48/80- or immunoglobulin E (IgE)-induced histamine release from mast cells. The inhibitory effect of gallic acid on the histamine release was mediated by the modulation of cAMP and intracellular calcium. Gallic acid decreased the phorbol 12-myristate 13-acetate plus calcium ionophore A23187-stimulated pro-inflammatory cytokine gene expression and production such as TNF-alpha and IL-6 in human mast cells. The inhibitory effect of gallic acid on the pro-inflammatory cytokine was nuclear factor-kappaB and p38 mitogen-activated protein kinase dependent. In addition, gallic acid inhibited compound 48/80-induced systemic allergic reaction and IgE-mediated local allergic reaction. The inhibitory activity of gallic acid on the allergic reaction and histamine release was found to be similar with disodium cromoglycate. Our findings provide evidence that gallic acid inhibits mast cell-derived inflammatory allergic reactions by blocking histamine release and pro-inflammatory cytokine expression, and suggest the mechanisms of action. Furthermore, in vivo and in vitro anti-allergic effect of gallic acid suggests a possible therapeutic application of this agent in inflammatory allergic diseases.     

Mast cells and basophils are essential for allergies: mechanisms of allergic inflammation and a proposed procedure for diagnosis

The current definition of allergy is a group of IgE-mediated diseases. However, a large portion of patients with clinical manifestations of allergies do not exhibit elevated serum levels of IgE (sIgEs). In this article, three key factors, ie soluble allergens, sIgEs and mast cells or basophils, representing the causative factors, messengers and primary effector cells in allergic inflammation, respectively, were discussed. Based on current knowledge on allergic diseases, we propose that allergic diseases are a group of diseases mediated through activated mast cells and/or basophils in sensitive individuals, and allergic diseases include four subgroups: (1) IgE dependent; (2) other immunoglobulin dependent; (3) non-immunoglobulin mediated; (4) mixture of the first three subgroups. According to our proposed definition, pseudo-allergic-reactions, in which mast cell or basophil activation is not mediated via IgE, or to a lesser extent via IgG or IgM, should be non-IgE-mediated allergic diseases. Specific allergen challenge tests (SACTs) are gold standard tests for diagnosing allergies in vivo, but risky. The identification of surface membrane activation markers of mast cells and basophils (CD203c, CCR3, CD63, etc) has led to development of the basophil activation test (BAT), an in vitro specific allergen challenge test (SACT). Based on currently available laboratory allergy tests, we here propose a laboratory examination procedure for allergy.     

β‐eudesmol suppresses allergic reactions via inhibiting mast cell degranulation

The regulatory effect of β‐eudesmol, which is an active constituent of Pyeongwee‐San (KMP6), is evaluated for allergic reactions induced by mast cell degranulation. Phorbol 12‐myristate 13‐acetate (PMA) plus calcium ionophore A23187‐stimulated human mast cell line, HMC‐1 cells, and compound 48/80‐stimulated rat peritoneal mast cells (RPMCs) are used as the in vitro models; mice models of systemic anaphylaxis, ear swelling, and IgE‐dependent passive cutaneous anaphylaxis (PCA) are used as the in vivo allergic models. The results demonstrate that β‐eudesmol suppressed the histamine and tryptase releases from the PMA plus calcium ionophore A23187‐stimulated HMC‐1 cells. β‐eudesmol inhibits the expression and activity of histidine decarboxylase in the activated HMC‐1 cells. In addition, β‐eudesmol inhibits the levels of histamine and tryptase released from the compound 48/80‐stimulated RPMCs. Furthermore, β‐eudesmol decreases the intracellular calcium level in the activated RPMCs. β‐eudesmol also decreases the compound 48/80‐induced mortality and ear swelling response. β‐eudesmol suppresses the serum levels of histamine, IgE, interleukin (IL)‐1β, IL‐4, IL‐5, IL‐6, IL‐13, and vascular endothelial growth factor (VEGF) under PCA mice as well as PCA reactions. Therefore, the results from this study indicate the potential of β‐eudesmol as an anti‐allergic drug with respect to its pharmacological properties against mast cell‐mediated allergic reactions.     

盐酸左卡巴斯汀滴眼液治疗过敏性结膜炎68例

目的评价盐酸左卡巴斯汀滴眼液治疗过敏性结膜炎的疗效和安全性.方法140例结膜炎患者随机分成2组.试验组68例用盐酸左卡巴斯汀滴眼液,对照组72例,用色甘酸钠滴眼液,用药均为每次1滴,qid,疗程均为10d.结果试验组用药10d后的缓解眼痒效果达75%,缓解充血效果达76%;总有效率达76%,对照组为71%,64%和71%,2组差异无显著性(P＞0.05).试验组不良反应发生率为4.4%,与对照组(1.4%)相比,差异无显著性(P＞0.05).结论盐酸左卡巴斯汀滴眼液治疗过敏性结膜炎疗效明显,无明显不良反应.     

Tofacitinib suppresses mast cell degranulation and attenuates experimental allergic conjunctivitis

BackgroundAllergic conjunctivitis (AC), a common eye inflammation that affects patients’ health and quality of life, is still a therapeutic challenge for ophthalmologists. Tofacitinib, a new Janus kinase (JAK) inhibitor, has been successfully used in the treatment of several disorders. Nonetheless, its effect in AC and the potential anti-allergic mechanisms are still unclear. The objective of the current study was to explore the roles of tofacitinib in preventing AC and elucidate the potential underlying mechanisms.MethodsTofacitinib was used topically in BALB/c mice with experimental allergic conjunctivitis (EAC). Ocular allergic symptoms and biological modifications were examined. To assess the anti-allergic mechanisms of tofacitinib, RBL-2H3 cells and HUVECs were cultured in vitro. The inhibitory effects and mechanisms of tofacitinib were studied and measured by real-time quantitative PCR, ELISA, western blot analysis, and flow cytometry.ResultsTopical administration of tofacitinib reduced the clinical symptoms of OVA-induced EAC, with a substantial mitigation in inflammatory cell infiltration, histamine release, and TNF-α mRNA as well as IL-4 mRNA expression. In vitro, tofacitinib repressed the degranulation and cytokine production in RBL-2H3 cells and reduced histamine-induced vascular hyperpermeability. The underlying mechanism might involve the downregulation of phosphorylation of JAK3/STATs signaling molecules in RBL-2H3 cells and HUVECs.ConclusionsOur findings provide evidence that tofacitinib prevented EAC by targeting the JAK3/STATs pathway. We recommend the use of tofacitinib as an innovative approach for the treatment of AC.     

治疗结膜炎的新喹诺酮类药物贝西沙星

贝西沙星是一种治疗细菌性结膜炎的广谱抗菌剂。与其他喹诺酮类药物相比,其对易引发结膜炎的G+菌和G-菌、厌氧菌具有等效或较强的抗菌作用,对于某些对喹诺酮类药物产生耐药性的菌种,同样具有抗菌作用。同时,贝西沙星通过抑制眼部致炎因子的表达,进行免疫调节,从而更好地发挥其抗菌作用。贝西沙星滴眼后能迅速进入眼部各组织,且具有较长的药效时间。文中对贝西沙星的药理作用、药动学及临床试验进展进行综述。     

Health economic impact of olopatadine compared to branded and generic sodium cromoglycate in the treatment of seasonal allergic conjunctivitis in the UK

ABSTRACT

Objective: This study estimated the health economic impact of olopatadine (Opatanol^*) compared to branded cromoglycate (Opticrom^?) and generic sodium cromoglycate in the treatment of seasonal allergic conjunctivitis (SAC) in the UK.

Design and setting: This was a modelling study performed from the perspective of the UK's National Health Service (NHS).

Methods: A decision model was constructed depicting the management of SAC sufferers who are 4 years of age or above over a typical allergy season of 4 months and considers the decision by a GP to initially treat a patient with olopatadine, branded or generic cromoglycate. The analysis assumed both drugs to be equally effective. Consequently, a cost-minimisation analysis was performed to identify the least costly alternative.

Main outcome measures and results: Starting treatment with olopatadine is expected to lead to a healthcare cost of £92 (95% CI: £46; £150) over 4 months compared to £109 (95% CI: £65; £166) with branded cromoglycate and £95 (95% CI: £51; £152) with generic cromoglycate, resulting in a 16% and 3% reduction in healthcare costs respectively over 4 months of treatment. This cost-difference is primarily due to fewer GP visits among olopatadine-treated patients.

Conclusion: Use of olopatadine instead of branded or generic cromoglycate affords an economic benefit to the NHS. Hence, within the limitations of the model, olopatadine is the preferred first-line treatment for use in SAC sufferers, since it is expected to lead to fewer GP visits, thereby releasing healthcare resources for alternative use.