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216


EQUINE VETERINARY EDUCATION / AE / APRIL 2018


showed a decrease in cortisol concentration; however, concentrations returned to a level similar to baseline values when the dose was given once a day (Dıaz et al. 2014). This


suggests that long-term therapeutic use of aerosolised fluticasone suppresses endogenous cortisol through its action over the hypothalamic–pituitary–adrenal axis. For long-term treatment, the lowest effective dose of fluticasone should be utilised and it should be combined with environmental management (Dıaz et al. 2014). Systemic absorption of inhaled glucocorticoids occurs via


the respiratory or gastrointestinal tract, and is reflected by the observed adrenal suppression in different studies (Rush et al. 1999, 2000; Dıaz et al. 2014). It has been documented that about 23% of the beclomethasone administered via the metered-dose inhaler is deposited and metabolised in the lower respiratory tract; meaning that the remaining may be absorbed from the lungs to systemic circulation, or swallowed from the nasopharynx (Rush et al. 1999). This brings some concerns about possible systemic side effects of circulating glucocorticoids after inhalation therapy; however, no studies have been performed in horses to determine the likelihood of adverse effects after the use of inhaled glucocorticoids. In man, fluticasone propionate was observed to have


poor oral absorption and low systemic bioavailability after intranasal administration, concluding that systemic side effects were unlikely (Daley-Yates and Baker 2001); however, this conclusion must be taken with caution in horses, since they have shown to be more sensitive to adrenal suppression than humans (Barnes 1995). It is important to mention that hygiene must be considered when administering inhaled glucocorticoids, since contaminated delivering devices could be a source for pathogens in the respiratory tract (Duvivier et al. 1997; Lavoie 2001). In man, there is a risk of oropharyngeal candidiasis with the long-term use of inhalation therapy, especially in elderly or immunosuppressed human patients (Barnes 1995; Battaglia et al. 2015); however, this is not reported in horses. To analyse better the possible side effects due to inhalation therapy with glucocorticoids in horses, studies comparing side effects in different body systems between inhalation and systemic administration need to be performed in horses. Extrapolating from human studies, complications in at-risk-populations of respiratory infections, ocular damage, or bony changes could arise; however, when compared with the use of systemic glucocorticoids, these side effects were less pronounced (Battaglia et al. 2015).


Inhalation therapy could be adequate for many horses


with IAD, where, unlike horses with RAO, a rapid effect is not needed to control severe bronchospasm in an acute crisis. Fluticasone propionate alone can be used to manage cases of IAD, and a suggested dose for an average sized mature horse is to start at a dose of 2000 lg every 12 h for one week, then 2000 lg once daily for one week, then 1500 lg once daily for another week, followed by 1500 lg every other day until discontinuation; and this treatment is reported up to 3 months in duration (Mazan 2009). In general, the same drugs used for the treatment of RAO are beneficial in cases of IAD; however, a positive effect is observed with lower dosages for shorter treatment durations in horses with IAD. Two to 4 weeks of glucocorticoid therapy is often prescribed (Rush 2002; Cou€


etil et al. 2007).


There is sufficient scientific evidence for the use of glucocorticoids in the management of both RAO and IAD in


© 2016 EVJ Ltd


horses, either by the enteral, parenteral or inhalation route. Dosages have been established based on clinical studies; however, the practitioner will encounter a diverse response depending on the case and management practices, leading to the use of different dosing regimens.


Glucocorticoids for the treatment of interstitial pneumonia Interstitial pneumonia is a cause of acute or chronic lower respiratory tract disease in horses. Even though infectious organisms or toxins have been implicated in the pathogenesis of the disease, it is often referred to as idiopathic due to the difficulty in identifying a causative agent (Wilkins et al. 2015). The inflammation in the lung parenchyma will cause structural changes in the lung, reducing the number of functional alveoli and therefore affecting ventilation. This reduction in lung compliance is associated with the loss of distensible alveoli, the presence of pulmonary oedema and fibrosis (Wilkins and Lascola 2015). Glucocorticoids are thought to work in decreasing the inflammation that precedes the development of fibrous tissue and early and aggressive use may lead to a better long-term outcome for cases of interstitial pneumonia (Spelta et al. 2013). The course of therapy is usually prolonged, ranging from 6 to 12 weeks, and is often accompanied by treatment with antimicrobial medications. Treatments described include dexamethasone i.m. or i.v. at 0.02–0.04 mg/kg bwt every 12–24 h, and prednisolone per os at 1 mg/kg bwt every 12–24 h (Wilkins and Lascola 2015). Equine multinodular pulmonary fibrosis is a chronic and progressive type of interstitial pneumonia associated with the presence of equine herpesvirus type 5 (Spelta et al. 2013; Kessell et al. 2014). Since an infectious organism is often the cause of multinodular pulmonary fibrosis in horses, glucocorticoid therapy is sometimes avoided due to its immunosuppressive effects; however, inhibition of the inflammatory response is a key factor to avoid irreversible damage to the lung (Niedermaier et al. 2010). Long-term therapy with systemic glucocorticoids in cases of interstitial pneumonia may put the animals at risk for developing gastric ulceration, or delay in healing of already existing ulcers, therefore gastric acid suppression may be indicated for the duration of the treatment (Boothe and Mealey 2012).


Gastrointestinal system


Inflammatory bowel disease Inflammatory bowel disease (IBD) is characterised by inflammatory cell infiltration of the bowel wall (Fig 2). Depending on the inflammatory cells involved, they are classified as granulomatous enteritis (GE), multisystemic eosinophilic epitheliotropic disease (MEED), eosinophilic enterocolitis, lymphocytic–plasmacytic enteritis (LPE) and basophilic enterocolitis (Davis 2009). Infiltration occurs in the mucosa and submucosa, and the cause may be associated with parasitic, infectious or neoplastic processes (Schumacher 2009). Horses will typically present with progressive weight loss and intermittent abdominal discomfort. Diarrhoea may or may not be present, and hypoproteinaemia is common due to intestinal protein loss. The clinical signs are similar regardless of the type of cellular infiltrate (Davis 2009; Schumacher 2009). Definitive diagnosis is based on results of histological examination of an intestinal biopsy specimen (Schumacher et al. 2000).


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