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TABLE 2: Treatment for the management of inflammatory bowel disease in horses using dexamethasone
Dose
(mg/kg bwt) Route 0.1
0.075 0.05
0.025 0.025
i.m. i.m. i.m.
Adjusted from Kalck (2009).
Fig 2: Thickening of the small intestinal wall (arrow) in a case of lymphocytic-plasmacytic enteritis.
Management of mature horses with inflammatory bowel
disease is typically unsuccessful long term (Barr 2006). Glucocorticoids are the drugs used most commonly to treat IBD because they reduce intestinal inflammation (Schumacher 2009). Since a prolonged and high dose course of therapy is often required, horses must be monitored for any adverse clinical signs, such as immunosuppression, gastric ulceration or increased susceptibility to infections (Barr 2006). Anecdotally, long-term use of systemic glucocorticoids has been related to the development of laminitis; however, there is no scientific evidence to support this. No relationship was found in a previous retrospective study of horses on long-term therapy with prednisolone and the occurrence of laminitis (Jordan et al. 2017). Even though prognosis for horses with IBD is poor, there
are case reports describing that long-term survival and parenteral use of dexamethasone appeared to produce better results (Duryea et al. 1997; McCue et al. 2003; Carmalt 2004). There are no large studies assessing the efficacy of glucocorticoids in the treatment of IBD using different protocols for each specific type of cellular infiltrate, therefore the presented dosing regimens are based on case reports, with a degree of variability among them. A prolonged, tapering course of glucocorticoids is recommended, and parenteral administration is initially necessary because absorption of orally administered medication may be poor (Barr 2006; Schumacher 2009). A suggested initial dose for dexamethasone is 0.05–0.1 mg/kg bwt i.m. for 2–4 weeks (Kemper et al. 2000; Schumacher 2009); however, most reported cases of IBD in horses have been fatal despite aggressive treatment with glucocorticoids (Schumacher 2009). For some cases, high doses of dexamethasone, up to 0.2 mg/kg bwt once daily, are recommended (Davis 2009). The dosing schedule should be adjusted to meet each horse’s needs, tapering or increasing it based on response to the treatment; as well as decreasing or even discontinuing the therapy if there is concern of adverse effects such as laminitis or secondary infections (Kalck 2009). A dosing schedule is described in Table 2. The suggested protocol can be adjusted based on clinical response; it is important to evaluate the clinical condition prior to decreasing the medication. Since the protocol for these cases is long and with high doses, owners should be aware of possible adverse effects such as delayed wound healing, gastric ulceration or immunosuppression, as well as the likelihood of relapses, in which case the dosage should
be reviewed. In horses in which clinical improvement is noted, maintenance with low doses of dexamethasone from 0.02 to 0.05 mg/kg bwt orally once daily can be attempted; however, signs may re-appear (McCue et al. 2003; Barr 2006). Prednisolone administered orally from 0.5 to 2.0 mg/kg
bwt once daily was proven to be ineffective in the treatment of equine granulomatous enteritis (Woods et al. 1993). Even though there is a lack of literature reporting success after treatment of IBD with orally administered prednisolone, the reported dose of this drug ranges from 0.2 to 4.4 mg/kg bwt orally every 12–24 h (Barr 2006; Kaikkonen et al. 2014). Clinical cases of horses with GE and LPE have been
reported to respond favourably to treatment with dexamethasone (Duryea et al. 1997; Kemper et al. 2000). However, in most of the published reports of horses with LPE, affected animals were subjected to euthanasia because of poor condition or lack of response to treatment (Kemper et al. 2000; Schumacher 2009). In a case report of LPE in an Arabian gelding, dexamethasone was administered daily starting at 0.1 mg/kg bwt i.v.; the dose was tapered by 10 mg weekly until a dose of 10 mg was reached. During the treatment, clinical signs improved for short periods and then returned, so the horse was ultimately subjected to euthanasia (Barr 2006). Another report of treatment of GE was reported to respond to long-term treatment with dexamethasone administered i.m., starting at 40 mg and tapering over a 16- week period. Five months after discontinuation of therapy, the horse was brighter and back to normal activity (Duryea et al. 1997). There are several reports of horses with MEED being
successfully treated with glucocorticoids. In one report, there was a positive response to treatment, initially with dexamethasone administered i.v., followed by subsequent oral administration; the horse was reported to remain clinically normal after discontinuation of treatment (Carmalt 2004). Another horse was treated with low doses of dexamethasone starting at 0.1 mg/kg bwt i.v. once daily and tapered to 0.018 mg/kg bwt once daily until treatment was stopped at Day 52. The horse was followed for 17 months and dexamethasone was adjusted intermittently based on appearance of eosinophilia (Carmalt 2004). In a case report of MEED in which the horse showed clinical improvement for at least 18 months, it was determined that the minimum effective dose of dexamethasone was 0.03 mg/kg bwt i.v. every 24 h for 14 days, after which it was gradually decreased (McCue et al. 2003). Since the type of cellular infiltrate varies among cases of
IBD, it may be inappropriate to compare the response to treatment among them (Kalck 2009). It is therefore important to mention that even though some dosing regimens are
© 2016 EVJ Ltd
Frequency Once daily
Once daily Once daily
i.m. or per os Once daily i.m. or per os
Duration
14–21 days 21 days 21 days 21 days
Every other day Maintenance
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