Han van der Kolk, DVM, PhD, dipl ECEIM
Aeres University of Applied Sciences, Dronten, the Netherlands [h.van.der.kolk@aeres.nl]
Equine Cushing’s diseaseEquine Metabolic SyndromeDisproportionate congenital short stature (or dwarfism) in the Friesian horse breedHypertrophic osteopathy (or Marie’s disease)Renal secondary hyperparathyroidismReferencesAbstract
Equine Cushing’s disease
Another remarkable clinical sign is the bulging of supraorbital fat seen in 20-60% of horses with Cushing’s disease. Major sequelae of an adenoma of the pars intermedia of the pituitary gland are secondary diabetes mellitus (and concurrent weight loss) and laminitis. It should be realised that horses with Cushing’s disease usually are not suffering from polyuria and polydipsia unless in association with secondary diabetes mellitus or diabetes insipidus. Other complications include hyperhidrosis [excessive sweating], infertility, galactorrhoea, delayed wound healing, bilateral blindness, depression, and seizures. Pregnant mares with Cushing’s disease and secondary diabetes mellitus might give birth to (underweight) foals with a very poor prognosis if the diabetes mellitus is not treated during pregnancy. The diagnosis is best confirmed using assessment of the basal plasma ACTH concentration or performing an overnight dexamethasone suppression test. Horses with hyperadrenocorticism have been shown to have resting hyperinsulinaemia and reduced tissue sensitivity to insulin (Beech and Garcia 1985). In addition, by using the euglycaemic hyperinsulinaemic clamp technique [*] it has been shown that horses with Cushing’s disease have a low basal rate of glucose metabolism associated with increased insulin resistance (Klinkhamer et al. 2011). With respect to treatment, preference should be given to dopamine agonists like pergolide or bromocriptine. It is important to realize that horses with Cushing’s disease only are not polyuric and polydipsic and might initially be more or less obese and as such might resemble horses with Equine Metabolic Syndrome.
Equine Metabolic Syndrome
The major sequela of Equine Metabolic Syndrome is laminitis. Unfortunately, it is difficult to reduce weight in affected horses by dietary restriction (“easy keepers”).
Horses with Equine Metabolic Syndrome have resting hyperinsulinaemia similar to horses with Cushing’s disease. In contrast to horses with Cushing’s disease the result of the dexamethasone suppression test is normal in horses affected with Equine Metabolic Syndrome. Remarkably, the euglycaemic hyperinsulinaemic clamp technique as gold standard for the sensitivity of tissues to insulin has not been applied to horses affected with Equine Metabolic Syndrome yet. Most effective preventive and treatment strategies are those associated with both increased physical activity and dietary-induced weight reduction.
Disproportionate congenital short stature (or dwarfism) in the Friesian horse breed
Affected animals have approximately 25% shorter fore- and hindlimbs and approximately 50% reduced bodyweight. In case of congenital dwarfism in the Friesian horse breed, a dysplastic metaphysis of the distal metacarpus and metatarsus is usually radiographically evident (Back et al. 2008), whereas no abnormalities were detected in the function of the hypothalamic-pituitary growth axis (de Graaf-Roelfsema et al. 2009). A B4GALT7 mutation identified affects the moieties of proteoglycans of the extracellular matrix (Leegwater et al 2016) associated with tendon laxity. Treatment of affected animals is supportive.
Hypertrophic osteopathy (or Marie’s disease)
Blood biochemistry might reveal increased activity of alkaline phosphatase. Treatment must be directed against elimination of the underlying cause if possible.
Renal secondary hyperparathyroidism
Cushingova bolest u konjaMetabolički sindrom u konjaNeproporcionalno kongenitalni nizak rast (ili patuljasti rast) kod frizijske pasmine konjaHipertrofična osteopatijaRenalni sekundarni hiperparatireoidizamReferences
Cushingova bolest u konja
Još jedan značajan klinički znak je ispupčenje supraorbitalnog sala koje se vidi u 20-60% konja s Cushingovom bolešću. Glavne posljedice adenoma pars intermedia hipofize su sekundarni dijabetes melitus (i istodobni gubitak težine) i laminitis. Treba imati na umu da konji s Cushingovom bolešću obično ne pate od poliurije i polidipsije osim ako nisu povezani sa sekundarnim dijabetes melitusom ili dijabetes insipidusom. Ostale komplikacije uključuju hiperhidrozu [pretjerano znojenje], neplodnost, galaktoreju, odgođeno zacjeljivanje rana, bilateralnu sljepoću, depresiju i napadaje. Gravidne kobile s Cushingovom bolešću i sekundarnim dijabetesom melitusom mogu roditi ždrebad (premale težine) s vrlo lošom prognozom ako se dijabetes melitus ne liječi tijekom trudnoće. Dijagnoza se najbolje potvrđuje procjenom bazalne koncentracije ACTH u plazmi ili provođenjem testa supresije deksametazonom tijekom noći. Pokazalo se da konji s hiperadrenokorticizmom imaju hiperinzulinemiju u mirovanju i smanjenu osjetljivost tkiva na inzulin (Beech i Garcia 1985). Osim toga, korištenjem tehnike euglikemične hiperinzulinemijske stezaljke [*] pokazano je da konji s Cushingovom bolešću imaju nisku bazalnu stopu metabolizma glukoze povezanu s povećanom inzulinskom rezistencijom (Klinkhamer i sur. 2011.). Što se tiče liječenja, prednost treba dati agonistima dopamina poput pergolida ili bromokriptina. Važno je shvatiti da samo konji s Cushingovom bolešću nisu poliurični i polidipsični te da u početku mogu biti više ili manje pretili i kao takvi mogu nalikovati konjima s metaboličkim sindromom konja.
Metabolički sindrom u konja
Glavna posljedica Metaboličkog sindroma konja je laminitis. Nažalost, teško je smanjiti težinu oboljelih konja ograničenjem prehrane („laki čuvari”).
Konji s metaboličkim sindromom konja imaju hiperinzulinemiju u mirovanju sličnu konjima s Cushingovom bolešću. Za razliku od konja s Cushingovom bolešću, rezultat testa supresije deksametazonom je normalan kod konja s metaboličkim sindromom konja. Zanimljivo je da tehnika euglikemične hiperinzulinemijske stezaljke kao zlatni standard za osjetljivost tkiva na inzulin još nije primijenjena na konje s metaboličkim sindromom konja. Najučinkovitije strategije prevencije i liječenja su one povezane s povećanom tjelesnom aktivnošću i smanjenjem tjelesne težine izazvanim prehranom.
Neproporcionalno kongenitalni nizak rast (ili patuljasti rast) kod frizijske pasmine konja
Zaražene životinje imaju približno 25% kraće prednje i stražnje udove i približno 50% smanjenu tjelesnu težinu. U slučaju kongenitalnog patuljastog rasta u frizijske pasmine konja, displastična metafiza distalnog metakarpusa i metatarzusa obično je radiografski evidentna (Back i sur. 2008), dok nisu otkrivene abnormalnosti u funkciji hipotalamus-hipofizna os rasta (de Graaf-Roelfsema i sur. 2009). Identificirana mutacija B4GALT7 utječe na dijelove proteoglikana izvanstaničnog matriksa (Leegwater i sur. 2016.) povezane s opuštenošću tetive. Liječenje oboljelih životinja je suportivno.
Hipertrofična osteopatija
Biokemija krvi može otkriti povećanu aktivnost alkalne fosfataze. Liječenje mora biti usmjereno protiv uklanjanja temeljnog uzroka ako je moguće.
Renalni sekundarni hiperparatireoidizam
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