Page 937 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition
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912                                        CHAPTER 6



  VetBooks.ir  axis more sensitive to decreases in serum calcium,   proopiomelanocortin   (POMC),   a   precursor
                                                          peptide that is split into adrenocorticotropic
           allowing more rapid mobilisation of calcium from
           bone in times of acute need. Calcium supplementa-
           tion should be provided during times of acute loss   hormone  (ACTH),  α-melanocyte-stimulating
                                                          hormone (α-MSH), corticotropin-like immuno-
           (e.g. during exertion that causes profuse sweating   reactive peptide and  β-endorphins. The reason
           or during early lactation).                    for the decrease in hypothalamic inhibition is
                                                          currently  unknown,  but  recent  studies  suggest
           Prognosis                                      that inflammation and oxidative stress over time
           If properly recognised and treated, the prognosis for   lead to neurodegeneration. Certain breeds, such
           recovery from hypocalcaemia is excellent. However,   as Morgan horses and ponies, may be genetically
           if hypocalcaemia is unrecognised in severely affected   predisposed to developing PPID.
           (e.g. recumbent) horses, the prognosis is poor, and   The exact consequences of the decreased inhibi-
           death may occur before the results of plasma calcium   tion of the melanotrophs and increased secretion of
           measurements are known. Horses with primary    ACTH, α-MSH and β-endorphins is poorly under-
           hypoparathyroidism can  be managed successfully   stood. The traditional view of PPID is that clini-
           with oral calcium supplementation.             cal signs are caused by overproduction of ACTH,
                                                          leading to excessive stimulation of the zona fas-
           PITUITARY PARS INTERMEDIA                      ciculata of the adrenal gland producing glucocor-
           DYSFUNCTION                                    ticoids, such as cortisol. However, baseline plasma
                                                          concentrations of cortisol are usually within the
           Other and previous names: equine Cushing’s disease,   normal range in horses with PPID. Recent studies
           pituitary adenoma, pituitary hypertrophy, pituitary   have suggested that clinical signs could be caused
           hyperplasia.                                   by a loss of the normal cortisol circadian rhythm or
                                                          by other metabolites and peptides also produced in
           Definition/overview                            excess (e.g. α-MSH).
           PPID is a common disease of older horses affect-
           ing more than 25% of horses older than 15 years  Clinical presentation
           of age. This condition, originally described as a   The traditional clinical presentation is a lethar-
           benign tumour of the pars intermedia of the pitu-  gic older horse (>15 years of age) with a pendulous
           itary gland, is probably more accurately described as   abdomen and long, shaggy hair coat that does not
           hypertrophy or hyperplasia (adenoma or adenoma-  shed normally in spring (hypertrichosis) (Fig. 6.9).
           tous  hyperplasia) of the pituitary gland. The main   Less advanced cases may have subtle clinical presen-
           clinical significance of the disease are the associated   tations including poor performance, loss of topline,
           complications such as laminitis and recurrent infec-  hoof changes in the absence of lameness and slightly
           tions. The latter is reflected in an increased incidence   delayed coat shedding. As the disease evolves, there
           of sole abscesses, non-healing skin lesions, dental   is a tendency for fat to accumulate in the crest of
           disease, GI parasitism and  non-responsive respira-  the neck, over the rump, in the sheath of geldings
           tory infections. In rare instances, the neurological   and behind the eyes. Despite this fat accumula-
           deficits, presumably due to the mass effect of a large   tion, weight loss can occur due to muscle wasting.
           tumour, may be the initial presenting clinical signs.  Affected horses may be hyperhidrotic, secreting
                                                          sweat that tends to be greasy (Fig. 6.10). The long
           Aetiology/pathophysiology                      hair coat traps sweat, exacerbating skin problems,
           PPID is caused by  neurodegeneration  of the   particularly  Dermatophilus congolensis  infection.
           inhibitory dopaminergic hypothalamic neurons   A  fairly uncommon manifestation is lactation in
           resulting in adenomas or adenomatous hyper-    non-pregnant mares probably related to altered
           plasia of the pars intermedia melanotroph popu-  prolactin secretion. While it is possible for affected
           lation. The  melanotroph population produces   mares to  carry foals  to  term,  mares are more
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