Equine Cushing-like syndrome or Hyperadrenocorticism is caused by excessive secre- tion of ACTH by the pituitary gland, secondary bilateral adrenocortical hyperplasia and associated hypercortisolemia. Equine Cushing-like syndrome is due to hyperpla- sia or adenoma formation of the pituitary pars intermedia. A possible cause is the reduction of negative regulation of dopamine on ACTH secretion because of a hypo- thalamic disease (Dybdal, 1997). Considering this etiopathogenesis a more appro- priate description of the disease is probably Pituitary Pars Intermedia Dysfunction (PPID) (Schott, 1997). PPID is relatively frequent in old horses (>18 years) with no apparent sex predisposition although authors have suggested that females are afflicted more than males (Boujon et al., 1993; Heinrichs, 1990). The characteristic clinical signs include: weight loss secondary to muscle wasting, exercise intolerance, pendu- lous abdomen, hirsutism and curly hair coat, polyuria and polydipsia, hyperhydrosis, delayed wound healing (Thompson et al., 1995) and bulging supraorbital fat pads as a result of fat redistribution. Less frequent symptoms are skin infections, urinary tract infections, gingivitis, periodontal infections, bronchopneumonia and chronic recurrent laminitis (Hillyer et al. 1992; Reed, 1998). Persistent hypercortisolism induces insulin resistance and associated glucose intolerance, thus hyperglycemia and hyperinsulinemia are possible (Beech e Garcia, 1985; Beech, 1987; Reed, 1998). Furthermore, infertility seems to be a common consequence of releasing inhibition of gonadothropic hormones (Love, 1993).
Equine cushing-like syndrome: diagnosis and therapy in two cases
SGORBINI, MICAELA;PANZANI, DUCCIO;CORAZZA, MICHELE
2004-01-01
Abstract
Equine Cushing-like syndrome or Hyperadrenocorticism is caused by excessive secre- tion of ACTH by the pituitary gland, secondary bilateral adrenocortical hyperplasia and associated hypercortisolemia. Equine Cushing-like syndrome is due to hyperpla- sia or adenoma formation of the pituitary pars intermedia. A possible cause is the reduction of negative regulation of dopamine on ACTH secretion because of a hypo- thalamic disease (Dybdal, 1997). Considering this etiopathogenesis a more appro- priate description of the disease is probably Pituitary Pars Intermedia Dysfunction (PPID) (Schott, 1997). PPID is relatively frequent in old horses (>18 years) with no apparent sex predisposition although authors have suggested that females are afflicted more than males (Boujon et al., 1993; Heinrichs, 1990). The characteristic clinical signs include: weight loss secondary to muscle wasting, exercise intolerance, pendu- lous abdomen, hirsutism and curly hair coat, polyuria and polydipsia, hyperhydrosis, delayed wound healing (Thompson et al., 1995) and bulging supraorbital fat pads as a result of fat redistribution. Less frequent symptoms are skin infections, urinary tract infections, gingivitis, periodontal infections, bronchopneumonia and chronic recurrent laminitis (Hillyer et al. 1992; Reed, 1998). Persistent hypercortisolism induces insulin resistance and associated glucose intolerance, thus hyperglycemia and hyperinsulinemia are possible (Beech e Garcia, 1985; Beech, 1987; Reed, 1998). Furthermore, infertility seems to be a common consequence of releasing inhibition of gonadothropic hormones (Love, 1993).I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
