ABSTRACT
From case studies in humans it is known that primary hypothyroidism (PH) may be associated with morphological and functional changes of the pituitary. There is no insight into the time scale of these changes. In this study, seven beagle dogs were followed up for 3 years after the induction of primary hypothyroidism. Three of these dogs were followed up for another 1.5 years while receiving l-thyroxine. Adenohypophyseal function was investigated at 2-month intervals with the combined intravenous injection of CRH, GHRH, GnRH, and TRH, and measurement of the plasma concentrations of ACTH, GH, LH, PRL, and TSH. In addition, after 2 years of hypothyroidism a single TRH-stimulation test and a somatostatin test were performed, with measurements of the same pituitary hormones. Every 6 months the pituitary gland was visualized by computed tomography (CT). Induction of PH led to high plasma TSH concentrations for a few months, where after concentrations gradually declined to values no longer significantly different from pre-PH values. A blunted response to stimulation of TSH release preceded this decline. Basal plasma GH concentrations increased during PH and there was a paradoxical hyperresponsiveness to TRH stimulation. Basal GH concentrations remained elevated and returned only to low values during l-thyroxine treatment. Basal PRL concentrations decreased significantly during PH and normalized after several months of l-thyroxine treatment. The pituitary gland became enlarged in all dogs. Histomorphology and immunohistochemical studies in 4 dogs, after 3 years of PH, revealed thyrotroph hyperplasia, large vacuolated thyroid deficiency cells, and decreased numbers of mammotrophs. Several cells stained for both GH and TSH. In conclusion, with time PH led to a loss of the TSH response to low T4 concentrations, hypersecretion of GH, and hyposecretion of PRL. The enlarged pituitaries were characterized by thyrotroph hyperplasia, large vacuolated thyroid deficiency cells, and double-staining cells, which are indicative of transdifferentiation.
Subject(s)
Cell Transdifferentiation , Dog Diseases/physiopathology , Hypothyroidism/physiopathology , Pituitary Gland, Anterior/physiopathology , Pituitary Gland/pathology , Prolactin/metabolism , Thyrotropin/metabolism , Animals , Dog Diseases/drug therapy , Dog Diseases/metabolism , Dog Diseases/pathology , Dogs , Female , Hyperpituitarism/etiology , Hyperpituitarism/metabolism , Hyperpituitarism/veterinary , Hypertrophy/etiology , Hypothyroidism/drug therapy , Hypothyroidism/etiology , Hypothyroidism/veterinary , Thyroid Function Tests , Thyroidectomy/adverse effects , Thyroxine/therapeutic useABSTRACT
A 13-year-old male, castrated, crossbred cat was referred for insulin-resistant diabetes mellitus. The cat had a ravenous appetite and a dull coat. Basal urinary corticoid/creatinine ratios were normal. In the low-dose dexamethasone suppression test there was no suppression of the (nonelevated) plasma cortisol concentration, whereas the (nonelevated) plasma adrenocorticotropic hormone (ACTH) concentration declined to low values. Basal plasma alpha-melanocyte-stimulating hormone (alpha-MSH) concentrations were highly elevated (> 1,500 ng/liter). Computed tomography revealed a pituitary tumor originating from the pars intermedia (PI). After microsurgical transsphenoidal hypophysectomy, the clinical signs resolved and the cat no longer required insulin administration. Microscopic examination of the surgical specimen revealed a pituitary adenoma originating from the PI with infiltration into the neural lobe. The adenoma immunostained intensely positive for alpha-MSH and only weakly for ACTH. It is concluded that the ACTH-independent cortisol production was probably due to the (weak) glucocorticorticotropic effects of the extremely high plasma concentration of alpha-MSH and related peptides.
Subject(s)
Adenoma/veterinary , Cat Diseases/pathology , Diabetes Mellitus, Type 1/veterinary , Pituitary Neoplasms/veterinary , alpha-MSH/metabolism , Adenoma/complications , Adenoma/pathology , Adenoma/surgery , Animals , Cat Diseases/metabolism , Cats , Diabetes Mellitus, Type 1/complications , Diabetes Mellitus, Type 1/metabolism , Diabetes Mellitus, Type 1/pathology , Immunohistochemistry/veterinary , Male , Pituitary Neoplasms/complications , Pituitary Neoplasms/pathology , Pituitary Neoplasms/surgery , alpha-MSH/bloodSubject(s)
Antidiarrheals/adverse effects , Diarrhea/veterinary , Dog Diseases/drug therapy , Dogs/genetics , Veterinary Drugs/adverse effects , Animals , Antidiarrheals/therapeutic use , Breeding , Diarrhea/drug therapy , Female , Incidence , Loperamide/adverse effects , Loperamide/therapeutic use , Male , Mutation , Veterinary Drugs/therapeutic useABSTRACT
A 9-year-old castrated male European shorthair cat with insulin-resistant diabetes was referred with the preliminary diagnosis of pituitary-dependent hyperadrenocorticism, based on measurements of urinary corticoids. Further studies revealed not only resistance of plasma concentrations of cortisol, adrenocorticotropic hormone (ACTH) and alpha-melanocyte-stimulating hormone (alpha-MSH) to suppression by a low dose of dexamethasone, but also elevated plasma concentrations of growth hormone (GH) and insulin-like growth factor I (IGF-I). Pituitary imaging with dynamic contrast-enhanced computed tomography demonstrated an enlarged pituitary gland and an adenoma. The cat underwent trans-sphenoidal hypophysectomy after which the insulin resistance disappeared. On histopathological and immunocytochemical examination of the surgical specimen a double adenoma was found, consisting of a corticotroph adenoma and a somatotroph adenoma separated by unaffected pituitary tissue.
Subject(s)
Adenoma/complications , Cat Diseases/pathology , Cushing Syndrome/etiology , Diabetes Mellitus/etiology , Pituitary Neoplasms/complications , Adenoma/pathology , Adenoma/veterinary , Adrenocorticotropic Hormone/blood , Adrenocorticotropic Hormone/metabolism , Animals , Cat Diseases/physiopathology , Cats , Cushing Syndrome/veterinary , Diabetes Mellitus/veterinary , Growth Hormone/blood , Growth Hormone/metabolism , Hydrocortisone/blood , Insulin Resistance , Insulin-Like Growth Factor I/analysis , Male , Pituitary Neoplasms/pathology , Pituitary Neoplasms/veterinary , alpha-MSH/bloodABSTRACT
REASONS FOR PERFORMING STUDY: The occurrence of unexpectedly high numbers of horses with neurological signs during two outbreaks of strangles required prompt in-depth researching of these cases, including the exploration of magnetic resonance imaging (MRI) as a possible diagnostic technique. OBJECTIVES: To describe the case series and assess the usefulness of MRI as an imaging modality for cases suspected of space-occupying lesions in the cerebral cavity. METHODS: Four cases suspected of suffering from cerebral damage due to Streptococcus equi subsp. equi infection were examined clinically, pathologically, bacteriologically, by clinical chemistry (3 cases) and MRI (2 cases). In one case, MRI findings were compared to images acquired using computer tomography (CT). RESULTS: In all cases, cerebral abscesses positive for Streptococcus equi subsp. equi were found, which explained the clinical signs. Although the lesions could be visualised with CT, MRI images were superior in representing the exact anatomic reality of the soft tissue lesions. CONCLUSIONS: The diagnosis of bastard strangles characterised by metastatic brain abscesses was confirmed. MRI appeared to be an excellent tool for the imaging of cerebral lesions in the horse. POTENTIAL CLINICAL RELEVANCE: The high incidence of neurological complications could not be explained but possibly indicated a change in virulence of certain strains of Streptococcus equi subsp. equi. MRI images were very detailed, permitting visualisation of much smaller lesions than demonstrated in this study and this could allow prompt clinical intervention in less advanced cases with a better prognosis. Further, MRI could assist in the surgical treatment of brain abscesses, as has been described earlier for CT.