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Results for “Adrenocortical Hyperfunction”

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Preliminary experience with the diagnostic value of the canine corticosteroid-induced alkaline phosphatase isoenzyme in hypercorticism and diabetes mellitus.

The present study communicates the interim experience with the diagnostic value of the canine corticosteroid-induced alkaline phosphatase isoenzyme (CIAP), qualitatively assessed by agarose gel electrophoresis, for the diagnosis of Hypercorticism (prolonged exposure to increased concentrations of exogenous or endogenous corticosteroids) and Diabetes mellitus. A total of 106 canine serum samples with a total alkaline phosphatase activity greater than 2.90 mu kat/l were included. CIAP was identified in 28 out of 29 cases of Hypercorticism, in 7 out of 9 cases of Diabetes mellitus, and in 33 out of 68 cases of various other diseases. Sensitivity and specificity with respect to Hypercorticism were 0.97 and 0.48, respectively, while for Diabetes mellitus sensitivity and specificity were 0.78 and 0.37. From this, the positive and the negative predictive values were calculated using standard formulas. The main conclusion may be summarized as follows: In the dog, only the negative finding of CIAP seems to be of diagnostic value in ruling out Hypercorticism as a cause for an increased total alkaline phosphatase activity.

Adrenocortical Hyperfunction↗

Hirsutes. I: Diagnosis.

Hirsutes, the coarse, androgen-dependent growth of hair in women, is a common problem faced by doctors. Whether a woman presents to a clinician or not depends on cultural and racial factors. The clinician must differentiate normal biological variation from cases of hirsutes. In the vast majority of cases, androgen excess is only found locally at the level of the hair follicle; that is, the hirsutism is idiopathic. Important causes of androgen excess, such as an ovarian tumour, need to be excluded. Part one describes the causes of hirsutism and how to differentiate them using history, examination and investigation.

Adrenocortical Hyperfunction↗

Cushing's syndrome with bilateral multinodular adrenal hyperplasia. Ultrastructural, histochemical, and immunohistochemical study.

An unusual case of Cushing's syndrome of a 59-year-old man with bilateral multinodular adrenal hyperplasia and microadenoma of the pituitary gland is presented. Failure to suppress plasma cortisol with large doses of dexamethasone may suggest autonomous growth of hyperplastic nodules of the adrenals, which were at first induced by prolonged stimuli of ACTH from the microadenoma of the pituitary gland. ACTH could not be detected in the microadenoma cells on paraffin sections, while Crooke's cells were strongly positive for ACTH. The interrelation between bilateral multinodular adrenal hyperplasia and pituitary microadenoma is discussed.

3-Hydroxysteroid Dehydrogenases↗

Failure to suppress adrenal function in congenital adrenal hyperplasia (21-hydroxylase deficiency). Three case reports.

Three patients, aged 14, 16, and 32 years respectively, with congenital adrenal hyperplasia (21-hydroxylase deficiency) are described. Excessive adrenal activity and ACTH secretion could not be suppressed with doses of corticosteroids sufficient to cause iatrogenic Cushing's syndrome, even though part of the steroid dosage was administered in the late evening. The resistance to feed-back suppression was of the same order as that seen in Cushing's syndrome. Adrenalectomy was performed in the 16-year-old girl, and was followed by a menarche. Adrenalectomy was considered inadvisable in the other two patients.

Adolescent↗

Adrenal hyperplasia.

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Adrenocortical Hyperfunction↗

Transsphenoidal hypophysectomy in beagle dogs: evaluation of a microsurgical technique.

OBJECTIVE: Assessment of a microsurgical technique for transsphenoidal hypophysectomy in dogs. STUDY DESIGN: Prospective study using physical examination, pituitary function testing, computed tomography (CT), and histological examination at autopsy. ANIMALS OR SAMPLE POPULATION: Eight laboratory beagle dogs. METHODS: Pituitary function was assessed before and at 10 weeks after hypophysectomy by combined administration of four releasing hormones (anterior pituitary), administration of haloperidol (pars intermedia), and infusion of hypertonic saline (posterior pituitary). RESULTS: CT imaging enabled accurate preoperative localization of the pituitary. Appropriate positioning and surgical technique facilitated exposure of the pituitary and its extraction without hemorrhage. Postoperative recovery was generally uncomplicated. None of the eight dogs had somatotropic, gonadotropic, lactotropic, melanotropic, or posterior pituitary responses to stimulation at 10 weeks after hypophysectomy. Four dogs (ACTH nonresponders) also had no corticotropic response and four (ACTH responders) had small but significant responses in the combined anterior pituitary function test. Adrenocortical atrophy was more pronounced in the ACTH nonresponders than in the responders. No residual pituitary tissue was found along the ventral hypothalamic diencephalon but nests of pituitary cells were found embedded in fibrous tissue in the sella turcica. CONCLUSIONS: The surgical technique proved to be safe and effective. Microscopic nests of pituitary cells in the sella turcica may be responsible for residual corticotropic response to hypophysiotropic stimulation after hypophysectomy. CLINICAL RELEVANCE: The surgical technique may be used in the treatment of dogs with pituitary-dependent hyperadrenocorticism. The corticotropic response is the most sensitive criterion in assessing completeness of hypophysectomy in dogs.

Adrenocortical Hyperfunction↗

Results of transsphenoidal hypophysectomy in 52 dogs with pituitary-dependent hyperadrenocorticism.

OBJECTIVE: To evaluate microsurgical transsphenoidal hypophysectomy in dogs with pituitary-dependent hyperadrenocorticism (PDH). STUDY DESIGN: Prospective study to evaluate the results (survival and disease-free interval, remission, recurrence) and complications of microsurgical transsphenoidal hypophysectomy by clinical follow-up, computed tomography (CT), and urinary corticoid-to-creatinine (C/C) ratios in dogs with PDH. The effect of surgical experience was investigated by comparing results of hypophysectomy cases 1 through 26 and 27 through 52. ANIMALS OR SAMPLE POPULATION: 52 dogs with PDH. RESULTS: Preoperative CT enabled accurate assessment of pituitary size (24 nonenlarged and 28 enlarged) and localization relative to intraoperative anatomic landmarks. Treatment failures included procedure-related mortalities (five dogs) and incomplete hypophysectomies (four dogs). The 1-year estimated survival rate was 84% (95% confidence interval [CI], 71% to 92%). The 2-year estimated survival rate was 80% (95% CI, 65% to 90%). In 43 dogs, the hyperadrenocorticism went into remission. Hyperadrenocorticism recurred in five dogs. The 1-year estimated relapse-free fraction was 92% (95% CI, 76% to 97%). The main complications were transient, mild, postoperative hypernatremia; transient reduction or cessation of tear production (25 eyes in 18 dogs); permanent (five dogs) or prolonged (nine dogs) diabetes insipidus; and secondary hypothyroidism. Normal tear production had resumed in all but one case after a median period of 10 weeks. In the second case series (27 through 52), the hospitalization period was shorter, the number of dry eyes fewer, the survival fraction greater, and the postoperative mortality lower than in the first series. In 15 dogs in which remission was obtained, postoperative CT images suggested the presence of small pituitary remnants; in 1 of these, hyperadrenocorticism recurred. In 46 dogs, the histological diagnosis was pituitary adenoma. CONCLUSIONS: Microsurgical transsphenoidal hypophysectomy in dogs with PDH is an effective method of treatment in specialized veterinary institutions having access to advanced pituitary imaging techniques. Postoperative CT findings do not correlate well with remission or subsequent recurrence of hyperadrenocorticism. CLINICAL RELEVANCE: The neurosurgeon performing hypophysectomies must master a learning curve and must be familiar with the most frequent complications of the operation to recognize them as early as possible and to treat them immediately and effectively. Urinary C/C ratios are sensitive indicators for the assessment of remission and recurrence of hyperadrenocorticism.

Adrenocortical Hyperfunction↗

Canine hypophysectomy using a ventral paramedian approach.

OBJECTIVE: To evaluate the degree of pituitary exposure, completeness of hypophysectomy, and perioperative morbidity associated with an alternative paramedian surgical approach and excisional technique for the canine pituitary gland. STUDY DESIGN: Experimental imaging, surgical, and endocrinologic study. ANIMAL POPULATION: Nine healthy, purpose-bred Beagle dogs. METHODS: Surgical landmarks for the pituitary were determined by computed tomography (CT), and then using a ventral paramedian approach medial to the rami of the mandible, the pituitary was exposed and removed en bloc by manipulation and ultrasonic aspiration. Efficacy of the procedure was evaluated using endocrinologic and pathologic observation. RESULTS: CT images allowed the precise location of surgical landmarks for hypophysectomy. Statistically significant decreases in secretion of all measured pituitary hormones except adrenocorticotropic hormone (ACTH) occurred after hypophysectomy. Despite the absence of gross evidence of residual pituitary tissue, immunohistochemical staining revealed residual pituitary cells in the sella turcica of most dogs. CONCLUSION: CT imaging and a paramedian approach facilitated surgical access to the pituitary gland by a transoral technique; however, use of an ultrasonic aspirator removed all visible pituitary glands but left cellular remnants capable of ACTH secretion in the sella turcica. CLINICAL RELEVANCE: Although this technique did not result in complete hypophysectomy, clinical use in dogs with pituitary-dependent hyperadrenocorticism is warranted because the goal is not complete hypophysectomy but removal of a pituitary tumor.

Adrenocortical Hyperfunction↗