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[Diagnosis of the causes and prevention of intrauterine fetal death in the second trimester of pregnancy in women with hyperandrogenism].

Differential diagnosis of the causes of intrauterine fetal death was carried out in 84 women; in 57 of them it was due to hyperandrogenism of various origins. 63.2% of patients suffered from mixed (combined ++ovario-adrenal) androgen hypersecretion, 33.3% from the adrenal and only 3.5% of women from the ovarian form of hyperandrogenism. Relationship between the frequency of intrauterine fetal death, the pregnancy term and the form of hyperandrogenism was revealed. Differential diagnosis of hyperandrogenism forms and preparatory pathogenetic therapy helped preserve the pregnancy and resulted in delivery of a viable healthy child in 77.4% of the examined women.

Adrenal Cortex↗

[Correlation of hydrocortisone and corticosterone content in assessing the functional state of the adrenal cortex in varying forms of hypercorticism].

Separate determination of hydrocortisone and corticosterone in the blood of patients with the hypercorticism symptom-complex showed that elevation of the corticosteroid concentration could occur on account of similar elevation of the concentration of both hormones, or one of the hormones alone. Analogous data were observed in patients after ACTH administration. Dexamethasone administration caused a reduction of the hydrocortisone and corticosterone concentration in patients with Itsenko-Cushing's disease, but to a lesser degree than in healthy individuals. Administration of the preparation to the patients with juvenile dyspituitrism decreased the cortizol level, but corticosterone chiefly; as to the patients with the hypothalamic syndrome--only the cortizol level was reduced, the level of corticosterone remaining unchanged. Thus, the evidence obtained before and after the administration of the ACTH preparations and dexamethasone permitted to assess the adrenal cortex function more fully and to defect disturbances of the corticosteroid secretion of interest of the understanding of the clinical symptoms of the disease.

11-Hydroxycorticosteroids↗

Influence of single peroral dose of aminoglutethimide on the rat adrenal cortex.

In female albino rats force fed with a single dose of 50 mg of aminoglutethimide (AG) lipoid adrenocortical hyperplasia was found within 24 h. In addition, a marked focal increase in cytoplasmic transparency was found which ultrastructurally appeared to result from optically empty vacuoles and membrane-bound spaces. Later, an increase occurred in the translucency of the cytoplasmic matrix, mitochondrial swelling, destruction of cell membranes and disappearance of adrenocortical cells presenting as cytolysis. Some of the damaged cortical cells contained protein vacuoles with fibrillar structures and occasionally also blood cells. All such changes were associated with a marked infiltration by neutrophilic granulocytes, the most severe of them resembling an acute purulent epinephritis. Ultrastructural examination showed blood monocytes with signs of initial phagocytic activity at sites of disintegration of adrenocortical cells. Focal decrease of dehydrogenase activity was demonstrated in areas of cellular destruction, while no alteration in acid phosphatase activity was detected. Moreover, an absolute increase in corticosterone production form endogeneous precursors in vitro was found which could be partially explained by an increase in adrenocortical size. Formation of 18-hydroxycorticosterone and aldosterone from 4-14C-progesterone was decreased. However, no appreciable changes were revealed in the zona glomerulosa. From these findings it may be assumed that high doses of AG not only block the conversion of cholesterol into pregnenolone, but also injure some other cellular enzymatic systems necessary for the integrity of the adrenocortical cell.

Adrenal Cortex↗

The nodular adrenal.

Nodules commonly occur in the human adrenal gland. They are best regarded as part of the ageing process, produced in response to adrenal vascular changes. Nodules exhibit a wide diversity of size and distribution and are seen not only in subjects with normal adrenal function but also in patients with hypercorticalism (Cushing's and Conn's syndromes). In these disorders, the nodules appear to be a consequence of the diseases, rather than being aetiological.

Adrenal Cortex↗

[Adrenocortical scintigraphy with 131I-19-iodocholesterol. Indications and results in 66 cases of hypercortisolism and hyperaldosteronism (author's transl)].

Scintigraphy was used in 66 patients with biochemically demonstrated hyperactivity of the adrenal cortex in order to determine the nature and site of the lesions. In cases of hypercortisolism, uptake was bilateral in 12 patients with Cushing's disease, unilateral in 7 patients with malignant or non-malignant tumours, and absent in 3 cases of large malignant tumours. In cases of hyperaldosteronism, scintigraphy performed during dexamethasone-induced ACTH suppression showed distinctly asymmetrical uptake in 13 patients with Conn's adenoma (confirmed by surgery as being on the good uptake side in 10 patients), symmetrical in 20 patients with biochemical findings indicating bilaterality, and intermediate in 9 patients. There was no false positive diagnosis of tumour. Scintigraphy appears to be of considerable value for locating adrenocortical lesions, especially small tumours.

19-Iodocholesterol↗

[Thiamine prevention of the corticosteroid reaction afer surgery].

Thiamine effect on the blood 11-HOCS, hydrocortisone and corticosterone levels were studied in patients subjected to herniotomy and/or appendectomy under local anaesthesia. Intramuscular injections of thiamine in a dose of 0.12 g one day and 1.5 to 2 hours before surgery reduced the corticosteroid reaction prior to the operation (psychogenic factor effect) and at the height of the surgery (operation trauma effect). The subsequent administration of the vitamin averted a decrease in the blood corticosteroid level within the postoperative period. Positive results of experimental and clinical studies allow recommending thiamine as an effective remedy for adrenal gland protection from functional exhaustion at surgical stress.

Adrenal Cortex↗

Cortical hyperplasia of the adrenal gland in the dog.

A survey of the adrenal glands of 151 dogs revealed 33 cases of nodular cortical hyperplasia and six cases of diffuse cortical hyperplasia. The gross, microscopic and ultrastructural changes seen in these two forms of the condition are compared. Detailed measurements indicate that a morphometric study is of some value in establishing a post mortem diagnosis of hyperadrenocorticalism. Cell counts show that, despite differences revealed by histological examination, cellular hypertrophy may be in important feature in both nodular and diffuse 'hyperplasia'. Electron micrography suggests that the ultrastructural changes in nodular hyperplasia are of a degenerative nature while in diffuse hyperplasia the increased quantity of endoplasmic reticulum present and the appearance of the other organelles indicate hyperactivity. This correlates well with the clinical evidence of hyperadrenocorticalism seen in the latter condition.

Adrenal Cortex↗

Use of urine cortisol:creatinine ratio versus adrenocorticotropic hormone stimulation testing for monitoring mitotane treatment of pituitary-dependent hyperadrenocorticism in dogs.

OBJECTIVE: To evaluate use of urine cortisol-to-creatinine ratio (UC:C) as a means of monitoring response to long-term mitotane treatment in dogs with pituitary-dependent hyperadrenocorticism. DESIGN: Prospective uncontrolled study. ANIMALS: 101 dogs with pituitary-dependent hyperadrenocorticism. PROCEDURE: Urine samples were obtained from dogs on the morning an ACTH stimulation test was performed, and owners were asked their opinion on the health of their dog to monitor response to mitotane treatment. Urine was assayed for cortisol and creatinine concentrations, and UC:C was calculated. The UC:C was compared with post-ACTH plasma cortisol concentration. RESULTS: Post-ACTH plasma cortisol concentration was used to categorize each dog's response to mitotane treatment. The UC:C did not correlate satisfactorily with results of ACTH stimulation testing. Twenty-seven of 85 (32%) dogs would have been incorrectly considered as having received appropriate doses using UC:C. In addition, 16 dogs that received overdoses could not be distinguished from 29 dogs that received appropriate doses. CLINICAL IMPLICATIONS: UC:C does not provide a consistent, correct assessment of mitotane-induced adrenocortical destruction. The ACTH stimulation test, although more time-consuming and expensive, is recommended for monitoring response to mitotane treatment.

Adrenal Cortex↗