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At least 73 records · Page 4Linked to original sources
PubMed1995

[The steroid content of the amniotic fluid in the 1st and 2nd pregnancy trimesters in 21-hydroxylase insufficiency and in fetal central nervous system defects].

A total of 103 samples of amniotic fluid obtained by transabdominal amniocentesis were examined, 52 of these from women at a high risk of giving birth to children with congenital adrenal hyperplasia due to 21-hydroxylase (21-OH) deficiency and 30 ones with fetuses with different neural tube malformations. 17-Hydroxyprogesterone was found to be a reliable marker indicating the disease in fetuses from the group at risk of hereditary 21-OH deficiency. This marker can be effectively used as early as in the 1 gestation trimester. Fetal CNS defects are associated with hypofunction of the adrenal cortex in the II gestation trimester, observed in 60-63% of cases with hydrocephalus, anencephaly, or microcephaly. Since the function of fetal adrenals is of paramount importance for the development and maturation of a fetus, it should be examined in case of developmental defects of the neural tube, in order to predict the effect of prenatal treatment.

17-alpha-Hydroxyprogesterone↗
PubMed1996

[Late-onset adrenomyeloneuropathy perplexed with spondylosis. A case report].

We reported a 60-year-old man with late-onset adrenomyeloneuropathy (AMN). He had been well until 10 years before entry, when he noticed numbness in the legs with gait difficulty; symptoms worsened gradually with additional urinary disturbance. Transient improvement occurred after cervical and lumbar spinal operation under the diagnosis of spinal spondylosis, while his spastic gait got worse. Neurological examination on admission disclosed bilateral horizontal nystagmus, ataxic and spastic gait, increased patellar tendon reflexes, Chaddock sign, and impaired deep sense in the lower limbs with positive Romberg sign. Abnormal laboratory data included hypofunction of the adrenal cortex and elevated saturated very long chain fatty acids (VLCFAs). Serum cholestanol level was normal and anti-HTLV-1 antibody was negative. T2-weighted MRI showed a high signal intensity lesion in the occipital white matter along the optic radiation. Electrophysiological tests suggested a brainstem lesion on auditory brainstem response, thoracic or lumbar lesion on somatosensory evoked potential, and peripheral neuropathy on nerve conduction study. In the present case, it should be emphasized that the determination of serum VLCFAs unveiled the diagnosis of AMN in old patients with spinal spondylosis or without apparent clinical symptoms of adrenocortical insufficiency.

Adrenoleukodystrophy↗
PubMed1988

Diseases of the adrenal cortex.

The adrenal cortex is functionally a three-dimensional gland that secretes glucocorticoids, mineralocorticoids, and sex steroids. Of these three classes of steroids only the gluco- and mineralocorticoid hormones are necessary to sustain life. The availability of sensitive and specific radioimmunoassays has permitted accurate measurement of practically every steroid hormone secreted by the adrenal cortex. As in other endocrinopathies, suppression studies are employed when hyperfunction is suspected, while provocative tests are used to detect hypofunction. These dynamic studies enable the clinician to evaluate the functional status of the adrenal cortex. The anatomic configuration of the adrenal cortices is delineated by high-resolution computed tomography (and magnetic resonance imaging), obviating the need for invasive procedures such as venography or arteriography. The disorders of the adrenal cortex can be viewed from the dual perspectives of hyperfunction and hypofunction. Clinical expressions of hyperfunctional adrenocortical syndromes include Cushing's syndrome, primary hyperaldosteronism, and the adrenogenital syndrome. The expressions of hypofunctional syndromes include Addison's disease and selective hypoaldosteronism. The diagnosis and treatment of these disorders are outlined in this issue.

Addison Disease↗
PubMed1986

[The thyroid gland and adrenal cortex in the large fetus and their role in the development of macrosomia].

In a morphological study of thyroid glands and adrenal cortex of large fetuses compared to the controls the authors revealed a significant increase of the thyroid gland functional activity, as well as of glomerular and fascicular zones of adrenal cortex. The functional tension of the thyroid gland appeared to be reduced in large fetuses with obesity. Hyperfunction of all zones of the adrenal cortex was also revealed in them. In medium height fetuses with obesity hypofunction of the thyroid gland, as well as hyperfunction of the fascicular and fetal adrenal cortex zones were present. Correlation-regression analysis has revealed close interrelations between the functional state of the thyroid gland, adrenal cortex and fetal mass.

Adrenal Cortex↗
PubMed1979

The effect of a low potassium diet on the glomerular zone of the adrenal cortex of rats.

Rats were fed on low potassium diets in order to observe the effect of dietary low potassium on the adrenal cortex. The authors clarified morphological changes of the hypofunctional glomerular zone and compared these changes with those of the hyperfunctional glomerular zone. Three weeks after or 2 months after the start of a low potassium diet, slight narrowing of the glomerular zone of the adrenal cortex was observed followed by miniaturization of cells, presence of binuclear cells and an increase of lipid with enlarged lipid drops. Electron microscope mainly disclosed changes of mitochondrial cristae consisting of markedly reduced, enlarged and irregularly dilated cristae with shortening or elongation. Granules appeared in mitochondria. Lysosomes or dense bodies were enlarged. The Golgi's apparatus was atrophied but endoplasmic reticulum did not show remarkable changes. These changes were directly opposite to those of the hyperfunctional glomerular zone noted after a pottasium load or seen in sodium deficiency. Consequently, these changes were considered to be the changes of the hypofunctional glomerular zone associated with decrease of aldosterone production.

Adrenal Cortex↗
PubMed1978

[Change in the adrenal cortex of rats in stress after hypophysectomy, thyroidectomy and castration].

To elucidate factors producing destructive changes in the adrenal cortex under severe stress, the following experiments were performed: 1) severe combined stress (KC) including unilateral adrenalectomy and fixation in supin position for 24 h (control group); 2)hypophysectomy KC; 3) thyroidectomy KC; 4) bilateral orchiectomy KC; 5) injection of vitamine "E" for 14 days + KC. The adrenals were studied by a complex of morphometrical and histochemical methods. Hypophysectomy prevented estructive changes in the adrenal cortex under KC. This effect was not connected with hypofunction of the thyroid gland and the testes, as their excision (in rats without hypophysectomy) did not prevent the development of necrobiotic changes in the adrenal cortex. A suggestion is made on a "corticolytic" effect of ACTH which reveals itself under severe stress. Destruction of adrenocorticocytes is supposed to result from activation of peroxide oxidation of lipids. This is indirectly supported by a large number of lipofuscin containing cells, by decrease in the activity of alkaline phosphatase and ATPh-ase, by activation of acid phosphatase and also by decreasing alterative phenomena at the injection of vitamine "E".

Adrenal Cortex↗