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[Clinical use in the radioimmunologic determination of plasmatic TSH].
Clinical value of plasma TSH radioimmunoassay in various thyroid diseases (primary hypothyroidism, hyperthyroidism and simple goiter) is discussed. In particular, the results obtained of plasma TSH after TRH administration either in thyroid disease either in various disorders of endocrinologic interest (massive obesity, Laurence-Moon Biedl's syndrome, true precocious puberty, congenital adrenal hyperplasia, Klinfelter's and Turner's syndromes) are discussed.
[Therapeutic value of ascorbic acid in the pre- and postoperative periods in complicated ulcer disease].
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[Functional tests used in diagnosis of different forms of hypercorticism].
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[Cushing's syndrome caused by multiple nodular hyperplasia of the adrenal cortex].
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[Morphology of the kidneys in arterial hypertension of adrenal genesis (according to biopsy findings)].
67 renal biopsies obtained in the course of adrenalectomy from patients with primary hyperaldosteronism, hypercorticism and pheochromocytoma were studied. Sclerotic affection of the arterioles and renal interstitium were found in long lasting adrenal arterial hypertension. This may cause residual postoperative hypertension. Endocrine nephropathy in primary hyperaldosteronism due to hypopotassemia and alcalosis manifests with vacuolar distrophy and atrophy of the epithelium, dilatation of tubular lumen, intratubular calcinosis and tubulointerstitial nephritis. Primary hyperaldosteronism was characterized by hypoplasia of the juxtaglomerular apparatus (JGA) but in massive spironolacton therapy signs of enhanced renin-secreting function of the glomerular efferent arteriola may be observed. In hypercorticism pyelonephritis is rather frequent. In patients with pheochromocytoma hypercatecholaminemia may result in JGA activation this being particularly evident in renal artery stenosis. Recurrent hypertension after pheochromocytoma removal in the absence of renal pathology may indicate recurrent tumor or missed second tumor.
[Clinical heterogeneity of X-linked adrenoleukodystrophy ].
X-linked adrenoleukodystrophy (X-ALD) is a relatively common world spread disease characterized by significant clinical heterogeneity. Clinico-biochemical examination in the Medico-genetic research center identified, 20 X-ALD cases in 17 families over 5 years. Prevalence of children (60%) and adolescence (25%) cerebral forms is explained, in part, by patients referring for medical-genetic counseling. Adrenomyeloneuropathy was diagnosed in one patient. In two healthy siblings presymptomatic stage was found. A main X-ALD biochemical marker is an increase of very long chain fatty acids (VLCFA) level, which does not depend on clinical form of the disease. Most interesting appeared to be a family including 5 patients in 3 generations with intrafamilial combination of childhood and adolescence cerebral forms, and atypically mild disease course in proband. Regarding symptoms of childhood and adolescence cerebral forms, attention has been drawn to 3 patients with tics, which mask organic nature of the disease on its initial stage. X-ALD is so far incurable, but its timely diagnosis provides an adequate medico-genetic help on the base of modern prenatal diagnosis.
[Function of the fetal adrenal cortex].
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[Primary aldosteronism].
The syndrome of primary aldosteronism is caused either by an aldosterone-producing adenoma or by idiopathic bilateral adrenal hyperplasia. Hypokalemic hypertension is the leading symptome of the disease. Diagnosis is by the combination of abnormally high and non-suppressible aldosterone values with undetectable or low renin values unresponsive to postural changes or salt restriction. Patients with aldosterone-producing adenoma normally show a fall in plasma aldosterone in response to posture and ACTH-dependent circadian rhythm of aldosterone, whereas bilateral hyperplasia is characterized by postural increases in plasma aldosterone and an ACTH-independent diurnal aldosterone rhythm. These creteria serve to differentiate between adenoma and hyperplasia. An aldosterone-producing adenoma can be localized by veinography, determination of aldosterone concentration in both adrenal veins and by 131I-cholesterol scintigraphy. In our hands the determination of aldosterone in blood from both adrenal veins is the most efficient procedure. In interpreting the results, however, rhythmic and sudden changes in adrenal hormone secretion should be considered. In cases where no adrenal venous blood is obtained, 131I-cholesterol scintigraphy may be used to localize adenoma. In patients with aldosterone-producing adenomas unilateral adrenalectomy should be performed, whereas patients with idiopathic bilateral hyperplasia should receive antihypertensive therapy. As rare instances of primary aldosteronism, a case of aldosterone-producing carcinoma of the adrenal cortex and a case of presumably unilateral adrenal hyperplasia are reported.
Identical male twins with congenital adrenal hyperplasia. Comparison of growth, serum and urinary steroids.
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Source of serum alkaline phosphatase in clinically normal and diseased dogs: a clinical study.
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[Corticosuprarenaloma in children].
Thirty-four cases of corticosurrenaloma with clinical onset before 15 years of age have been studied. Higher frequency in girls (65 percent of the cases) and in young age (80 percent before 5 years of age, 43 percent before 2 years), association with personal or familial other tumors and malformations, are noticeable features. Virilism is the major manifestation in children (83 percent of the cases), either isolated or associated with hypercortisolism and/or feminization. Hormonal assays are of little value, and the dynamic adrenal tests are of some help only in small tumors or isolated hypercortisolism. Radiological diagnosis by urography with cavography, arteriography, is easy in most cases. Evaluation of prognosis is very difficult. Clinical and biological data are not significant, histological data are often of little help. Only a very large mass, and occurrence of metastases (liver, lungs) evidence malignancy. This series does not allow to assess definitely the best therapeutic regimen. Surgery has to be performed as soon as possible. The effects of radiations have not yet been ascertained. High doses of op'DDD have led to a sustained remission of the tumor or metastases in 2 patients, and perhaps to a longer survival in 4 others.
[Adverse effects of inhaled corticosteroids are dose-dependent].
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[The most common forms of endocrine-based hypertension].
Endocrine (adrenal) hypertension (primary aldosteronism, hypercortisolism and pheochromocytoma) had been considered for a long time as a rare cause of arterial hypertension. However, recent studies have shown a frequent incidence of primary aldosteronism among hypertensive subjects and therefore it is necessary to exclude primary aldosteronism in all subjects with severe hypertension. On the contrary, pheochromocytoma and hypercortisolism may be often overlooked in patients with incidentally found adrenal tumor and thus they can cause unexpected per- and postoperative complications.
[Primary hyperaldosteronism].
Primary hyperaldosteronism (PHA), autonomic secretion of aldosterone by the adrenal gland, is rare. PHA usually results in therapy-resistant hypertension and is often but not always accompanied by hypokalaemia. Common causes of PHA are an aldosterone-producing adenoma, idiopathic aldosterone hypersecretion, unilateral hyperplasia or a genetic variant: glucocorticoid-remediable aldosteronism (GRA). The diagnosis should be phased and first of all requires a biochemical confirmation of the presence of PHA. In PHA patients, plasma renin is invariably suppressed. Blood should be collected under standardised conditions while the patient is not using beta-blockers or centrally-acting antihypertensive medication. Patients with a suppressed plasma renin and an elevated plasma aldosterone concentration have PHA. In patients with a suppressed plasma renin and a high-normal plasma aldosterone concentration a confirming test should be performed in which PHA is diagnosed if aldosterone is not suppressed following volume expansion with sodium chloride. The cause of PHA is determined by means of a CT scan or MRI of the adrenal glands to find a unilateral adenoma. If the CT scan or MRI is normal, adrenal vein aldosterone sampling may be considered as a next step in order to demonstrate lateralisation of aldosterone production. The hypertension and hypokalaemia of all forms of PHA respond well to spironolactone therapy. In the case of a unilateral adenoma or unilateral hyperplasia, adrenalectomy is the treatment of choice. For GRA, dexamethasone in doses that reduce the corticotropin (ACTH) level is indicated.
Pemphigus vulgaris; hyperadrenalism with osteoporosis.
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[Experimental study on hyperadrenalism; studies on blood coagulation].
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Primary neoplasms of the adrenal gland; diagnosis and surgical management.
Tumors of the adrenal glands produce hormones which cause a variety of symptoms and signs including high blood pressure, excessive growth of hair on the body and precocious sexual development. By recently developed tests, it has been possible to differentiate high blood pressure due to these tumors from hypertension due to other causes. Removal of these tumors will often alleviate changes caused by them. Localization of the tumor and appraisal of the condition of the contralateral gland should be carried out preoperatively if possible. In this, several kinds of roentgen studies are helpful. Infusions of drugs during operation can be used to control the blood pressure which otherwise would vary widely. During a ten-year period (1942 to 1951) there were observed at the Los Angeles County General Hospital 100 proved cases of non-secreting and secreting primary neoplasms of the adrenal glands. In addition, there were three cases of Cushing's syndrome due to bilateral adrenal cortical hyperplasia, and ten probable cases (four, pheochromocytomas; five, Cushing's syndrome; one, adrenogenital syndrome) in which operation was not done.