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Results for “Adrenocortical Hyperfunction”

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PubMed2001

[Diagnosis and surgical treatment of arterial hypertension of adrenal origin].

230 patients with arterial hypertension of adrenal origin were treated. 205 of them underwent adrenalectomy with surrounding paranephral fat. There were no lethal outcomes. Endogenic adrenocorticism was diagnosed in 134 patients. Cushing's syndrom was in 96 patients, Cushing's disease--in 34, ACTH-ectopic syndrome--in 2, adrenocortical cancer--in 2. Primary hyperaldosteronism was diagnosed in 42 cases: idiopathic hyperaldosteronism in 23 patients, aldosteronproducing adenoma (Conn's syndrome)--in 19. Tumors of chromaffine tissue were defected in 30 patients. All the patients underwent complex examination (hormonal profile, US, CT, MRT, angiography if it was necessary). Symptomatic arterial hypertension of adrenal origin was diagnosed during one year in 10% patients only because of absence of typical clinical picture. Use of complex examination has permitted to make a correct topical diagnosis and to choose optimum treatment policy in all the cases.

ACTH Syndrome, Ectopic↗
PubMed1975

[Hypercorticism].

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Adrenocortical Hyperfunction↗
PubMed2001

[Endocrine myopathies].

Disturbances in the endocrine system induce a myopathy by acting on protein synthesis or on energetic metabolic pathways. Thus, a proximal myopathy is seen in hypercorticism, hyper- or hypothyroidism and acromegaly. On the other hand, endocrine disorders modify the transsarcolemmal balance in electrolytes, inducing generalized paresia, as in adrenal insufficiency or in thyrotoxic periodic paralysis. The diagnosis is usually easy if a muscle disorder occurs in a complete clinical feature of endocrinopathy but a myopathy may reveal it. Moreover, the steroid myopathy induced by iatrogenic glucocorticoid excess may lead to confusion in patients treated for an inflammatory myopathy. The treatment of endocrine myopathies is based on the correction of the hormonal disorder.

Acromegaly↗
PubMed2001

[Polycystic ovary syndrome of extra-ovarian origin. Review].

An established fact in the polycystic ovarian syndrome (POS) is an abnormal ovarian steroidogenesis. Though this suggest an intrinsic ovarian defect, the syndrome could also be influenced by factors outside the ovaries. Although of unknown etiology, the POS is one of the most frequent endocrine disorders in the gynecologic practice. The disorder is characterized by ultrasound findings of enlarged polycystic ovaries, hyperandrogenism, menstrual disorders, obesity and including the appearance of infertility. There are a series of mechanisms involved in the extraovarian androgen increase in patients with POS. Among these mechanisms are implicated those of central and peripheral origin, genetic factors and adrenocortical dysfunction. In the same way, the alterations produced could imply genetic, molecular biological, biochemical, physiological and endocrinological factors. Sometimes all these factors could interact at the same time. The high serum androgen level could stop the pituitary gonadotropin production, either as a direct mechanism or as a result of its peripheral conversion. The increased androgens also explain the manifestations of clinical acne, hirsutism, and the detention in follicular ovarian maturation. All these manifestations are related with the menstrual disorders, anovulation, and infertility that these patients develop. The characteristics of the extraovarian POS include the 17-hydroxyprogesterone elevation in response to the ACTH test and the dexamethasone suppression of adrenal androgens. It is possible to improve the ovarian function in some patients with POS. This could be achieved with clomiphene citrate associated with glucocorticoids to induce ovulation.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed2001

[Elevated hormone levels without endocrinopathy: hypercortisoluria and hypoglycemia as facticious disorders].

A 29-year-old female patient with weight gain and intermittent hypertension was suspected of having Cushing's syndrome due to conspicuous hypercortisoluria. Specific laboratory tests demonstrated that the urine samples contained prednisolone, which had resulted in a false positive elevation of urine-free cortisol measurements. The patient admitted to having taken prednisolone tablets and also to having added them to several urine collections. In a 21-year-old male patient with unexplained hypoglycaemia, hypoglycaemia was recorded during a 72-hour fast together with an elevated level of plasma insulin and a low level of plasma C-peptide. The presence of insulin autoantibodies could be excluded, making a diagnosis of factitious hypoglycaemia highly likely. Both patients were confronted with the factitious disorder and received psychiatric counselling, after which no further problems arose. Where excessive hormone levels occur, the possibility of a factitious disorder needs to be considered. In such cases, specific supplementary laboratory tests may prove helpful.

Adrenocortical Hyperfunction↗
PubMed1975

[Value of retropneumoperitoneum in the exploration of Cushing's syndrome. 155 cases].

The study is based upon 155 cases of Cushing's syndrome and shows the diagnostic value ognosis of the suprarenal lesion responsible was possible. Bilateral suprarenal hyperplasia was always recognised with accuracy. Pneumoretroperituneum is the technique of choice for the surveillance of the therapeutic effects of synthetic anti-cortisols (especially O.P.'D.D.D.).

Adenoma↗
PubMed2001

[Adrenocortical macronodular hyperplasia with massive enlargement of the gland. A rare variant of autonomous hypercortisolism].

OBJECTIVE: To present a case of Cushing's syndrome due to massive adrenocortical macronodular hyperplasia that gave the gland the appearance of a pseudotumor. METHODS: In a review of the surgical pathology of the adrenal gland recently performed in our hospital, 82 adrenalectomy specimens obtained from 1978-1998 were found. Of these 82 surgical specimens, 44 (53.6%) were cortical pathologies and 10 of these (12.1%) were hyperplasia. There was only one with massive adrenocortical macronodular hyperplasia. A 53-year-old male, chronic alcoholic with cushingoid obesity and hypercortisolism is described. RESULTS: Ultrasound and CT assessment showed enlarged, asymmetrical adrenal glands and macronodules. The analytical and MRI study of the sella turcica showed primary adrenal hypercortisolism. Adrenalectomy of the dominant gland (the left adrenal whose activity was demonstrated on the 131Iodine scintiscan) was performed. The postoperative cortisol levels returned to normal and remain normal up to the present time, 18 months after surgery. The surgical specimen weighed 104 gms and was completely macronodular. CONCLUSIONS: Massive adrenocortical macronodular hyperplasia is a rare cause of pituitary-independent autonomous primary adrenal hypercortisolism. It is always bilateral. Adrenal weight is significantly increased (total weight of both adrenals 60-180 gms) and present yellow or golden, non-encapsulated nodules of a few millimeters to up to 4 cms, comprised of cells with scanty activity, therefore massive enlargement of the glands is necessary to produce Cushing's syndrome. The clinical, biochemical and surgical aspects can cause confusion and can be suggestive of an adrenocortical neoplasm. Treatment is by adrenalectomy.

Adrenal Cortex↗
PubMed1975

Immunity to Hammondia hammondi infection in cats.

Acquisition of immunity to Hammondia hammondi, a newly recognized coccidian of cats, was studied in 18 specific-pathogen-free cats. One cat was given a single oral inoculation, 11 cats were given 2 oral inoculations, and 1 cat was given 3 oral inoculations of homogenized mouse carcasses containing H hammondi. In all cats, oocyst shedding began 6 to 9 days after the 1st inoculation. Oocyst shedding peaked at 1 to 2 days after the onset of shedding and lasted for 1 to 2 weeks. None of the cats became sick. Of the 11 cats inoculated twice (between 2-51 days after the 1st inoculation), 5 shed oocysts 7 to 14 days after the repeat inoculation; however, fewer oocysts were shed at this time. One cat that was inoculated thrice (14 and 51 days after the 1st inoculation) shed oocysts 14 to 17 days after the 3rd inoculation but not after the 2nd inoculation. Spontaneous oocyst shedding was studied in 9 of these 13 H hammondi-infected cats for 5 months. Two cats spontaneously shed oocysts: One cat (inoculated only once) spontaneously re-shed oocysts 21 to 24, 31 to 33, 49 to 50, and 118 to 120 days after inoculation; The other cat (inoculated twice-the 2nd time, 6 days after the 1st inoculation) re-shed oocysts 38 to 48, 85 to 89, and 133 to 136 days after the 1st inoculation. The course of H hammondi infection was studied in 5 cats given weekly injections of 6-methyl prednisolone acetate for at least 7 weeks, starting 18 days before inoculation in 2 cats, and starting 14, 34, and 45 day after inoculation in 3 cats. The induced hyperadrenocorticism did not affect the prepatent period or induce parasitism of extraintestinal organs. The 3 cats infected for 14, 34, and 45 days, re-shed oocysts after hyperadrenocorticism was induced. It was concluded that immunity to H hammondi infection in cats is less stable than immunity to the related coccidian, Toxoplasma gondii.

Adrenocortical Hyperfunction↗
PubMed1975

[Bartter's disease associated with hypercorticism, phosphate and magnesium deficiencies and familial renal tubular disease].

A new case of Bartter's syndrome is described. There is a context of other cases of familial renal tubular disease with a sex-linked heredity. In this case, the Bartter's syndrome is associated with magnesium deficiency and hypomagnesemia, with a ricket and severe phosphate deficiency, and finally with an hypercorticism. The basal secretion rate of cortisol agree with a Cushing's syndrome. This hypercorticism is corrected by aminogluthetimide. The influence of the hyperreninism on the hypercorticism is discussed.

Adrenocortical Hyperfunction↗