The natural history of cushing's syndrome

Plotz, Charles M.; Knowlton, Abbie I.; Ragan, Charles

doi:10.1016/0002-9343(52)90027-2

Cited by 723 publications

(240 citation statements)

References 63 publications

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“…6 " 15 Since corticosteroids are lipogenic in " 22 and since they are increased in Type A individuals under certain situations 23 and in individuals exposed to stress or other environmental challenges, 2425 it is possible that much of the elevated cholesterol associated with coronary heart disease, Type A behavior, and stress could be the result of increased corticosteroids or increased responsiveness to corticosteroids.…”

mentioning

confidence: 99%

Relationship between cortisol and cholesterol in men with coronary artery disease and type A behavior.

Schwertner¹,

Troxler²,

Uhl³

et al. 1984

Arteriosclerosis

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To further understand the hormonal mechanisms linking behavior pattern and coronary artery disease (CAD), we Investigated the relationship between 0930-hour plasma cortisol and cholesterol In relatively young males who had undergone coronary anglography and In a subgroup of Individuals who had undergone the structured interview for classification of behavior pattern. A statistically significant association (p < 0.05) was found between cortisol and cholesterol for Individuals who had either minimal CAD (20% to 49% narrowing) or significant CAD (3=50% narrowing), but not for subjects without CAD. An association between cortisol and cholesterol was also found to be significant S ince serum cholesterol is one of the most important risk factors for coronary heart disease, numerous studies have been made to identify factors that control its levels in blood. Extensive evidence now indicates that cholesterol metabolism is controlled by a complex system involving genetics, sex, diet, and age. Some evidence also indicates that behavior pattern may have an influence on cholesterol concentrations. Individuals with Type A behavior, for instance, have higher serum cholesterol concentrations and have more severe and extensive coronary atherosclerosis than do Type B individuals.

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mentioning

confidence: 99%

Relationship between cortisol and cholesterol in men with coronary artery disease and type A behavior.

Schwertner¹,

Troxler²,

Uhl³

et al. 1984

Arteriosclerosis

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“…However, the exact mechanism has not been defined. In a review of natural Cushing's syndrome cases [11], infections accounted for approximately one half of the deaths in the autopsied cases with Cushing's syndrome. Nine patients were found to have tuberculosis, which is a similar rate to that found in the general autopsy population.…”

Section: Discussionmentioning

confidence: 99%

Adrenal Tuberculosis in Cushing's Disease with Bilateral Macronodular Adrenocortical Hyperplasia

et al. 2006

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Abstract. Cushing's disease is a disorder of hypercortisolism caused by a pituitary micro-or macro-adenoma. Most patients with Cushing's disease have a bilateral adrenal enlargement, which depends on the duration of the disease, as a result of the long standing ACTH stimulation of both adrenal glands. However, in macronodular adrenocortical hyperplasia (MNH) that is caused by Cushing's disease, if the MNH gains autonomy, a bilateral adrenalectomy, as well as the removal of pituitary adenoma, is often essential. We encountered a patient diagnosed with Cushing's disease with bilateral adrenal tuberculosis simulating MNH. She had taken anti-tuberculosis medications one year prior to admission due to spinal tuberculosis. Sellar MRI revealed a pituitary macroadenoma, but adrenal CT showed enlargement in both adrenal glands that appeared to be MNH. A hormonal study and bilateral inferior petrosal sinus sampling revealed Cushing's disease. Therefore, she underwent trans-sphenoidal surgery of the pituitary mass. The pituitary surgery was successful and the serum cortisol returned to normal range. However, the adrenal mass rapidly enlarged after removing the pituitary tumor without showing evidence of a recurrence or adrenal autonomy of hypercortisolism. Accordingly, a laparoscopic left adrenalectomy was performed to examine the nature of the mass. The resected left adrenal gland was pathologically determined to have a lesion of tuberculosis with some part of the intact cortex. So we assumed that the cause of rapid adrenal enlargement might be due to adrenal tuberculosis. In summary, to the best of our knowledge, this is the first case of Cushing's disease coexisting with both adrenal tuberculosis simulating a bilateral MNH.

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“…All those comorbidities, together with the typical hypercoagulable state due to alterations of clotting factors (17), severely impair the cardiovascular profile of patients with Cushing's syndrome, leading to an increased incidence of cardiovascular events and mortality, if left untreated (18,19). Considering that the cardio-metabolic impairment in those patients is often associated with an increased rate of severe infectious complications (20), an increased incidence of osteoporotic fractures, and psychiatric disorders (21), it is clear that patients with Cushing's syndrome are characterized by a life-threating disease that requires a precise causative diagnosis and a rapid therapeutic strategy. A comprehensive review on the complications of Cushing's syndrome and their treatment has been recently published elsewhere (19) and is beyond the scope of this review.…”

Section: Clinical Spectrum Of Adrenal Cushing's Syndromementioning

confidence: 99%

cAMP signaling in cortisol-producing adrenal adenoma

Calebiro

Dalmazi

Bathon

et al. 2015

European Journal of Endocrinology

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The cAMP signaling pathway is one of the major players in the regulation of growth and hormonal secretion in adrenocortical cells. Although its role in the pathogenesis of adrenocortical hyperplasia associated with Cushing's syndrome has been clarified, a clear involvement of the cAMP signaling pathway and of one of its major downstream effectors, the protein kinase A (PKA), in sporadic adrenocortical adenomas remained elusive until recently. During the last year, a report by our group and three additional independent groups showed that somatic mutations of PRKACA, the gene coding for the catalytic subunit a of PKA, are a common genetic alteration in patients with Cushing's syndrome due to adrenal adenomas, occurring in 35-65% of the patients. In vitro studies revealed that those mutations are able to disrupt the association between catalytic and regulatory subunits of PKA, leading to a cAMP-independent activity of the enzyme. Despite somatic PRKACA mutations being a common finding in patients with clinically manifest Cushing's syndrome, the pathogenesis of adrenocortical adenomas associated with subclinical hypercortisolism seems to rely on a different molecular background. In this review, the role of cAMP/PKA signaling in the regulation of adrenocortical cell function and its alterations in cortisolproducing adrenocortical adenomas will be summarized, with particular focus on recent developments.

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The natural history of cushing's syndrome

Cited by 723 publications

References 63 publications

Relationship between cortisol and cholesterol in men with coronary artery disease and type A behavior.

Relationship between cortisol and cholesterol in men with coronary artery disease and type A behavior.

Adrenal Tuberculosis in Cushing's Disease with Bilateral Macronodular Adrenocortical Hyperplasia

cAMP signaling in cortisol-producing adrenal adenoma

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