Stress-induced Cushing's syndrome in fur-chewing chinchillas

One of the most serious problems in the chinchilla industry is 'fur-chewing', when the chinchilla bites off areas of its own or some other animal's fur. The condition generally develops in both genders at the age of 6-8 months. In chinchilla farms in Croatia an incidence of 15-20% has been observed. A pathomorphological, microbiological and parasitological investigation was conducted on eleven 6- to 11-month-old chinchillas of both sexes with clinical symptoms of 'fur-chewing' and three chinchillas without such signs. Histopathology of the adrenal glands and of the chewed skin revealed changes typical of Cushing's syndrome in 'fur-chewed' chinchillas, such as hyperkeratinisation of the epidermis, epidermal atrophy, pronounced follicular and sebaceous gland atrophy, hyperkeratinisation of the follicles with comedo formations and the presence of calcium salts in subcutis.

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Investigation of atrophic adrenal glands in Cushing's syndrome model rats induced by the administration of dexamethasone

Endocrine Abstracts ◽

10.1530/endoabs.49.ep4 ◽

2017 ◽

Author(s):

Toshiro Seki ◽

Atsushi Yasuda ◽

Natsumi Kitajima ◽

Masami Seki ◽

Masayuki Oki ◽

...

Keyword(s):

Cushing’S Syndrome ◽

Adrenal Glands ◽

Cushing's Syndrome

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Pitfalls in the diagnosis and management of Cushing's syndrome

Neurosurgical FOCUS ◽

10.3171/2014.11.focus14704 ◽

2015 ◽

Vol 38 (2) ◽

pp. E4 ◽

Cited By ~ 34

Author(s):

Vivek Bansal ◽

Nadine El Asmar ◽

Warren R. Selman ◽

Baha M. Arafah

Keyword(s):

Cushing’S Syndrome ◽

Cushing’S Disease ◽

Salivary Cortisol ◽

Clinical Symptoms ◽

Cushing's Syndrome ◽

Cushing's Disease ◽

Biochemical Tests ◽

Late Night ◽

Late Night Salivary Cortisol ◽

Free Cortisol

Despite many recent advances, the management of patients with Cushing's disease continues to be challenging. Cushing's syndrome is a complex metabolic disorder that is a result of excess glucocorticoids. Excluding the exogenous causes, adrenocorticotropic hormone–secreting pituitary adenomas account for nearly 70% of all cases of Cushing's syndrome. The suspicion, diagnosis, and differential diagnosis require a logical systematic approach with attention paid to key details at each investigational step. A diagnosis of endogenous Cushing's syndrome is usually suspected in patients with clinical symptoms and confirmed by using multiple biochemical tests. Each of the biochemical tests used to establish the diagnosis has limitations that need to be considered for proper interpretation. Although some tests determine the total daily urinary excretion of cortisol, many others rely on measurements of serum cortisol at baseline and after stimulation (e.g., after corticotropin-releasing hormone) or suppression (e.g., dexamethasone) with agents that influence the hypothalamic-pituitary-adrenal axis. Other tests (e.g., measurements of late-night salivary cortisol concentration) rely on alterations in the diurnal rhythm of cortisol secretion. Because more than 90% of the cortisol in the circulation is protein bound, any alteration in the binding proteins (transcortin and albumin) will automatically influence the measured level and confound the interpretation of stimulation and suppression data, which are the basis for establishing the diagnosis of Cushing's syndrome. Although measuring late-night salivary cortisol seems to be an excellent initial test for hypercortisolism, it may be confounded by poor sampling methods and contamination. Measurements of 24-hour urinary free-cortisol excretion could be misleading in the presence of some pathological and physiological conditions. Dexamethasone suppression tests can be affected by illnesses that alter the absorption of the drug (e.g., malabsorption, celiac disease) and by the concurrent use of medications that interfere with its metabolism (e.g., inducers and inhibitors of the P450 enzyme system). In this review, the authors aim to review the pitfalls commonly encountered in the workup of patients suspected to have hypercortisolism. The optimal diagnosis and therapy for patients with Cushing's disease require the thorough and close coordination and involvement of all members of the management team.

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STUDIES ON THE IN VITRO PRODUCTION OF CORTICOSTEROIDS BY ADRENAL GLANDS FROM NORMOTENSIVE INDIVIDUALS AND HYPERTENSIVE PATIENTS

Canadian Journal of Biochemistry and Physiology ◽

10.1139/y62-032 ◽

1962 ◽

Vol 40 (1) ◽

pp. 285-301 ◽

Cited By ~ 1

Author(s):

Jean Davignon ◽

Erich Koiw ◽

Wojciech Nowaczynski ◽

Gilles Tremblay ◽

Jacques Genest

Keyword(s):

Cushing’S Syndrome ◽

Adrenal Glands ◽

Cushing's Syndrome ◽

The Other ◽

Malignant Hypertension ◽

Unit Weight ◽

Chromatographic Technique ◽

Acth Stimulation ◽

The Mean

The production of aldosterone and other corticosteroids by adrenal glands surgically removed from 5 normotensive subjects with renal disease of various types, 11 patients with arterial hypertension, and 2 with Cushing's syndrome was investigated in vitro by the incubation chromatographic technique. The rate of steroid formation per unit weight of tissue was markedly lower in severe and malignant hypertension and slightly higher in benign hypertension as compared with the rate in normotensive controls. The amount of steroid released varied widely from one gland to the other and showed marked overlapping between the various groups; these variations were most prominent in benign hypertension, less in the normotensive group, and least evident in severe and malignant hypertension. The response of steroidogenesis to ACTH stimulation in vitro was slightly reduced in severe and malignant hypertension. The mean output of aldosterone by adrenal glands from hypertensives was slightly above the mean value obtained with normotensive control glands. The percentage of aldosterone formation in respect to total steroid production was roughly correlated with the severity of hypertension. In four hyperplastic adrenals obtained from two cases of Cushing's syndrome, the in vitro formation of steroids per unit weight of tissue and the response to ACTH did not differ significantly from that found in glands obtained from the other patients under study. The value of in vitro studies for the assessment of the functional capacity of the adrenal cortex is discussed.

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ACTH-independent massive bilateral adrenal disease (AIMBAD): A subtype of Cushing's syndrome with major diagnostic and therapeutic implications

Acta Endocrinologica ◽

10.1530/eje.0.1310067 ◽

1994 ◽

Vol 131 (1) ◽

pp. 67-73 ◽

Cited By ~ 55

Author(s):

Steven A Lieberman ◽

T Ross Eccleshall ◽

David Feldman

Keyword(s):

Cushing’S Syndrome ◽

Adrenal Glands ◽

Medical Center ◽

Serum Cortisol ◽

Cushing's Syndrome ◽

Bilateral Adrenalectomy ◽

Preoperative Treatment ◽

Therapeutic Implications ◽

Adrenal Imaging ◽

Adrenal Disease

Lieberman SA, Eccleshall TR, Feldman D. ACTH-independent massive bilateral adrenal disease (AIMBAD): a subtype of Cushing's syndrome with major diagnostic and therapeutic implications. Eur J Endocrinol 1994:131:67–73. ISSN 0804–4643 A 49-year-old man with classic manifestations of Cushing's syndrome had undetectable levels of ACTH, lack of suppression of hypercortisolism with dexamethasone in doses of 2, 8, or 16 mg per day, bilaterally enlarged adrenal glands on MRI, and bilateral adrenal uptake of iodocholesterol. Preoperative treatment with ketoconazole lowered blood pressure and serum cortisol and produced symptoms of steroid withdrawal. Bilateral adrenalectomy revealed massively enlarged adrenal glands (left: 199 g, right: 93 g). Sequencing of the gene encoding the stimulatory G protein, Gsα, did not show either of two activating mutations previously reported in patients with McCune–Albright syndrome or acromegaly. Twenty-three previous cases of Cushing's syndrome due to ACTH-independent massive bilateral adrenal disease (AIMBAD) have been reported. AIMBAD may cause confusion in the differential diagnosis of Cushing's syndrome as endocrine testing suggests a unilateral, ACTHindependent process while adrenal imaging demonstrates bilateral abnormalities. Bilateral adrenalectomy is curative and appears to carry little risk of Nelson's syndrome. The pathogenesis of AIMBAD appears to be heterogeneous, as recent reports have demonstrated GIP-mediated hypercortisolism and familial AIMBAD. Transition from Cushing's disease to ACTH-independence is not supported by the available data. Future cases of AIMBAD should be investigated carefully to further elucidate the pathogenesis of this disorder. David Feldman, Division of Endocrinology, Dept. of Medicine, Room S-005, Stanford University Medical Center, Stanford, CA 94305, USA

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Hypophosphatemia as Unusual Cause of ARDS in Cushing’s Syndrome Secondary to Ectopic CRH Production. A Case Report

The Scientific World JOURNAL ◽

10.1100/tsw.2008.20 ◽

2008 ◽

Vol 8 ◽

pp. 138-144 ◽

Cited By ~ 4

Author(s):

Stefania Mondello ◽

Vincenzo Fodale ◽

Salvatore Cannav ◽

Carmela Aloisi ◽

Barbara Almoto ◽

...

Keyword(s):

Case Report ◽

Cushing’S Syndrome ◽

Clinical Symptoms ◽

Laboratory Data ◽

Blood Gases ◽

Recovery Phase ◽

Cushing's Syndrome ◽

Surgical Removal ◽

Arterial Blood ◽

Underlying Disorder

Hypophosphatemia is an unusual cause of acute respiratory distress syndrome (ARDS). We describe a hypophosphatemia-related ARDS case report of a 50-year-old woman with ACTH dependent Cushing's syndrome secondary to ectopic CRH production. The patient clinically showed hypotension tachypnea and increasing dyspnea. Laboratory data showed carbohydrate intolerance, severe hypokalemia, and hypophosphatemia. Arterial blood gases measurement revealed hypocapnia and elevation in bicarbonate values. Chest X-ray showed diffuse bilateral alveolar infiltrates similar to acute pulmonary edema and Kerley's striae. Chest CT scan evidenced diffuse ground glass opacification, bilateral patchy consolidation, and fibrosis, compatible with the recovery phase of ARDS. Clinical symptoms and laboratory examinations supported the diagnosis of ARDS. The patient was managed with supplemental potassium, octreotide, and oxygen therapy. Hypophosphatemia was managed by treating the underlying disorder. Successive surgical removal of the adrenal gland led to complete resolution of Cushing's syndrome. In conclusion, although rare and associated with specific risk factors, hypophosphatemia should be suspected in patients who develop unexplained ARDS.

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FAMILIAL CUSHING'S SYNDROME

Acta Endocrinologica ◽

10.1530/acta.0.0870139 ◽

1978 ◽

Vol 87 (1) ◽

pp. 139-147 ◽

Cited By ~ 23

Author(s):

Bartolomé Arce ◽

Manuel Licea ◽

Santiago Hung ◽

Rubén Padrón

Keyword(s):

Short Stature ◽

Carbohydrate Metabolism ◽

Cushing’S Syndrome ◽

Adrenal Glands ◽

Clinical Manifestations ◽

Cushing's Syndrome ◽

Adrenal Carcinoma ◽

Adenomatous Hyperplasia

ABSTRACT Cushing's syndrome has been demonstrated in four of seven siblings with clinical manifestations appearing around puberty in three of the four siblings. The only other associated findings in these cases were short stature and disturbed carbohydrate metabolism. Adenomatous hyperplasia of the adrenal glands was demonstrated in 3 of the patients, and a virilizing adrenal carcinoma in the fourth sibling. The pathogenesis of the adrenocortical disorders in these siblings is discussed.

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