scholarly journals Is diabetes in Cushing's syndrome only a consequence of hypercortisolism?

2014 ◽  
Vol 170 (2) ◽  
pp. 311-319 ◽  
Author(s):  
Carla Giordano ◽  
Valentina Guarnotta ◽  
Rosario Pivonello ◽  
Marco Calogero Amato ◽  
Chiara Simeoli ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Cushing’S Syndrome ◽  
Cushing's Syndrome ◽  
Visceral Adiposity Index ◽  
Metabolic Complications ◽  
Family History Of Diabetes ◽  
Pituitary Disease ◽  
History Of ◽  
Adrenal Disease

ObjectiveDiabetes mellitus (DM) is one of the most frequent complications of Cushing's syndrome (CS). The aim of this study was to define the changes in insulin sensitivity and/or secretion in relation to glucose tolerance categories in newly diagnosed CS patients.DesignCross-sectional study on 140 patients with CS.MethodsA total of 113 women (80 with pituitary disease and 33 with adrenal disease, aged 41.7±15.7 years) and 27 men (19 with pituitary disease and eight with adrenal disease, aged 38.1±20.01 years) at diagnosis were divided according to glucose tolerance into normal glucose tolerance (CS/NGT), impaired fasting glucose and/or impaired glucose tolerance (CS/prediabetes), and diabetes (CS/DM) groups.ResultsSeventy-one patients had CS/NGT (49.3%), 26 (18.5%) had CS/prediabetes and 43 (30.8%) had CS/DM. Significant increasing trends in the prevalence of family history of diabetes (P<0.001), metabolic syndrome (P<0.001), age (P<0.001) and waist circumference (P=0.043) and decreasing trends in HOMA-β (P<0.001) and oral disposition index (DIo) (P<0.002) were observed among the groups. No significant trends in fasting insulin levels, area under the curve for insulin (AUCINS), Matsuda index of insulin sensitivity (ISI-Matsuda) and visceral adiposity index were detected.ConclusionsImpairment of glucose tolerance is characterized by the inability of β-cells to adequately compensate for insulin resistance through increased insulin secretion. Age, genetic predisposition and lifestyle, in combination with the duration and degree of hypercortisolism, strongly contribute to the impairment of glucose tolerance in patients with a natural history of CS. A careful phenotypic evaluation of glucose tolerance defects in patients with CS proves useful for the identification of those at a high risk of metabolic complications.

scholarly journals Natural history of glucose tolerance, beta-cell function and peripheral insulin sensitivity in cystic fibrosis patients with fasting euglycemia

2003 ◽  
Vol 149 (1) ◽  
pp. 53-59 ◽  
Author(s):  
F Lombardo ◽  
F De Luca ◽  
M Rosano ◽  
C Sferlazzas ◽  
C Lucanto ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Insulin Sensitivity ◽  
Natural History ◽  
Glucose Tolerance ◽  
Pancreatic Beta Cells ◽  
Cell Function ◽  
Glucose Levels ◽  
Peripheral Insulin Resistance ◽  
History Of ◽  
Over Time

OBJECTIVE: The loss of pancreatic beta-cells is thought to be one of the principal causes of diabetes mellitus (DM) in cystic fibrosis (CF), but the role of peripheral insulin resistance (IR) in the pathogenesis of DM in CF remains unclear. The aim of this study was to evaluate whether eventual changes of glucose tolerance (GT) over time were associated with modifications of insulin secretion or sensitivity. METHODS: Plasma glucose and insulin responses to an oral GT test (OGTT) were investigated and reinvestigated 13 Years later in 14 CF patients with initial and persistent fasting euglycemia and no history of insulin treatment. Insulin sensitivity (IS) at both tests was assessed on the basis of insulin and glucose levels both in the fasting state and during OGTTs. RESULTS: From the 1st to the 2nd OGTT: (a) the prevalence of DM responses significantly increased; (b) the areas beneath the respective glucose and insulin curves significantly increased and decreased respectively; (c) IR and IS indices decreased and increased respectively, even in the patients who developed DM; (d) pulmonary function significantly worsened in the entire series, especially in the patients who developed DM. CONCLUSIONS: (i) the natural history of glyco-metabolic status in CF is characterized by deteriorating GT over time; (ii) insulinopenia plays a prominent role in the pathogenesis of GT worsening; (iii) IR does not play any significant part in the pathogenesis of DM development; (iv) deterioration of lung function tests is more severe in the subjects who develop DM over time.

scholarly journals Arterial thrombosis as primary presentation of endogenous Cushing’s syndrome

2019 ◽  
Vol 12 (2) ◽  
pp. bcr-2018-227491
Author(s):  
Vijay Alexander ◽  
Maria Koshy ◽  
Riddhi Dasgupta ◽  
Ronald Albert Carey
Keyword(s):  
Cushing’S Syndrome ◽  
Arterial Thrombosis ◽  
Clinical Manifestations ◽  
Dynamic Mri ◽  
Cushing's Syndrome ◽  
Positron Emission ◽  
History Of ◽  
Laboratory Investigations ◽  
Primary Presentation

Cushing’s syndrome is known to present with a characteristic set of clinical manifestations and complications, well described in literature. However, hypercoagulability remains an under recognised entity in Cushing’s syndrome. A 31-year-old woman from Southern India presented with history of fever, left upper quadrant pain and progressive breathing difficulty for 3 weeks. Clinical examination revealed discriminatory features of Cushing’s syndrome. Laboratory investigations showed biochemical features of endogenous ACTH-dependent Cushing’s syndrome. Imaging of the abdomen revealed splenic collection, left-sided empyema and extensive arterial thrombosis. Gadolinium enhanced dynamic MRI of the pituitary gland revealed no evidence of an adenoma while a Ga-68 DOTATATE positron emission tomography CT scan ruled out an ectopic Cushing’s. A diagnosis of endogenous Cushing’s syndrome causing a prothrombotic state with extensive arterial thrombosis was made. She was initiated on oral anticoagulation and oral ketoconazole for medical adrenal suppression. She subsequently underwent bilateral adrenalectomy and was well at follow-up.

scholarly journals A Natural History of Adrenocorticotropin-Independent Bilateral Adrenal Macronodular Hyperplasia (AIMAH) from Preclinical to Clinically Overt Cushing's Syndrome.

2001 ◽  
Vol 48 (6) ◽  
pp. 677-683 ◽  
Author(s):  
AKIKO OHASHI ◽  
YUYA YAMADA ◽  
KATSUHIKO SAKAGUCHI ◽  
TORU INOUE ◽  
MASAHARU KUBO ◽  
...  
Keyword(s):  
Natural History ◽  
Cushing’S Syndrome ◽  
Cushing's Syndrome ◽  
History Of

Subclinical Cushing’s Syndrome in women with adrenal incidentalomas is associated with adipose tissue dysfunction

2016 ◽  
Vol 62 (5) ◽  
pp. 72-73
Author(s):  
Stavroula A. Paschou ◽  
Markella Nezi ◽  
Fotini Dimitropoulou ◽  
Dimitrios Ioannidis ◽  
Argyro Panagiotakou ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Cushing’S Syndrome ◽  
Clinical Signs ◽  
Cushing's Syndrome ◽  
Visceral Adiposity Index ◽  
Adrenal Incidentalomas ◽  
Subclinical Cushing’S Syndrome ◽  
Adipose Tissue Dysfunction ◽  
Mass Size ◽  
And Function

Introduction. The visceral adiposity index (VAI) is a mathematical formula based on simple anthropometric and biochemical parameters and reflects the distribution and function of the adipose tissue.Aim: to investigate the possible association between the presence of subclinical Cushing’s syndrome (SCS) and VAI in patients with adrenal incidentalomas.Patients and methods. We studied 258 patients with adrenal incidentalomas. The diagnosis of SCS was based on a post-LDDST cortisol level ≥1.8 mg/dl combined with an abnormal result of at least one other test of the HPA axis, in the absence of clinical signs. The VAI index was calculated as following: Women VAI= [WC/36.58+(1.89×BMI)] ×(TG/0.81)×(1.52/HDL), Men VAI= [WC/39.68+(1.88×BMI)] ×(TG/1.03)×(1.31/HDL).Results. 122 patients were excluded from the analysis due to overt metabolic problems (8 with BMI>39, 82 with metabolic syndrome and 34 with type 2 diabetes). Among 136 patients who were included in the analysis (42M/94W, 56.9±9.7 y), SCS was diagnosed in 24 (17.6%). Patients with SCS presented with significantly higher levels of insulin (12.4±4.6 vs 9.9±3.2 μIU/ml, p=0.036) and triglycerides (114±36 vs 97±34 mg/dl, p=0.023), larger size of tumors (3.26±0.88 vs 2.28±1.06 cm, p<0.001) and higher calculated VAI (1.77±0.83 vs 1.39±0.69, p=0.045). Regression analysis revealed that the presence of SCS was positively associated with VAI [OR (95% CI) 1.888 (1.051–3.394), p=0.034] but when gender subgroup analysis followed, this was shown only in women [OR (95% CI) 2.284 (1.135–4.595), p=0.021]. Another important prognostic factor for the probability of SCS was the mass size [OR (95% CI) 2.237 (1.441–3.472), p<0.001].Conclusion. SCS in women with adrenal incidentalomas is associated with adipose tissue dysfunction.

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

1994 ◽  
Vol 131 (1) ◽  
pp. 67-73 ◽  
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

scholarly journals Increased risk of osteoporotic fractures in patients with Cushing's syndrome

2002 ◽  
pp. 51-56 ◽  
Author(s):  
P Vestergaard ◽  
J Lindholm ◽  
JO Jorgensen ◽  
C Hagen ◽  
HC Hoeck ◽  
...  
Keyword(s):  
Fracture Risk ◽  
Cushing’S Syndrome ◽  
Osteoporotic Fractures ◽  
Cushing's Syndrome ◽  
Time Interval ◽  
Pituitary Disease ◽  
Background Population ◽  
Increased Risk ◽  
And Gender ◽  
Self Administered Questionnaire

OBJECTIVE: To evaluate if fracture risk was increased in patients with Cushing's syndrome due to the increased endogenous cortisol production. DESIGN: Cohort. METHODS: A self-administered questionnaire was mailed to 125 patients with Cushing's syndrome diagnosed between 1985 and 1999 in Denmark. The response of each patient was compared with that of three age- and gender-matched control subjects randomly drawn among respondents to the same questionnaire from the background population. RESULTS: One hundred and four patients (83%) responded. The median age of the patients was 48 years (range 19-85 years). Sixty-eight had pituitary disease, 28 had adrenal disease, four had had both pituitary and adrenal surgery while four had not undergone surgery at the time of the study. The median time from diagnosis to surgery was 0.2 (range 0-3) years. Eighty-six percent were cured following surgery. There was an increased fracture risk within the last 2 years prior to diagnosis (incidence rate ratio 6.0, 95% confidence intervals (CI): 2.1-17.2). More than 2 years prior to diagnosis and following diagnosis there was no difference in fracture risk between patients and controls. The patients had more low-energy fractures than the controls (relative risk 5.4, 95% CI: 1.4-20.1). There was no difference in fracture risk between patients with adrenal or pituitary disease. CONCLUSIONS: Patients with Cushing's syndrome had an increased fracture risk in a narrow time interval before diagnosis, while no increase in fracture risk could be demonstrated after diagnosis and treatment.

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