<b>Pre‐clinical Cushing's syndrome: an unexpected frequent cause of poor glycaemic control in obese diabetic patients</b>

Leibowitz, Gil; Tsur, Anat; Chayen, S.; Salameh, Mohammad; Raz, Itamar; Cerasi, Erol; Gross, David J.

doi:10.1046/j.1365-2265.1996.737558.x

Cited by 176 publications

(133 citation statements)

References 24 publications

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“…It is not uncommon that Cushing's syndrome is diagnosed only in advanced disease states several years after the onset of symptoms, and so the disease is typically associated with substantial morbidity and mortality (1,2). Mild forms of Cushing's syndrome, however, probably often remain undiagnosed in obese diabetic patients (3,4). Therefore, reliable and convenient screening tests for Cushing's disease are of particular clinical importance.…”

Section: Introductionmentioning

confidence: 99%

Measurement of late-night salivary cortisol with an automated immunoassay system

Vogeser¹,

Durner²,

Seliger³

et al. 2006

Clinical Chemistry and Laboratory Medicine (CCLM)

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Background: Measurement of late-night salivary cortisol concentrations is increasingly used as a screening test in suspected Cushing's syndrome. Cortisol concentrations are typically extremely low in latenight samples and discordant assay-specific reference ranges have been reported. Therefore, the aim of our study was to assess the analytical performance of the first automated cortisol immunoassay specified for salivary measurements and to establish late-night sampling reference-range data for this test. Methods: Salivary cortisol was measured using the Roche Cobas Cortisol assay (Roche Diagnostics). Five salivary pools in different concentration ranges were used to assess the inter-assay imprecision of this test in a two-centre evaluation protocol including two reagent lots. Linearity was tested by serial dilution. Salivary samples were obtained at 23:00 h from 100 apparently healthy volunteers using a commercially available salivary sampling device (Salivette, Sarstedt). A subset of 20 samples was used for method comparison with isotope dilution liquid chromatography-tandem mass spectrometry. Results: Inter-assay coefficients of variation (ns20) between 11.6% and 40.4% were found for mean cortisol concentrations between 12.9 and 2.6 nmol/L, with an estimated functional sensitivity of approximately 5.0 nmol/L. The test also gave linear results in the lowest concentration range between 1.0 and 8.3 nmol/L. Mean late-night salivary cortisol of 5.0 nmol/L was found for healthy individuals; the absolute range was 1.4-16.7 nmol/L, and the 95th percentile was 8.9 nmol/L. Substantially lower concentrations were found with isotope dilution LC-MS/MS compared to immunoassay results (mean concentrations 1.8 and 4.4 nmol/L, respectively). Conclusions: The automated assay investigated was found to offer acceptable analytical performance in the very low concentration range required for latenight salivary cortisol, despite a very short turnaround time. Using this assay, late-night salivary

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Section: Introductionmentioning

confidence: 99%

Measurement of late-night salivary cortisol with an automated immunoassay system

Vogeser¹,

Durner²,

Seliger³

et al. 2006

Clinical Chemistry and Laboratory Medicine (CCLM)

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“…Pathologic Cushing's syndrome may be an unsuspected finding in patients with type 2 diabetes mellitus with a prevalence as high as 3% (43,44,45,46,47). The converse is also true in that patients with diabetes mellitus with poor glycemic control may have an activated HPA axis (48).…”

Section: Type 2 Diabetes Insulin Resistance and The Metabolic Syndromementioning

confidence: 92%

DIAGNOSIS OF ENDOCRINE DISEASE: Differentiation of pathologic/neoplastic hypercortisolism (Cushing’s syndrome) from physiologic/non-neoplastic hypercortisolism (formerly known as pseudo-Cushing’s syndrome)

Findling

Raff

2017

European Journal of Endocrinology

106

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Endogenous hypercortisolism (Cushing's syndrome) usually implies the presence of a pathologic condition caused by either an ACTH-secreting neoplasm or autonomous cortisol secretion from a benign or malignant adrenal neoplasm. However, sustained or intermittent hypercortisolism may also accompany many medical disorders that stimulate physiologic/nonneoplastic activation of the HPA axis (formerly known as pseudo-Cushing's syndrome); these two entities may share indistinguishable clinical and biochemical features. A thorough history and physical examination is often the best (and sometimes only) way to exclude pathologic/neoplastic hypercortisolism. The presence of alcoholism, renal failure, poorly controlled diabetes and severe neuropsychiatric disorders should always raise suspicion that the presence of hypercortisolism may be related to physiologic/non-neoplastic Cushing's syndrome. As late-night salivary cortisol and low-dose dexamethasone suppression have good sensitivity and negative predictive value, normal studies exclude Cushing's syndrome of any form. However, these tests have imperfect specificity and additional testing over time with clinical follow-up is often needed. When there is persistent diagnostic uncertainty, secondary tests such as the DDAVP stimulation test and the dexamethasone-CRH test may provide evidence for the presence or absence of an ACTH-secreting tumor. This review will define and characterize the numerous causes of physiologic/non-neoplastic hypercortisolism and provide a rational clinical and biochemical approach to distinguish it from pathologic/neoplastic hypercortisolism (true Cushing's syndrome).

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“…Leibowitz et al [13] reported three patients with sub-CS in a study of 90 overweight patients (body mass index > 25 kg/m 2 ) with poorly controlled diabetes (HbA1c > 9%). Catargi et al [14] reported three patients with subCD and one patient with subCS in a group of 200 overweight patients (body mass index > 25 kg/m 2 ) with poorly controlled diabetes (HbA1c > 8%).…”

Section: Characteristics Of Suspected Subcd Patientsmentioning

confidence: 99%

The Frequency of Type 2 Diabetic Patients who Meet the Endocrinological Screening Criteria of Subclinical Cushing's Disease

et al. 2010

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Pre‐clinical Cushing's syndrome: an unexpected frequent cause of poor glycaemic control in obese diabetic patients

Cited by 176 publications

References 24 publications

Measurement of late-night salivary cortisol with an automated immunoassay system

Measurement of late-night salivary cortisol with an automated immunoassay system

DIAGNOSIS OF ENDOCRINE DISEASE: Differentiation of pathologic/neoplastic hypercortisolism (Cushing’s syndrome) from physiologic/non-neoplastic hypercortisolism (formerly known as pseudo-Cushing’s syndrome)

The Frequency of Type 2 Diabetic Patients who Meet the Endocrinological Screening Criteria of Subclinical Cushing's Disease

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