Posted on November 25, 2013 by MaryO
Is Diabetes in Cushing syndrome only a consequence of hypercortisolism?
Source
C Giordano, Dipartimento di Medicina Interna e Specialistica (Di.Bi.Mi.S) Sezione di Endocrinologia e Malattie del Metabolismo, University of Palermo, Palermo, Italy.
Abstract
OBJECTIVE:
Diabetes mellitus (DM) is one of the most frequent complications of Cushing syndrome (CS). Aim of the study was to define the changes in insulin sensitivity and/or secretion in relation to glucose tolerance categories in newly diagnosed CS patients.
DESIGN:
Cross-sectional study on 140 patients with CS.
METHODS:
113 women (80 with pituitary disease and 33 with adrenal disease, aged 41.7±15.7 yr) and 27 men (19 with pituitary disease and 8 with adrenal disease, aged 38.1±20.01 yr) 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).
RESULTS:
71 patients belonged to CS/NGT (49.3%), 26 (18.5%) to CS/prediabetes and 43 (30.8%) to 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 HOMAβ (p<0.001)and Oral Dispositional Index (DIo) (p<0.002) were observed among the groups. No significant trend in fasting insulin, AUC INS, ISI-Matsuda and VAI was detected.
CONCLUSIONS:
Impairment of glucose tolerance is characterized by the inability of β-cells to adequately compensate insulin resistance through increased insulin secretion. Age, genetic predisposition and lifestyle, in combination with duration and degree of hypercortisolism, strongly contribute to the impairment of glucose tolerance in the natural history of CS. A careful phenotypic evaluation of glucose tolerance defects in patients with CS proves useful for the identification of patients at high risk for metabolic complications.
- PMID:
- 24255133
- [PubMed – as supplied by publisher]
Filed under: adrenal, Cushing's, pituitary | Tagged: abstract, adrenal, Conditions and Diseases, Cushing's Syndrome, diabetes, diabetes mellitus, glucose tolerance, health, hypercortisolism, Impaired glucose tolerance, Insulin, Insulin resistance, Journal of Endocrinology, metabolic syndrome, pituitary | Leave a comment »
Posted on November 14, 2013 by MaryO
Osteoporosis International, 11/14/2013 Clinical Article
Trementino L, et al. – Bone loss and fractures are a common complication of CS.
The authors investigate the role of gender, disease etiology, duration, and degree of hypercortisolism as well as the impact of glucocorticoid receptor (GR) polymorphisms on the development of bone complications in CS.
While GR gene variants as well as gender and disease etiology seem not to play a role, the degree and duration of hypercortisolism seem to be the major determinants of bone loss and fractures in this group of patients.
More investigations are needed to understand the real impact of these determinants on the development of bone complications in patients with hypercortisolism.
Read more
Filed under: Cushing's | Tagged: abstract, Bone, Bone density, Complications, Conditions and Diseases, Cushing's Syndrome, Disease, health, osteoporosis | Leave a comment »
Posted on November 7, 2013 by MaryO
Source
Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, University of Oxford, Headington, Oxford OX3 7EJ, UK.
Abstract
BACKGROUND:
Conventional glucocorticoid (GC) replacement for patients with adrenal insufficiency (AI) is inadequate. Patients with AI continue to have increased mortality and morbidity and compromised quality of life despite treatment and monitoring.
OBJECTIVES:
i) To review current management of AI and the unmet medical need based on literature and treatment experience and ii) to offer practical advice for managing AI in specific clinical situations.
METHODS:
The review considers the most urgent questions endocrinologists face in managing AI and presents generalised patient cases with suggested strategies for treatment.
RESULTS:
Optimisation and individualisation of GC replacement remain a challenge because available therapies do not mimic physiological cortisol patterns. While increased mortality and morbidity appear related to inadequate GC replacement, there are no objective measures to guide dose selection and optimisation. Physicians must rely on experience to recognise the clinical signs, which are not unique to AI, of inadequate treatment. The increased demand for corticosteroids during periods of stress can result in a life-threatening adrenal crisis (AC) in a patient with AI. Education is paramount for patients and their caregivers to anticipate, recognise and provide proper early treatment to prevent or reduce the occurrence of ACs.
CONCLUSIONS:
This review highlights and offers suggestions to address the challenges endocrinologists encounter in treating patients with AI. New preparations are being developed to better mimic normal physiological cortisol levels with convenient, once-daily dosing which may improve treatment outcomes.
- PMID:
- 24031090
- [PubMed – in process]
- PMCID:
- PMC3805018
- [Available on 2013/12/1]
From http://www.mdlinx.com/endocrinology/newsl-article.cfm/4829245/ZZ4747461521296427210947/?news_id=2364&newsdt=110713&subspec_id=1509&utm_source=Focus-On&utm_medium=newsletter&utm_content=Top-New-Article&utm_campaign=article-section
Filed under: adrenal, adrenal crisis, Treatments | Tagged: abstract, adrenal insufficiency, AI, glucocorticoids | Leave a comment »
Posted on October 5, 2013 by MaryO
- Katrin Ritzel,
- Felix Beuschlein,
- Anne Mickisch,
- Andrea Osswald,
- Harald J. Schneider,
- Jochen Schopohl and
- Martin Reincke
–Author Affiliations
Medizinische Klinik und Poliklinik IV, Klinikum der Universität München, D-80336 München, Germany
- Address all correspondence and requests for reprints to: Martin Reincke, M.D., Medizinische Klinik und Poliklinik IV, Klinikum der Universität München, Ziemssenstrasse 1, D-80336 München, Germany. E-mail:Martin.Reincke@med.uni-muenchen.de.
Abstract
Background: The outcome of bilateral adrenalectomy (BADx) in patients with Cushing’s syndrome (CS) is not well characterized.
Methods: A literature search was performed with the search terms “bilateral adrenalectomy” or “total adrenalectomy” and “Cushing’s” or “Cushing.” Immediate and long-term outcomes after BADx in CS were analyzed using descriptive statistics (median [range]).
Results: From 549 screened publications, 37 studies met inclusion criteria (1320 patients, 82% having Cushing’s disease [CD], 13% having ectopic CS, and 5% having primary adrenal hyperplasia).
Surgical morbidity and mortality of BADx (23 studies, 739 patients) were 18% (6–31) and 3% (0–15), respectively. In patients with CD, surgical mortality was below 1%. Although residual cortisol secretion due to accessory adrenal tissue or adrenal remnants was found in 3–34% (5 studies, 236 patients), less than 2% had a relapse of CS.
Symptoms of hypercortisolism (eg, hypertension, obesity, or depression) improved in the majority of the patients after BADx (7 studies, 195 patients). The number of adrenal crises per 100 patient-years was 9.3 (6 studies, 203 patients).
Nelson’s syndrome occurred in 21% (0–47) of the patients (24 studies, 768 patients). Mortality (23 studies, 690 patients) was 17% (0–88) at a follow-up of 41 months (14–294). Remarkably, 46% of the patients died in the first year after surgery. The median ages at death were 62 years (CD) and 53 years (ectopic CS).
Conclusion: BADx is relatively safe and provides adequate success. Excess mortality within the first year after surgery suggests that intensive clinical care for patients after BADx is warranted.
- Copyright © 2013 by The Endocrine Society
From http://jcem.endojournals.org/content/98/10/3939.abstract
Filed under: adrenal, Cushing's, pituitary, Treatments | Tagged: abstract, adrenal, bilateral laparoscopic adrenalectomy, BLA, cortisol, Cushing's, depression, ectopic, hypercortisolism, hypertension, mortality, Nelson's syndrome, obesity, primary adrenal hyperplasia, transsphenoidal | Leave a comment »
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