Hormonal Evaluation of the Patient with an Incidentally Discovered Adrenal Mass

Desforges, Jane F.; Ross, Nathan S.; Aron, David C.

doi:10.1056/nejm199011153232007

Cited by 284 publications

(23 citation statements)

References 31 publications

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“…Recent literature suggests that 10%–20% of solid AIs demonstrate a subclinical hormonal dysfunction, which may place patients at a higher risk for metabolic derangements such as IR [83]. Subclinical hypercortisolism is the most common abnormality detected in patients with AIs, with an average incidence of 9% [84]. Patients with AIs have a higher prevalence of diabetes or glucose intolerance (20%–75%), compared with the general population [85].…”

Section: Muscle Insulin Resistance and Endocrine Diseasementioning

confidence: 99%

Skeletal Muscle Insulin Resistance in Endocrine Disease

Peppa

Koliaki

Nikolopoulos

et al. 2010

Journal of Biomedicine and Biotechnology

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We summarize the existing literature data concerning the involvement of skeletal muscle (SM) in whole body glucose homeostasis and the contribution of SM insulin resistance (IR) to the metabolic derangements observed in several endocrine disorders, including polycystic ovary syndrome (PCOS), adrenal disorders and thyroid function abnormalities. IR in PCOS is associated with a unique postbinding defect in insulin receptor signaling in general and in SM in particular, due to a complex interaction between genetic and environmental factors. Adrenal hormone excess is also associated with disrupted insulin action in peripheral tissues, such as SM. Furthermore, both hyper- and hypothyroidism are thought to be insulin resistant states, due to insulin receptor and postreceptor defects. Further studies are definitely needed in order to unravel the underlying pathogenetic mechanisms. In summary, the principal mechanisms involved in muscle IR in the endocrine diseases reviewed herein include abnormal phosphorylation of insulin signaling proteins, altered muscle fiber composition, reduced transcapillary insulin delivery, decreased glycogen synthesis, and impaired mitochondrial oxidative metabolism.

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Section: Muscle Insulin Resistance and Endocrine Diseasementioning

confidence: 99%

Skeletal Muscle Insulin Resistance in Endocrine Disease

Peppa

Koliaki

Nikolopoulos

et al. 2010

Journal of Biomedicine and Biotechnology

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“…[3] Published literature recommends re-evaluation imaging to be performed at intervals ranging from 3 to 12 months after the initial diagnosis. [3647–50] Considering the radiation exposure, MRI may be preferred over CT.…”

Section: Introductionmentioning

confidence: 99%

Current concepts in the management of adrenal incidentalomas

Kanagarajah¹,

Ayyathurai²,

Manoharan³

et al. 2012

Urol Ann

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Adrenal tumors are among the commonest incidental findings discovered. The increased incidence of diagnosing adrenal incidentalomas is due to the widespread availability and use of noninvasive imaging studies. Extensive research has been conducted to define a cost-effective diagnostic and therapeutic protocol to guide physicians in managing incidental adrenal lesions. However, there is little consensus on the optimal management strategy. Published literature to date, describes a wide spectrum of treatment options ranging from excision of all adrenal lesions regardless of the size and functional status to extensive hormonal and radiological evaluation to avoid surgery. In this review, we present a comprehensive overview of the presentation, evaluation and management of adrenal incidentalomas. Additionally, we propose a management algorithm to optimally manage these tumors.

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“…In autopsy studies adrenal incidentalomas were seen in 1.9–8.7% [6, 7]. It is estimated that they are discovered in about 2% of abdominal CT scans [8]. 7% of these adrenal masses produce aldosterone, 0.035% glucocorticosteroids, and 6.5% are pheochromocytomas or 0.058% adrenal carcinomas [8].…”

Section: Introductionmentioning

confidence: 99%

“…It is estimated that they are discovered in about 2% of abdominal CT scans [8]. 7% of these adrenal masses produce aldosterone, 0.035% glucocorticosteroids, and 6.5% are pheochromocytomas or 0.058% adrenal carcinomas [8]. Androgen or estrogen production is rarely reported.…”

Section: Introductionmentioning

confidence: 99%

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Adrenocortical Carcinoma Evolving after Diagnosis of Preclinical Cushing’s Syndrome in an Adrenal Incidentaloma

Höfle

Gasser²,

Lhotta³

et al. 1998

Horm Res Paediatr

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A 43-year-old female patient underwent abdominal ultrasonography and CT scan because of uncharacteristic abdominal pain. A 3-cm homogeneous adrenal tumor was diagnosed. The endocrine tests revealed an adrenal preclinical Cushing’s syndrome (PCS). Due to the latent hormone excess we decided to operate on the adrenal tumor. Since the tumor was small, laparoscopic adrenalectomy was performed. Histological evaluation showed an adrenocortical tumor of undetermined nature. Four months later the patient presented with a metastasizing cortisol- and androgen-producing adrenocortical carcinoma (ACC). After pretreatment with ketoconazole to suppress the biosynthesis of adrenal steroids under substitution with hydrocortisone, we reduced the tumor load by surgery. Postoperatively we continued ketoconazole and started o,p′-dichlorodiphenyldichloroethane as well as chemotherapy with doxorubicin and suramin. However, the patient died from ACC 7 months after adrenalectomy. It is known from several reports that PCS may persist clinically silently or may progress to full-blown Cushing’s syndrome. This is the first time a malignant course of PCS is described. Independent of the initial therapeutic strategy of PCS, i.e. surgery or regular follow-up visits, we must be aware that also relatively small adrenal tumors can harbor malignancy.

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Hormonal Evaluation of the Patient with an Incidentally Discovered Adrenal Mass

Cited by 284 publications

References 31 publications

Skeletal Muscle Insulin Resistance in Endocrine Disease

Skeletal Muscle Insulin Resistance in Endocrine Disease

Current concepts in the management of adrenal incidentalomas

Adrenocortical Carcinoma Evolving after Diagnosis of Preclinical Cushing’s Syndrome in an Adrenal Incidentaloma

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