Mini-review: pheochromocytomas causing the ectopic ACTH syndrome

Ballav, Chitrabhanu; Naziat, Auditi; Mihai, Radu; Karavitaki, Niki; Ansorge, Olaf; Grossman, Ashley

doi:10.1007/s12020-012-9646-7

Cited by 47 publications

(59 citation statements)

References 24 publications

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“…This was unlikely in our patient as the histology of the background adrenal was normal. There are several clinical manifestations of hypercortisolism, but in a perioperative patient such as ours, important considerations need to be borne in mind, including hypertension, glucose intolerance and hypokalaemia necessitating preoperative treatment 4. Hypercortisolism causes tissue fragility and may increase the risk of perioperative bleeding 1.…”

Section: Discussionmentioning

confidence: 99%

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Phaeochromocytoma with hypercortisolism and hypercalcaemia

et al. 2015

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SUMMARYWe report a case of phaeochromocytoma associated with hypercortisolism and hypercalcaemia in a 62-year-old man. The patient presented to clinic, with a 3-year history of exertional headaches, and a 4-month history of increasing fatigue, sweating and palpitations, loss of appetite and weight, and sleepiness. He did not have a medical, family or social history that could account for these symptoms. 24 h urinary catecholamines, plasma metanephrines, 24 h urinary cortisol and adjusted serum calcium, were elevated. Overnight low-dose dexamethasone suppression test did not suppress morning plasma cortisol. Serum intact parathyroid hormone and parathyroid hormone-related peptide were low, and adrenocorticotropic hormone was normal. The patient was treated with intravenous 0.9% sodium chloride and disodium pamidronate to control hypercalcaemia. CT showed a 10 cm left adrenal mass. Following inpatient treatment with phenoxybenzamine, he underwent a left adrenectomy and histology confirmed a phaeochromocytoma. Postoperatively, he required long-term steroids for contralateral adrenal suppression. Adjusted serum calcium returned to normal postoperatively. BACKGROUND

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Section: Discussionmentioning

confidence: 99%

“…Rarely, these tumours are associated with hypercortisolism, and this may occur through ectopic secretion of ACTH or CRH by the adrenal medullary tumour 4 5. Furthermore, phaeochromocytomas may be associated with adrenal cortical hyperplasia in the same gland, thought to be due to paracrine stimulation from the phaeochromocytoma.…”

Section: Discussionmentioning

confidence: 99%

Phaeochromocytoma with hypercortisolism and hypercalcaemia

et al. 2015

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“…Paraneoplastic CS syndrome due to ACTH secretion from MTC appears to be relatively rare as it was only detected in 10/1640 patients with MTCs (0.6%) (Barbosa et al 2005). Phaeochromocytomas secreting ACTH are considered to be even rarer, accounting for approximately 5.2% of all cases of ectopic ACTH related CS (Ballav et al 2012). Pancreatic NETs associated with PN-CS account for up to 10% of ectopic CS.…”

Section: Cushing's Syndrome (Cs)mentioning

confidence: 99%

Paraneoplastic endocrine syndromes

Dimitriadis

Angelousi

Weickert

et al. 2017

Endocrine-Related Cancer

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The majority of neoplasms are responsible for symptoms caused by mass effects to surrounding tissues and/or through the development of metastases. However, occasionally neoplasms, with or without endocrine differentiation, acquire the ability to secrete a variety of bioactive substances or induce immune cross-reactivity with the normal tissues that can lead to the development of characteristic clinical syndromes. These syndromes are named endocrine paraneoplastic syndromes when the specific secretory components (hormones, peptides or cytokines) are unrelated to the anticipated tissue or organ of origin. Endocrine paraneoplastic syndromes can complicate the patient's clinical course, response to treatment, impact prognosis and even be confused as metastatic spread. These syndromes can precede, occur concomitantly or present at a later stage of tumour development, and along with the secreted substances constitute the biological 'fingerprint' of the tumour. Their detection can facilitate early diagnosis of the underlying neoplasia, monitor response to treatment and/or detect early recurrences following successful initial management. Although when associated with tumours of low malignant potential they usually do not affect long-term outcome, in cases of highly malignant tumours, endocrine paraneoplastic syndromes are usually associated with poorer survival outcomes. Recent medical advances have not only improved our understanding of paraneoplastic syndrome pathogenesis in general but also enhanced their diagnosis and treatment. Yet, given the rarity of endocrine paraneoplastic syndromes, there is a paucity of prospective clinical trials to guide management. The development of well-designed prospective multicentre trials remains a priority in the field in order to fully characterise these syndromes and provide evidence-based diagnostic and therapeutic protocols.

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“…Neuroendocrine tumors of the thyroid usually are medullary thyroid cancer and often are caused by germline mutations in the rearranged during transfection (RET) proto-oncogene [222]. Many other organs can harbor ACTH-secreting neuroendocrine tumors, and for each organ, for instance, the prostate, pancreas, adrenal medulla/pheochromocytoma, one would have to consider the respective pathogenesis [223][224][225].…”

Section: Genetic Aspects Of Cushing's Syndromementioning

confidence: 99%

Endocrine Hypertension and Chronic Kidney Disease

Koch

Pamporaki

Kantorovich

2014

Chronic Kidney Disease and Hypertension

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IntroductionEndocrine forms of secondary hypertension (HTN) have traditionally included syndromes of mineralocorticoid excess with primary aldosteronism (PA) representing the most common etiology, followed by Cushing's syndrome (CS), and pheochromocytoma. Besides these conditions of hormonal excess, there are also other rare conditions such as congenital adrenal hyperplasia (11β-hydroxylase, 17α-hydroxylase deficiency), apparent mineralocorticoid excess, Geller syndrome (mineralocorticoid receptor (MR) activation), Liddle syndrome, pseudohypoaldosteronism type 2, and Chrousos syndrome that can cause HTN [1-4] (see Fig. 16.1).When considering the current obesity epidemic, with its many hormonal derangements (e.g., deficiencies of testosterone, vitamin D, growth hormone), the hitherto estimated prevalence rates of approximately 10 % for endocrine HTN are likely to be an underestimate. Potential nonadrenal causes of endocrine HTN include excess production of growth hormone (acromegaly), thyroid hormone, and parathyroid hormone, as well as insulin resistance, hypothyroidism, and overstimulation of central MRs [1,. These "nontraditional" forms of endocrine HTN will not be discussed in detail in this chapter.Cutoffs of systolic and diastolic blood pressure (BP) for defining HTN along with reference ranges for hormonal assays among various patient populations are 186 C. A. Koch et al. all important to consider when applying existing or emerging data to clinical patient scenarios. HTN guidelines by various societies have been recently revisited [41][42][43][44][45][46]. The American Society of Hypertension/International Society of Hypertension (ASH/ISH) guidelines reaffirm the traditional threshold of 140/90 mmHg as a cutoff for defining an elevated BP and state that individuals with a BP of 140-159/90-99 mmHg and no other risk factors are considered at low risk. On the other hand, the Joint National Committee (JNC 8) suggests a systolic blood pressure (SBP) of 150 mmHg as a worrisome threshold, especially for those 80 years and older. For the diastolic BP goal, both the ASH/ISH and JNC 8 guidelines view 90 mmHg as the cutoff; the exception are diabetic hypertensives for whom the cutoff is 85 mmHg. From epidemiologic studies and drug trials, there appears no sound evidence to continue recommending a BP of 140/90 mmHg as the cutoff to initiate antihypertensive treatment; moreover, any increased benefit from additional antihypertensive medications can be nonexistent or negligible, particularly in the face of increased likelihood of adverse effects. .1 Inherited endocrine condition related to mineralocorticoid excess. The picture shows the molecular pathways involved in dysregulation of NaCl homeostasis located in the distalrenal tubules. AME apparent mineralocorticoid excess; GRA glucocorticoid-remediable aldosteronism; PHA2 pseudohypoaldosteronism type 2; MR mineralocorticoid receptor; WNK with-no-lysine ( K) kinase 1,4; ROMK renal outer medullary potassium channel; ENaC epithelial sodium channel; KLHL3 kelch-like 3; C...

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Mini-review: pheochromocytomas causing the ectopic ACTH syndrome

Cited by 47 publications

References 24 publications

Phaeochromocytoma with hypercortisolism and hypercalcaemia

Phaeochromocytoma with hypercortisolism and hypercalcaemia

Paraneoplastic endocrine syndromes

Endocrine Hypertension and Chronic Kidney Disease

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