A Case of Ectopic ACTH Syndrome Associated with Metastatic Prostate Cancer

Abstract Objective: Ectopic ACTH production from malignancy is a rare etiology of Cushing’s syndrome. The most common tumors associated with this syndrome include small cell lung cancer, pancreatic neuroendocrine tumors, pheochromoctoma, thymic carcinoma, and bronchial carcinoma. Metastatic prostate cancer does not commonly produce ACTH. Here, we present a rare case of Cushing’s syndrome due to metastatic prostate cancer. Case Report: Patient is a 64 year old man with a 2 year history of castrate-resistant prostate cancer who was admitted for the 2nd time in 1 month for profound weakness and new onset hypokalemia. Initial analysis revealed hypertension with systolic blood pressure in the 150s, potassium in the mid 2s, an ACTH level of >1000pg/mL, and a 24-hr urine cortisol of almost 10,000mcg/24hrs. This was confirmed on repeat analysis. Metyrapone was initiated for treatment of hypercortisolemia and systemic chemotherapy with Cisplatin/Irinotecan was started to treat metastatic prostate cancer. ACTH and 24-hr urine cortisol levels returned to normal within a few weeks of therapy. The patient was able to discontinue Metyrapone following systemic chemotherapy treatment. Subsequent labs following discontinuation of metyrapone confirmed ongoing resolution of hypercortisolemia. Conclusion: This case represents an extremely rare cause of Cushing’s syndrome. Metastatic prostate cancer can rarely produce ACTH and cause clinical Cushing’s syndrome. Ectopic Cushing’s syndrome is often due to very aggressive tumors and is associated with a poor prognosis. Rapid recognition and treatment of this condition can be lifesaving.

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Ectopic ACTH Syndrome by Prostate Cancer; An Autopsy Case

Nihon Naika Gakkai Zasshi ◽

10.2169/naika.98.2586 ◽

2009 ◽

Vol 98 (10) ◽

pp. 2586-2588

Author(s):

Nao Yamamoto ◽

Mihoko Yamada ◽

Yuichiro Sudo ◽

Tetsunari Hase ◽

Daijuro Hayashi ◽

...

Keyword(s):

Prostate Cancer ◽

Ectopic Acth Syndrome ◽

Autopsy Case ◽

Ectopic Acth

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New-Onset Resistant Hypertension in a Newly Diagnosed Prostate Cancer Patient

American Journal of Hypertension ◽

10.1093/ajh/hpz125 ◽

2019 ◽

Vol 32 (12) ◽

pp. 1214-1217

Author(s):

Nattawat Klomjit ◽

Daniel J Rowan ◽

Andrea G Kattah ◽

Irina Bancos ◽

Sandra J Taler

Keyword(s):

Prostate Cancer ◽

Plasma Renin Activity ◽

Resistant Hypertension ◽

Prostate Gland ◽

Plasma Renin ◽

Renin Activity ◽

Ectopic Acth Syndrome ◽

Chronic Hypertension ◽

Ectopic Acth ◽

New Onset

Abstract BACKGROUND New onset resistant hypertension in a previously stable patient with chronic hypertension should lead to consideration of secondary causes. Electrolyte abnormalities are useful clues for identifying some common causes, especially mineralocorticoid excess. CASE PRESENTATION We report the case of a 69-year-old man who developed severe resistant hypertension despite the use of 6 antihypertensive medications, including diuretics. He had metabolic alkalosis and hypokalemia with suppressed plasma renin activity and serum aldosterone. Concurrently, he was diagnosed with small cell neuroendocrine carcinoma of the prostate gland, a rare form of prostate cancer. Despite absence of typical Cushingoid features, investigation confirmed the diagnosis of ectopic adrenocorticotropic hormone (ACTH) syndrome from neuroendocrine prostate cancer. Because of the severity of his hypercortisolism, he underwent urgent bilateral adrenalectomy for hormonal and symptomatic control. Blood pressure improved significantly and he was dismissed with a single antihypertensive agent. Unfortunately, the patient died from his cancer 1 month later. CONCLUSION Primary and secondary hyperaldosteronism are usually diagnosed based on measurements of aldosterone and plasma renin activity. However, if plasma renin activity and aldosterone are both low, rare causes of mineralocorticoid excess such as ectopic ACTH syndrome should be entertained.

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Adrenocortical Ultrastructure in Ectopic Acth Syndrome

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100091172 ◽

1976 ◽

Vol 34 ◽

pp. 238-239

Author(s):

K. Kovacs ◽

E. Horvath ◽

W. Singer

Keyword(s):

Adrenal Cortex ◽

Zona Glomerulosa ◽

Ectopic Acth Syndrome ◽

Pituitary Neoplasms ◽

Electron Microscopic ◽

Adrenocortical Cells ◽

Cell Hyperplasia ◽

Ectopic Acth ◽

Ectopic Acth Production ◽

Microscopic Findings

Secretion of ACTH by non-pituitary neoplasms is recognized with increasing frequency. While the clinical and biochemical changes associated with ectopic ACTH production have been extensively studied recently, relatively little attention was focused on the morphology of the adrenal cortex and, to our knowledge, the fine structure of the adrenocortical cells in cases of ectopic ACTH syndrome has not been described so far. We report here the electron microscopic findings in the adrenal cortex of a 50-year-old man with a pancreatic apudoma. The patient showed the characteristic clinical and biochemical features of ectopic ACTH syndrome and because of extensive hypercorticism, underwent bilateral adrenalectomy.By light microscopy, the adrenal cortices showed extensive compact cell hyperplasia and lipid depletion. The zona glomerulosa was present in small foci and, except for a few places, fasciculata cells were noted under the fibrous capsule.

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Electron Microscopic investigation of crooke’s change in the pituitaries of patients with hypercorticism

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100156225 ◽

1989 ◽

Vol 47 ◽

pp. 848-849

Author(s):

E. Horvath ◽

K. Kovacs ◽

L. Stefaneanu ◽

N. Losinski

Keyword(s):

Nucleolar Organizer ◽

Microscopic Investigation ◽

Electron Microscopic Investigation ◽

Ectopic Acth Syndrome ◽

Nucleolar Organizer Regions ◽

Electron Microscopic ◽

Human Pituitary ◽

Ectopic Acth ◽

Crooke’S Hyalinization

Human pituitary corticotropins have unique morphologic markers: bundles of type-1 filaments, measuring approximately 70 A in width and representing cytokeratin. The extreme ring-like accumulation of type-1 filaments, known as Crooke's hyalinization, signals functional suppression of the corticotropins and occurs in endogenous and exogenous glucocorticoid excess, caused by ACTH-secreting pituitary adenoma, glucocorticoid secreting adrenocortical tumor, ectopic ACTH-syndrome and administration of pharmacologic doses of glucocorticoids. Cells of autonomous corticotroph adenomas usually do not show Crooke's hyalin change. A minority of these tumors, however, retains sensitivity to the negative feed-back effect of elevated blood glucocorticoid levels and display typical Crooke’s change.In the present study pituitary corticotropins in various phases of Crooke's hyalinization were investigated in patients with glucocorticoid excess of various origin, applying histology, immunocytochemistry, count of argyrophilic nucleolar organizer regions (AgNOR), and transmission electron microscopy.

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