Severe Cushing's syndrome due to ectopic ACTH secretion from small cell lung carcinoma with adrenal metastases

2021 ◽  
Author(s):  
Aristidis Diamantopoulos ◽  
Marina Koulenti ◽  
Eirini Sampanioti ◽  
Eirini Evangelatou ◽  
Efstathios Dimitropoulos ◽  
...  
Keyword(s):  
Lung Carcinoma ◽  
Small Cell Lung Carcinoma ◽  
Cushing's Syndrome ◽  
Small Cell ◽  
Small Cell Lung ◽  
Adrenal Metastases ◽  
Acth Secretion ◽  
Ectopic Acth ◽  
Cell Lung Carcinoma ◽  
Ectopic Acth Secretion

scholarly journals Expression of somatostatin and dopamine receptors in ACTH-producing tumours

2010 ◽  
Vol 56 (1) ◽  
pp. 14-18
Author(s):  
I I Dedov ◽  
E I Marova ◽  
A Iu Abrosimov ◽  
A M Lapshina ◽  
A Iu Grigor'ev ◽  
...  
Keyword(s):  
Dopamine Receptors ◽  
Lung Carcinoma ◽  
Small Cell Lung Carcinoma ◽  
Somatostatin Receptors ◽  
Small Cell ◽  
Cushing's Disease ◽  
Small Cell Lung ◽  
Ectopic Acth ◽  
Cell Lung Carcinoma ◽  
Carcinoid Tumours

This study was designed to compare immunoexpression of somatostatin receptors (SR)1-5 and dopamine receptors 2 (DR2) in pituitary and non-pituitary ectopic ACTH-producing tumours. A total of 35 patients were enrolled in the study including 21 with Cushing's disease (CD) and 14 with ACTH-ectopic syndrome (ACTH-ES) associated with carcinoid tumours of lungs (n=11), kidney (n=1), thymus (n=1) and with small-cell lung carcinoma (n=1). All patients with corticotropinomas exhibited expression of SR 1-5 dominated by SR-1 (57%). 81% of these tumours expressed two and more SR subtypes. DR2 expression was documented in 52% of the tumours and co-expression of DR2 with different SR subtypes in 29%. Neoplasms associated with ACTH-ES expressed SR with the predominance of SR-3 (72%). Half of these tumours co-expressed two and more SR subtypes. Expression of DR2 was demonstrated in 50% of the neoplasms associated with ACTH-ES; 38% of them co-expressed SR and DF2.

Adrenal metastases in small cell lung carcinoma

Lung Cancer ◽  
1999 ◽  
Vol 25 ◽  
pp. S35
Author(s):  
M.M. Vaslamatzis ◽  
S. Pavlidou ◽  
E. Patila ◽  
S. Xynogalas ◽  
V. Philadetaki ◽  
...  
Keyword(s):  
Lung Carcinoma ◽  
Small Cell Lung Carcinoma ◽  
Small Cell ◽  
Small Cell Lung ◽  
Adrenal Metastases ◽  
Cell Lung Carcinoma

scholarly journals A case of recurrent non-small-cell lung carcinoma and paraneoplastic Cushing's syndrome

Lung Cancer ◽  
2006 ◽  
Vol 51 (2) ◽  
pp. 251-255 ◽  
Author(s):  
I. Noorlander ◽  
J.W. Elte ◽  
O.C. Manintveld ◽  
K.G. Tournoy ◽  
M.M. Praet ◽  
...  
Keyword(s):  
Cushing’S Syndrome ◽  
Lung Carcinoma ◽  
Small Cell Lung Carcinoma ◽  
Cushing's Syndrome ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma

scholarly journals Ectopic Cushing’s Syndrome Secondary to Metastatic Paraganglioma

2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
R. Daya ◽  
C. Wingfield ◽  
P. Sotshononda ◽  
F. Seedat ◽  
S. Bulbulia ◽  
...  
Keyword(s):  
Neuroendocrine Tumors ◽  
Cushing’S Syndrome ◽  
Case Reports ◽  
Small Cell Lung Carcinoma ◽  
Cushing's Syndrome ◽  
Acth Secretion ◽  
Ectopic Acth ◽  
Cell Lung Carcinoma ◽  
Ectopic Acth Secretion ◽  
Ectopic Cushing’S Syndrome

Paraneoplastic or ectopic Cushing’s syndrome (CS) is a rare cause of endogenous hypercortisolism. It is due to ectopic adrenocorticotropic hormone (ACTH) secretion and has been reported in association with a variety of neuroendocrine tumors such as small-cell lung carcinoma, carcinoid tumors, and medullary carcinoma of the thyroid. Paragangliomas (PGLs) are rare neuroendocrine tumors that can secrete catecholamines. Case reports and reports of ectopic ACTH secretion from metastatic PGLs causing CS are exceedingly rare. We present a case of a 38-year-old female, who presented with typical signs, symptoms, and complications of CS, secondary to a PGL with widespread metastases, which eventually led to her demise.

scholarly journals Development of Delayed Paraneoplastic ACTH Syndrome in Small Cell Lung Carcinoma

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A995-A996
Author(s):  
Misbah Azmath ◽  
Susan Tannenbaum ◽  
Pamela Taxel
Keyword(s):  
Lung Carcinoma ◽  
Small Cell Lung Carcinoma ◽  
Small Cell ◽  
Response To Therapy ◽  
Prognostic Impact ◽  
Tumor Type ◽  
Small Cell Lung ◽  
Ectopic Acth ◽  
Cell Lung Carcinoma ◽  
Cortisol Levels

Abstract Background: Paraneoplastic/ectopic ACTH syndrome (EAS) is a rare but well-recognized syndrome in small cell lung carcinoma (SCLC), occurring in 1-5% of cases (1) and most often at diagnosis. We present a patient with SCLC who developed paraneoplastic ACTH syndrome 9 months after initiation of treatment. Case: A 73 year old female with long history of smoking and COPD (on home O2) and SCLC seen during hospitalization with severe muscle cramps, generalized weakness, hypertension and hypokalemia. Eleven months prior, she was diagnosed with SCLC after presenting with left superior mediastinum, supraclavicular and neck lymphadenopathy. She received 4 cycles of chemotherapy and immune checkpoint inhibitor (ICI) therapy (atezolizumab) was also initiated and continued throughout. Good response to therapy occurred until nine months post initiation, when relapse in same regions was identified on repeat PETCT. Physical examination revealed new onset resistant hypertension up to 240/120mmHg, and extensive bilateral lower extremity edema. Labs showed hypokalemia of 2.3 mmol/l and metabolic alkalosis with serum bicarbonate 43 mmol/l. Further investigations showed a random cortisol of 97.1 ug/dl with repeat of 175.9 ug/dl the following AM. ACTH was 374.1pg/ml. TSH was 0.25 uU/ml with low normal T4 and T3. Pituitary MRI showed no evidence of hypophysitis or enlargement. Repeat biopsy of cervical lymph node was unchanged from initial biopsy with two notable differences: morphology showed a “more organized, trabecular pattern” and MIB-1 staining had declined from 70-80% to 20%, and tumor cells stained positive for ACTH. She did not respond to octreotide, but did respond to ketoconazole (hypokalemia, edema improved and cortisol levels decreased to 24.2 ug/dl). However, hepatotoxicity occurred and thus it was discontinued with rapid rise of cortisol. As she was not a candidate for bilateral adrenalectomy, we started metyrapone with lowering of cortisol levels within 4 doses. However, new cavitary lesions on chest CT developed with concern for disseminated fungal infection. Patient elected for hospice and passed away the following day. Conclusion: We present an unusual case of paraneoplastic ACTH syndrome that developed after immunotherapy in SCLC. In summary, the relapse of SCLC while on immune therapy was associated pathologically by differentiation into a neuroendocrine tumor type and biochemically by a considerable ACTH production. We conclude that ACTH production with subsequent severe hypercortisolism causing immunosuppression may be a novel mechanism by which SCLC can evade immunotherapy. Reference: (1) Nagy-Mignotte H, Shestaeva O, Moro-Sibilot D et al. Prognostic impact of paraneoplastic cushing’s syndrome in small-cell lung cancer. J Thorac Oncol. 2014 Apr,9.

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