Abstract
Dual ectopic secretion of adrenocorticotropic hormone (ACTH) and growth hormone-releasing hormone (GHRH) by a single neuroendocrine tumor (NET) is extremely rare. We report a 43-year-old woman presenting with acral enlargement, weight gain, hyperpigmentation, and proximal muscle weakness. Laboratory evaluation revealed elevated cortisol, ACTH, and insulin-like growth factor 1 (IGF-1), consistent with concurrent Cushing syndrome and acromegaly. Imaging demonstrated a left hilar mass, and biopsy confirmed a pulmonary NET with immunohistochemical (IHC) positivity for synaptophysin and chromogranin. Pituitary magnetic resonance imaging (MRI) showed diffuse hyperplasia, suggesting trophic stimulation rather than a primary pituitary adenoma. Surgical resection resulted in normalization of hormone levels, marked clinical improvement, and regression of pituitary enlargement. Although direct histologic confirmation of tumor-derived GHRH was unavailable, the reversible pituitary hyperplasia favors ectopic GHRH-mediated stimulation rather than primary ectopic GH secretion. IHC of the resected tumor demonstrated ACTH positivity, supporting ectopic ACTH secretion. This case highlights the importance of recognizing dual hormone–secreting NETs in patients presenting with overlapping endocrine syndromes, as early detection and complete resection can lead to remission.
Keywords: neuroendocrine tumor, ACTH, GHRH, pulmonary carcinoid, Cushing syndrome, acromegaly, ectopic hormone secretion
Introduction
Neuroendocrine tumors (NETs) are a diverse group of neoplasms arising from neuroendocrine cells distributed throughout the body [1]. While many NETs are non-functional, a subset secretes bioactive hormones, resulting in distinct clinical syndromes. Among functional NETs, secretion of either adrenocorticotropic hormone (ACTH) or growth hormone-releasing hormone (GHRH) is rare [2].
The incidence of NETs varies by anatomical location. Epidemiological data suggest age-adjusted incidence rates per 100 000 population of 3.65 for gastroenteropancreatic NETs, 0.43 for pancreatic NETs, 0.2 to 2.0 for bronchial NETs, and 0.4 for thymic NETs [3]. Pulmonary NETs account for approximately 25% of all NETs and 2% of primary lung malignancies and are classified as typical carcinoids (TC) and atypical carcinoids (AC), with TC being 5 to 10 times more prevalent than AC [4].
Ectopic ACTH secretion from NETs can cause Cushing syndrome, characterized by hypercortisolism, centripetal obesity, hypertension, hyperglycemia, and round facies [5]. In contrast, ectopic GHRH secretion is a rare cause of acromegaly, leading to pituitary somatotroph hyperplasia with acral enlargement, coarsened facial features, and associated with metabolic complications [6]. While isolated ectopic secretion of ACTH or GHRH has been reported, simultaneous ectopic secretion of both hormones by a single tumor is exceedingly rare. Tadokoro et al described a pancreatic NET initially considered nonfunctional that later evolved to secrete both ACTH and GHRH, resulting in combined Cushing syndrome and acromegaly [2].
Here, we report a unique case of a pulmonary NET co-secreting ACTH and GHRH, presenting with overlapping features of Cushing syndrome and acromegaly, likely the first such case documented in the literature.
Case presentation
A 43-year-old woman presented to the Endocrinology Clinic of a tertiary care center in Rajasthan, India, with a 2-year history of acral enlargement, weight gain, hyperpigmentation of the skin, lips, and tongue, knee pain, backache, and increased snoring. She also reported proximal muscle weakness, manifested as difficulty rising from a seated position.
She had been newly diagnosed with diabetes mellitus and hypertension approximately 1 month prior to presentation. There was no clinical or echocardiographic evidence of cardiomyopathy, and evaluation did not reveal osteoporosis or menstrual irregularities.
Her past medical history was notable for a bronchoscopic excision of a carcinoid tumor from the left bronchus 10 years prior. There was no family history suggestive of multiple endocrine neoplasia (MEN) or other hereditary endocrine disorders. She denied any history of smoking, alcohol consumption, tobacco use, or illicit drug use.
Diagnostic assessment
At presentation, clinical examination revealed a blood pressure of 140/95 mmHg, pulse rate of 83 beats per minute, and body mass index (BMI) of 29.89 kg/m2. She exhibited classic features of acromegaly, including acral enlargement and coarse facial features, along with diffuse hyperpigmentation and proximal muscle weakness, suggestive of concurrent Cushing syndrome (Fig. 1A–1D).
Figure 1.
(A) Clinical photograph showing enlargement of hands with hyperpigmentation of skin on the dorsum of the hand. (B) Enlargement of the feet with dorsal hyperpigmentation. (C) Characteristic coarse facial features with an enlarged nose and thickened lips. (D) Enlarged tongue (macroglossia) with mucosal and perioral hyperpigmentation.
Laboratory investigations confirmed biochemical hypercortisolism. The 8 Am serum cortisol was 18.1 µg/dL (499.5 nmol/L) (reference range: 4.46 to 22.7 µg/dL [123 to 625 nmol/L]), and midnight serum cortisol was 18.4 µg/dL (507.6 nmol/L) (reference range: <7.5 µg/dL [<207 nmol/L]), indicating loss of diurnal variation. An overnight 1-mg dexamethasone suppression test showed a lack of suppression (post-dexamethasone cortisol 17.9 µg/dL; 494.0 nmol/L; normal <1.8 µg/dL [<50 nmol/L]). In addition, 24-hour urinary free cortisol (UFC) was markedly elevated at 450 µg/24 hours (1240 nmol/24 hours) (reference range: 3.5 to 45 µg/24 hours [10 to 124 nmol/24 hours]). Plasma ACTH was significantly elevated at 341 pg/mL (75.0 pmol/L) (reference range: ≤46 pg/mL [≤10.1 pmol/L]), consistent with ACTH-dependent Cushing syndrome (Table 1).
Table 1.
Laboratory findings of the patient on admission
| Parameter | Result | Reference range |
|---|---|---|
| Hormones | ||
| Serum cortisol (8 Am) | 18.1 µg/dL (499.5 nmol/L) | 4.46 to 22.7 µg/dL (123 to 625 nmol/L) |
| Serum cortisol (midnight) | 18.4 µg/dL (507.6 nmol/L) | <7.5 µg/dL (<207 nmol/L) |
| 24-hour UFC | 450 µg/24 hours (1240 nmol/24 hours) | 3.5 to 45 µg/24 hours (10 to 124 nmol/24 hours) |
| Plasma ACTH | 341.0 pg/mL (75.0 pmol/L) | ≤46 pg/mL (≤10.1 pmol/L) |
| IGF-1 | 792 ng/mL (1038 nmol/L) | 65 to 200 ng/mL (85 to 260 nmol/L) |
| GH | 12.8 ng/mL (3.8 nmol/L) | 0 to 5 ng/mL (0 to 1.5 nmol/L) |
| Plasma GHRH | 6.85 pg/mL (2.3 pmol/L) | 5 to 18 pg/mL [1.7 to 6.0 pmol/L] |
| Renal function test | ||
| BUN | 28 mg/dL (10.0 mmol/L) | 15 to 37 mg/dL (5.4 to 13.2 mmol/L) |
| Serum creatinine | 0.5 mg/dL (44.2 µmol/L) | 0.5 to 1.0 mg/dL (44 to 88 µmol/L) |
| Sodium | 135 mEq/L (135 mmol/L) | 135 to 145 mEq/L (135 to 145 mmol/L) |
| Potassium | 4.3 mEq/L (4.3 mmol/L) | 3.5 to 5.5 mEq/L (3.5 to 5.5 mmol/L) |
| Chloride | 101 mEq/L (101 mmol/L) | 99 to 109 mEq/L (99 to 109 mmol/L) |
| Liver function test | ||
| SGOT (AST) | 19 U/L | 15 to 46 U/L |
| SGPT (ALT) | 23 U/L | <35 U/L |
| Albumin | 4.2 g/dL (42 g/L) | 3.5 to 5.0 g/dL (35 to 50 g/L) |
| Globulin | 2.9 g/dL (29 g/L) | 2.0 to 3.5 g/dL (20 to 35 g/L) |
| Biochemistry | ||
| HbA1c | 6.7% | <5.7% (<39 mmol/mol) |
| Complete blood count | ||
| Hemoglobin | 12.1 g/dL (121 g/L) | 12.0 to 15.5 g/dL (120 to 155 g/L) |
| TLC | 5.97 × 103/µL (5.97 × 109/L) | 4.0 to 11.0 × 103/µL (4.0 to 11.0 × 109/L) |
| Platelet count | 471 × 103/µL (471 × 109/L) | 150 to 450 × 103/µL (150 to 450 × 109/L) |
Values in parentheses are International System of Units (SI). Abbreviations: ACTH, adrenocorticotropic hormone; IGF-1: insulin-like growth factor 1; GH, growth hormone; SGOT (AST), serum glutamic oxaloacetic transaminase (aspartate aminotransferase); SGPT (ALT), serum glutamic pyruvic transaminase (alanine aminotransferase); HbA1c, glycated hemoglobin; UFC, urinary free cortisol; GHRH, growth hormone-releasing hormone; BUN, blood urea nitrogen; TLC, total leukocyte count.
Evaluation for acromegaly demonstrated an elevated insulin-like growth factor 1 (IGF-1) level of 792 ng/mL (1038 nmol/L) (reference range: 65 to 200 ng/mL [85 to 260 nmol/L]) and random growth hormone (GH) level of 12.8 ng/mL (3.8 nmol/L) (reference range: 0 to 5 ng/mL [0 to 1.5 nmol/L]). Chest radiography showed mediastinal widening, and computed tomography of the thorax revealed a left hilar mass (Fig. 2A and 2B). Given suspicion of ectopic hormone secretion from a neuroendocrine tumor, plasma GHRH was measured and found to be inappropriately normal at 6.85 pg/mL (2.3 pmol/L) (reference range: 5 to 18 pg/mL [1.7 to 6.0 pmol/L]) (Table 1).
Figure 2.
(A) Chest radiograph showing mediastinal widening (B) contrast-enhanced CT of the thorax showing a large lobulated mediastinal (123 × 70 × 137 mm) mass extending into the left upper lobe.
Given the characteristic clinical features and IGF-1 levels >1.3× the upper limit of normal, the diagnosis of acromegaly was considered established; therefore, oral glucose tolerance testing for GH suppression was not performed, consistent with current guideline recommendations [7, 8].
Biopsy of the mediastinal mass confirmed a neuroendocrine tumor with low-grade nuclear features, with immunohistochemistry positive for synaptophysin and chromogranin (Fig. 3A and 3B). Dynamic contrast-enhanced pituitary magnetic resonance imaging (MRI) performed on a 3-T scanner demonstrated diffuse symmetric pituitary enlargement, with an estimated height of 11.2 mm, consistent with pituitary hyperplasia (Fig. 4A and 4B).
Figure 3.
Sections from the mediastinal mass showing features consistent with a low-grade neuroendocrine tumor. (A) IHC demonstrates focal positivity for chromogranin (×40). (B) IHC demonstrates diffuse and strong positivity for synaptophysin (×40). (C) Histopathological examination of the resected specimen showing an atypical pulmonary neuroendocrine tumor with low-grade nuclei, 5 to 6 mitoses per 10 HPF, and a MIB-1 (Ki-67) index of ∼3% (hematoxylin and eosin stain, ×40). (D) IHC demonstrates ACTH positivity, seen as fine granular cytoplasmic staining in tumor cells, consistent with ACTH expression (×40).
Figure 4.
Dynamic contrast-enhanced 3T pituitary MRI. Panels (A) and (B) Preoperative sagittal and coronal T1-weighted post-contrast images showing diffuse, symmetric pituitary enlargement with homogeneous enhancement, consistent with pituitary hyperplasia (arrows). Panels (C) and (D) Postoperative sagittal and coronal T1-weighted post-contrast images demonstrate resolution of pituitary hyperplasia and normalization of pituitary size (arrows).
Treatment
The patient underwent successful surgical excision of the mediastinal tumor via a thoracic approach (Fig. 5A and 5B). Perioperative stress-dose glucocorticoids were administered. On postoperative day 3, glucocorticoids were withheld for 24 hours, and serum cortisol was low at 3.4 µg/dL (93.8 nmol/L); therefore, glucocorticoid replacement was continued.
Figure 5.
Intraoperative image [Panel (A) and (B)] showing complete surgical excision of the mediastinal neuroendocrine tumor via a left thoracic approach.
At the 3-month postoperative follow-up, after withholding glucocorticoid replacement for 24 hours, the 8 Am serum cortisol was 6.5 µg/dL (179.3 nmol/L), suggesting partial recovery of hypothalamic–pituitary–adrenal axis function. A cosyntropin (Synacthen) stimulation test was planned but could not be performed because the patient was lost to follow-up. At a subsequent 9-month follow-up, after withholding glucocorticoids for 24 hours, the 8 Am serum cortisol remained suppressed at 0.9 µg/dL (24.8 nmol/L), consistent with persistent adrenal insufficiency. Glucocorticoid replacement was therefore continued, and reassessment of hypothalamic–pituitary–adrenal axis function with cosyntropin stimulation testing is planned at future follow-up.
Histopathological examination of the resected specimen revealed an atypical pulmonary neuroendocrine tumor with low-grade nuclear features, 5 to 6 mitoses per 10 high-power fields, and a Ki-67 (MIB-1) labeling index of 3% (Fig. 3C). Immunohistochemistry showed positivity for synaptophysin and chromogranin, confirming neuroendocrine differentiation, and diffused cytoplasmic ACTH positivity, supporting ectopic ACTH secretion (Fig. 3D). According to the 2021 World Health Organization classification of thoracic tumors, these findings were consistent with a well-differentiated, intermediate-grade atypical carcinoid tumor [7].
Outcome and follow-up
Following surgical resection of the mediastinal tumor, the patient demonstrated marked clinical improvement. In the immediate postoperative period, serum cortisol decreased from 18.1 µg/dL (499.5 nmol/L) preoperatively to 3.4 µg/dL (93.8 nmol/L), indicating prompt resolution of hypercortisolism with development of secondary adrenal insufficiency. Concurrently, GH levels declined from 12.8 ng/mL (3.8 nmol/L) to 1.2 ng/mL (0.36 nmol/L) by the fifth postoperative day, reflecting effective suppression of excess GH secretion (Table 2).
Table 2.
Biochemical parameters on admission, in the immediate postoperative period, and at follow-up
| Parameter | On admission | Immediate post-op | Post-op day 5 | 3-Month follow-up | Reference range |
|---|---|---|---|---|---|
| GH | 12.8 ng/mL (3.8 nmol/L) | NA | 1.2 ng/mL (0.36 nmol/L) | NA | 0 to 5 ng/mL (0 to 1.5 nmol/L) |
| IGF-1 | 792 ng/mL (1038 nmol/L) | NA | NA | 112 ng/mL (147 nmol/L) | 65 to 200 ng/mL (85 to 260 nmol/L) |
| Serum cortisol | 18.1 µg/dL (499.5 nmol/L) | 3.4 µg/dL (93.8 nmol/L) | NA | 6.5 µg/dL (179.3 nmol/L) | 4.46 to 22.7 µg/dL (123 to 625 nmol/L) |
| ACTH | 341.0 pg/mL (75.0 pmol/L) | NA | NA | NA | ≤46 pg/mL (≤10.1 pmol/L) |
| HbA1c | 6.7% | NA | NA | 5.4% | <5.7% (<39 mmol/mol) |
Values in parentheses are International System of Units (SI). Abbreviations: ACTH, adrenocorticotropic hormone; IGF-1, insulin-like growth factor 1; GH, growth hormone; HbA1c, glycated hemoglobin; NA, not available.
At the 3-month postoperative follow-up, the patient reported sustained symptomatic relief, including resolution of joint pain, improved muscle strength, better glycemic control, and normalization of blood pressure without further antihypertensive adjustment. Hyperpigmentation of the skin, lips, and tongue had completely resolved (Fig. 6A–6C). Laboratory evaluation showed biochemical normalization, with IGF-1 decreasing from 792 ng/mL (1038 nmol/L) to 112 ng/mL (147 nmol/L) and glycated hemoglobin (HbA1c) improving from 7.0% to 5.4% (Table 2).
Figure 6.
Postoperative resolution of hyperpigmentation and acromegaloid features following surgical resection. (A) Resolution of facial coarsening. (B) Marked improvement in pigmentation over the dorsum of the hands. (C) Resolution of hyperpigmentation and soft-tissue swelling over the feet.
At the same visit, after withholding glucocorticoid replacement for 24 hours, the 8 Am serum cortisol was 6.5 µg/dL (179.3 nmol/L), suggesting partial recovery of hypothalamic–pituitary–adrenal axis function (Table 2). A cosyntropin (Synacthen) stimulation test was planned but could not be performed because the patient was lost to follow-up.
Follow-up pituitary MRI demonstrated complete resolution of pituitary hyperplasia, with pituitary height reduced to 4.4 mm, confirming reversibility of pituitary changes consistent with ectopic GHRH-mediated stimulation (Fig. 4C and 4D).
At the 9-month postoperative follow-up, after withholding glucocorticoids for 24 hours, the 8 Am serum cortisol remained suppressed at 0.9 µg/dL (24.8 nmol/L), consistent with persistent adrenal insufficiency, and glucocorticoid replacement therapy was continued.
Given the diagnosis of atypical carcinoid tumor and its potential for recurrence or metastasis, the patient is planned for functional imaging with a gallium-68-labeled 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetraacetic acid-d-PhelTyr3-Thr8-OC (68Ga-DOTATATE) positron emission tomography-computed tomography (PET/CT) scan to evaluate residual disease, assess for distant metastases, and guide long-term surveillance.
Discussion
Neuroendocrine tumors are uncommon neoplasms capable of producing various hormonal syndromes depending on their secretory profile. Pulmonary carcinoids are the most frequent thoracic NETs, and subsets are functional, most often secreting ACTH. GHRH secretion is far less common, and to our knowledge, concurrent ACTH secretion with clinical and radiologic features suggestive of ectopic GHRH activity arising from a pulmonary carcinoid has not been previously documented.
In our patient, the coexistence of biochemical hypercortisolism and growth hormone excess required a structured evaluation including targeted hormonal assays, cross-sectional imaging, and histopathology. Elevated ACTH levels confirmed ACTH-dependent Cushing syndrome, while inappropriately normal (non-suppressed) GHRH levels in the context of acromegaly suggested an ectopic source. Imaging revealed a left hilar mass, and histopathology established the diagnosis of an atypical carcinoid tumor, a well-differentiated, intermediate-grade NET positive for synaptophysin and chromogranin.
Functional pulmonary carcinoids, particularly atypical subtypes, tend to present at more advanced stages than nonfunctional tumors [3]. The mitotic index in our patient (5 to 6 per 10 high-power fields) and Ki-67 index (3%) indicated intermediate proliferative activity, associated with higher recurrence and metastatic potential than typical carcinoids but still more favorable than high-grade neuroendocrine carcinomas [9]. Surgical resection remains the treatment of choice and offers curative potential in localized disease [4]. In this case, tumor removal resulted in rapid biochemical remission of both hormonal syndromes and radiologic resolution of pituitary hyperplasia, highlighting the reversibility of pituitary changes secondary to ectopic GHRH stimulation.
An important differential consideration is primary ectopic GH secretion. However, ectopic GH production would be expected to suppress hypothalamic GHRH release and reduce pituitary somatotroph stimulation through negative feedback and therefore would not typically result in diffuse pituitary hyperplasia. In contrast, sustained ectopic GHRH stimulation leads to somatotroph hyperplasia and symmetric pituitary enlargement, which was observed preoperatively and completely resolved after tumor resection in our patient. This reversible pituitary enlargement supports a trophic mechanism more consistent with ectopic GHRH activity than primary ectopic GH secretion.
Similar to previously described cases of ectopic GHRH secretion from bronchial carcinoids, surgical removal normalized GH and IGF-1 levels and reversed pituitary hypertrophy, but in our case, this occurred alongside resolution of ACTH-dependent hypercortisolism [1].
Reports of dual ectopic secretion of ACTH and GHRH are exceedingly rare. Southgate et al described ectopic secretion of both hormones from an adenoid cystic carcinoma of pulmonary origin, resulting in acromegaly and hypercortisolism complicated by pituitary infarction [10]. More recently, Tadokoro et al reported a metastatic pancreatic neuroendocrine tumor that evolved to secrete both ACTH and GHRH with biochemical and immunohistochemical confirmation [2]. However, comparable cases arising from pulmonary neuroendocrine tumors, particularly carcinoid tumors, have not been previously described.
Limitations of this report include the limited availability of plasma GHRH estimation, which is not routinely performed and was within the low-normal range in our patient. Because of limited assay availability and the patient's rapid postoperative biochemical and clinical improvement, repeat postoperative GHRH measurement was not performed. Tumor immunohistochemistry for GHRH was also not performed because validated staining is not available in India, precluding direct histopathologic confirmation of tumor-derived GHRH secretion. The interpretation of ectopic GHRH activity was therefore based on concordant clinical, biochemical, and radiologic findings, including elevated GH and IGF-1 levels, pituitary hyperplasia on initial imaging, and complete resolution after tumor resection.
Furthermore, inferior petrosal sinus sampling (IPSS) was not performed because the procedure is unavailable at our institute, limiting biochemical localization of ACTH secretion. Nevertheless, ectopic ACTH secretion was supported by markedly elevated ACTH levels and confirmed by immunohistochemical ACTH positivity in the resected tumor.
Additional limitations include the absence of genetic or molecular analyses and the need for longer follow-up to assess recurrence risk. Given the intermediate-grade histology and potential for late metastasis, the patient is scheduled for 68Ga-DOTATATE PET-CT to evaluate residual or metastatic disease and guide long-term surveillance.
Despite these limitations, this case expands the clinical spectrum of functional pulmonary carcinoids and underscores the importance of considering dual ectopic hormone secretion in patients presenting with overlapping features of Cushing syndrome and acromegaly.
Learning points
Concurrent ectopic ACTH secretion with features suggestive of ectopic GHRH activity is rare and should be considered in patients with overlapping Cushing syndrome and acromegaly.
Pituitary hyperplasia due to ectopic GHRH stimulation can be completely resolved after tumor resection.
Surgical resection is curative in localized disease and leads to rapid biochemical and clinical improvement.
Comprehensive hormonal and imaging evaluation is essential in patients with overlapping endocrine syndromes.
Acknowledgements
The authors express their sincere gratitude to the Departments of Pathology, Biochemistry, and Surgical Oncology of Nims University for their valuable support in the diagnostic and management process. The authors also thank the nursing staff for their dedicated patient care and assistance. Special appreciation is extended to the patient and family for their cooperation and consent to share this case for academic and clinical learning purposes.
Contributor Information
Dogga Sudhakar, Department of Endocrinology, National Institute of Medical Sciences and Research, Nims University Rajasthan, Jaipur 303121, India.
Sourav Debnath, Department of Pharmacy Practice, Nims Institute of Pharmacy, Nims University Rajasthan, Jaipur 303121, India.
Nishant Jain, Department of Endocrinology, National Institute of Medical Sciences and Research, Nims University Rajasthan, Jaipur 303121, India.
Naveen Sharma, Department of Surgical Oncology, National Institute of Medical Sciences and Research, Nims University Rajasthan, Jaipur 303121, India.
Mahaveer Singh, Department of Endocrinology, National Institute of Medical Sciences and Research, Nims University Rajasthan, Jaipur 303121, India.
Contributors
All authors made individual contributions to the authorship. D.S. and M.S. managed the patient and prepared the manuscript. S.D. contributed to data collection and literature review. N.J. and N.S. assisted in histopathology interpretation and follow-up. All authors reviewed and approved the final manuscript.
Funding
No public or commercial funding.
Disclosures
None declared.
Informed patient consent for publication
Signed informed consent was obtained directly from the patient.
Data availability
Data sharing is not applicable to this article because no datasets were generated or analysed in the course of this study.
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Data Availability Statement
Data sharing is not applicable to this article because no datasets were generated or analysed in the course of this study.