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Lack of Utility of ¹¹¹In-Pentetreotide Scintigraphy in Localizing Ectopic ACTH Producing Tumors: Follow-Up of 18 Patients

Developmental Endocrinology Branch, National Institute of Child Health and Human Development (D.J.T., G.P.C., L.K.N.); Departments of Radiology (C.C., J.L.D., J.C.) and Nursing (N.M.), Clinical Center, National Institutes of Health, Bethesda, Maryland 20892

	Abstract

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Octreotide scintigraphy has been advocated as the principal imaging modality for localizing ectopic ACTH-secreting tumors in Cushing’s syndrome. To assess its usefulness we reviewed the course of 18 consecutive patients with ectopic ACTH-producing tumor. Imaging included ¹¹¹In-pentetreotide scintigraphy, computed tomography (CT), and/or magnetic resonance imaging (MRI). Tumor was detected initially in 7/18 patients, and in 3/18 during follow-up. No ACTH-secreting tumor was detected by octreotide scintigraphy when CT/MRI were negative. Seventeen of forty octreotide scintigrams were abnormal. CT and/or MRI confirmed tumors in 10, but demonstrated nonendocrine lesions in association with 6 false positive octreotide scintigrams. Hepatic venous sampling for ACTH refuted one lesion detected by octreotide and CT scans. Twenty-three of forty octreotide scintigrams were normal. Of these, 8 were false negative, as CT and/or MRI detected tumor; 10 agreed with negative CT and MRI, and 5 correctly refuted false positive CT and/or MRI scans. Repeated CT/MR, but not octreotide scintigraphy, led to tumor resection in 2 patients. We conclude that octreotide scintigraphy does not offer greater sensitivity than CT/MRI and that false positive scans are common. Although octreotide scintigraphy may be helpful in selected cases, it is not a significant advance over conventional imaging for ectopic ACTH-secreting tumors.

	Introduction

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CUSHING’S SYNDROME due to autonomous ACTH production from an extrapituitary source, first described in 1969, causes about 5–10% of Cushing’s syndrome (1, 2). Bronchial and thymic carcinoid, pheochromocytoma, and gastrinoma are common causative tumors (3). After biochemical diagnosis of ectopic Cushing’s syndrome, optimal treatment includes localization and removal of the ACTH-secreting tumor. However, computed tomography (CT) or magnetic resonance imaging (MRI) (4, 5) never localizes approximately 33% of ectopic ACTH-producing tumors.

Recent case reports and small series suggest that imaging after injection of ¹¹¹In-pentetreotide or other radioactive-labeled analogs of somatostatin can identify ectopic ACTH-producing tumors, particularly those more than 2 cm in diameter (6, 7, 8, 9, 10). Consequently, a major review recommended octreotide scintigraphy as the primary test, as its sensitivity may be greater than CT or MRI (11).

Octreotide scintigraphy is based on the finding that carcinoid tumors commonly express somatostatin receptors (12, 13). Because the usefulness of octreotide imaging has rarely been evaluated for imaging small (<2 cm) tumors or occult masses not visualized by conventional radiography, we retrospectively analyzed our experience with 18 consecutive patients with ectopic ACTH secreting tumors.

	Subjects and Methods

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Patients

A retrospective case review identified 18 consecutive patients (9 male, 9 female; ages 20–79 yr) with ectopic ACTH secretion who had had at least one octreotide scintigram between 1994–1998 at the National Institutes of Health Clinical Center. Patients had ACTH-dependent hypercortisolism according to standard criteria: urine free cortisol more than 300 nmol/day; normal 70–300 nmol/day; 0800 h ACTH more than 3 pmol/L, normal 1–6 pmol/L. CRH stimulation and overnight 8 mg dexamethasone suppression tests were consistent with ectopic ACTH secretion in all patients (14, 15). Based on published criteria, inferior petrosal sinus sampling (IPSS) results were diagnostic of a nonpituitary source of ACTH in 15 patients (16). IPSS was not performed in 3 patients (nos. 10, 13, and 17; Table 1), in whom the diagnosis of ectopic Cushing’s syndrome was based on historical and/or biochemical criteria. Patient 10 presented with recurrent Cushing’s syndrome 11 yr after resection of an ACTH-containing bronchial carcinoid. Patient 13 was diagnosed with ACTH-dependent hypercortisolism during follow-up for sporadic (non-MEN I) metastatic gastrinoma. Patient 17 was severely obese (450 lb), so that neither IPSS nor imaging studies could be performed on initial evaluation. An ACTH-staining bronchial carcinoid was ultimately excised from this patient after adrenalectomy, weight loss, and imaging.

Clinical features included weight gain (100%) and other features of Cushing’s syndrome. Hypertension was present in 11 patients (61%) and hypokalemia in 5 (28%). Infections affected 4 patients (22%) and included cellulitis of the lower extremities, pneumocystis pneumonia, oral candidiasis, urinary tract infections, and pneumonia (unknown organism). Urine-free cortisol levels (RIA) were markedly elevated in nonadrenalectomized cases [mean 7500 nmol/day, range 410–28,100 nmol/day; normal range 70–300 nmol/day (or 2,717, range 150–10,185 ug/day; normal range 24–108 ug/day)]. Random plasma ACTH levels were very high [mean 48, normal range 5–340 pmol/L; normal range 1–6 pmol/L (or mean 218, range 22 to 1,557 pg/mL, normal range 6–26 pg/mL)].

Imaging

Patients were imaged 4 and 24 h after injection with 6 mCi ¹¹¹In-pentetreotide (Octreoscan) using Trionix (Twinburg, OH) or ADAC (Milipitas, CA) dual- or triple-headed cameras with medium-energy parallel hole collimators centered over both ¹¹¹Indium photon peaks (173 and 247 KeV) with 20% windows. At 4 h, whole body, planar spot, and SPECT images were obtained, and at 24 h, spot and SPECT images were repeated. For SPECT, 120 sequential, 30-sec images using dual headed cameras, or 120 sequential, 40-sec images using triple headed cameras were obtained. The images were reconstructed with the manufacturers’ software by using a standard filtered back projection algorithm. Hamming (Trionix) or Hanning (ADAC) filters were used. Scintigraphy was regarded as abnormal if nonphysiological uptake was observed at both 4 and 24 h. Scintigrams were initially interpreted by one of three Nuclear Medicine physicians, without knowledge of the CT or MRI results. Two observers (C.C.C. and J.A.C.) reviewed the results, one who had knowledge of the patients’ radiology results and subsequent clinical course, and one who did not. The octreotide scintigraphy interpretation was altered retrospectively in only one case (5), as shown in Table 1. True and false positivity and negativity were defined on the basis of biopsy or unequivocal anatomical imaging (CT/MRI).

CT was performed with a Hi Speed Advantage Scanner (GE Medical Systems, Milwaukee, WI) scanner. Section thickness was 5 mm through the chest and upper abdomen to the adrenals and 10 mm through the lower abdomen and pelvis. All sections were contiguous. A contrast agent was administered orally. Most studies were performed during a bolus (130 mL injected at 2 mL/sec) of nonionic water-soluble contrast, given at the radiologist’s discretion.

MRI was obtained with a 0.5-T scanner (Picker, Highland Heights, OH). T1-weighted spin-echo (SE) imaging was performed with a repetition time (TR) of 300 msec, echo time (TE) of 10 msec (TR/TE = 300/10), and eight excitations. T2-weighted SE imaging was performed with TR/TE of 2000/80 and two excitations. Short inversion time inversion-recovery (STIR) imaging was performed with a TR of 1,600 msec, TE of 30 msec, inversion time of 100 msec, and four excitations. Images were obtained in the coronal and axial planes.

CT and MRI scan results were interpreted by a single author (J.L.D.). On some occasions interpretation of the CT or MRI scans was done with knowledge of the other scan, hence these modalities are considered together and compared with octreotide scintigraphy. We defined an "abnormal" CT or MR study as one where the imaging results were sufficiently convincing to prompt further action, such as venous sampling, biopsy, or surgical exploration. In one patient (5), a tumor found on imaging was thought to be definite, but no action was deemed necessary on clinical grounds. Where tumors were not evident on CT or MRI, they were considered "occult."

	Results

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Clinical, imaging, and pathological data for the 18 patients are summarized in Table 1. Ten patients had a single imaging evaluation, and the other eight patients had follow-up imaging on up to five occasions.

Initial imaging

Initial imaging with CT and/or MRI revealed evidence of a neuroendocrine tumor in seven patients (3, 4, 7, 10, 13, 15, 17). This led to surgical resection of an ACTH-staining neuroendocrine tumor and cure of hypercortisolism in five cases (3, 4, 7, 15, 17). The tumors ranged in size from 1.5–3.0 cm. Surgery was not indicated in two patients with metastatic disease (10, 13).

In six of the seven patients with abnormal CT and/or MRI, concurrent octreotide scintigraphy was abnormal (3, 7, 10, 13, 15, 17). Case 4 had positive CT and MRI with false negative octreotide scintigraphy. The lower neck lesion of case 15 was detected on CT chest images.

False positive octreotide scintigraphy corresponded to a liver lesion on CT, refuted by negative hepatic venous sampling for ACTH (5) and an area of inflammatory consolidation on MRI (11). Three patients with negative (9, 16) or false positive initial octreotide imaging (11) did not undergo follow-up.

Follow-up imaging

The remaining eight patients with initially occult tumors (1, 2, 6, 8, 12, 14, 18) were re-evaluated, generally at 6-month intervals. In two of these cases follow-up CT and/or MRI localized a biopsy-proven ACTH source (12, 14). Unbiopsied, but highly likely CT/MRI tumor detection was also noted in another patient (2) with recurrent thoracic tumor after lobectomy for a bronchial carcinoid. Follow-up octreotide scintigraphy after an initial normal scan did not localize an ACTH-secreting tumor in any patient.

The follow-up period was 7–42 months in these patients. Discontinued follow-up related to disseminated incurable disease (13, 14) or failure to return for unknown reasons (5, 10).

Outcome of management

Of the 15 patients with new onset Cushing’s syndrome, tumor was localized in 8. Cure was obtained by removal of an ACTH source in 3 patients (3, 7, 15). One patient (4) had an ACTH-positive pancreatic carcinoid excised but did not return for biochemical follow-up. The remaining 4 patients had an ACTH-secreting tumor removed, but they had either already been adrenalectomized (12, 17) or were not cured because of metastases (13, 14). Of the 3 patients with recurrent Cushing’s syndrome (2, 5, 10), tumor was localized with CT and MRI in 2 (2, 10) and with octreotide scintigraphy in 1 patient (10).

Patient 13 had skeletal lesions from metastatic gastrinoma detected by octreotide scintigraphy and Tc 99m MDP imaging, which were not detected by CT. Although this did not influence management (chemotherapy), such a finding could alter management of a patient where surgery was contemplated. In two patients (10, 14), metastatic disease only, rather than primary tumor, was detected by imaging.

Reflecting the difficulty in achieving either initial localization or cure of hypercortisolism, 7 of the 18 cases were ultimately treated with bilateral adrenalectomy. Other noncured patients were treated with inhibitors of adrenal steroidogenesis.

Final diagnoses

Final diagnoses included bronchial carcinoid (six patients, 33%), bronchial carcinoid tumorlets (12) (reported elsewhere; 17), metastatic gastrinoma (13), pancreatic carcinoid (4), lymphatic spread of a previously resected bronchial carcinoid (5), metastatic neuroendocrine tumor involving the liver and lung (14), neuroendocrine carcinoma inside the carotid sheath (noncarotid body) (15), and undiagnosed (six patients, 33%).

Comparison of octreotide scintigraphy and conventional imaging

A comparison of the results of octreotide scintigraphy with CT and MRI scanning is shown in Table 2. There were 17 abnormal octreotide scintigrams. Ten were true positive identifying ACTH-secreting tumor, and seven were false positives. Biopsy confirmed an ACTH-containing tumor identified by nine positive scans, and MRI showing nodal metastases from previously excised neuroendocrine tumor confirmed an additional case (10). Octreotide scintigraphy did not reveal more extensive tumor than CT and/or MRI did in any patient, except for the skeletal metastatic gastrinoma lesions (13). Four false positive octreotide scintigrams were associated with nonendocrine lesions on CT or MRI (radiation fibrosis in three scans and an inflammatory lesion in one scan). Three false positive octreotide scintigrams prompted further investigation. The results included 1), a left upper quadrant lesion, shown to be an accessory spleen on liver/spleen scan; 2), a hepatic lesion, also seen on CT but not associated with an elevation of hepatic venous plasma ACTH; and 3), a lesion in the right upper quadrant not associated with a lesion on CT, which was not seen on subsequent octreotide scintigraphy.

	Discussion

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Ultimately, CT and/or MRI scanning identified the source of ectopic ACTH secretion in 10 of the 18 patients. Six of these tumors were also detected by octreotide scintigraphy. Octreotide scintigraphy did not alter management in any case by identifying more extensive tumor than that shown on conventional imaging. Additionally, repeated CT/MRI, but not octreotide scintigraphy, subsequently detected tumors in cases that were initially occult. False positive octreotide scans were seen in 4 cases due to radiation fibrosis or lung inflammation.

At initial evaluation, 61% of patients had undetectable ACTH-secreting tumor, representing occult cases. Eventually, with follow-up, tumor was localized in 56% of these patients, although cure by ablation of the ectopic ACTH source was achieved in only 17%. This outcome reflects persistent ACTH secretion from tumor elsewhere (28%) or, in 39% of cases, inability to localize the ACTH source.

Overall performance of the 3 imaging modalities was suboptimal, as 8 of 18 (44%) patients did not have their tumor detected. This highlights the need for better imaging capabilities; the difficulty of localizing ectopic ACTH-secreting tumors is inadequately emphasized in the literature.

Early detection of ectopic ACTH-producing tumors may avoid adrenalectomy and reduce the risk from metastatic neuroendocrine tumor. ¹¹¹In-pentetreotide scintigraphy offered the promise of high sensitivity neuroendocrine tumor detection in these patients. The value of octreotide scintigraphy has been demonstrated in gastrinomas (18, 19). Carcinoid tumors, common sources of ectopic ACTH production, often express somatostatin receptors (12, 13). Apart from CT/MRI imaging, the only other technique that has been evaluated for the detection of ectopic ACTH-secreting tumors is selective venous sampling, which has been of limited value when conventional radiologic imaging is unrevealing (4, 5, 20).

We studied patients with bronchial carcinoid, the commonest cause of ectopic Cushing’s syndrome, as well as other forms of neuroendocrine tumor arising in the chest or abdomen. However, no known cases of thymic carcinoid, medullary thyroid carcinoma, pheochromocytoma, or small cell carcinoma of the lung were included in this study, hence the value of octreotide scintigraphy in these tumors was not assessed. However, ACTH-secreting thymic carcinoids are almost always larger than 2 cm on presentation (4, 21), and the other tumors are also usually in this size range and may be identified by biochemical markers. Thus, unlocalized cases in this series probably represent small bronchial carcinoids.

The recent introduction of octreotide scintigraphy and the relative rarity of ectopic Cushing’s syndrome limit the relevant literature. Several case reports describe detection of nonoccult ectopic ACTH-secreting tumor with octreotide scintigraphy (7, 8, 9, 10, 22, 23, 24). De Herder and coworkers (24) reported that eight of nine patients with an ectopic ACTH-secreting tumor were detected with ¹²³I-Tyr3-octreotide or ¹¹¹InDTPA-D-Phe1-octreotide imaging (24). However, only one of these cases was occult, and in that case scintigraphy failed (21). Where details are given, the octreotide imaging technique in those reports appears similar to that used in our patients (19).

Although octreotide scintigraphy did not add significant sensitivity to CT/MRI in this series, it is conceivable that a technique relying on in vivo receptor labeling may add to the specificity of diagnoses made with CT/MRI. This would be analogous to functional information derived from MRI, where certain features on T2 and STIR images help distinguish small central carcinoids from pulmonary vasculature (3). However, the frequency of ACTH-secreting tumors in patients with negative octreotide scintigraphy and positive CT and MRI scans suggests that octreotide imaging cannot be relied on for improving the specificity of anatomical studies.

The relatively poor results of octreotide scintigraphy in vivo are at odds with the in vitro finding of somatostatin receptors in the majority (up to 87%) of carcinoid tumors, the major cause of occult ectopic ACTH-secreting neoplasms (12, 13). We speculate that the imaging technique may be limited by the small size of ectopic ACTH-secreting tumors, the specific somatostatin receptor subtype expressed by the tumors, or the amount of isotope administered, 6 mCi (26, 27). The smallest tumor detected by octreotide scintigraphy in our series was 1.6 cm; the smallest other reported tumor detected was 0.6 cm (9). Only one other tumor of less than 1 cm was detected on octreotide scintigraphy (7); other reported tumor sizes were 1.0–3.0 cm (10, 25, 28, 29, 30).

In these 18 patients, octreotide scintigraphy did not detect otherwise occult ectopic ACTH-secreting tumors. False positive scintigrams without corroborative CT/MRI evidence of neuroendocrine tumor were generally explainable by nonendocrine processes. Overall, as octreotide scintigraphy did not enhance efforts to localize ACTH-secreting tumors or manage ectopic Cushing’s syndrome, we do not recommend that CT and MRI be replaced by octreotide scintigraphy.

	Footnotes

 
Address for correspondence and requests for reprints to: Dr. Lynnette K. Nieman, National Institutes of Health, Building 10, Room 10N262, 10 Center Drive Bethesda, Maryland 20892-1862.

Received September 22, 1998.

Revised December 11, 1998.

Accepted December 17, 1998.

	References

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