Cyclical Cushing’s Syndrome Due to Bronchial Carcinoid: Early Diagnosis and Prompt Treatment : The Endocrinologist

Journal Logo

You can read the full text of this article if you:

Access through Ovid
00019616-200803000-00013ReviewThe EndocrinologistThe Endocrinologist© 2008 Lippincott Williams & Wilkins, Inc.18March 2008 p 95-100Cyclical Cushing’s Syndrome Due to Bronchial CarcinoidEarly Diagnosis and Prompt TreatmentCME Review Article #6Hamid, Zulekha MD‡†; Faas, Fred H. MD*†*Professor of Medicine, Division of Endocrinology, Department of Medicine University of Arkansas for Medical Sciences; †Staff Physician, Central Arkansas Veterans Healthcare System, Little Rock, Arkansas; and ‡Physician, Little Rock Diagnostic Clinic, Little Rock, Arkansas.The authors have disclosed that they have no significant relationships with or financial interests in any commercial organizations pertaining to this educational activity.All staff in a position to control the content of this CME activity have disclosed that they have no financial relationships with, or financial interests in, any commercial companies pertaining to this educational activity.Lippincott CME Institute has identified and resolved all faculty and staff conflicts of interest regarding this educational activity.Reprints: Fred H. Faas, MD, 4301 W Markham Slot 587 Little Rock, AR 72205. E-mail: [email protected] Editor’s Note:This article is the 6th of 18 that will be published in 2008 for which a total of up to 18 AMA PRA Category 1 Credits™ can be earned. Instructions for how credits can be earned precede the CME Examination at the back of this issue.AbstractWe hereby describe a patient with cyclical Cushing’s syndrome due to ectopic production of adrenocorticotropic hormone (ACTH) by a bronchial carcinoid tumor, accurately diagnosed and treated within a short period of time. In addition we describe for the first time careful assessment of cortisol levels in the postoperative period without hormone replacement demonstrating limited need for steroid replacement. A 43-year-old female patient was referred for evaluation of Cushing’s syndrome. The diagnosis was made 2 months prior, because of the symptoms and elevated serum cortisol and urine free cortisol after a dexamethasone suppression test. Her symptoms improved and results of our laboratory studies were normal. Two months later symptoms developed again with elevated urine free cortisol and a paradoxical response to low and high-dose dexamethasone suppression test. The corticotrophin releasing hormone test suggested a nonpituitary origin. Magnetic resonance imaging of the pituitary was negative. Computed tomography and magnetic resonance imaging of the chest revealed a nodule in the right lung. Octreotide scan showed increased uptake in that area. She had a right lobectomy. Pathology revealed carcinoid tumor with ACTH staining. The cortisol levels were reduced, but steroid supplementation was not required for 2 weeks, supporting the cyclical nature of disease. This is a rare case of cyclical CS due to a bronchial carcinoid. High index of clinical suspicion and careful repeated laboratory evaluation over time is required to establish the diagnosis. Careful postoperative monitoring of cortisol values is needed. After resection of the ectopic source of ACTH, steroid supplementation may not always be needed.Learning ObjectivesDescribe this patient’s presenting symptoms, the test results suggesting a nonpituitary origin of ACTH secretion, and the final outcome.Contrast the causes and origin of typical and cyclical Cushing’s disease.Predict whether patients treated surgically for cyclical Cushing’s disease will routinely require steroid supplementation.Cushing’s syndrome is a rare disorder caused by excessive cortisol production. In the majority of cases it is caused by Cushing’s disease due to an adrenocorticotropic hormone (ACTH) secreting pituitary adenoma. Other etiologies include excessive cortisol production by the adrenal gland, nonpituitary secretion of ACTH or, very rarely, corticotrophin-releasing hormone. Despite various medical tools available for the diagnosis, Cushing’s syndrome still presents a challenge in clinical practice. To further add to the complexity of the disease, some cases have intermittent secretion of excess cortisol resulting in high peaks of serum cortisol followed by periods of completely normal cortisol levels. This phenomenon, known as cyclical Cushing’s syndrome, was first described by Bailey in 19711 in a patient with a malignant bronchial carcinoid tumor diagnosed at the autopsy. Clinicians should be aware of the existence of the cyclical Cushing’s syndrome as it often leads to misdiagnosis and treatment delay.We describe a patient with cyclical Cushing’s syndrome due to ectopic production of ACTH by a bronchial carcinoid tumor successfully treated in a short period of time. We highlight the challenges in the diagnosis and treatment of this complex condition.CASE REPORTA 43-year-old white female patient was referred for further evaluation of Cushing’s syndrome. She developed numbness of hands and legs, worsening of acne, weight gain, muscle weakness, hirsuitism, easy bruising, hypertension, and pedal edema. She had an extensive cardiac and renal workup including echocardiogram and computed tomography (CT) imaging of the abdomen and pelvis. There was no conclusive diagnosis. A work up for Cushing’s syndrome revealed an abnormal overnight dexamethasone suppression test (DST) with an elevated morning cortisol of 20 μg/dL after the administration of 1 mg of dexamethasone the night before. Following a low-dose DST (0.5 mg every 6 hours for 48 hours) the 8:00 am serum cortisol values were 58 and 74 μg/dL at 24 and 48 hours with an elevated urine free cortisol (UFC) of 1022 μg/24 on the second day (Table 1).JOURNAL/endst/04.03/00019616-200803000-00013/table1-13/v/2021-02-17T201845Z/r/image-tiff Laboratory Investigation by Referring PhysicianThe patient was referred to our clinic for further evaluation and treatment. Before her visit she noticed improvement in her symptoms with reduction in weight, resolution of acne, and significant improvement in pedal edema and muscle weakness. Physical examination showed that she was overweight with abdominal obesity and a few purplish striae on her lower abdomen. Laboratory studies carried out in our clinic were completely normal (Table 2).JOURNAL/endst/04.03/00019616-200803000-00013/table2-13/v/2021-02-17T201845Z/r/image-tiff Laboratory Data on Presentation to Our Clinic: Basal Values of Plasma Cortisol, ACTH, and Urine Free CortisolTwo months later she presented again with similar symptoms and was found to have 3 elevated 24-hour UFCs of 189 μg/24, 237 μg/24, and 529 μg/24 (normal range <45 μg/24) and elevated 17OH corticosteroids of 37.2 mg/24 (normal range 4–14 mg/24) (Table 3). Her serum ACTH fluctuated between 33 and 38 pg/mL (normal range 10–60 pg/mL). She also had an elevated fasting blood sugar of 155 mg/dL with a HgA1C of 7.7%. The results suggested ACTH-dependant hypercortisolism with a cyclical pattern of cortisol secretion. To confirm the diagnosis we performed a DST. A low-dose DST (0.5 mg dexamethasone every 6 hours for 48 hours) showed a paradoxical rise in the UFC with a baseline UFC of 119 to 356, and 790 μg/24 hr at 24 and 48 hours. A similar response was found with high-dose DST (2 mg dexamethasone every 6 hours for 48 hours) with a baseline UFC of 378 to 829 and 1183 μg/24 at 24 and 48 hours (Table 4). An ACTH level at the end of the DST was 118 pg/mL. Magnetic resonance imaging (MRI) of the pituitary gland was normal. An intravenous high-dose DST suggested suppression of ACTH with the cortisol going from 37 μg/dL before the test to 11 μg/dL at the end of the test (Table 5). A corticotrophin releasing hormone (CRH) stimulation test was performed. Cortisol levels did not rise after the intravenous administration of 100 μg CRH (from 31 μg to 32 μg) and the rise in ACTH level was only 14% (from 63 to 72 pg/mL) suggesting a nonpituitary origin of ACTH secretion (Table 6). To identify the source of ectopic ACTH secretion, a CT of the chest, abdomen, and pelvis was performed which revealed a 2.3- × 1.6-cm nodule in the right lower lobe. This was confirmed by MRI of the chest. An octreotide scan revealed pathologic uptake in the same region of the right lower lobe of the lung (Fig. 1). Serum calcitonin was normal at <2 pg/mL (normal range 0–15 pg/mL) and urinary 5-hydroxyindole acetic acid was normal at 6 mg/24 hr (normal range 0–15 mg/24 hr). She underwent right lobectomy for a bronchial carcinoid tumor. Pathology results confirmed the diagnosis and showed positive staining for ACTH (Fig. 2). After surgery her cortisol levels were reduced and normal diurnal variation returned (Fig. 3). Steroid supplementation was not required for 2 weeks after the operation, supporting the cyclical nature of the disease. The serum cortisol showed a gradual decline. She subsequently had symptoms of weakness and fatigue and was started on steroids at another hospital. She took hydrocortisone for about a month and, when last seen, was off of steroids for about a year. She was seen again 1 year after her surgery. Her physical appearance was dramatically different. She had lost significant weight (from 212 lb to 170 lb) with resolution of diabetes—HgA1C = 5.6% on no therapy. The symptoms of acne, hirsuitism, and pedal edema also resolved. The buffalo hump and striae improved (Fig. 4). A cosyntropin test was normal—baseline cortisol 9.9, 30 minutes 23.7 and 60 minutes 28.6 μg/dL with an ACTH of 11 pg/mL. The 24-hour UFC was normal at 17.1 μg/24, reflecting complete cure of her disease by surgery.JOURNAL/endst/04.03/00019616-200803000-00013/table3-13/v/2021-02-17T201845Z/r/image-tiff Laboratory Data After Recurrence of Symptoms: Random Values of Plasma Cortisol, ACTH, and Urine Free CortisolJOURNAL/endst/04.03/00019616-200803000-00013/table4-13/v/2021-02-17T201845Z/r/image-tiff Laboratory Data After Recurrence of SymptomsJOURNAL/endst/04.03/00019616-200803000-00013/table5-13/v/2021-02-17T201845Z/r/image-tiff Laboratory Data After Recurrence of Symptoms: High-Dose Dexamethasone Suppression Test (1 mg/hr Intravenous Dexamethasone for 7 hr)JOURNAL/endst/04.03/00019616-200803000-00013/table6-13/v/2021-02-17T201845Z/r/image-tiff Laboratory Data After Recurrence of Symptoms: Human CRH Test (100 μg Given as Intravenous Bolus)JOURNAL/endst/04.03/00019616-200803000-00013/figure1-13/v/2021-02-17T201845Z/r/image-tiff A, Preoperative imaging studies. CT of the chest: 2.3- × 1.6-cm noncalcified nodule in the right lower lobe. MRI of the chest, 2.5- × 1.4-cm enhancing mass in the right lower lobe corresponding to mass seen on CT. C, Octreotide scan, a focus of increased uptake within the right hilar region, which correlates with the mass on the CT and MRI of the chest.JOURNAL/endst/04.03/00019616-200803000-00013/figure2-13/v/2021-02-17T201845Z/r/image-png Carcinoid tumor with scattered positive immunostaining for ACTH.JOURNAL/endst/04.03/00019616-200803000-00013/figure3-13/v/2021-02-17T201845Z/r/image-tiff Cortisol values after surgery.JOURNAL/endst/04.03/00019616-200803000-00013/figure4-13/v/2021-02-17T201845Z/r/image-png Patient’s feature before and after surgery showing resolution of buffalo hump and striae.DISCUSSIONCyclical Cushing’s syndrome is a disorder in which there is rhythmic secretion of ACTH resulting in cyclic variation in adrenal steroid production. The timing of fluctuation can vary from few days to several months.1–3 Pituitary function may be normal between episodes and investigations are only abnormal when performed during the period of excess secretion. Clinical presentation is very variable and patients usually present with episodes of biochemical and clinical remission alternating with episodes of frank symptoms. The neuroendocrine mechanism of periodicity of cortisol overproduction is still poorly understood. One of the explanations for cyclic Cushing’s syndrome due to pituitary origin is the cyclical changes in central dopaminergic tone as a trigger for periodic ACTH secretion.4 Another theory is the episodic hemorrhage in the tumor causing temporary damage of actively secreting cells5 or the synchronous growth and death of ACTH secreting tumor cells.6In the majority of cases cyclic Cushing’s syndrome is caused by an ACTH secreting pituitary adenoma. From our review of literature about 16 cases were related to pituitary adenomas.2,3,7 Ectopic ACTH secretion and adrenal etiology for cyclical Cushing’s syndrome have been described in adrenal pheochromocytoma,8 adrenal adenoma,2,9 thymic carcinoid,5,10 oncocytic carcinoid of the kidney,11 malignant carcinoid tumor of the lung,12 and bronchial neuroendocrine tumors.1,13,14 There is a higher than expected incidence of carcinoid tumor causing cyclical Cushing’s disease compared with the reported incidence of typical Cushing’s syndrome due to a carcinoid tumor as the ectopic source. Seven cases of carcinoid tumors causing cyclical Cushing’s disease are reported—3 due to bronchial carcinoid,1,13,14 1 due to malignant bronchial carcinoid,12 2 due to thymic carcinoid,5,10 and 1 due to oncocytic carcinoid of kidney.11 Several patients thought to have cyclical Cushing’s disease underwent pituitary surgery.3 However, they continued to have persistent elevated cortisol because of either incomplete surgery or the presence of an ectopic source. Distinguishing between these 2 possibilities can be very difficult.The diagnosis of cyclical Cushing’s syndrome is often challenging and often diagnosed incorrectly. Normal pituitary/adrenal axis dynamics between symptomatic cycles make cyclical Cushing’s syndrome a difficult diagnosis. The timing of the tests performed can be critical. A DST conducted on the downward slope of the periodic curve would give the erroneous impression that the decreased cortisol production resulted from the dexamethasone, when in fact the decrease was due to periodicity, whereas suppression testing on the upward slope results in a paradoxical response. Endocrine testing may not be conclusive in differentiating pituitary from ectopic sources. A paradoxical response to dexamethasone has been reported in patients with cyclical Cushing’s disease.15 Diagnosis of cyclical Cushing’s syndrome should be actively sought in individuals with variable cortisol values, paradoxical or inconsistent responses to dexamethasone, and apparent spontaneous remission of the Cushingoid state. After diagnosis, careful differential diagnosis as to the etiology is essential to distinguish between pituitary Cushing’s syndrome and that due to an ectopic ACTH source.Our case confirms the challenges of the diagnosis of cyclical Cushing’s syndrome due to ectopic ACTH secretion. She demonstrated remission of her symptoms with normal laboratory values between her episodes. She also demonstrated paradoxical increases in cortisol levels on several occasions leading to the suspicion of cyclic Cushing’s syndrome. She showed suppression of serum free cortisol on a high dose intravenous dexamethasone test, which suggested a pituitary source. However, she had no response to a CRH test, which suggested an ectopic source. We did not perform petrosal sinus sampling as our patient demonstrated good laboratory evidence of ectopic ACTH secretion and CT and MRI scans showed a pulmonary lesion. Octreotide scan was confirmatory. Four cases of cyclical Cushing’s syndrome due to a bronchial carcinoid tumor are described in literature.1,12–14 One patient died and bronchial carcinoid was diagnosed at autopsy.1 In other patients the diagnosis was made after several years. In our patient the diagnosis was made in less than a year and she received treatment very early in the course of her disease. Currently she has had complete resolution of her symptoms with normal laboratory studies.Another unique aspect in our patient was the resumption of diurnal variation of cortisol production immediately after surgery. No patients have previously been reported (Fig. 3). Patients with either pituitary Cushing’s disease or Cushing’s syndrome due to the ectopic ACTH syndrome require exogenous steroids because of pituitary adrenal axis suppression from the excess steroids. In cyclic Cushing’s disease, the pituitary/adrenal axis may not be suppressed depending on the frequency and the extent of the cycle allowing for periods during which time the pituitary/adrenal axis may be normal. Our patient was monitored more closely postoperatively without hormonal supplementation than any previously reported cases. She did not exhibit any signs of adrenal insufficiency for several weeks. However, over time, she developed evidence of some suppression and required a brief period of cortisol replacement. This is likely due to recovery of the adrenal axis between cyclic episodes.CONCLUSIONBronchial carcinoid is rare etiology of cyclical Cushing’s syndrome. The subtleties and complexities that one can encounter in the diagnosis cannot be overemphasized. A high index of clinical suspicion and repeated laboratory evaluation over time is required to establish the diagnosis. Treatment usually results in cure and reduction in morbidity. Routine postoperative steroid supplementation in these patients may not be required because of the relatively intact pituitary/adrenal axis between cyclic episodes.REFERENCES1. Bailey RE. Periodic hormonogenesis—a new phenomenon. Periodicity in function of a hormone producing tumor in Man. J Clin Endocrinol Metab. 1971;32:317–327.[Context Link][CrossRef][Medline Link]2. Shapiro MS, Shenkman L. Variable hormonogenesis in Cushing’s syndrome. Q J Med. 1991;79:351–363.[Context Link][Medline Link]3. Atkinson AB, Kennedy AL, Carson DJ, et al. Five cases of cyclical Cushing’s syndrome. BMJ. 1985;291:1453–1457.[Context Link][CrossRef][Medline Link]4. Watanobe H, Aoki R, Takebe K, et al. In vivo and in vitro studies in a patient with cyclical Cushing’s disease showing some responsiveness to bromocriptine. Horm Res. 1991;36:227–234.[Context Link][CrossRef][Medline Link]5. Thorner MO, Martin WH, Ragan GE, et al. A case of ectopic ACTH syndrome: diagnostic difficulties caused by intermittent hormone secretion. Acta Endocrinol. 1982;99:364–370.[Context Link][Medline Link]6. Jordan RM, Ramos-Gabatin A, Kendall JW, et al. Dynamics of adrenocorticotropin (ACTH) secretion in cyclic Cushing’s syndrome: evidence for more than one abnormal ACTH biorhythm. J Clin Endocrinol Metab. 1982;55:531–537.[Context Link][CrossRef][Medline Link]7. Velkeniers B, Beckers A, Stevenaert A, et al. Cyclical Cushing’s disease. A case report. Pathol Res Pract. 1991;187:603–607.[Context Link][CrossRef][Medline Link]8. Terzolo M, Ali A, Pia A, et al. Cyclic Cushing’s syndrome due to ectopic ACTH secretion by an adrenal pheochromocytoma. Endocrinol Invest. 1994;17:869–874.[Context Link]9. Blau N, Miller WE, Miller ER Jr, et al. Spontaneous remission of Cushing’s syndrome in a patient with an adrenal adenoma. J Clin Endocrinol Metab. 1975;40:659–663.[Context Link][CrossRef][Medline Link]10. Meinardi JR, Van Den Berg G, Wolffenbuttel BHR, et al. Cyclical Cushing’s syndrome due to an atypical thymic carcinoid. Neth J Med. 2006;64:23–27.[Context Link][Medline Link]11. Hannah J, Lippe B, Lai-Goldman M, et al. Oncocytic carcinoid of the kidney associated with periodic Cushing’s syndrome. Cancer. 1988;61:2136–2140.[Context Link][CrossRef][Medline Link]12. Chajek T, Romanoff H. Cushing syndrome with cyclical edema and periodic secretion of corticosteroids. Arch Intern Med. 1976;136:441–443.[Context Link][CrossRef][Medline Link]13. Arnaldi G, Mancini T, Kola B, et al. Cyclical Cushing’s syndrome in a patient with a bronchial neuroendocrine tumor (typical carcinoid) expressing ghrelin and growth hormone secretagogue receptors. J Clin Endocrinol Metab. 2003;88:5834–5840.[Context Link][Full Text][CrossRef][Medline Link]14. Shapiro MS, Gutman A, Bruderman I, Myers B, et al. Cushing’s syndrome associated with a bronchial adenoma. Possible periodic hormonogenesis. Isr J Med Sci. 1975;11:919–924.[Context Link][Medline Link]15. Brown RD, Van Loon GR, Orth DN, et al. Cushing’s disease with periodic hormonogenesis: one explanation for paradoxical response to dexamethasone. J Clin Endocrinol Metab. 1973;36:445–451.[Context Link][CrossRef][Medline Link]cyclical Cushing’s disease; bronchial carcinoid; adrenal insufficiency00019616-200803000-0001300006090_2006_64_23_meinardi_carcinoid_|00019616-200803000-00013#xpointer(id(citation_FROM_JRF_ID_d4258e744_citationRF_FLOATING))|11065405||ovftdb|SL000060902006642311065405citation_FROM_JRF_ID_d4258e744_citationRF_FLOATING[Medline Link]1642143900019616-200803000-0001300002808_1988_61_2136_hannah_associated_|00019616-200803000-00013#xpointer(id(citation_FROM_JRF_ID_d4258e782_citationRF_FLOATING))|11065213||ovftdb|SL00002808198861213611065213citation_FROM_JRF_ID_d4258e782_citationRF_FLOATING[CrossRef]10.1002%2F1097-0142%2819880515%2961%3A10%3C2136%3A%3AAID-CNCR2820611034%3E3.0.CO%3B2-P00019616-200803000-0001300002808_1988_61_2136_hannah_associated_|00019616-200803000-00013#xpointer(id(citation_FROM_JRF_ID_d4258e782_citationRF_FLOATING))|11065405||ovftdb|SL00002808198861213611065405citation_FROM_JRF_ID_d4258e782_citationRF_FLOATING[Medline Link]328264300019616-200803000-0001300000779_1976_136_441_chajek_corticosteroids_|00019616-200803000-00013#xpointer(id(citation_FROM_JRF_ID_d4258e819_citationRF_FLOATING))|11065213||ovftdb|SL00000779197613644111065213citation_FROM_JRF_ID_d4258e819_citationRF_FLOATING[CrossRef]10.1001%2Farchinte.136.4.44100019616-200803000-0001300000779_1976_136_441_chajek_corticosteroids_|00019616-200803000-00013#xpointer(id(citation_FROM_JRF_ID_d4258e819_citationRF_FLOATING))|11065405||ovftdb|SL00000779197613644111065405citation_FROM_JRF_ID_d4258e819_citationRF_FLOATING[Medline Link]126755200019616-200803000-0001300004678_2003_88_5834_arnaldi_neuroendocrine_|00019616-200803000-00013#xpointer(id(citation_FROM_JRF_ID_d4258e849_citationRF_FLOATING))|11065404||ovftdb|SL00004678200388583411065404citation_FROM_JRF_ID_d4258e849_citationRF_FLOATING[Full Text]00004678-200312000-0004100019616-200803000-0001300004678_2003_88_5834_arnaldi_neuroendocrine_|00019616-200803000-00013#xpointer(id(citation_FROM_JRF_ID_d4258e849_citationRF_FLOATING))|11065213||ovftdb|SL00004678200388583411065213citation_FROM_JRF_ID_d4258e849_citationRF_FLOATING[CrossRef]10.1210%2Fjc.2003-03051400019616-200803000-0001300004678_2003_88_5834_arnaldi_neuroendocrine_|00019616-200803000-00013#xpointer(id(citation_FROM_JRF_ID_d4258e849_citationRF_FLOATING))|11065405||ovftdb|SL00004678200388583411065405citation_FROM_JRF_ID_d4258e849_citationRF_FLOATING[Medline Link]1467117700019616-200803000-0001300004445_1975_11_919_shapiro_hormonogenesis_|00019616-200803000-00013#xpointer(id(citation_FROM_JRF_ID_d4258e886_citationRF_FLOATING))|11065405||ovftdb|SL0000444519751191911065405citation_FROM_JRF_ID_d4258e886_citationRF_FLOATING[Medline Link]118436500019616-200803000-0001300004678_1973_36_445_brown_hormonogenesis_|00019616-200803000-00013#xpointer(id(citation_FROM_JRF_ID_d4258e928_citationRF_FLOATING))|11065213||ovftdb|SL0000467819733644511065213citation_FROM_JRF_ID_d4258e928_citationRF_FLOATING[CrossRef]10.1210%2Fjcem-36-3-44500019616-200803000-0001300004678_1973_36_445_brown_hormonogenesis_|00019616-200803000-00013#xpointer(id(citation_FROM_JRF_ID_d4258e928_citationRF_FLOATING))|11065405||ovftdb|SL0000467819733644511065405citation_FROM_JRF_ID_d4258e928_citationRF_FLOATING[Medline Link]434660300019616-200803000-0001300004678_1971_32_317_bailey_hormonogenesis_|00019616-200803000-00013#xpointer(id(citation_FROM_JRF_ID_d4258e427_citationRF_FLOATING))|11065213||ovftdb|SL0000467819713231711065213citation_FROM_JRF_ID_d4258e427_citationRF_FLOATING[CrossRef]10.1210%2Fjcem-32-3-31700019616-200803000-0001300004678_1971_32_317_bailey_hormonogenesis_|00019616-200803000-00013#xpointer(id(citation_FROM_JRF_ID_d4258e427_citationRF_FLOATING))|11065405||ovftdb|SL0000467819713231711065405citation_FROM_JRF_ID_d4258e427_citationRF_FLOATING[Medline Link]432239000019616-200803000-0001300006865_1991_79_351_shapiro_hormonogenesis_|00019616-200803000-00013#xpointer(id(citation_FROM_JRF_ID_d4258e452_citationRF_FLOATING))|11065405||ovftdb|SL0000686519917935111065405citation_FROM_JRF_ID_d4258e452_citationRF_FLOATING[Medline Link]164948000019616-200803000-0001300002418_1985_291_1453_atkinson_cyclical_|00019616-200803000-00013#xpointer(id(citation_FROM_JRF_ID_d4258e482_citationRF_FLOATING))|11065213||ovftdb|SL000024181985291145311065213citation_FROM_JRF_ID_d4258e482_citationRF_FLOATING[CrossRef]10.1136%2Fbmj.291.6507.145300019616-200803000-0001300002418_1985_291_1453_atkinson_cyclical_|00019616-200803000-00013#xpointer(id(citation_FROM_JRF_ID_d4258e482_citationRF_FLOATING))|11065405||ovftdb|SL000024181985291145311065405citation_FROM_JRF_ID_d4258e482_citationRF_FLOATING[Medline Link]299854000019616-200803000-0001300004137_1991_36_227_watanobe_responsiveness_|00019616-200803000-00013#xpointer(id(citation_FROM_JRF_ID_d4258e519_citationRF_FLOATING))|11065213||ovftdb|SL0000413719913622711065213citation_FROM_JRF_ID_d4258e519_citationRF_FLOATING[CrossRef]10.1159%2F00018216900019616-200803000-0001300004137_1991_36_227_watanobe_responsiveness_|00019616-200803000-00013#xpointer(id(citation_FROM_JRF_ID_d4258e519_citationRF_FLOATING))|11065405||ovftdb|SL0000413719913622711065405citation_FROM_JRF_ID_d4258e519_citationRF_FLOATING[Medline Link]166838100019616-200803000-0001300000067_1982_99_364_thorner_difficulties_|00019616-200803000-00013#xpointer(id(citation_FROM_JRF_ID_d4258e557_citationRF_FLOATING))|11065405||ovftdb|SL0000006719829936411065405citation_FROM_JRF_ID_d4258e557_citationRF_FLOATING[Medline Link]628042700019616-200803000-0001300004678_1982_55_531_jordan_adrenocrticotrophin_|00019616-200803000-00013#xpointer(id(citation_FROM_JRF_ID_d4258e594_citationRF_FLOATING))|11065213||ovftdb|SL0000467819825553111065213citation_FROM_JRF_ID_d4258e594_citationRF_FLOATING[CrossRef]10.1210%2Fjcem-55-3-53100019616-200803000-0001300004678_1982_55_531_jordan_adrenocrticotrophin_|00019616-200803000-00013#xpointer(id(citation_FROM_JRF_ID_d4258e594_citationRF_FLOATING))|11065405||ovftdb|SL0000467819825553111065405citation_FROM_JRF_ID_d4258e594_citationRF_FLOATING[Medline Link]628478300019616-200803000-0001300006586_1991_187_603_velkeniers_cyclical_|00019616-200803000-00013#xpointer(id(citation_FROM_JRF_ID_d4258e631_citationRF_FLOATING))|11065213||ovftdb|SL00006586199118760311065213citation_FROM_JRF_ID_d4258e631_citationRF_FLOATING[CrossRef]10.1016%2FS0344-0338%2811%2980154-800019616-200803000-0001300006586_1991_187_603_velkeniers_cyclical_|00019616-200803000-00013#xpointer(id(citation_FROM_JRF_ID_d4258e631_citationRF_FLOATING))|11065405||ovftdb|SL00006586199118760311065405citation_FROM_JRF_ID_d4258e631_citationRF_FLOATING[Medline Link]165640900019616-200803000-0001300004678_1975_40_659_blau_spontaneous_|00019616-200803000-00013#xpointer(id(citation_FROM_JRF_ID_d4258e705_citationRF_FLOATING))|11065213||ovftdb|SL0000467819754065911065213citation_FROM_JRF_ID_d4258e705_citationRF_FLOATING[CrossRef]10.1210%2Fjcem-40-4-65900019616-200803000-0001300004678_1975_40_659_blau_spontaneous_|00019616-200803000-00013#xpointer(id(citation_FROM_JRF_ID_d4258e705_citationRF_FLOATING))|11065405||ovftdb|SL0000467819754065911065405citation_FROM_JRF_ID_d4258e705_citationRF_FLOATING[Medline Link]1127076 Laboratory Investigation by Referring Physician Laboratory Data on Presentation to Our Clinic: Basal Values of Plasma Cortisol, ACTH, and Urine Free Cortisol Laboratory Data After Recurrence of Symptoms: Random Values of Plasma Cortisol, ACTH, and Urine Free Cortisol Laboratory Data After Recurrence of Symptoms Laboratory Data After Recurrence of Symptoms: High-Dose Dexamethasone Suppression Test (1 mg/hr Intravenous Dexamethasone for 7 hr) Laboratory Data After Recurrence of Symptoms: Human CRH Test (100 μg Given as Intravenous Bolus) A, Preoperative imaging studies. CT of the chest: 2.3- × 1.6-cm noncalcified nodule in the right lower lobe. MRI of the chest, 2.5- × 1.4-cm enhancing mass in the right lower lobe corresponding to mass seen on CT. C, Octreotide scan, a focus of increased uptake within the right hilar region, which correlates with the mass on the CT and MRI of the chest. Carcinoid tumor with scattered positive immunostaining for ACTH. Cortisol values after surgery. Patient’s feature before and after surgery showing resolution of buffalo hump and striae.Cyclical Cushing’s Syndrome Due to Bronchial Carcinoid: Early Diagnosis and Prompt TreatmentHamid Zulekha MD; Faas, Fred H. MDCME Review Article #6CME Review Article #6218p 95-100