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PubMed1992

[A case of Cushing syndrome caused by ACTH producing atypical lung carcinoid tumor].

A forty-one-year-old male who was found to have lung carcinoid tumor showed clinical features of Cushing syndrome. At the age of 38 years during a regular check-up, a chest roentgenogram showed multiple nodular shadows in the bilateral lung, and he was admitted to hospital. By open lung biopsy, he was diagnosed as having malignant carcinoid or small cell carcinoma of the lung. The abnormal lung shadows did not respond to chemotherapy (CDDP + VDS). The clinical course after discharge was uneventful until the age of 41 years, when he was readmitted to our hospital because of brain metastasis. Physical examination revealed moon face and central obesity. Plasma ACTH level was high and dexamethasone suppression test showed no cortisol suppression on 8 mg dexamethasone administration. Therefore, it was thought that the patient had ACTH producing ectopic tumor which led to Cushing syndrome. We measured the molecular weight of ACTH by column chromatography and found he had a big ACTH (molecular weight about 22,000). Reexamining him clinically and histologically, we concluded that the patient had atypical carcinoid tumor in the lung which might produce ACTH causing Cushing syndrome with metastasis to the brain.

Adrenocorticotropic Hormone↗
PubMed1961

[Cushing syndrome].

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Cushing Syndrome↗
PubMed2003

Discriminatory value of the low-dose dexamethasone suppression test in establishing the diagnosis and differential diagnosis of Cushing's syndrome.

Cushing's syndrome requires a screening test of high sensitivity, followed by biochemical evaluation of the source of the tumor when the cause is ACTH dependent. The high-dose dexamethasone suppression test is still in common use as an aid in differential diagnosis, although its value has been queried. We have routinely used the low-dose dexamethasone suppression test for many years in the diagnosis of Cushing's syndrome but noticed that patients with pituitary-dependent Cushing's syndrome or Cushing's disease, usually showed some degree of suppression of their serum cortisol, compared to those with the ectopic ACTH syndrome. We therefore analyzed retrospectively the serum cortisol responses during the low-dose dexamethasone suppression test and the high-dose dexamethasone suppression test in 245 patients with ACTH-dependent Cushing's syndrome and compared the diagnostic utility of each test either alone or in combination with a standard test using CRH. Evaluation of the serum cortisol response at 24 and 48 h during the low-dose dexamethasone suppression test correctly identified 98% of patients with ACTH-dependent Cushing's syndrome and distinguished between pituitary and ectopic causes with a sensitivity of 82% and a specificity of 79%. In the same patients, the serum cortisol response to the high-dose dexamethasone suppression test had a slightly higher sensitivity (91%) and specificity (80%). However, the combined criteria of a more than 30% suppression of serum cortisol during the low-dose dexamethasone suppression test and/or a more than 20% increase in the CRH test had a significantly higher sensitivity (97%) and specificity (94%) than either the high-dose dexamethasone or the CRH tests alone in the differential diagnosis of ACTH-dependent Cushing's syndrome. It produced equivalent information to that when high-dose and CRH test results were combined. We therefore conclude that in our patient series, the serum cortisol response during the low-dose dexamethasone suppression test is highly sensitive in diagnosing Cushing's syndrome and, combined with the results of the serum cortisol response to the CRH test, offered a safe and cost-effective test in the differential diagnosis of ACTH-dependent Cushing's syndrome. There does not appear to be any necessity for retaining the high-dose dexamethasone suppression test in this diagnostic work-up.

Adrenocorticotropic Hormone↗
PubMed1996

[A case of ACTH-producing thymic carcinoid tumor with Cushing syndrome].

ACTH-producing thymic carcinoid tumor with Cushing syndrome in a 41-year-old male was reported. Plasma ACTH and cortisol was high, and chest X-ray film and CT scan revealed a tumor mass in the anterior mediastinum. Extended thymectomy with pretracheal lymph node dissection was performed. The microscopic findings revealed that the mass was carcinoid tumor with metastasis of anterior mediastinal lymph node. ACTH and cortisol were restored to normal range 1 week after operation. Unfortunately, he admitted seven months later because of high level of ACTH and right supraclavicular lymph nodes swelling. He underwent right neck dissection. Pathological examination proved metastatic carcinoid tumors in the dissected nodes. It is important to perform supraclavicular lymph node dissection together with extended thymectomy for thymic carcinoid tumor.

Adrenocorticotropic Hormone↗
PubMed2003

Diagnosis and surgical treatment of ectopic adrenocorticotropic hormone-producing pulmonary tumors accompanied by Cushing syndrome.

Malignant pulmonary tumors are rarely accompanied by Cushing syndrome. We encountered 4 patients with adrenocorticotropic hormone (ACTH)-producing pulmonary tumors (3 with carcinoid and 1 with small cell carcinoma). All patients were females aged 33-76 years. In the 4 patients, diagnostic methods, surgical procedures, stage, outcome, and immunohistological findings were evaluated. Subtotal resection of the anterior lobe of the pituitary gland had been performed in 3 patients. However, ACTH did not decrease, and further examination revealed pulmonary tumors. Preoperative blood sampling by catheter examination was performed in 2 patients, of whom 1 showed increased ACTH. Intraoperative blood sampling showed increased ACTH in 1 patient. Lobectomy combined with mediastinal lymph node dissection was performed in 3 patients and lobectomy alone (video-assisted thoracoscopic surgery) in 1. All patients showed a decrease in ACTH after operation without tumor recurrence. Diagnosis is possible by measuring ACTH in pulmonary arterial wedge blood obtained by catherization or in pulmonary venous blood obtained during operation. Surgical resection is effective for ectopic ACTH-producing pulmonary tumors.

Adrenocorticotropic Hormone↗
PubMed1996

[Food-dependent Cushing syndrome: a new entity of organic hypercorticism].

Diagnosis of Cushing's syndrome is quite difficult in endocrinology. Spontaneous Cushing's syndrome is usually divided into two subgroups, one which is dependent on corticotropin (ACTH) and another one which is not. In the first class are Cushing's disease, the ectopic corticotropin syndrome and the rare ectopic corticotropin-releasing hormone (CRH) syndrome; these ACTH-dependent Cushing's syndrome have usually diffusely enlarged adrenal glands. In the second class are cortisol producing unilateral adrenocortical adenomas or carcinomas, and the recent Cushing's syndrome with food dependent periodic hormonogenesis. This food dependent Cushing's syndrome is an ACTH-independent Cushing's syndrome with multinodular enlargement of both adrenal glands. Pathogenesis is an aberrant adrenal sensitivity to physiologic secretion of gastric inhibitory peptide (GIP). Ectopic expression of GIP receptors on adrenal cells involve pathologic food induced cortisol secretion. Food dependent Cushing's syndrome is a new cause of Cushing's syndrome. Food induced cortisol secretion may have to be explored in the ACTH-independent Cushing's syndrome.

Adrenocortical Hyperfunction↗
PubMed1984

Bilateral primary pigmented nodular adrenocortical disease. Rare cause of the Cushing syndrome.

Four patients (two males and two females, ages 12-21 years) had clinical features of the Cushing syndrome. Results of biochemical tests (in three patients tested) suggested the presence of an autonomously functioning adrenocortical neoplasm. However, radiologic examination of the adrenals did not show an adrenal tumor. The four patients underwent curative bilateral total adrenalectomy and did not manifest the Nelson syndrome postoperatively (follow-up, 2-22 years). The adrenal pathologic findings in these patients were similar. Gross findings included: 1) decreased, normal, or slightly increased total gland weight; 2) studding of the external and cut surfaces by small (less than 4 mm) black, brown, dark-green , red, or (rarely) yellow nodules; and 3) cortical atrophy and disorganization of the normal zonation between the nodules. Microscopically, the nodules were composed predominantly of enlarged, globular, cortical cells with granular eosinophilic cytoplasm that often contained lipofuscin. Twenty-four similar cases have been reported. Findings in these plus our four cases identify a special type of adrenocortical pathology associated with Cushing syndrome, for which we suggest the name "primary pigmented nodular adrenocortical disease."

Adolescent↗
PubMed1985

Growth in Cushing syndrome.

Pre- and post-operative growth was analysed in eight children with Cushing syndrome. Six children had Cushing's disease; three of them were treated by bilateral adrenalectomy and three by transphenoidal pituitary adenectomy. One child had an adrenocortical adenoma and another primary adrenocortical nodular dysplasia. The typical cushingoid habitus was not always present during hypercortisolism. In contrast, abnormal deceleration of longitudinal growth and increase in relative weight were constant. The slowing of growth started 0.2-5.1 years before diagnosis. In four children these changes concurred. In three others the excessive weight gain preceded the slowing of growth, by 2.5-7.0 years. In one patient the deceleration appeared first; this was a girl with concomitant coeliac disease. This pattern of growth change occurring before (normal slowing of growth in) late puberty should raise the possibility of hypercortisolism. There was a suggestion of a better growth recovery in Cushing disease after pituitary adenectomy than after bilateral adrenalectomy.

Adolescent↗
PubMed1989

[Adrenocortical carcinoma with Cushing syndrome: report of a case].

We report a 45-year-old female with left adrenocortical carcinoma resulting in Cushing syndrome. She visited the 3rd Department of Internal Medicine, Kanazawa University Hospital with complaints of moon face, amenorrhea and hypertension. A diagnosis of left adrenal tumor with Cushing syndrome was made and she was transferred to our clinic. Left thoracoabdominal adrenalectomy was performed. The histologic report was compatible with adrenocortical carcinoma with no invasion into adjunctive tissues. She is now on endocrinologic study and is being administered 1,1-dichloro-2-[o-chlorophenyl]-2[p-chlorophenyl] ethane. There is no evidence of local recurrence or remote metastasis.

Adrenal Cortex Neoplasms↗
PubMed1998

Drug-induced Cushing syndrome in a patient with ulcerative colitis after betamethasone enema: evaluation of plasma drug concentration.

The authors report the induction of Cushing syndrome by daily betamethasone enema in a patient with ulcerative colitis, and they determine for the first time the pharmacokinetic profile of betamethasone after rectal dosing. The authors found high plasma concentrations of betamethasone, which could have been enough to cause Cushing syndrome. Suppression of the hypothalamus-pituitary-adrenal axis disappeared after the dose schedule was changed from every day to three times a week. These findings suggest that a considerable amount of betamethasone is absorbed after rectal dosing.

Administration, Rectal↗
PubMed1953

[Cushing syndrome].

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Cushing Syndrome↗
PubMedDate not supplied

Corticotropin-releasing hormone test: improvement of the diagnostic accuracy of simultaneous and bilateral inferior petrosal sinus sampling in patients with Cushing syndrome.

Twenty-six consecutive patients with ACTH-dependent Cushing syndrome were subjected to simultaneous, bilateral inferior petrosal sinus sampling for ACTH assay before and after ACTH-releasing hormone (CRH) stimulation. The baseline ACTH inferior petrosal sinus/periphery (IPS/P) ratio was > or = 2 in 12 of 26 patients (46%), whereas the CRH-stimulated IPS/P ratio was > or = 3 in 19 of 26 patients (73%). A pituitary adenoma, ACTH-secreting at immunostaining, was surgically proved in all of the 19 patients who had an ACTH IPS/P ratio > or = 2 basally or > or = 3 after the CRH test but also in three other patients who did not have such ratios. The value of the basal IPS/P ratio and the complete lack of ACTH increase after CRH led to the diagnosis of an ectopic ACTH syndrome in four patients: a bronchial carcinoid was found in three patients, and the site of the tumor was still unknown in the other. In conclusion, the CRH test improved the diagnostic accuracy of inferior petrosal sinus sampling from 61.5% (12 pituitary, 4 ectopic) to 92.0% (19 pituitary, 4 ectopic). Thus it should be performed during the diagnostic process.

ACTH Syndrome, Ectopic↗
PubMed1992

Urine free cortisol in the high-dose dexamethasone suppression test for the differential diagnosis of the Cushing syndrome.

OBJECTIVE: To develop criteria for interpreting the high-dose dexamethasone suppression test using urine free cortisol as an end point for the differential diagnosis of the Cushing syndrome. DESIGN: Retrospective review. SETTING: Inpatient research ward. PATIENTS: Patients (118) with surgically confirmed causes of the Cushing syndrome: 94 with pituitary disease, 14 with primary adrenal disease, and 10 with ectopic adrenocorticotropic hormone (ACTH) secretion. MAIN OUTCOME MEASURES: The sensitivity, specificity, and diagnostic accuracy were determined for the high-dose dexamethasone suppression test using urine free cortisol and using 17-hydroxysteroid excretion. For each analysis, patients with pituitary disease were considered to be "diseased" and patients with nonpituitary disease were considered to be "non-diseased". The level of suppression that gave 100% specificity was determined for each steroid. RESULTS: The accuracy of urine free cortisol when used as an end point in the high-dose dexamethasone suppression test was equivalent to that of 17-hydroxysteroid excretion. At all levels of sensitivity and specificity, however, the degree of suppression of urine free cortisol used for the diagnosis of pituitary disease was greater than that of 17-hydroxysteroid excretion. The likelihood ratios for pituitary disease based on urine free cortisol suppression of greater than 50%, of greater than 80%, and of greater than 90% were 4.2, 10.1, and "infinite," respectively. Suppression of urine free cortisol greater than 90% or suppression of 17-hydroxysteroid excretion greater than 64% was associated with 100% specificity. When these criteria were combined, the percentage of correct predictions (102 of 118 [86%; 95% CI, 78% to 92%]) was higher than that obtained using either steroid alone (89 of 118 [75%; CI, 65% to 83%]) (P = 0.009) and higher than that obtained using the traditional criterion of 50% suppression for 17-hydroxysteroid excretion (95 of 118 [80%; CI, 71% to 87%]) (P = 0.016). CONCLUSIONS: In the high-dose dexamethasone suppression test, the degree of suppression of urine free cortisol used for the diagnosis of pituitary disease is greater than that traditionally used for 17-hydroxysteroid excretion. The diagnostic performance of the test is improved by measuring both urine free cortisol and 17-hydroxysteroid excretion and by requiring greater suppression of both steroids.

17-Hydroxycorticosteroids↗