Literature DB >> 10523219

Paradoxical response to dexamethasone in the diagnosis of primary pigmented nodular adrenocortical disease.

C A Stratakis1, N Sarlis, L S Kirschner, J A Carney, J L Doppman, L K Nieman, G P Chrousos, D A Papanicolaou.   

Abstract

BACKGROUND: Primary pigmented nodular adrenocortical disease causes the Cushing syndrome in children and young adults and is most frequently associated with the Carney complex.
OBJECTIVE: To evaluate diagnostic tests for primary pigmented nodular adrenocortical disease.
DESIGN: Retrospective cohort study.
SETTING: Tertiary care center. PATIENTS: 21 patients with primary pigmented nodular adrenocortical disease. The control groups consisted of 9 patients with macronodular adrenocortical disease and 15 patients with primary unilateral adrenocortical disease (single adenomas). MEASUREMENTS: Clinical characteristics, radiologic imaging, and a 6-day Liddle test with determination of urinary free cortisol and 17-hydroxycorticosteroid excretion.
RESULTS: Adrenal imaging and other tests were of limited value for the diagnosis of primary pigmented nodular adrenocortical disease. The Liddle test, however, distinguished patients with this disorder from those with other primary adrenocortical lesions. An increase of 50% or more in urinary free cortisol levels on day 6 of the Liddle test identified 9 of 13 patients (69.2% [95% CI, 46.6% to 91.8%]) with primary pigmented nodular adrenocortical disease, excluded all patients with macronodular adrenocortical disease, and was present in only 3 of the 15 patients with single adrenocortical adenomas (20% [CI, 0% to 40.2%]). An increase in urinary free cortisol excretion of 100% or more on day 6 of the Liddle test identified only patients with primary pigmented nodular adrenocortical disease.
CONCLUSIONS: Patients with primary pigmented nodular adrenocortical disease responded to dexamethasone with a paradoxical increase in glucocorticoid excretion during the Liddle test. This feature distinguishes such patients from those who have the Cushing syndrome caused by other primary adrenal disorders and may lead to timely detection of the Carney complex (a potentially fatal disorder) in asymptomatic patients.

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Year:  1999        PMID: 10523219     DOI: 10.7326/0003-4819-131-8-199910190-00006

Source DB:  PubMed          Journal:  Ann Intern Med        ISSN: 0003-4819            Impact factor:   25.391


  60 in total

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2.  A novel splice site mutation of the PRKAR1A gene, C.440+5 G>C, in a Chinese family with Carney complex.

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4.  A six month mitotane course induced sustained correction of hypercortisolism in a young woman with PPNAD and Carney complex.

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Review 5.  Neonatal Cushing Syndrome: A Rare but Potentially Devastating Disease.

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6.  Deletions of the PRKAR1A locus at 17q24.2-q24.3 in Carney complex: genotype-phenotype correlations and implications for genetic testing.

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Review 7.  Genetics of Cushing's Syndrome.

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10.  Primary pigmented nodular adrenocortical disease presenting with a unilateral adrenocortical nodule treated with bilateral laparoscopic adrenalectomy: a case report.

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