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Letters to the Editor |
Cedars-Sinai Medical Center Los Angeles, California 90048
Dimitris A. Papanicolaou
NICHD, NIH Bethesda, Maryland 20892
Mericq and Cutler (1) recently reported that high fluid intake increased urine free cortisol (UFC) excretion in normal subjects. They hypothesized that an increase in urinary volume would reduce the fraction of filtered cortisol that is either reabsorbed or metabolized and thus increase the UFC. They also speculated that patients with polyuria would have elevated UFC levels and would be incorrectly considered as having Cushing syndrome, if only UFC were measured. They suggested that patients with polyuria should undergo alternative testing including an overnight dexamethasone suppression test, diurnal plasma cortisol levels, or urinary 17-hydroxycorticosteroid (17-OHCS) excretion. We report a patient with psychogenic polydipsia with elevated UFC but not Cushing syndrome.
A 37-yr-old male presented with complaints of obesity, decreased libido, polydipsia, polyuria, polyphagia, sweating, and feeling warm. The patient’s only medication was Paroxetine, taken intermittently for anxiety. On physical examination, he lacked stigmata of Cushing syndrome, including the absence of a buffalo hump, supraclavicular filling, striae, thin skin, ecchymoses, facial plethora, or proximal muscle wasting. He had generalized, rather than central obesity. Because his 24-h urinary volume was 8–12 liters, he underwent a water deprivation test. His baseline urine osmolality was 81 mmol/kg, with a corresponding serum osmolality of 282 mmol/kg. After 8 h of water deprivation, his urine osmolality rose to 667 mmol/kg with a serum osmolality of 295 mmol/kg, consistent with psychogenic polydipsia, rather than diabetes insipidus. The patient was evaluated for Cushing syndrome and was found to have UFC levels of 335 and 519 nmol/day (nl, 55–248 nmol/day). Computed tomography scan and magnetic resonance imaging failed to show a pituitary or adrenal tumor.
The patient was referred to the National Institutes of Health for further studies to distinguish between Cushing syndrome and a pseudo-Cushing state. The patient’s serum cortisol suppressed to 28 nmol/L during a 1-mg overnight dexamethasone suppression test. Diurnal plasma cortisol values were: 2330, 86 nmol/L; 0000, 66 nmol/L; 0730, 182 nmol/L; 0800, 171 nmol/L, consistent with a normal diurnal cortisol variation (2). UFCs were 552 and 651 nmol/day (normal, 66–298); urine volume was 7 and 7.5 L/day, respectively. 17-OHCS were 10.5 mg/day, (normal, 3–10 mg/day) (4 mg/day per gram of daily excreted creatinine). During a loperamide suppression test (3), plasma cortisol suppressed from a baseline of 604 nmol/L to 39 nmol/L, 210 min after loperamide administration. A dexamethasone-CRH test (4) showed undetectable levels of plasma cortisol and ACTH at all times following oCRH. The above tests are all consistent with a pseudo-Cushing state. On psychiatric consultation, the patient was found to suffer from anxiety and a personality disorder with obsessive-compulsive elements. He refused further psychiatric intervention.
The patient continued to believe he had Cushing syndrome and sought medical treatment at Cedars-Sinai Medical Center. His urinary volume was still in the 8–12 L range. His UFC was 621 nmol/day (normal, 30–232 nmol/day), while his 17-OHCS excretion was 6.9 mg/day, (normal, 3–10 mg/d) (2.5 mg/d per gram of daily excreted creatinine). Of note, his 24-h urinary creatinine was elevated (in proportion to the elevation of his UFC) at 233, 280, and 210 µmol/kg/day (nl, 140–190 µmol/kg/day). The patient was reassured that the diagnosis of Cushing syndrome was highly unlikely and was instructed to restrict his fluid intake to 2 L/day.
We conclude that this patient’s increase in UFC was secondary to increased urinary volume resulting from psychogenic polydipsia. He lacked the physical stigmata of Cushing syndrome, and detailed endocrinologic evaluation argued against Cushing syndrome. Unlike the volunteers who were given excess fluid acutely and had normal urinary creatinine excretion (1), this patient had an elevated urinary creatinine excretion, which suggests that psychogenic polydipsia results in the inability to reabsorb creatinine and cortisol (loss of the renal medullary gradient), rather than an inability to metabolize cortisol. Realization that excess fluid intake can elevate UFC levels would prevent patients from undergoing prolonged and expensive evaluations for Cushing syndrome based on elevated urinary free cortisol excretion alone.
Footnotes
Address correspondence to: Theodore C. Friedman, M.D., Ph.D., Division of Endocrinology, Cedars-Sinai Medical Center, D-2019, 8700 Beverly Boulevard, Los Angeles, California 90048.
Received March 19, 1998.
References
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