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Diagnosis of hypopituitarism

INTRODUCTION

The diagnosis of hypopituitarism, defined as deficient secretion of one or more pituitary hormones because of pituitary or hypothalamic disease, is made by documenting subnormal secretion of these pituitary hormones in defined circumstances. Each pituitary hormone must be tested separately, since there is a variable pattern of hormone deficiency among patients with hypopituitarism.

The impetus to measure pituitary hormones is the suspicion that the secretion of one or more may be subnormal. This suspicion can be based upon the knowledge that the patient has either a lesion known to cause hypopituitarism or a symptom known to be caused by hypopituitarism. (See "Causes of hypopituitarism" and "Clinical manifestations of hypopituitarism".) The knowledge that the patient has a lesion that can cause hypopituitarism, eg, a sellar mass, is by itself sufficient reason to test for hypopituitarism because some patients with hypopituitarism have no symptoms.

CORTICOTROPIN

For normal health, the basal secretion of corticotropin (ACTH) must be sufficient to maintain the serum cortisol concentration within the normal range. For survival, it must increase to raise serum cortisol concentrations in times of physical stress.

Basal ACTH secretion — To test basal ACTH secretion, serum cortisol should be measured at 8 to 9 AM, and the results should be interpreted as follows:

  • A serum cortisol value of ≤3 mcg/dL (83 nmol/L; normal range 5 to 25 mcg/dL [138 to 690 nmol/L]), confirmed by a second determination, is strong evidence of cortisol deficiency, which in a patient with a disorder known to cause hypopituitarism is usually the result of that disorder. Such a finding in the absence of any known cause of hypopituitarism mandates measurement of serum ACTH. A serum ACTH value not higher than normal is inappropriately low and establishes the diagnosis of secondary adrenal deficiency (ie, pituitary or hypothalamic disease). A value higher than normal documents primary adrenal insufficiency (ie, adrenal disease). (See "Diagnosis of adrenal insufficiency in adults".)
  • A serum cortisol value of ≥18 mcg/dL (497 nmol/L) indicates that basal ACTH secretion is sufficient and also that it is probably sufficient for times of physical stress.
  • A serum cortisol value >3 mcg/dL (83 nmol/L) but <18 mcg/dL (497 nmol/L) that is persistent on repeat determination is an indication to evaluate ACTH reserve.

         

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Literature review current through: Apr 2013. | This topic last updated: Jun 29, 2012.
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References
Top
  1. Spark RF. Simplified assessment of pituitary-adrenal reserve. Measurement of serum 11-deoxycortisol and cortisol after metyrapone. Ann Intern Med 1971; 75:717.
  2. Jubiz W, Meikle AW, West CD, Tyler FH. Single-dose metyrapone test. Arch Intern Med 1970; 125:472.
  3. Landon J, Greenwood FC, Stamp TC, Wynn V. The plasma sugar, free fatty acid, cortisol, and growth hormone response to insulin, and the comparison of this procedure with other tests of pituitary and adrenal function. II. In patients with hypothalamic or pituitary dysfunction or anorexia nervosa. J Clin Invest 1966; 45:437.
  4. Streeten DH, Anderson GH Jr, Bonaventura MM. The potential for serious consequences from misinterpreting normal responses to the rapid adrenocorticotropin test. J Clin Endocrinol Metab 1996; 81:285.
  5. Soule SG, Fahie-Wilson M, Tomlinson S. Failure of the short ACTH test to unequivocally diagnose long-standing symptomatic secondary hypoadrenalism. Clin Endocrinol (Oxf) 1996; 44:137.
  6. Dickstein G, Shechner C, Nicholson WE, et al. Adrenocorticotropin stimulation test: effects of basal cortisol level, time of day, and suggested new sensitive low dose test. J Clin Endocrinol Metab 1991; 72:773.
  7. Mayenknecht J, Diederich S, Bähr V, et al. Comparison of low and high dose corticotropin stimulation tests in patients with pituitary disease. J Clin Endocrinol Metab 1998; 83:1558.
  8. Soule S, Van Zyl Smit C, Parolis G, et al. The low dose ACTH stimulation test is less sensitive than the overnight metyrapone test for the diagnosis of secondary hypoadrenalism. Clin Endocrinol (Oxf) 2000; 53:221.
  9. Nye EJ, Grice JE, Hockings GI, et al. Adrenocorticotropin stimulation tests in patients with hypothalamic-pituitary disease: low dose, standard high dose and 8-h infusion tests. Clin Endocrinol (Oxf) 2001; 55:625.
  10. Suliman AM, Smith TP, Labib M, et al. The low-dose ACTH test does not provide a useful assessment of the hypothalamic-pituitary-adrenal axis in secondary adrenal insufficiency. Clin Endocrinol (Oxf) 2002; 56:533.
  11. Hartman ML, Crowe BJ, Biller BM, et al. Which patients do not require a GH stimulation test for the diagnosis of adult GH deficiency? J Clin Endocrinol Metab 2002; 87:477.
  12. Biller BM, Samuels MH, Zagar A, et al. Sensitivity and specificity of six tests for the diagnosis of adult GH deficiency. J Clin Endocrinol Metab 2002; 87:2067.