Thomas B. Repas, DO, FACP, FACE, CDE, is an endocrinologist, lipidologist and physician nutrition specialist in clinical practice at the Regional Medical Clinic Endocrinology and Diabetes Education Center in Rapid City, SD. Dr. Repas is the former chairman of the professional diabetes advisory committees of the Wyoming and the Wisconsin Diabetes Prevention and Control Programs. He is board certified in the areas of endocrinology, diabetes and metabolism, clinical lipidology, internal medicine and nutrition, and is also a certified diabetes educator.

Hyponatremia is a clue to hypopituitarism

I was requested to see an inpatient who was incidentally found to have a 2.2-cm pituitary macroadenoma. The patient was a male in his mid-70s who also had hyponatremia with serum sodiums ranging between 124 nmol/L and 129 mmol/L (135-145 mmol/L). In my consult note, I mentioned that hyponatremia in the presence of a pituitary macroadenoma was concerning for central adrenal insufficiency.

The neurosurgeons, however, had been consulted before I had the opportunity to see the patient. One of the neurosurgeons questioned my concern about the hyponatremia possibly being a sign of central adrenal insufficiency. He told me that hyponatremia in association with a pituitary incidentaloma is “very unusual.” They were concerned the patient may have syndrome of inappropriate antidiuretic hormone secretion and ordered a CT of the chest to evaluate for other reasons to explain the hyponatremia.

It is true that central adrenal insufficiency is a less common cause of hyponatremia compared with other more common causes such as fluid overload, diuretic therapy, cirrhosis, congestive heart failure and syndrome of inappropriate antidiuretic hormone. However, in a patient with a pituitary macroadenoma, our index of suspicion should be much higher.

Often, hyponatremia is the only clue that a patient has hypopituitarism. Unlike primary adrenal insufficiency, central adrenal insufficiency does not present with hyperkalemia because adrenal mineralocorticoid production is relatively adrenocorticotropic hormone-independent. It has been reported that as many as 40% to 89% of those with hypopituitarism also have hyponatremia.

Further evaluation of our patient revealed two cortisols of 2.6 mcg/dL and 4.1 mcg/dL (5-25 mcg/dL) and a morning adrenocorticotropic hormone level that was undetectable. The patient had not received any corticosteroids beforehand, which could have also explained such results. He had a very low free thyroxine of 0.44 ng/dL (0.8-1.8 ng/dL); low-normal free triiodothyronine; and inappropriately “normal” thyroid-stimulating hormone of 1.92 mIU/L (0.3-5.0 mIU/L). Furthermore, insulin-like growth factor I was very low; follicle-stimulating hormone was normal; luteinizing hormone was low; total testosterone was very low, in the 30 ng/dL range (240-950 ng/dL); and prolactin was 7.2 ng/mL (3-13 ng/mL).

I diagnosed panhypopituitarism and began replacement therapy with hydrocortisone and levothyroxine. I usually proceed with stimulation testing before initiating treatment; however, in this patient’s case I was certain he had the diagnosis. I did not want to delay treatment any longer, so I initiated hydrocortisone. In patients who do not have as clear a picture as this patient, however, we should always perform stimulation testing to confirm the diagnosis before beginning glucocorticoid replacement therapy.

The patient’s serum sodium levels slowly trended upward. He will be coming to see me in the near future as an outpatient so we can further discuss his diagnosis, management and replacement of other hormonal deficiencies.

Hypopituitarism with central adrenal insufficiency can sometimes present with hyponatremia. It is not “very unusual” and should be considered as a possible diagnosis among the many potential causes of hyponatremia.

For more information:

  • Diederich S. European Journal of Endocrinology. 2003;148:609-617.