Endocrine Abstracts (2013) 32 P956 | DOI: 10.1530/endoabs.32.P956

Hyponatremia as a first sign of panhypopituitarism: empty sella

Adriana Dokupilová1, Jana Kollerová2 & Juraj Payer2


1Cardiology Department, Nitra, Slovakia; 2Department of Internal Medicine, Bratislava, Slovakia.


Introduction: Hyponatremia is the most common disorder of electrolytes encountered in clinical practice, occurring in up to 15–30% of both acutely and chronically hospitalized patients. Although most cases are mild and relatively asymptomatic, it is important clinically because: i) acute severe hyponatremia can cause substantial morbidity and mortality, ii) mortality is higher in patients with hyponatremia who have a wide range of underlying diseases and iii) overly rapid correction of chronic hyponatremia can cause severe neurologic deficits and death.

Hyponatremia as the presenting manifestation of empty sella syndrome is rare. The term empty sella makes reference to the herniation of the subarachnoid space within the sella in patients with no history of pituitary tumor, surgery or radiotherapy. Although it is not usually associated with endocrine abnormalities, different degrees of hypopituitarism and mild hyperprolactinemia have been reported. Its clinical presentation resembles that of the syndrome of inappropriate antidiuretic hormone (ADH) secretion, but fluid restriction alone is unable to correct this problem. The cause of ADH secretion in hyponatremia associated with hypopituitarism is related to adrenocortical deficiency. The glucocorticoid deficit is not an osmotic, but a physiological stimulus for ADH secretion. Glucocorticoids have been shown to reverse the impaired water diuresis of this disorder by increasing the renal excretion of solutefree water. Glucocorticoid substitution is the mainstay treatment in this setting, but there are no practical guidelines for optimal glucocorticoid correction. In reviewing the literature, the dosage of hormone substitution has varied. Frequent monitoring of natremia is necessary to prevent neurologic deficits and myelinolysis.

Case report: A 38-year-old patient was admitted to our Department in April/May 2011 due to dyspepsia, nauzea and vomiting. Patient had a history of treatment with NSA (nimesulid) 14 day before admission, after falling down he complained of the pain in the right thorax. On the date of admission he had following laboratory findings: severe hyponatremia 118.8 (reference range RR 135–145 mmol/l), low serum osmolality 240 (275–295 mOsm/kg), urine osmolality 547 (50–1400 mmol/kg), uTSH 2.92 (0.3–4.2 μIU/ml), serum cortisol level at 0900 h was 616 (500 nmol/l and more), mild anaemia Hb 117 (130–180 g/l). He suffered from asthma and had meningitis in 1994. He had no liver and renal disease and never drank alcohol, he denied any history of using diuretics. His weight was 71 kg, his height was 171 cm, pulse rate 58 beats/min, respiratory rate 19/min, blood pressure 110/70 mmHg, temperature 36.7 °C. He was clinically euvolemic. Patient underwent gastroscopy with conclusion: minimal antrumgastritis and dysmotility like dyspepsia. Colonoscopy was without pathologic findings. CT of thorax and abdomen was without traumatic or other pathological changes, as well as CT of brain. After water restriction the serum natrium level normalised and patient was discharged. According to baseline laboratory findings, thyroid and severe adrenocortical deficiency was excluded. The follow up laboratory findings in June 2011 were: Na 134.5 (135–145 mmol/l), K 4.69 (3.6–5.3 mmol/l), ACTH 18 (7.2–63.3 pg/ml), IGF1 46.8 (109–284 ng/ml), low level of gonadotropins FSH 2.68 IU/l, LH 1.31 IU/l, very low serum testosteron 0.89 (8.69–29 nmol/l), uTSH 2.92 (0.3–4.2 μIU/ml), fT4 8.7 (12–22 pmol/l), aTPO 5.43 (5–34 IU/ml), aTG <10 (10–115 IU/ml), cortisol 298 (more than 500 nmol/l), prolactin 15.6 (4.0–15.2 ng/ml), MRI of hypophysis shown empty sella. We suggested panhypopituitarism – ACTH deficiency, TSH deficiency, gonadotropin deficiency and GH deficiency. Patient was tested at 5th Department of Internal Medicine University Hospital in Bratislava, where our suspicion was confirmed. Patient was started treatment with hydrocortison in daily dose 15 mg, levothyroxin in daily dose 75 μg, testosteron replacement therapy every 2–3 weeks and growth hormone replacement terapy with complete restitution of laboratory findings. Nowadays patient is feeling healthy and using all recommended medication.

Conclusion: Hyponatremia is the most common electrolyte disorder. Its frequency is higher in females, the elderly, and in patients who are hospitalized. Complete differential diagnosis including endocrinology laboratory and imaging techniques is necessary to obtain a correct diagnosis and following treatment.

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