#1925 A rare cause of hyponatremia due to adrenal insufficiency in a patient with small cell lung cancer

Abstract Background and Aims Hyponatremia is the most frequent electrolyte disorder. Small Cell Lung Cancer (SCLC) release often antidiuretic hormone paraneoplastically. But Adrenal insufficiency is a rare cause of hyponatremia in SCLC. Prior one can cause euvolemic hyponatremia, latter one can cause hypovolemic hyponatremia. Opposite treatments should be applied for each one. So They should be investigated carefully before starting the treatment. Method A male patient who had metastatic SCLC was admitted to the emergency. After physical examination blood and urine tests were provided. Results A 52-year-old male patient who had metastatic SCLC was admitted to the emergency unit because of fatigue, weakness and confusion. On physical examination the patient's face was darkened but his conjunctiva was pale, his tongue and mucous membranes were dry. The blood pressure was 90/60 mm Hg. The test results provided were as follows: Glucose 106 mg/dL, creatinine 0.42 mg/dL, urea 38.1 mg/dL, sodium 109 mmol/L, potassium 3.3 mmol/L, white blood cells 9760 /mm3, hemoglobin: 9 g/dL, platelets: 176000/mm3. The patient had no chemotherapy during the last three months. He also did not have a history of antihypertensive treatment. The echocardiographic examination revealed that the ejection fraction was 60%. The abdominal computerized tomography scan showed multiple metastasis of the tumor, but adrenal glands were free of metastasis. The sodium deficit was calculated targeting to 120 mmol/L and therapy was started. The patient's weight was 70 kg. The calculated sodium deficit was 420 mmol. Since the hyponatremia was chronic, the deficit was planned to be given in 24 hours. Potassium was also given. During hospitalization, on day 2nd the patient's blood and urine tests were as follows: Creatinine 0.58 mg/dL, urine creatinine 22.8 mg/dL, 24-hour urine volume 2200 mL, 24-hour creatinine clearance 60 ml/min. Urine sodium concentration 105.6 mmol/L, serum sodium 114 mmol/L, sodium clearance: 1.41 ml/min. Fractional sodium excretion was 2.3%. Although the treatment was continued for 6 days, with the same dose of 420 mEq sodium given for each day, the serum sodium concentration reached to 115 mmol/L on day 6. (Totally, 2520 mEq of sodium was given for 6 days). Therefore, hyponatremia was thought to be due to urinary loss of sodium. The fractional sodium excretion of 2.3% supported this. All these findings suggested the diagnosis of renal salt wasting in this patient. We decided to give the patient fludrocortisone (Astonin H 0.1 mg) twice a day orally in addition to sodium chloride tablets (approximately 1.5 gram = 25-30 mmol). During the follow-up of the patient, the both fludrocortisone pills and salt tablets increased to 2 × 2, finally, when reached the level of sodium is above 130 mmol/L, salt tablets were stopped. One thing need to be noted here; hyponatremia did not improve unless giving fludrocortisone. But after this, although more sodium was given during sodium replacement, there was no increase in fractionated sodium excretion, on the contrary, it decreased. On day 14th, Fractional sodium elimination was 1.7%. Serum Na: 133 mmol/L. The patient was advised to take fludrocortisone tablets twice a day orally and was discharged from hospital on day 15th when serum sodium concentration was 138 mmol/L. If a patient with serum cortisol level below 4 mcg/dl have been evaluated as adrenal insufficiency regardless of ACTH level in sera.; additionally, hyperpigmentation and hyponatremia due to salt wasting through the kidneys led us to diagnose. The hyponatremia resolved only after added fludrocortisone. Conclusion However SCLC can give rise euvolemic hyponatremia producing ADH generally, besides, SCLC can cause adrenal insufficiency leading to serious hypovolemic hyponatremia. Diagnose is of crucial importance for correct treatment which can be only achieved by replacing the both sodium and fludrocortisone.