Endocrine Abstracts

JOINT2444

Introduction: Parhon’s syndrome, also known as the syndrome of inappropriate antidiuretic hormone secretion (SIADH) or antidiabetes insipidus, is a rare disorder characterized by excessive secretion of antidiuretic hormone (ADH) from the posterior pituitary gland or an ectopic source. This results in dilutional hyponatremia, which requires hospitalization in 15–20% of cases.

Materials and methods: Patient S., a 66-year-old male, has been hospitalized multiple times since March 2024 due to recurrent episodes of hyponatremia, with serum sodium levels dropping to 108 mmol/l, accompanied by seizures and falls. Parhon’s syndrome was suspected.

Results: In June 2024, the patient was admitted to the Department of Neuroendocrinology at the Endocrinology Research Centre. Hormonal studies showed no evidence of hypothyroidism (TSH: 0.487 mIU/l, free T4: 16.8 pmol/l)or adrenal insufficiency (ACTH: 28 pg/ml, cortisol: 326.7 nmol/L). Heart failure was ruled out (NT-proBNP: 10 pg/ml; reference range: 0–125 pg/ml). Upon admission, laboratory findings included serum sodium of 119.9 mmol/l, blood osmolality of 247–249 mOsm/kg (reference: 280–300), and urine osmolality of 415–603 mOsm/kg (reference: 300–1200). Initial treatment involved an infusion of 3% NaCl, followed by oral therapy with 0.9% solution of NaCl. After five days, sodium stabilized at 133.6 mmol/lwith fluid restriction (800 mL/day) and furosemide (80 mg/day). As prior imaging showed no brain, thoracic, or abdominal tumors, further tests were done to explore a possible ectopic ADH source. A whole-body PET/CT (June 2024) revealed a hypermetabolic lesion in the right back, diagnosed as elastofibroma, but a follow-up PET/CT (July 2024) showed no tumors. A core biopsy failed due to insufficient tissue visibility. A surgeon suggested the 18F-FDG uptake was due to nonspecific changes from prior falls linked to hyponatremia. With fluid restriction, furosemide (80 mg/day), and NaCl (200 mL/day), serum sodium levels remained stable (138–141 mmol/L). Reducing furosemide to 40 mg/day led to sodium levels of 135–138 mmol/l, but stopping it caused a drop to 132.8 mmol/l, requiring reintroduction at 40 mg/day to maintain normal levels. Ongoing sodium monitoring was advised.

Conclusions: Despite the absence of a confirmed source of ADH hypersecretion, this case underscores the importance of early diagnosis, understanding the pathophysiology of Parhon’s syndrome, and implementing an effective treatment strategy. Proper management prevents severe complications associated with hyponatremia and inappropriate therapy, ultimately improving the patient’s quality of life.