Table 1.

Etiology in adipsic hypernatremia and ROHHAD (NET) syndrome.

Cause	Adipsic Hypernatremia (Average Serum Sodium Level: 157.1 ± 15.2 mM in Pediatric and Adult Patients) (Ref. [28])	ROHHAD (NET) Syndrome (Dysnatremia: 45.5% (15/33 Cases), Shown in 5~10 Years Old) (Ref. [15])
Genetic or innate factor	Structural defect in central septal lesion of brain (septo-optic dysplasia, agenesis of cortex, etc. (Refs. [4,5]))	Some candidate genes (PHOX2B, BDNF, RAI-1, etc.) have been analyzed but not confirmed. (Ref. [15])
Associated Tumor	Craniopharyngioma, germinoma, etc., in hypothalamus and pituitary lesion	Neural crest tumor (neuroblastoma, ganglioblastoma, etc.)
Inflammatory factors	Viral encephalitis (CMV, HHV-6, or COVID-19) (Refs. [8,9,10])	Similar symptoms to COVID-19 (Ref. [10])
Immunological factors	Autoantibodies:	Autoantibodies:
	Anti-Nax antibody Anti-subfornical antibody (Refs. [11,12,28])	Anti-hypothalamus, anti-pituitary Anti-subfornical antibody Anti-ZSCAN1(in ROHHAD-NET) (Refs. [21,28,29,30])
	Area:	Area:
	CVOs (SFO and OVLT) and their neural network area (SON, ARC, PVN, etc.) (Refs. [11,12,28])	Hypothalamus, brainstem, pontine tegmentum, midbrain, pons, upper cervical cord, thalamus (Ref. [18])
	Infiltrated or related immunological cells:	Infiltrated or related immunological cells:
	Deposition of the C3 component and infiltration of inflammatory cells Apoptosis in SFO and OVLT	Dense perivascular lymphocytic infiltrate CD20+ B-cells, patchy nodular parenchymal lymphocytic infiltrate CD8+ T-cells (Ref. [18])