Pituitary · 2026
Sustained remission of chronic post-traumatic arginine vasopressin deficiency despite absent posterior pituitary bright spot on MRI: a case series.
СтатьяКлинический случайНазвание и аннотация: Перевод в очереди
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Yamaki Tomohiro, Oka Nobuo, Ito Daisuke, Kobayashi Shigeki
Аннотация
BACKGROUND: Absence of the posterior pituitary bright spot (PPBS) on T1-weighted MRI is often observed in chronic post-traumatic arginine vasopressin deficiency (AVP-D), but its association with permanent AVP-D remains unclear.
CASE PRESENTATION: We report five patients with chronic-phase post-traumatic AVP-D (156-965 days post-injury) who were transferred to our rehabilitation center. All patients had received long-term desmopressin therapy and exhibited persistent absence of the PPBS on T1-weighted MRI at admission. Despite these findings, desmopressin therapy was successfully tapered and discontinued in all five cases. Case 3 presented a diagnostic challenge, in which resolution of post-traumatic AVP-D was obscured by concomitant adrenal insufficiency and was confirmed only after stabilization of glucocorticoid replacement. In Cases 3, 4, and 5, detectable plasma arginine vasopressin levels (1.0-1.9 pg/mL) were observed following desmopressin withdrawal despite persistent radiologic absence of the PPBS. All patients maintained stable water balance without desmopressin therapy, with no recurrence of polyuria or clinically significant hypernatremia during follow-up.
CONCLUSION: Endogenous vasopressin secretion may be retained in selected patients with chronic TBI, even when MRI suggests persistent neurohypophyseal abnormalities. Our cases demonstrate that absence of the PPBS is not a definitive marker of lifelong post-traumatic AVP-D. These observations support periodic reassessment and supervised trial discontinuation of desmopressin therapy in the neurorehabilitation setting, suggesting that preserved endogenous vasopressin function may remain unrecognized years after the initial insult.
CASE PRESENTATION: We report five patients with chronic-phase post-traumatic AVP-D (156-965 days post-injury) who were transferred to our rehabilitation center. All patients had received long-term desmopressin therapy and exhibited persistent absence of the PPBS on T1-weighted MRI at admission. Despite these findings, desmopressin therapy was successfully tapered and discontinued in all five cases. Case 3 presented a diagnostic challenge, in which resolution of post-traumatic AVP-D was obscured by concomitant adrenal insufficiency and was confirmed only after stabilization of glucocorticoid replacement. In Cases 3, 4, and 5, detectable plasma arginine vasopressin levels (1.0-1.9 pg/mL) were observed following desmopressin withdrawal despite persistent radiologic absence of the PPBS. All patients maintained stable water balance without desmopressin therapy, with no recurrence of polyuria or clinically significant hypernatremia during follow-up.
CONCLUSION: Endogenous vasopressin secretion may be retained in selected patients with chronic TBI, even when MRI suggests persistent neurohypophyseal abnormalities. Our cases demonstrate that absence of the PPBS is not a definitive marker of lifelong post-traumatic AVP-D. These observations support periodic reassessment and supervised trial discontinuation of desmopressin therapy in the neurorehabilitation setting, suggesting that preserved endogenous vasopressin function may remain unrecognized years after the initial insult.