Successful Treatment of Lithium-Induced Nephrogenic Diabetes Insipidus with Celecoxib: A Promising Therapeutic Option.

BACKGROUND Nephrogenic diabetic insipidus (NDI) poses a challenge in clinical management, particularly when associated with lithium ingestion. Non-selective non-steroidal anti-inflammatory drugs (NSAIDs) have been widely used for the treatment of numerous diseases worldwide, including NDI. However, many studies have reported the diverse adverse effects of long-term use of non-selective NSAIDs. Celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, is a better drug to relieve pain and inflammation in terms of long-term safety and efficacy than non-selective NSAIDs. Nevertheless, there are few reports describing the effectiveness of celecoxib in treating NDI. CASE REPORT We report a case of a 46-year-old woman with schizophrenia who presented with severe hypernatremia and refractory polyuria due to lithium-induced NDI. Cessation of lithium ingestion and traditional treatments, including trichlormethiazide and desmopressin, yielded minimal improvement in her hypernatremia and polyuria. Her sodium level needed to be strictly controlled with the infusion of dextrose 5% in water. Given the safety of celecoxib, we decided to initiate celecoxib as the treatment of lithium-induced NDI instead of indomethacin. Notably, the introduction of celecoxib led to a substantial and sustained amelioration of polyuria and hypernatremia without any celecoxib-associated adverse effects. Even after transfer to another hospital, stability in serum sodium levels persisted with celecoxib. CONCLUSIONS We presented a case of lithium-induced NDI successfully treated with celecoxib, a selective COX-2 inhibitor. To the best of our knowledge, this is the first reported case of successful treatment of lithium-induced NDI with celecoxib, and suggests celecoxib is a viable therapeutic option warranting further exploration. Physicians should consider its use when faced with the challenging management of lithium-induced NDI.

Ipsilateral Visual Loss Caused by Optic Nerve Compression between a Tuberculum Sellae Meningioma and the Internal Carotid Artery.

We report a rare case of ipsilateral visual loss caused by compression of the optic nerve between a tuberculum sellae meningioma (TSM) and the internal carotid artery (ICA). The patient was a 70-year-old female who presented with a 2-year history of left visual disturbance with a TSM on magnetic resonance imaging. No tumor infiltration to the optic canal was identified in the preoperative images. Extended endoscopic transsphenoidal surgery was performed and showed no infiltration to the optic canal. The tumor was removed completely, and optic nerve compression was found between the TSM and atherosclerotic ICA. This report shows an atypical case in which compression of the optic nerve between a TSM and the ICA caused ipsilateral visual loss despite no infiltration to the optic canal.