Diabetes insipidus following neurosurgery at a university hospital in Western Saudi Arabia.

OBJECTIVES: To review the incidence, spectrum of clinical manifestation, course, risk factors, as well as treatment of diabetes insipidus (DI) following neurosurgery of the pituitary gland. METHODS: The files of 24 patients that underwent neurosurgery for sellar lesions, or tumor near the hypothalamus or pituitary gland at the Department of Neurosurgery, King Abdulaziz University Hospital, Jeddah, Kingdom of Saudi Arabia were retrospectively reviewed between January 2011 to December 2014. A total of 24 patients were studied, and were divided into 2 groups namely; DI and non-DI. Patient characteristics were studied using descriptive statistics. The differences in proportion between the 2 groups were found out using Z-test for proportion in 2 populations. The mean differences in the hormonal abnormalities for the 2 groups were assessed using independent t-test. All statistics are considered statistically significant when p less than 0.05. RESULTS: During hospitalization, 13 (54.2%) out of 24 patient that underwent neurosurgery had manifestations of DI, which was transient in 5 (38.8%) and permanent in 8 (61.2%). The DI subgroup contained higher prevalence of prolactinoma, craniopharyngioma, pre-operative panhypopituitarism, and macroadenoma in MRI imaging and transphenoidal surgery. Furthermore, urine osmolality was significantly lower in the DI group post-operatively with a significant p=0.023. It was recognized that the permanent DI documented more significant numbers than other studies. CONCLUSION: In our study group, it was recognized that permanent DI meant that our patients needed desmopressin for more than 3 months, which documented a more significant number than other studies.

Pseudotumor cerebri and prolactin secreting pituitary adenoma. Association or coincidence?

The occurrence of pseudotumor cerebri (PTC) and hyperprolactinemia related to a prolactinoma are extremely rare, and the link between these pathologies has not been examined adequately in the post-MRI era. We report a patient with a small intrasellar prolactinoma who also developed PTC. Magnetic resonance venography did not show any evidence of compression of the cavernous or any other sinuses. She initially responded to treatment with acetazolamide and cabergoline. However 9 months later, her PTC symptoms recurred despite a normal serum prolactin level and a mild reduction of the pituitary tumor size on MRI. She improved after a lumboperitoneal shunt. We conclude that the findings in our patient do not support an association between PTC and hyperprolactinemia or prolactinoma. However, the case supports the need for clinicians to consider the diagnosis of PTC when patients with small pituitary lesions exhibit raised intracranial pressure features.