MON-012 Panhypopituitarism and Arginine-vasopressin Deficiency in a Case of Toxoplasma Encephalitis Secondary to AIDS

Abstract Disclosure: C. Man: None. R.J. Freedman: None. I. Mbaga: None. V. Loseva: None. Introduction: While the prevalence of Toxoplasma gondii infection in the general population is relatively high, symptomatic disease primarily occurs in immunocompromised hosts, notably HIV-positive patients who are not receiving antiretroviral therapy. In most cases, patients present with encephalitis, followed by ocular disease and pneumonia, which occur less frequently. Cases of toxoplasmic encephalitis and pituitary dysfunction have been described mostly in children, in the setting of congenital disease, but reports of this association in adults are limited. Case report: We present the case of a 31-year-old male patient with no significant past medical history, who was brought to the emergency department for confusion and lethargy that had progressively worsened over the last days. On arrival, he was found to be hypothermic, tachycardic, and hypotensive, requiring intubation for airway protection and vasopressor support due to persistent hypotension. An MRI of the brain revealed multiple lesions that were hyperintense on T2-weighted images and exhibited ring enhancement on T1-weighted images, the largest of which was located in the left frontal lobe, measuring 4 × 3.2 × 2.8 cm. There was also extensive vasogenic edema and a stable 3-mm rightward midline shift. Despite appropriate ICU management, the patient remained hypernatremic, raising suspicion for arginine-vasopressin (AVP) deficiency. For a sodium level of 171 mEq/L, the urinary output was 3L/24 hours, and the urinary osmolality was 126 mOsm/kg. Pituitary function testing revealed panhypopituitarism with cortisol < 3 mcg/dL, fT4 0.4 ng/dL (NV: 0.93-1.7), TSH inappropriately normal of 0.69 mcIU/mL (NV: 0.27-4.2), FSH < 0.3 mIU/mL, LH < 0.3 mIU/mL, total testosterone 3 ng/dL (NV: 300-1080), and an IGF-1 Z-score of -2.5 SD. Simultaneously, the patient was diagnosed with HIV (viral load > 500,000 copies/mL, CD4+ 5 cells/mcL). A lumbar puncture confirmed encephalitis with positive PCR for Toxoplasma gondii. The patient was started on a 6-week regimen of Atovaquone, Leucovorin, and Pyrimethamine. Antiretroviral therapy was initiated several weeks later to avoid immune reconstitution inflammatory syndrome. Recovery was slow and partial. By week 5, the patient was able to eat independently, though he remained mostly nonverbal. At 8 weeks post-presentation, he continued to require substitution with desmopressin, at a decreased dose compared to initially, corticosteroids, and levothyroxine. Conclusion: The incidence of toxoplasmic encephalitis (TE) has significantly declined with the advancement of antiretroviral therapy. However, untreated or undiagnosed HIV-positive patients remain at high risk, with up to 30% developing TE. A high clinical suspicion of endocrine deficiencies in such cases is essential for timely diagnosis and treatment. Presentation: Monday, July 14, 2025