Primary Pituitary Abscess: Two Case Reports.

Introduction Pituitary abscess is a rare disorder that represents a small fraction of all pituitary lesions. In this report, we present two additional cases with unique features to promote awareness and prompt surgical intervention. Case Presentations A 42-year-old male presented with headache, photophobia, subjective fever, dizziness, imbalance, nausea, and vomiting. A pituitary hormone panel confirmed hypothyroidism and suggested central hypogonadism and secondary adrenal insufficiency. Magnetic resonance imaging (MRI) showed a large sellar mass measuring 2.5 cm × 1.8 cm × 1.6 cm (CC × XT × AP). A 76-year-old woman presented with several months of headaches and unsteady gait in the setting of a known previously asymptomatic sellar lesion, measuring 1.8 cm × 1.2 cm × 1.5 cm (XT × CC × AP). Repeat MRI demonstrated possible hemorrhage within the lesion. In both cases, a preliminary diagnosis of pituitary macroadenoma was made, but transsphenoidal surgery revealed an encapsulated abscess; cultures obtained from the abscesses stained for gram-positive bacteria. Conclusion Pituitary abscess is a rare, potentially life-threatening disorder that may be easily mistaken for other sellar lesions. In this review, we contribute two additional cases of pituitary abscesses to increase awareness and emphasize the importance of proper diagnosis and management.

A case of pituitary apoplexy mimicking viral meningitis.

Pituitary apoplexy (PA) is a clinical syndrome caused by ischemia or hemorrhage of the pituitary gland, typically in the context of an adenoma. It typically presents with a thunderclap headache and sterile cerebral spinal fluid (CSF). The authors identify a case of PA, which initially presented with the signs and symptoms of viral meningitis. Presentation of Case: A 44-year-old man presented to the emergency department with headache, nuchal rigidity, fever, and delirium. The patient reported a 10-year history of chronic that were partially responsive to acetaminophen. Four days after admission, the patient developed right-sided cranial nerve III, IV, and VI palsies. Labs revealed anemia and hyponatremia. The CSF was leukocytic, lymphocyte-predominant, and had elevated protein. In addition to these results, negative CSF bacterial cultures led the care team to believe this case was viral meningoencephalitis. Routine MRI of the brain at presentation revealed a 3.1×2.5×3.2 (craniocaudal×anterior posterior×transverse) expansile mass centered within the sella turcica. An endocrine workup revealed hypopituitarism. The diagnosis of PA was then made. A microscopic transsphenoidal resection of the sellar mass was performed, and histopathologic analysis confirmed necrotic pituitary adenoma tissue. Following an uncomplicated procedure, the patient recovered fully from his cranial nerve palsies and continues to do well. Discussion: Because life-threatening hypotension from acute adrenal insufficiency can be caused by PA, timely diagnosis is crucial. When a patient presents with meningism, PA should be included in the differential diagnosis. Conclusion: This report illustrates a case of PA presenting with symptoms and a CSF profile classically associated with viral meningitis.

A novel pipeline of 2-(benzenesulfonamide)-N-(4-hydroxyphenyl) acetamide analgesics that lack hepatotoxicity and retain antipyresis.

Although acetaminophen (ApAP) is one of the most commonly used medicines worldwide, hepatotoxicity is a risk with overdose or in patients with compromised liver function. ApAP overdose is the most common cause of acute fulminant hepatic failure. Oxidation of ApAP to N-acetyl-p-benzoquinone imine (NAPQI) is the mechanism for hepatotoxicity. 1 is a non-hepatotoxic, metabolically unstable lipophilic ApAP analog that is not antipyretic. The newly synthesized 3 is a non-hepatotoxic ApAP analog that is stable, lipophilic, and retains analgesia and antipyresis. Intraperitoneal or po administration of the new chemical entities (NCEs), 3b and 3r, in concentrations equal to a toxic dose of ApAP did not result in the formation of NAPQI. Unlike livers from NCE-treated mice, the livers from ApAP-treated mice demonstrated large amounts of nitrotyrosine, a marker of mitochondrial free radical formation, and loss of hepatic tight junction integrity. Given the widespread use of ApAP, hepatotoxicity risk with overuse, and the ongoing opioid epidemic, these NCEs represent a novel, non-narcotic therapeutic pipeline.