Chronic encapsulated expanding hematoma in nonfunctioning pituitary adenoma.

The diagnosis and treatment of pituitary macroadenomas with entire hematoma fluid accumulation are problematic. Such lesions are often difficult to completely resect, and recurrence is not uncommon. We present five cases of pituitary macroadenomas entirely composed of hematoma fluid and investigated their histopathology to clarify the mechanism of the hematoma fluid accumulation. Five patients with pituitary adenoma and significant intra-tumor hematoma underwent transsphenoidal resection and were retrospectively reviewed for their clinical status, findings on magnetic resonance imaging (MRI), intraoperative findings, and histopathology. The specific surgical techniques used to address these cases were also reviewed. All patients were diagnosed with nonfunctioning pituitary adenomas by histopathological examination. MRI showed all tumors extended to the cavernous sinus. Histopathology showed tumor tissues were located between the thick granulation tissue and the pseudocapsule of the tumor. The thick granulation tissues were composed of collagenous layers, neovascular vessels, and necrotic red blood cells, indicating repeat hemorrhage from the granulation tissues. The boundary between adenoma and normal pituitary gland was identified during surgical removal in four patients and was not identified in the other patient who showed a recurrence 2 years later. Clinical and histopathological findings indicate hematoma fluid accumulation in the present cases is caused by repeat hemorrhage from the reactive granulation tissues and can be regarded as a chronic encapsulated expanding hematoma. In these cases, the boundary between adenoma and normal pituitary gland should be identified before puncturing the hematoma fluid to minimize the risk of tumor recurrence.

Aortic wall inflammation due to Takayasu arteritis imaged with 18F-FDG PET coregistered with enhanced CT.

UNLABELLED: The purpose of this study was to evaluate the ability of (18)F-FDG PET to identify aortitis and to localize and follow disease activity in patients with Takayasu arteritis. The value of using (18)F-FDG PET coregistered with enhanced CT in determining vascular lesion sites and inflammatory activity was assessed. METHODS: Takayasu arteritis was diagnosed according to the predefined criteria. Eleven patients with Takayasu arteritis in the active stage, 3 patients with Takayasu arteritis in the inactive stage, and 6 healthy subjects underwent (18)F-FDG PET coregistered with enhanced CT and the inflammatory vascular lesion was evaluated by using the standardized uptake value (SUV) of (18)F-FDG accumulation as an index. Two patients with active disease were analyzed by sequential (18)F-FDG PET scans during treatment. RESULTS: The (18)F-FDG PET revealed intense (18)F-FDG accumulation (SUV > or = 2.7) in the vasculature of 2 of the 11 cases in the active stage of Takayasu arteritis. The other 9 patients in the active stage revealed weak (18)F-FDG accumulation (2.3 > or = SUV > or = 1.2). No significant (18)F-FDG accumulation was observed in the patients with inactive disease (SUV < or = 1.2) and 6 control healthy subjects (SUV < 1.3). Given the cutoff SUV is 1.3, the sensitivity of (18)F-FDG PET analysis of Takayasu arteritis is 90.9% and the specificity is 88.8%. (18)F-FDG PET coregistered with enhanced CT localized (18)F-FDG accumulation in the aortic wall in the patients with Takayasu arteritis who had weak (18)F-FDG accumulation that could not otherwise be identified anatomically. Finally, (18)F-FDG accumulation resolved with therapy in 2 active cases. The disappearance of (18)F-FDG accumulation did not coincide with the level of general inflammatory markers. CONCLUSION: The (18)F-FDG PET images coregistered with enhanced CT images showed the distribution and inflammatory activity in the aorta, its branches, and the pulmonary artery in patients with active Takayasu arteritis, even those who had weak (18)F-FDG accumulation. The intensity of accumulation decreased in response to therapy.

Plasma concentrations of atrial and brain natriuretic peptides in a case with hypertensive encephalopathy.

Hemodynamic mechanism for brain edema forrmation in patients with hypertensive encephalopathy is unclear. Potential roles of natriuretic peptides in the pathogenesis of hypertensive encephalopathy are discussed. A 32-year-old man presented with slight left hemiparesis. He was slightly confused, and his blood pressure was extremely high. Cranial plain computerized tomography scans revealed diffuse brain edema mainly in the supratentorial white matter region. Blood examination revealed that plasma concentrations of atrial and brain natriuretic peptides were significantly high. His left hemiparesis disappeared within a day, but he tended to be agitated. His altered mental status, however, resolved with control of blood pressure. Serial magnetic resonance imagings demonstrated that the magnitude of brain edema was attenuated in proportion to decline in plasma concentrations of natriuretic peptides. This case suggests that significant elevation of plasma concentrations of natriuretic peptides may contribute to an acute rise in blood pressure, and that these peptides potentially play an important role in development of brain edema in hypertensive encephalopathy.