This study decribes the treatment of a 37-year old female patient, with a history of poorly treated arterial hypertension (AH), referred to surgical consultation with right lower back pain, vertigo, headache, sweating and palpitations. During hospitalization, blood pressure (BP) ranged between 130/80 mm Hg and 190/120 mm Hg. The remainder of the clinical examination was normal. Thoracoabdominal scanner showed adrenal mass measuring 55x45x65 mm compressing the inferior vena cava and the right renal vein. The assay of urinary vanilmandelic acid (VMA) was 11.8mg/24hours. The assay of catecholamines in the blood was not performed. The diagnosis of pheochromocytoma was retained and surgical indication was determined. During pre-anaesthesia consultation, clinical examination showed good general condition, blood pressure (BP) to190/120 mmHg, normal cardiopulmonary auscultation and prediction criterion of easy intubation (Mallampati II). The patient underwent preoperative treatment with alpha-blockers and beta-blockers, and calcium channel blocker. Adrenalectomy was performed using midline laparotomy. The patient didn?t have hemodynamic instability during mobilization and tumor resection. The postoperative course was uneventful. She was discharged home on postoperative day 7. At 3 months? follow-up, the patient had no clinical signs and blood pressure was normal. Anesthesia for the surgical treatment of pheochromocytoma is feasible even in resource-limited settings. An adequate preoperative preparation of the patient helps prevent complications.

The development of rebound thymic hyperplasia (RTH) has been reported in patients who have recovered from stressful conditions such as surgery and steroid therapy. We report a case of RTH following the resolution of hypercortisolism after adrenalectomy for the treatment of adrenocortical adenoma in a patient with Cushing syndrome.

The initial description of Carney complex (CNC) in 1985 included myxomas, spotty skin pigmentation, and endocrine overactivity (of the adrenal, the pituitary, and the testis). In 1997, thyroid neoplasms were found in 3 patients with CNC and involvement of the gland in the syndrome was apparent. Herein, we describe the clinical, pathologic, and follow-up findings in 26 patients with CNC and a disorder of the thyroid gland. The patients were predominantly middle-aged women with an asymptomatic thyroid mass. Four patients had hyperthyroidism, which was caused by follicular hyperplasia in 2 patients and by toxic adenoma in 2 others. Pathologic findings included benign lesions (follicular hyperplasia, nodular hyperplasia, and follicular adenoma) in 16 patients and carcinomas (follicular or papillary) in 10 patients. The follicular carcinomas had unusual features, multifocality, bilaterality, and lymph node metastasis. The tumor was fatal in 3 of 4 patients with a tumor ≥3 cm in diameter. One patient had an unusual multifocal microscopic follicular hyperplasia. Detection and treatment of the thyroid neoplasms in patients with CNC requires long-term follow-up of patients with the syndrome.

This study aimed to explore the efficacy of propofol to treat malignant pheochromocytoma (PCC) in vitro and in vivo. In vitro, PC12 cells were treated with different concentrations of propofol (0, 1, 5, and 10 μg/mL) for specific times followed by a MTT assay to detect cell proliferation. Transwell assays were performed to assess the function of propofol on the migration and invasion of PC12 cells, and flow cytometry to analyze cell apoptosis and cell cycle progression. Quantitative real-time polymerase chain reaction was carried out to analyze the expression level of mRNA (Bcl-2, Bax, and CyclinE). The levels of Bcl-2, Bax, CyclinE, FOXO1, FOXO3, Bim, procaspase-3, and active caspase-3 were determined by western blotting. In vivo, the effects of propofol on PCC tumor growth were detected by transplanted mouse model. Transferase dUTP nick-end labeling was performed to detect tissue cell apoptosis. The results indicated that propofol inhibited PC12 cell proliferation, prevented cell migration and invasion, and induced the apoptosis of PC12 cells in a dose- and time-dependent manner. Propofol treatment increased the expression of Bax and decreased that of Bcl-2. In addition, propofol significantly induced the G1/S phase arrest in PC12 cells, and the expression of Cyclin E was reduced. Moreover, the levels of FOXO1, FOXO3, Bim, procaspase-3, and active caspase-3 were enhanced by propofol treatment. In vivo, propofol treatment significantly reduced the PCC tumor growth and induced tissue cell apoptosis. In conclusion, propofol has potent anti-PCC activity in vitro and in vivo, and is a potential small-molecule drug for treating malignant PCC.