A case of fatal myxedema coma with electrocardiogram Osborne J-wave in a patient initially diagnosed with hypothyroidism.

Myxedema coma is a life-threatening endocrine emergency with a high mortality rate resulting from severe insufficiency of thyroid hormones. Intravenous levothyroxine replacement is considered the standard therapy for myxedema coma in many countries. In Japan, however, although there are diagnostic criteria highly suggestive or diagnostic for myxedema coma, no management strategy has been established, despite the availability of levothyroxine. Here we report a 75-year-old man with a history of Alzheimer's disease and schizophrenia who developed somnolence and generalized edema. Except for a pulse rate of 60 bpm, his vital signs and blood oxygen level were stable. Thyroid studies showed an elevated serum thyrotropin level of 219.2 µU/mL and a decreased serum free-thyroxine level of 0.15 ng/dL. On this basis he was diagnosed as having hypothyroidism rather than being highly suggestive for myxedema coma. Daily oral levothyroxine 25 µg was initiated and increased to 50 µg 3 days later. Seven days after being started on levothyroxine, the patient suddenly developed impaired consciousness, hypoxemia, hypotension, hypothermia, and hyponatremia. Electrocardiography revealed junctional bradycardia with Osborne J-wave. Myxedema coma was therefore diagnosed. He went into cardiac arrest in the emergency room but was resuscitated. Despite subsequent intravenous administration of hydrocortisone and levothyroxine, as well as intensive supportive care, he eventually died 12 hours after hospital admission. This case illustrates some of the challenges associated with the management of patients with signs highly suggestive/diagnostic of myxedema coma, including the optimal loading dosage and intervention timing of thyroid hormone replacement.

Endoscopic Endonasal Removal of Large Calcified Pituitary Adenoma: Case Report and Review of the Literature.

BACKGROUND: Large calcified intrasellar masses, called pituitary stones, have been reported as calcified pituitary adenomas in the literature. Although relatively rare, calcified pituitary adenomas appear in various formations. Thus, whether the lesion is removable-and, if so, which approach is appropriate-mainly depends on its formation and quality. CASE DESCRIPTION: A 46-year-old woman presented with visual loss and amenorrhea. Although computed tomography showed a uniformly calcified sellar tumor, magnetic resonance imaging displayed heterogenous intensity on T2-weighted images and mild gadolinium enhancement, suggesting that the lesion was a mixture of pituitary adenoma and fine calcification. Thus, we undertook tumor resection via an endoscopic endonasal approach, which resulted in total removal. The pathological diagnosis was a pituitary adenoma with rich calcification. CONCLUSIONS: We report a rare case of a large pituitary stone that was successfully removed via an endoscopic endonasal approach. This could therefore be a feasible, effective technique for the removal of pituitary stones, although careful analysis of preoperative magnetic resonance imaging is required.

Unusual Magnetic Resonance Imaging Findings of a Glioblastoma Arising During Treatment with Lenvatinib for Thyroid Cancer.

BACKGROUND: Glioblastoma (GBM) is a lesion radiologically characterized by magnetic resonance imaging findings, such as ring enhancement with extensive perifocal edema and a butterfly appearance extending into the bilateral lobes. However, these characteristic findings could be changed by antiangiogenic therapy, with decreased contrast enhancement and improved perifocal edema. Herein, we report a case of GBM that arose during treatment with a tyrosine kinase inhibitor for another cancer. CASE DESCRIPTION: A 57-year-old man presented with seizures. Until the seizure onset, he had been treated with the multireceptor tyrosine kinase inhibitor lenvatinib for 4 years for thyroid cancer and its metastasis to the thoracic vertebral body. Magnetic resonance imaging revealed a slightly high intensity lesion in the left frontal base area on T2-weighted or fluid-attenuated inversion recovery images, and the lesion showed only faint enhancement on T1-weighted images after gadolinium administration. Total resection was performed and the histopathologic diagnosis was GBM. However, grade IV histology was observed in only a limited area, and most of the specimen showed lower grade histology with moderate vascularization that lacked microvascular proliferation. CONCLUSIONS: Lenvatinib, which is antiangiogenic, might have affected the radiologic characteristics, as well as the pathology of the tumor. Brain tumors arising during treatment with receptor tyrosine kinases for other cancers could show atypical imaging findings.