A purely extradural lumbar nerve root cavernoma mimicking acute myeloid leukemia recurrence: Case report and literature review.

BACKGROUND: Myeloid sarcoma (MS) is a malignant tumor that usually occurs concomitantly with or following acute myeloid leukemia (AML). Cavernomas are benign congenital malformations that are unusual in the spine and exceedingly rare in pure extradural locations. CASE DESCRIPTION: We report a 73-year-old female with a previous medical history of AML in remission for 3 years who presented with symptoms of low back pain and right lower extremity radiculopathy. A magnetic resonance scan showed an extradural, foraminal lesion centered at the L2 level involving the right L2 nerve root. In view of the history of AML, this lesion was potentially considered MS, a form of AML relapse. Surgery consisting of a right L1 and L2 hemilaminectomy facilitated gross total resection of the purely extradural lesion the proved histologically to be a cavernoma. CONCLUSION: In patients with a history of leukemia, MS must be considered in the differential diagnosis for any epidural or nerve root lesion that appears following treatment. Although rare, cavernomas must be considered among the differential diagnoses for epidural nerve root lesions in the setting of AML.

Fever-triggered Brugada syndrome in an adult patient presenting with hemophagocytic syndrome induced by Chlamydophila pneumoniae.

A previously healthy 29-year-old man was admitted to our hospital, with a 4-day history of fever (>39°C), rigours, diaphoresis, fatigue and retro-orbital headache. On examination, he was febrile (37.8°C) and tachycardic (110 bpm). Laboratory work up revealed bicytopenia (white cell count 1.37×10(9)/L, platelets 60×10(9)/L) and an increase in C reactive protein (9 mg/dL). The ECG showed ST segment elevation in V1, V2 and V3 leads. The patient was admitted and investigation was initiated revealing prolonged fever (>7 days), pancytopenia, hepatosplenomegaly, hyperferritinemia, hypertriglyceridemia, hypofibrinogenemia, elevated soluble CD25 and hemophagocytosis in bone marrow. Therefore, the patient presented 7 of the 8 diagnostic criteria of hemophagocytic syndrome. Laboratorial investigation for infectious causes was negative, except for IgA and IgG Chlamydophila pneumoniae. ECG re-evaluation on the day of discharge showed no ST segment elevation and no other abnormalities. Genetic testing for known mutations associated with hemophagocytic syndrome and Brugada syndrome did not show any mutations in these genes.