[Childhood medulloblastoma]. / Le médulloblastome de l'enfant.

Medulloblastoma is one of the most common malignant childhood brain tumors. It is a primitive neuroectodermal tumor (PNET) and predominantly arises in the cerebellum and 4th ventricle. Most cases of medulloblastoma are sporadic, but some predisposition syndromes are known, such as SUFU and Gorlin syndromes. Most often intracranial hypertension reveals the disease typically with headache and vomiting. However, the frequent atypical presentation should not delay neuroradiological investigations. Brain and spinal MRI can establish the diagnosis of posterior fossa tumor and define the extent of the disease. CSF study completes the staging. Histologic examination of the tumor confirms the diagnosis of medulloblastoma. Patients are classified into 2 risk groups: standard-risk medulloblastoma, defined by nonmetastatic disease treated by total or subtotal tumor resection; and high-risk patients who have disseminated disease and/or residual disease. Tumor molecular genetic findings allow the use of emerging prognostic factors and may ultimately contribute to the development of targeted therapy. Current treatment in the oldest children combines surgical resection followed by radiotherapy and chemotherapy. The aim of recent studies was to increase survival and decrease sequelae by reducing CSI in older children with standard risk medulloblastoma. Treatment in younger patients is as much as possible restricted to surgery and chemotherapy. However, long-term sequelae after treatment for medulloblastoma remain frequent and the detection and treatment of those sequelae is an essential part of the follow-up of the patients.

[Pneumonia due to adenovirus type 7: a case report in a healthy infant]. / Pneumopathie hypoxémiante à adénovirus de type 7 chez un nourrisson sans déficit immunitaire.

A 15-month-old boy treated with amoxicillin and clavulanic acid therapy for 8 days was admitted for persistent gastroenteritis and fever. He received ceftriaxone for pneumonia modified on day 4 for cefotaxime and josamycin due to extension of alveolar lesions. On day 7, persistent fever and worsened respiratory distress led to addition of rifampicin. The child was then admitted to an intensive care unit. A hemophagocytic syndrome was suspected based on clinical signs and laboratory findings and confirmed by cytological examination of bone marrow. Adenovirus type 7 was identified by polymerase chain reaction and culture of bronchoalveolar fluid. Prognosis was good within 3 weeks. B and T immunologic evaluations were normal 5 months after the infection. This case of severe adenovirus pneumonia was associated with hemophagocytic syndrome in a child without identified primary immunodeficiency. Adenovirus type 3 and 7 are most frequently responsible for severe or fatal respiratory infections.