Intracranial haemorrhage among Chinese children with immune thrombocytopenia in a Hong Kong regional hospital.

OBJECTIVE: To evaluate potential risk factors, presenting symptoms, management, and outcomes of intracranial haemorrhage in Chinese children with immune thrombocytopenia managed in a regional hospital. DESIGN: Retrospective case series. SETTING: A regional hospital in Hong Kong. PATIENTS: All paediatric patients with immune thrombocytopenia complicated by intracranial haemorrhage in the period January 1996 to December 2009. RESULTS: Nine episodes of intracranial haemorrhage were reported in eight patients (aged 0.9 to 19 years) with immune thrombocytopenia; three of the patients had acute immune thrombocytopenia and the other five had chronic immune thrombocytopenia. Intracranial haemorrhage occurred as early as the initial presentation with immune thrombocytopenia (n=2) and as late as up to 5 years after the diagnosis. The median platelet count at the time of intracranial haemorrhage was 12 x 10(9) /L (<10 x 10(9) /L [n=4]; 10-20 x 10(9) /L [n=2]; >20 x 10(9) /L [n=3]). The bleeding was considered spontaneous in six episodes, while head trauma (n=2) and vascular malformation (n=1) were identified in three patients with mild-to-moderate thrombocytopenia (42-82 x 10(9) /L) at the time of the bleed. Headache and mucosal bleeding were the commonest presenting symptoms (n=5). All patients received multimodal treatment after diagnosis of intracranial haemorrhage, and included platelet transfusion (n=8), intravenous immunoglobulin (n=6), methylprednisolone (n=4), and splenectomy (n=4); three individuals underwent neurosurgical interventions. One (11%) patient died of posterior fossa bleeding and one (11%) had neurological sequelae. All survivors achieved remission of their immune thrombocytopenia with a median follow-up of 5.3 years. CONCLUSION: Intracranial haemorrhage can occur anytime during the course of immune thrombocytopenia. A high index of suspicion for intracranial haemorrhage should be maintained during follow-up, as favourable outcomes can be achieved after early and vigorous interventions.

Recombination-deficient mutants of Salmonella typhimurium are avirulent and sensitive to the oxidative burst of macrophages.

Mutations in the genes recA and recBC were constructed in the virulent Salmonella typhimurium strain 14028s. Both the recA and recBC mutants were attenuated in mice. The mutants were also sensitive to killing by macrophages in vitro. The recombination mutants were no longer macrophage sensitive in a variant line of J774 macrophage-like cells that fail to generate superoxide. This suggests that repair of DNA damage by Salmonella is necessary for full virulence in vivo and that the oxidative burst of phagocytes is one source of such DNA damage.