Idiopathic purpura fulminans in dengue hemorrhagic fever.

Purpura fulminans is a rapidly progressive thrombotic disease that has been described during both severe bacterial and viral infections. Disseminated intravascular coagulation (DIC), antiphospholipid antibodies and acquired or congenital C and S protein deficiency are thought to play a role in its pathogenesis. Here we report the case of a 4-year-old girl who developed gangrene of all her fingers and toes following dengue shock syndrome complicated by DIC and also discuss its management.

Dengue viral infections as a cause of encephalopathy.

The aim of this study was to determine the clinical characteristics and poor prognostic factors associated with high mortality in dengue encephalopathy. Fifteen patients with confirmed dengue infections, who developed encephalopathy, were recruited from two tertiary care hospitals in Colombo, Sri Lanka. Among the factors that contributed to encephalopathy were: Acute liver failure (73%), electrolyte imbalances (80%) and shock (40%). Five (33.3%) patients developed seizures. Disseminated intravascular coagulation was seen in five (33.3%). Secondary bacterial infections were observed in 8 (53.3%) of our patients. The overall mortality rate was 47%.

Experience with the oral iron chelator deferiprone in transfusion-dependent children.

OBJECTIVE: To establish efficacy and safety of deferiprone. DESIGN: Prospective study. SETTING: The Lady Ridgeway Hospital for Children, Colombo. PATIENTS: Transfusion-dependent children in the age group 1 to 15 years. INTERVENTION: Patients were given 75 mg/kg/day of deferiprone orally in divided doses. MEASUREMENTS: Efficacy of deferiprone therapy was assessed by 4 to 6 monthly serum ferritin (SF) assays. Safety of therapy was assessed by 4-weekly white cell counts and serum alanine aminotransferase (ALT) levels. The Z-score was used to assess the significance of the difference between the mean initial and final SF level. RESULTS: 82 patients received deferiprone therapy for a mean duration of 30 +/- 14 months. Initial SF levels ranged from 1115 to 12,165 micrograms/l with a mean of 5156 +/- 2631 micrograms/l. Final SF levels ranged from 312 to 15,285 micrograms/l with a mean of 2809 +/- 2380 micrograms/l (Z score 5.99; p < 0.001). Two (2.4%) children developed agranulocytosis which reverted to normal on discontinuation of treatment. 41 (50%) developed arthropathy and in 17 this was severe enough to require discontinuation of therapy. Serum ALT levels were raised in 35 (43%) patients but reverted to pretreatment values or lower despite continuation of deferiprone therapy. There was one death in a 9-year old child who developed diabetes mellitus and heart failure despite deferiprone therapy for 3 years. CONCLUSIONS: A final SF level < 2500 micrograms/l was achieved in 52% children. Severe arthropathy and agranulocytosis may necessitate permanent discontinuation of therapy.