From January 1994 to January 1998, 26 patients of unstable thoracolumbar burst fracture were treated by a short segment posterior instrumentation (pedicular screw plate/rod system), reduction and fusion in Kuala Lumpur and Universiti Kebangsaan Malaysia Hospital. Majority of them were young and in a productive age group (mean age were 30 year-old). The mean duration of follow-up was 24.4 months. The injuries were caused by fall from height (69%) and motor vehicle accident (31%). Most of the fracture occurred at 1st and 2nd lumbar vertebrae (24/26). Twelve of the patients did not have neurological deficits. Out of 14 patients with neurological deficits, 64.4% of them showed an improvement of at least one Frankel's grade. There was no defect correlation between canal compromise and neurological deficit. Kyphotic angle improved from 20 degrees to 7 degrees immediately after surgery. In the last follow-up average kyphotic angle was 9 degrees with average lost of 2 degrees. The average length of hospitalization following surgery was 24 days. A posterolateral bony fusion was achieved in all cases at an average of 3 months. Complication included 2 loosening and 3 misplacement of pedicle screw fixation. We concluded that short-segment fixation with posterolateral decompression and fusion is effective in the treatment of unstable thoracolumbar burst fracture.
Mutations in the hepatitis B virus (HBV) genome can potentially lead to vaccination failure, diagnostic escape, and disease progression. However, there are no reports on viral gene expression and large hepatitis B surface antigen (HBsAg) antigenicity alterations due to mutations in HBV isolated from a Bangladeshi population. Here, we sequenced the full genome of the HBV isolated from a clinically infected patient in Bangladesh. The open reading frames (ORFs) (P, S, C, and X) of the isolated HBV strain were successfully amplified and cloned into a mammalian expression vector. The HBV isolate was identified as genotype C (sub-genotype C2), serotype adr, and evolutionarily related to strains isolated in Indonesia, Malaysia, and China. Clinically significant mutations, such as preS1 C2964A, reverse transcriptase domain I91L, and small HBsAg N3S, were identified. The viral P, S, C, and X genes were expressed in HEK-293T and HepG2 cells by transient transfection with a native subcellular distribution pattern analyzed by immunofluorescence assay. Western blotting of large HBsAg using preS1 antibody showed no staining, and preS1 ELISA showed a significant reduction in reactivity due to amino acid mutations. This mutated preS1 sequence has been identified in several Asian countries. To our knowledge, this is the first report investigating changes in large HBsAg antigenicity due to preS1 mutations.