The mCSA was a strong predictor of the preoperative walking ability, leg and back pain, and was directly related to the quality of life of patients with central spinal stenosis.

The vertebral body fracture is the most frequent bone fragility fracture. In spite of this there is considerable uncertainty about the frequency, extent and severity of the acute pain and even more about the duration of pain, the magnitude of disability and how much daily life is disturbed in the post-fracture period. The aim of the present study was to follow the course of pain, disability, ADL and QoL in patients during the year after an acute low energy vertebral body fracture. The study design was a longitudinal cohort study with prospective data collection. All the patients over 40 years admitted to the emergency unit because of back pain with a radiologically acute vertebral body fracture were eligible. A total of 107 patients were followed for a year. The pain, disability (von Korff pain and disability scores), ADL (Hannover ADL score), and QoL (EQ-5D) were measured after 3 weeks, 3, 6 and 12 months. Two-thirds of the patients were women, and were similar in average age, as the men around 75 years. A total of 65.4% of the fractures were due to a level fall or a minor trauma, whereas 34.6% had no recollection of trauma or a specific event as the cause of the fracture. A total of 76.6% of the fractured patients were immediately mobilized and allowed to return home while the remaining were hospitalized. The average pain intensity score after 3 weeks was 70.9 (SD 19.3), the disability score 68.9 (SD 23.6), the ADL score 37.7 (SD 22.1) and EQ-5D score of 0.37 (SD 0.37). The largest improvements, 10-15%, occurred between the initial visit and the 3 months followup and were quite similar for all the measures. From 3 months, all the outcome measures leveled out or tended to deteriorate resulting in a mean pain intensity score of 60.5, disability score of 53.9, ADL score of 47.6, and EQ-5D score 0.52 after 12 months. After a whole year the fractured patients' condition was similar to the preoperative condition of patients with a herniated lumbar disc, central lumbar spinal stenosis or in patients 100% work disabled due to back or neck problems. Instead of the generally believed good prognosis for the greater majority of those fractured, the acute vertebral body fracture was the beginning of a long-lasting severe deterioration of their health.

The level of the acute osteoporotic vertebral fracture, fracture type and grade of fracture deformation were determined in 107 consecutive patients and related to pain, disability, activities of daily living (ADL) and quality of life (QoL) after 3 weeks, 3, 6 and 12 months. Two-thirds of the fractured patients were women and with a similar average age, around 75 years, as the men. Fifty-eight of the acute fractures were located in the thoracic spine and 49 in the lumbar spine and predominantly at the Th12 and L1 levels. Sixty-nine percent of the fractures were wedge, 19% concave and 12% crush fractures. There were 22 mildly, 50 moderately and 35 severely deformed vertebrae. The grade of fracture deformation was not related to gender, age or fracture location. Severely deformed vertebrae predominantly (92%) occurred among the crush fracture type. One year after the fracture, irrespective of fracture level, fracture type or grade of fracture deformation, 4/5 still had pronounced pain and deteriorated QoL. Initial severe fracture deformation by far was the worst prognostic factor for severe lasting pain and disability, and deterioration of ADL and QoL. Factors like fracture level, lumbar fractures tended to improve steadily while thoracic deteriorated, type of fracture, the wedge and concave resulting in less pain and better QoL than the crush fracture type and gender influenced to a lesser extent the outcomes during the year after the acute fracture.

No abstract

Serum amyloid A (SAA) was markedly increased in the plasma and in the liver upon acute inflammation induced by intraperitoneal injection of lipopolysaccharide (LPS) in mice, and SAA in the plasma was exclusively associated with HDL. In contrast, no HDL was present in the plasma and only a small amount of SAA was found in the VLDL/LDL fraction (d , 1.063 g/ml) after the induction of inflammation in ABCA1-knockout (KO) mice, although SAA increased in the liver. Primary hepatocytes isolated from LPS-treated wild-type (WT) and ABCA1-KO mice both secreted SAA into the medium. SAA secreted from WT hepatocytes was associated with HDL, whereas SAA from ABCA1-KO hepatocytes was recovered in the fraction that was .1.21 g/ml. The behavior of apolipoprotein A-I (apoA-I) was the same as that of SAA in HDL biogenesis by WT and ABCA1-KO mouse hepatocytes. Lipid-free SAA and apoA-I both stabilized ABCA1 and caused cellular lipid release in WT mouse-derived fibroblasts, but not in ABCA1-KO mousederived fibroblasts, in vitro when added exogenously. We conclude that both SAA and apoA-I generate HDL largely in hepatocytes only in the presence of ABCA1, likely being secreted in a lipid-free form to interact with cellular ABCA1. In the absence of ABCA1, nonlipidated SAA is seemingly removed rapidly from the extracellular space.-Hu, W., S. Abe-Dohmae, M. Tsujita, N. Iwamoto, O. Ogikubo, T. Otsuka, Y. Kumon, and S. Yokoyama. Biogenesis of HDL by SAA is dependent on ABCA1 in the liver in vivo. J. Lipid Res. 2008. 49: 386-393.