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- Fritzell, Peter, et al.
(författare)
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Cost-effectiveness of lumbar fusion and nonsurgical treatment for chronic low back pain in the Swedish lumbar spine study : A multicenter, randomized, controlled trial from the Swedish Lumbar Spine Study Group
- 2004
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Ingår i: Spine. - : Lippincott Williams & Wilkins. - 0362-2436 .- 1528-1159. ; 29:4, s. 421-434
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Tidskriftsartikel (refereegranskat)abstract
- Study Design. A cost-effectiveness study was performed from the societal and health care perspectives. Objective. To evaluate the costs-effectiveness of lumbar fusion for chronic low back pain (CLBP) during a 2-year follow-up. Summary of Background Data. A full economic evaluation comparing costs related to treatment effects in patients with CLBP is lacking. Patients and Methods. A total of 284 of 294 patients with CLBP for at least 2 years were randomized to either lumbar fusion or a nonsurgical control group. Costs for the health care sector ( direct costs), and costs associated with production losses ( indirect costs) were calculated. Societal total costs were identified as the sum of direct and indirect costs. Treatment effects were measured using patient global assessment of improvement, back pain ( VAS), functional disability (Owestry), and return to work. Results. The societal total cost per patient ( standard deviations) in the surgical group was significantly higher than in the nonsurgical group: Swedish kroner (SEK) 704,000 ( 254,000) vs. SEK 636,000 ( 208,000). The cost per patient for the health care sector was significantly higher for the surgical group, SEK 123,000 ( 60,100) vs. 65,200 ( 38,400) for the control group. All treatment effects were significantly better after surgery. The incremental cost-effectiveness ratio ( ICER), illustrating the extra cost per extra effect unit gained by using fusion instead of nonsurgical treatment, were for improvement: SEK 2,600 ( 600 - 5,900), for back pain: SEK 5,200 ( 1,100 - 11,500), for Oswestry: SEK 11,300 ( 1,200 - 48,000), and for return to work: SEK 4,100 ( 100 21,400). Conclusion. For both the society and the health care sectors, the 2-year costs for lumbar fusion was significantly higher compared with nonsurgical treatment but all treatment effects were significantly in favor of surgery. The probability of lumbar fusion being cost-effective increased with the value put on extra effect units gained by using surgery.
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- Bergdahl, I A, et al.
(författare)
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Increased mortality in COPD among construction workers exposed to inorganic dust.
- 2004
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Ingår i: European Respiratory Journal. - 0903-1936 .- 1399-3003. ; 23:3, s. 402-406
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Tidskriftsartikel (refereegranskat)abstract
- The aim of this study was to find out if occupational exposure to dust, fumes or gases, especially among never-smokers, increased the mortality from chronic obstructive pulmonary disease (COPD). A cohort of 317,629 Swedish male construction workers was followed from 1971 to 1999. Exposure to inorganic dust (asbestos, man-made mineral fibres, dust from cement, concrete and quartz), gases and irritants (epoxy resins, isocyanates and organic solvents), fumes (asphalt fumes, diesel exhaust and metal fumes), and wood dust was based on a job-exposure matrix. An internal control group with "unexposed" construction workers was used, and the analyses were adjusted for age and smoking. When all subjects were analysed, there was an increased mortality from COPD among those with any airborne exposure (relative risk 1.12 (95% confidence interval (CI) 1.03-1.22)). In a Poisson regression model, including smoking, age and the major exposure groups, exposure to inorganic dust was associated with an increased risk (hazard ratio (HR) 1.10 (95% CI 1.06-1.14)), especially among never-smokers (HR 2.30 (95% CI 1.07-4.96)). The fraction of COPD among the exposed attributable to any airborne exposure was estimated as 10.7% overall and 52.6% among never-smokers. In conclusion, occupational exposure among construction workers increases mortality due to chronic obstructive pulmonary disease, even among never-smokers.
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- Hedlund, Petter, et al.
(författare)
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Erectile dysfunction in cyclic CMP-dependent kinase I-deficient mice
- 2000
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : National Academy of Sciences; 1999. - 0027-8424 .- 1091-6490. ; 97:5, s. 2349-2354
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Tidskriftsartikel (refereegranskat)abstract
- The generation of nitric oxide (NO) in penile erectile tissue and the subsequent elevation of cyclic GMP (cGMP) levels are important for normal penile erection. Current treatments of erectile dysfunction elevate either cGMP levels by blocking cGMP degrading phosphodiesterase 5 or cyclic AMP (cAMP) levels by intrapenile injection of prostaglandin E1. The molecular target or targets of cGMP in erectile tissue and the role of cAMP for normal penile erection are not known. Herein, we report that mice lacking cGMP-dependent kinase I (cGKI) have a very low ability to reproduce and that their corpora cavernosa fail to relax on activation of the NO/cGMP signaling cascade. Elevation of cAMP by forskolin, however, induces similar relaxation in normal and cGKI-null corpus cavernosum. In addition, sperm derived from cGKI-null mice is normal, can undergo acrosomal reactions, and can efficiently fertilize eggs. Altogether, these data identify cGKI as the downstream target of cGMP in erectile tissue and provide evidence that cAMP signaling cannot compensate for the absence of the cGMP/cGKI signaling cascade in vivo.Penile erection is produced by an increased blood flow to the corpus cavernosum (CC), made possible by opening of penile resistance vessels (helicine arteries), relaxation of the CC cells, and occlusion of the venous outflow (1). The erectile response in several animal models depends on nitric oxide (NO), produced by nerves as well as vascular endothelium (1, 2–4). NO activates soluble guanylate cyclase, which leads to the production of cyclic GMP (cGMP). cGMP signals via three different receptors in eukaryotic cells, including ion channels, phosphodiesterases, and protein kinases (5). At present, however, the molecular targets that are activated by cGMP and finally execute the relaxation of penile smooth muscle are not known. In addition, two different cGMP-dependent protein kinases (cGKI and cGKII) have been identified in mammals (6, 7). cGKII is expressed in the small intestine, brain, and cartilage (8–10), whereas high levels of cGKI are found in vascular and intestinal smooth muscle, platelets, Purkinje cells of the cerebellum, and CC cells (11, 12). Inactivation of cGKI in mice abolished both NO/cGMP-dependent relaxation of vascular and intestinal smooth muscle and inhibition of platelet aggregation, causing hypertension, intestinal dysmotility, and abnormal hemostasis (13). In the present study, we investigated the function of cGKI in erectile tissue and the capability of cGKI-deficient mice to reproduce. Furthermore, we analyzed whether a cross-talk exists between the cGMP and cyclic AMP (cAMP) signaling cascades in smooth muscle (5, 14), i.e., whether cAMP can cause relaxation via cGKI.
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- Javid, D., et al.
(författare)
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Is the efficacy of the Cloward procedure overestimated? Technique of evaluation affects the outcome
- 2001
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Ingår i: European spine journal. - : Springer Science and Business Media LLC. - 0940-6719 .- 1432-0932. ; 10:3, s. 222-227
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Tidskriftsartikel (refereegranskat)abstract
- The purpose of the present study was to investigate the influence of the evaluation technique on the outcome of the Cloward procedure in cervical radiculopathy. The retrospective study included 94 consecutive patients operated on with anterior decompression and fusion with heterologous bone (Surgibone, Unilab). There were 56 men and 38 women, with a mean age of 48 years (range 27-78 years). Sixty-six patients had a single-level fusion, 26 a two-level fusion and one patient had a three-level fusion. The follow-up rate was 91/94 (97%) and evaluation was performed by an independent observer. Pain was quantified by visual analogue scale (VAS, range 0-100), functional disability by the new functional index Cervical Spine Functional Score (CSFS, range 0-100) and by the Neck Pain Disability Index (NPDI, range 0-100). The overall clinical outcome was assessed as excellent, good, fair or poor by both the patient and by the independent observer using Odom's criteria. At a mean follow-up of 26 months (range 12-56 months) the mean pain index was 39 (range 0-98), the mean CSFS 39 (range 0-85) and the mean NPDI 32 (range 0-76). The classification of the observer was 37% excellent, 40% good, 17% fair and 6% poor, and that of the patient was 53% excellent, 23% good, 20% fair and 4% poor. In the group classified as good by the observer, all scores were above 40, suggesting considerable remaining symptoms, and only 50% had returned to work. The results suggest that previous reports on the Cloward procedure using categorizations into excellent, good, fair or poor have overestimated the efficacy of the procedure. Only an excellent, but not a good, result as classified by the patient or an independent observer reflects a successful outcome. Neither of the variables studied seems independently sufficient for a balanced reflection of the outcome. The results suggest pain (VAS) as the primary outcome measurement, which, combined with the overall evaluation by the independent observer and work status, gives a multidimensional expression of the outcome.
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- Li, Xiang, et al.
(författare)
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Interleukin-10 mediates the protective effect of Linomide by reducing CXC chemokine production in endotoxin-induced liver injury
- 2004
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Ingår i: British Journal of Pharmacology. - : Wiley. - 1476-5381 .- 0007-1188. ; 143:7, s. 865-871
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Tidskriftsartikel (refereegranskat)abstract
- 1 The immunomodulator Linomide has been shown to protect against septic liver injury by reducing hepatic accumulation of leukocytes although the detailed anti-inflammatory mechanisms remain elusive. This study examined the effect of Linomide on the production of CXC chemokines, including macrophage inflammatory protein-2 (MIP-2) and cytokine-induced neutrophil chemoattractant (KC) and interleukin-10 (IL-10) in lipopolysaccharide (LPS)/D-galactosamine (Gal)-induced liver injury in mice. 2 It was found that pretreatment with 300 mg kg(-1) of Linomide markedly Suppressed leukocyte recruitment, perfusion failure, and hepatocellular damage and apoptosis in the liver of endotoxemic mice. 3 Administration of Linomide inhibited endotoxin-induced gene expression of MIP-2 and KC and significantly reduced the hepatic production of MIP-2 and KC by 63 and 80%, respectively. Moreover, it was found that Linomide increased the liver content of IL-10 by more than three-fold in endotoxemic mice. 4 The protective effect of Linomide against endotoxin-induced inflammation and liver injury was abolished in IL-10-deficient mice, suggesting that the beneficial effect of Linomide is dependent on the function of IL-10. 5 Taken together, these novel findings suggest that the protective effect of Linomide is mediated via local upregulation of IL-10, which in turn decreases the generation of CXC chemokines and pathological recruitment of leukocytes in the liver of endotoxemic mice.
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