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Anterior spinal fusion for thoracolumbar scoliosis: comprehensive assessment of radiographic, clinical, and pulmonary outcomes on 2-years follow-up

Verma, Kushagra; Auerbach, Joshua D; Kean, Kristin E; Chamas, Firas; Vorsanger, Matthew; Lonner, Baron S
BACKGROUND: There is a continued role for anterior spinal fusion (ASF) in the treatment of thoracolumbar scoliosis. Despite numerous previous reports of ASF in the treatment of thoracolumbar scoliosis, no single study has simultaneously evaluated clinical, radiographic, and pulmonary function outcomes. METHODS: Retrospective review of 31 consecutive thoracolumbar adolescent idiopathic scoliosis patients (Lenke type 5) who underwent ASF by a single surgeon. Patient records were comprehensively assessed for Scoliosis Research Society (SRS)-22 score, apical trunk rotation, radiographic changes, and pulmonary function before surgery and at 2-years follow-up. RESULTS: Thoracolumbar/lumbar curve correction averaged from 45 to 11 degrees (74%) and spontaneous correction of thoracic curves averaged from 26 to 15 degrees (42%). Instrumented segment lordosis increased by 11 degrees, whereas proximal junction kyphosis increased by 3 degrees. No significant changes were noted in T2-T12 kyphosis, distal junctional kyphosis, T12-S1 lumbar lordosis, or coronal balance. Thoracolumbar apical trunk rotation improved from 12 to 3 degrees. Average SRS scores significantly improved from 3.9 to 4.4. SRS assessments of self-image and pain also improved significantly from 3.6 to 4.5 and from 4.1 to 4.6, respectively. Absolute and percent predicted forced vital capacity and forced expiratory volume in 1 second were unchanged. Two patients suffered mild intercostal neuralgia postthoracotomy. There were no other complications. CONCLUSIONS: The thoracoabdominal anterior approach for thoracolumbar scoliosis facilitates excellent clinical and radiographic outcomes, minimal blood loss, powerful apical trunk rotation correction, relative maintenance of lordosis, relatively short fusion constructs, and improved SRS-22 performance, without significant pulmonary function impairment at 2 years. It continues to be an efficacious treatment for thoracolumbar scoliosis. LEVEL OF EVIDENCE: Level IV
PMID: 20864850
ISSN: 1539-2570
CID: 113662

Decreased production of nitric oxide by peripheral blood mononuclear cells of patients with peripheral vascular disease

Jacob, Theresa; Ascher, Enrico; Vorsanger, Matthew; Hingorani, Anil; Kallakuri, Shreedhar; Yorkovich, William; Schuzter, Richard
Although prior studies have implicated nitric oxide (NO), a molecular messenger, in the development and progression of atherosclerosis, most of these studies have centered on atherosclerotic plaques. The current investigation determines whether a correlation exists between the presence of altered levels of NO production by peripheral blood mononuclear cells (PBMCs) and atherosclerotic disease. Venous blood was collected from 8 surgical patients having severe peripheral vascular disease and 8 healthy controls. PBMCs were separated by gradient centrifugation, diluted to 10(5) cells per mL, and cultured. Lipopolysaccharide (LPS), at doses of 10, 25, and 50 ng/mL, was used to stimulate NO production. Total nitric oxide assay was performed to determine the levels of NO produced by PBMCs at 24 and 48 hours. When stimulated by LPS there was an increase in NO production in the PBMCs cultured from control as well as patient samples, as compared to basal NO levels. However, the data demonstrate a significant decrease in the nitric oxide production in the patients with atherosclerosis as compared to that in the control group (p < 0.05). The differential production of nitric oxide by PBMCs of patients with atherosclerotic disease and healthy controls not only suggests that it has a role in the pathogenesis of this disease but also underlines its systemic nature. Blood cells circulating in the body with altered levels of NO production could have profound effects in the microvascular environment mediating molecular pathways and signaling cascades that activate and augment atherosclerosis.
PMID: 15806279
ISSN: 1538-5744
CID: 471902