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Article Outcomes of patients receiving long-term corticosteroid therapy who undergo percutaneous vertebroplasty. free! 2007
Koch CA, Layton KF, Kallmes DF. · Mayo Clinic College of Medicine, Rochester, MI 55905, USA. · AJNR Am J Neuroradiol. · Pubmed #17353337 links to free full text
Abstract: BACKGROUND AND PURPOSE: The purpose of this study was to determine the efficacy and rate of complications in patients undergoing percutaneous vertebroplasty (PVP) for vertebral compression fractures as a result of secondary osteoporosis caused by long-term corticosteroid use compared with patients with primary osteoporosis treated with PVP. MATERIALS AND METHODS: A retrospective review of all patients undergoing PVP was conducted to identify patients who also received long-term corticosteroid therapy. Outcomes including pain, periprocedural complications, and frequency of new fractures in patients receiving corticosteroids were compared with control patients undergoing PVP for primary osteoporosis. RESULTS: Sixty-eight patients receiving long-term corticosteroid therapy underwent 79 PVP procedures. Patients treated with corticosteroids undergoing PVP were significantly younger and more likely to be male compared with control subjects. Patients receiving long-term corticosteroid treatment experienced significant pain relief immediately postprocedure and at 1 week, 1 month, 6 months, 1 year and 2 years postprocedure (P < .0001 at all time points). Patients receiving corticosteroids experienced similar decreases in pain from baseline compared with control subjects at all follow-up time points (P > .05). The complication rate for patients receiving corticosteroids was 4.4% compared with 3.4% for control subjects (P = .60). Patients on long-term corticosteroid treatment did not have an increased risk of new fractures after PVP compared with control subjects (P = .68). CONCLUSIONS: Percutaneous vertebroplasty performed for vertebral compression fractures as a result of long-term corticosteroid therapy is as safe and effective in relieving pain as PVP performed in patients with vertebral compression fractures as a result of primary osteoporosis.
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Article Compound heterozygous mutations of the SBDS gene in a patient with Shwachman-Diamond syndrome, type 1 diabetes mellitus and osteoporosis. 2006
Rosendahl J, Teich N, Mossner J, Edelmann J, Koch CA. · Medizinische Klinik und Poliklinik II, Universitatsklinikum Leipzig, Leipzig, Germany. · Pancreatology. · Pubmed #17106217 No free full text.
Abstract: Shwachman-Diamond syndrome (SDS) is characterized by exocrine pancreatic insufficiency, skeletal abnormalities and hematological dysfunction. The genetic analysis of the SBDS gene and the long-term follow-up of a 37-year-old man with SDS, osteoporosis and type 1 diabetes are reported. Analysis of the SBDS gene revealed a compound heterozygous genotype with 7 mutations. This genotype is the result of the inheritance of abnormal alleles from both healthy parents. We identified putatively non-functional gene conversions from the SBDS pseudogene into the otherwise normal SBDS gene in each of the parentally inherited alleles. The association of SDS and type 1 diabetes mellitus seems to be coincidental and not associated to distinct mutations of the SBDS gene. Osteoporosis in patients with SDS may be the result of a primary defect of the bone metabolism and not of a nutritional problem, although our patient had chronic hypophosphatemia. The long-term follow-up of this patient provides interesting insights into the course of SDS, showing the complexity of genotype-phenotype correlations and the possible influence of other modifying genes and/or environmental factors that might determine the phenotypic presentation of SDS in an individual patient.
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Minor Chiari malformation type 1 and osteoporosis. 2000
Koch CA, Heiss JD, Pacak K, Krakoff J, Winer KK, Wassermann EM. · No affiliation provided · Neurosurg Rev. · Pubmed #11086745 No free full text.
This publication has no abstract.
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Retraction Rapid increase in bone mineral density in a child with osteoporosis and autoimmune hypoparathyroidism treated with PTH 1-34. 2001
Koch CA. · Pediatric and Reproductive Endocrinology Branch, National Institute of Child Health and Human Development; National Institutes of Health, Building 10, Bethesda, MD 20892, U.S.A. · Exp Clin Endocrinol Diabetes. · Pubmed #11571675 No free full text.
Abstract: We describe a 16-year-old girl with autoimmune polyglandular syndrome type 1 including hypoparathyroidism, who had osteoporosis that improved rapidly with parathyroid hormone replacement therapy. Patients with hypoparathyroidism usually have high bone mass. Our patient developed vertebral compression fractures at age 10, shortly after hypoparathyroidism was diagnosed. She continued to have low lumbar bone mass until age 16, when a dual energy x-ray absorptiometry (DEXA) revealed a Z score of - 2.2 SD. Several factors including decreased physical activity, total body magnesium depletion, and intermittent ketoconazole and short-term prednisone treatment, may have contributed to the development and progression of osteoporosis. Therapy with synthetic human parathyroid hormone (PTH) 1-34 rapidly normalized lumbar bone mass, as assessed by DEXA.
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