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Blockmans D.,University Hospital Gasthuisberg
Annals of the New York Academy of Sciences | Year: 2011

[18F]Fluorodeoxyglucose positron emission tomography (FDG PET) can be used to visualize large-vessel inflammation in giant-cell arteritis, Takayasu arteritis, and other types of aortitis. In patients with symptoms compatible with polymyalgia rheumatica, findings of increased FDG-uptake in the shoulders, hips, as well as the spinous processes of the cervical and lumbar spine, may suggest this diagnosis. In patients with giant-cell arteritis, there is increased metabolic activity within the aortic wall on FDG PET scintigraphy, indicating inflammation of the aorta, which may be a predictor of a higher potential for aortic dilatation. © 2011 New York Academy of Sciences.. Source


Wildiers H.,University Hospital Gasthuisberg | Reiser M.,Klinik i fur Innere Medizin
Critical Reviews in Oncology/Hematology | Year: 2011

Early studies suggested a link between chemotherapy dosing and outcomes in breast cancer and aggressive non-Hodgkin's lymphoma. To help define the impact of relative dose intensity (RDI) and the role of growth factor support, we conducted a systematic literature review. Many breast cancer patients do not achieve planned RDI. Older age, obesity and febrile neutropenia are associated with reduced RDI, which leads to worse survival in several studies, particularly those including anthracyclines. G-CSF prophylaxis improved RDI in most, but not all, studies. There may be a threshold above which increasing RDI does not further improve outcomes (~85% for CMF and anthracycline-based regimens). For lymphoma, there is strong evidence that patients benefit from full-dose chemotherapy, with RDI reductions associated with reduced survival. The definition of " full dose" is, however, unclear. Older age and higher disease stage may be associated with reduced RDI, and G-CSF improved the chances of higher RDI in most studies. © 2010 Elsevier Ireland Ltd. Source


Lichtenstein G.R.,University of Pennsylvania | Rutgeerts P.,University Hospital Gasthuisberg
Inflammatory Bowel Diseases | Year: 2010

Treatment of patients with ulcerative colitis (UC) has traditionally focused on improving symptoms, with the main objective of inducing and maintaining symptomatic remission. However, new evidence suggests that concentrating exclusively on clinical outcome measures may not be adequate to achieve long-term treatment success. Indeed, physicians should also be assessing the reduction of endoscopic activity,with the intention of achieving completemucosal healing (defined as the absence of all mucosal ulceration, both microscopic and macroscopic, providing a sigmoidoscopy score of 0, as assessed on the Ulcerative Colitis Disease Activity Index). As a consequence of the customary reliance on symptomatic outcome measures, relatively few clinical trials have used mucosal healing or a composite including mucosal healing as a primary endpoint. This situation may soon change as new guidelines recommend the incorporation of mucosal healing into the primary endpoint of all new clinical trials in patients with UC. These recommendations are derived, in part, from data that have illustrated a correlation between mucosal healing and several important factors including long-term remission rates, disease-related complications (e.g., risk of colorectal cancer), healthcare utilization (e.g., need for colectomy), and patient quality of life.We already have drugs available to us that can effectively induce and maintain complete mucosal healing over long periods of time. This review evaluates the effect of medical therapy on mucosal healing in patients with UC and explores the importance of this outcome measure, both from the patient's perspective and clinical trial experience. Copyright © 2009 Crohn's & Colitis Foundation of America, Inc. Source


Lievens Y.,University Hospital Gasthuisberg
Breast | Year: 2010

A large amount of clinical evidence has recently accumulated supporting the efficacy and safety of hypofractionated radiotherapy for post-operative breast cancer. These schedules, typically delivering a lower total dose in fewer, but larger than 2 Gy fractions, are more convenient for the patients by limiting the number of treatment attendances. Moreover, the reduced resource use in terms of personnel and machine time is advantageous for radiotherapy departments and translates into lower treatment costs. In order to formally validate this therapeutic approach from a societal perspective, however, cost-effectiveness evaluations weighing long-term outcome against the societal costs incurred until many years after treatment are needed. © 2010 Elsevier Ltd. Source


Jaeken J.,University Hospital Gasthuisberg
Handbook of Clinical Neurology | Year: 2013

Congenital disorders of glycosylation (CDG) are genetic diseases due to defects in the synthesis or the attachment of the glycan moiety of glycoproteins and glycolipids. They can be divided into four groups: disorders of protein N-glycosylation, disorders of protein O-glycosylation, disorders of lipid glycosylation, and disorders of other glycosylation pathways and of multiple glycosylation pathways. Of the more than 40 reported CDG, some 80% are neurological or have an important neurological component. By far the most common neurological CDG is phosphomannomutase 2 deficiency. Isoelectrofocusing of serum transferrin, the most widely used screening test, picks up only CDG associated with sialic acid deficiency of N-linked glycans. Predominant neurological signs and symptoms are psychomotor retardation, epilepsy, hypotonia, hyporeflexia, strabismus, retinitis pigmentosa, polyneuropathy, myopathy, and cerebellar hypotrophy/hypoplasia. All known neurological CDG have an autosomal recessive inheritance except for IAP-CDG, an X-linked pure mental retardation syndrome. No curative or effective treatment is available for neurological CDG. Since at least 1% of the genome is involved in glycosylation, it is likely that the large majority of CDG is yet to be discovered. In 2008, a novel nomenclature was introduced using the gene symbol followed by -CDG, e.g., CDG-Ia becomes PMM2-CDG. CDG should be looked for in any unexplained neurological syndrome. © 2013 Elsevier B.V. Source

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