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Falun, Sweden

Geijer M.,Skane University Hospital | Lindqvist U.,Uppsala University | Husmark T.,Falu Lasarett | Alenius G.-M.,Umea University | And 3 more authors.
Journal of Rheumatology | Year: 2015

Objective. To describe early radiographic findings in patients from the Swedish psoriatic arthritis (SwePsA) registry, progression of destruction, correlations with clinical disease variables, and predictors of destruction. Methods. Hand and foot radiographs were available for 72 of 197 SwePsA patients followed for 5 years. Clinical data were collected according to the SwePsA protocol. Results. Disease characteristics and clinical improvement were similar in men and women. Radiographic abnormalities were more pronounced in men. Total Wassenberg radiographic score at baseline was 0 in 45% of men and 51% of women. One man and one woman had a score > 10. At 5 years, total score was 0 in 14% of men and 40% of women (p = 0.018); 17% of men and 7% of women had scores > 10. Mean total scores for men and women had increased. Baseline erythrocyte sedimentation rate was associated with baseline total radiographic score. In men, swollen joint count was positively, and in women tender joint count negatively, correlated to total radiographic score. After 5 years, only male scores, mainly hand scores, significantly correlated with 28-joint Disease Activity Score and Disease Activity Index for Psoriatic Arthritis scores, swollen joint count, and dactylitis. Achieving remission or minimal disease activity after 5 years protected against structural damage, mainly in men. Conclusion. Radiographic progression in early PsA was generally slow but substantial. Male sex appears to be a risk factor for early radiographic damage while the presence of baseline radiographic damage and dactylitis developing during followup seem to predict further destruction. Hand and foot radiograph scoring cannot be substituted with clinical signs. The Journal of Rheumatology Copyright © 2015. All rights reserved. Source

Nagtegaal I.D.,Radboud University Nijmegen | Tot T.,Falu Lasarett | Jayne D.G.,St James University Hospital | McShane P.,University of Leeds | And 6 more authors.
Journal of Clinical Oncology | Year: 2011

Purpose: New editions of the TNM staging system for colorectal cancer have been subject to extensive criticism. In the current study, we evaluate each edition of TNM and analyze stage migration caused by the different versions. Patients and Methods: Two independent test populations were used: participants derived from a randomized surgical trial from the United Kingdom (n = 455) and patients from a population-based series from Sweden (n = 505). All slides from these patient cases were reviewed with special attention for the presence of tumor deposits. Tumor deposits were classified according to the fifth, sixth, and seventh editions of TNM and correlated with prognosis. Results: Every change in edition of TNM led to a stage migration of between 33% and 64% in patients with tumor deposits. Reproducibility was best in the fifth edition of TNM. The prognostic value of the seventh edition was best only when all tumor deposits irrespective of size or contour were included as lymph nodes. The prognostic value of the fifth edition was better than that of the sixth. Conclusion: We demonstrate there is a place for tumor deposits in the staging of patients with colorectal cancer. However, many questions remain about their definition and the reproducibility and use of this category in special situations, such as after neoadjuvant treatment. These should be the subject of additional research before use as a factor in TNM staging. This work demonstrates the necessity of testing modifications before their introduction. © 2011 by American Society of Clinical Oncology. Source

Herrmann B.,Uppsala University | Eden D.,Uppsala University | Hadad R.,Orebro University | Christerson L.,Uppsala University | And 6 more authors.
Sexually Transmitted Diseases | Year: 2012

A new variant of Chlamydia trachomatis (nvCT) was discovered in Sweden in 2006, and it could not be detected by diagnostic systems from Abbott and Roche, whereas the third system used, from Becton Dickinson (BD), detects nvCT. We analyzed 3648 samples from 2 counties that used Roche and 2 counties that used BD methods from 2007 to 2011. After implementation of a Roche method that detects nvCT, its proportion has decreased and converged in the 4 counties but are still at different levels in Roche and BD counties. Future studies are needed to see if nvCT will decline further. Copyright © 2012 American Sexually Transmitted Diseases Association. Source

Borg J.,Karolinska Institutet | Ward A.B.,North Staffordshire Rehabilitation Center | Wissel J.,Kliniken Beelitz GmbH | Kulkarni J.,Royal Infirmary | And 9 more authors.
Journal of Rehabilitation Medicine | Year: 2011

Objective: This report describes the design of a study aiming to provide evidence for the extended use of botulinum toxin A (BOTOX®, Allergan Inc.) in focal post-stroke upper and lower limb spasticity and to evaluate the impact of incorporating botulinum toxin A treatment into the rehabilitation of patients with spasticity. Design: international, prospective, randomized, double-blind, placebo-controlled study with an open-label extension. Methods: Approximately 300 adults with a stroke occurring ≥ 3 months before screening, presenting with symptoms and signs of an upper motor neuron syndrome and focal spasticity-related functional impairment, were randomized to botulinum toxin A + standard care or placebo+standard care. Study medication was administered at baseline and again at Week 12 if required, with follow-up to 52 weeks. The primary endpoint was the number of patients who achieved their investigator-rated principal active functional goal (as measured by Goal Attainment Scaling), at 10 weeks after the second injection (Weeks 22-34) or at the 24-week visit if no second injection was administered. Secondary endpoints included changes from baseline in level of goal achievement, health-related quality of life and resource utilization. Conclusion: The BOTOX® Economic Spasticity Trial (BEST) will provide information regarding clinical and costeffectiveness of botulinum toxin + standard care vs standard care alone in patients with upper and/or lower limb poststroke spasticity typically seen in clinical practice. © 2011 The Authors. Source

Bjursell M.K.,Karolinska Institutet | Blom H.J.,VU University Amsterdam | Cayuela J.A.,Sahlgrenska University Hospital | Engvall M.L.,Karolinska Institutet | And 16 more authors.
American Journal of Human Genetics | Year: 2011

Four inborn errors of metabolism (IEMs) are known to cause hypermethioninemia by directly interfering with the methionine cycle. Hypermethioninemia is occasionally discovered incidentally, but it is often disregarded as an unspecific finding, particularly if liver disease is involved. In many individuals the hypermethioninemia resolves without further deterioration, but it can also represent an early sign of a severe, progressive neurodevelopmental disorder. Further investigation of unclear hypermethioninemia is therefore important. We studied two siblings affected by severe developmental delay and liver dysfunction. Biochemical analysis revealed increased plasma levels of methionine, S-adenosylmethionine (AdoMet), and S-adenosylhomocysteine (AdoHcy) but normal or mildly elevated homocysteine (Hcy) levels, indicating a block in the methionine cycle. We excluded S-adenosylhomocysteine hydrolase (SAHH) deficiency, which causes a similar biochemical phenotype, by using genetic and biochemical techniques and hypothesized that there was a functional block in the SAHH enzyme as a result of a recessive mutation in a different gene. Using exome sequencing, we identified a homozygous c.902C>A (p.Ala301Glu) missense mutation in the adenosine kinase gene (ADK), the function of which fits perfectly with this hypothesis. Increased urinary adenosine excretion confirmed ADK deficiency in the siblings. Four additional individuals from two unrelated families with a similar presentation were identified and shown to have a homozygous c.653A>C (p.Asp218Ala) and c.38G>A (p.Gly13Glu) mutation, respectively, in the same gene. All three missense mutations were deleterious, as shown by activity measurements on recombinant enzymes. ADK deficiency is a previously undescribed, severe IEM shedding light on a functional link between the methionine cycle and adenosine metabolism. © 2011 The American Society of Human Genetics. Source

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