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Träfflista för sökning "hsv:(MEDICIN OCH HÄLSOVETENSKAP) hsv:(Klinisk medicin) hsv:(Reumatologi och inflammation) "

Sökning: hsv:(MEDICIN OCH HÄLSOVETENSKAP) hsv:(Klinisk medicin) hsv:(Reumatologi och inflammation)

  • Resultat 61-70 av 4388
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61.
  • Silfverberg, T., et al. (författare)
  • Haematopoietic stem cell transplantation for treatment of relapsing-remitting multiple sclerosis in Sweden: an observational cohort study
  • 2023
  • Ingår i: Journal of Neurology Neurosurgery and Psychiatry. - : BMJ Publishing Group Ltd. - 0022-3050 .- 1468-330X.
  • Tidskriftsartikel (refereegranskat)abstract
    • BackgroundA growing evidence base supports the use of autologous haematopoietic stem cell transplantation (aHSCT) for treatment of relapsing-remitting multiple sclerosis (RRMS), but it has not yet been integrated into most national clinical guidelines. The objective of this study was to assess efficacy and safety when aHSCT is implemented in routine healthcare.MethodsWe assessed 231 patients and the final analysis included 174 RRMS patients who were treated with aHSCT in Sweden before 1 January 2020. Efficacy was evaluated by performing a retrospective analysis of prospectively collected data from the Swedish MS registry. Procedure-related safety was assessed by analysing data from electronic patient records covering a period of 100 days following aHSCT.ResultsWith a median follow-up time of 5.5 (IQR: 3.4-7.5) years, the Kaplan-Meier estimate for no evidence of disease activity was 73% (95% CI 66% to 81%) at 5 years and 65% (95% CI 57% to 75%) at 10 years. Out of the 149 patients with baseline disability, 80 (54%) improved, 55 (37%) were stable and 14 (9%) deteriorated. The mean number of adverse events per patient was 1.7 (& PLUSMN;SD: 1.5) for grade 3 events and 0.06 (& PLUSMN;SD: 0.3) for grade 4 events. Febrile neutropenia was the most common adverse event, affecting 68% of patients. There was no treatment-related mortality.ConclusionsTreatment with aHSCT for RRMS is associated with freedom from disease activity in a majority of patients, with acceptable adverse events. This procedure should be considered a standard of care for patients with highly active RRMS.
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62.
  • Svärd, Anna, et al. (författare)
  • Presence and immunoreactivity of Aggregatibacter actinomycetemcomitans in rheumatoid arthritis
  • 2024
  • Ingår i: Pathogens. - : MDPI. - 2076-0817. ; 13:5, s. 368-368
  • Tidskriftsartikel (refereegranskat)abstract
    • The presence of periodontal pathogens is associated with an increased prevalence of rheumatoid arthritis (RA). The systemic antibody response to epitopes of these bacteria is often used asa proxy to study correlations between bacteria and RA. The primary aim of the present study is toexamine the correlation between the presence of Aggregatibacter actinomycetemcomitans (Aa) in theoral cavity and serum antibodies against the leukotoxin (LtxA) produced by this bacterium. Thesalivary presence of Aa was analyzed with quantitative PCR and serum LtxA ab in a cell culturebased neutralization assay. The analyses were performed on samples from a well-characterized RAcohort (n = 189) and a reference population of blood donors (n = 101). Salivary Aa was present in15% of the RA patients and 6% of the blood donors. LtxA ab were detected in 19% of RA-sera andin 16% of sera from blood donors. The correlation between salivary Aa and serum LtxA ab wassurprisingly low (rho = 0.55 [95% CI: 0.40, 0.68]). The presence of salivary Aa showed no significantassociation with any of the RA-associated parameters documented in the cohort. A limitation of thepresent study is the relatively low number of individuals with detectable concentrations of Aa insaliva. Moreover, in the comparison of detectable Aa prevalence between RA patients and blooddonors, we assumed that the two groups were equivalent in other Aa prognostic factors. These limitations must be taken into consideration when the result from the study is interpreted. We concludethat a systemic immune response to Aa LtxA does not fully reflect the prevalence of Aa in saliva. Inaddition, the association between RA-associated parameters and the presence of Aa was negligiblein the present RA cohort.
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63.
  • Tyrberg, Tobias, et al. (författare)
  • Serum and cerebrospinal fluid neurofilament light chain in patients with central nervous system infections caused by varicella-zoster virus.
  • 2020
  • Ingår i: Journal of neurovirology. - : Springer Science and Business Media LLC. - 1538-2443 .- 1355-0284. ; 26:5, s. 719-726
  • Tidskriftsartikel (refereegranskat)abstract
    • Varicella-zoster virus (VZV) is a common cause of viral central nervous system (CNS) infection, and patients may suffer from severe neurological sequelae. The biomarker neurofilament light chain (NFL) is used for assessment of neuronal damage and is normally measured in cerebrospinal fluid (CSF). Novel methods have given the possibility to measure NFL in serum instead, which could be a convenient tool to estimate severity of disease and prognosis in VZV CNS infections. Here, we investigate the correlation of serum and CSF NFL in patients with VZV CNS infection and the association of NFL levels in serum and CSF with different VZV CNS entities. NFL in serum and CSF was measured in 61 patients who were retrospectively identified with neurological symptoms and VZV DNA in CSF detected by PCR. Thirty-three herpes zoster patients and 40 healthy blood donors served as control groups. NFL levels in serum and CSF correlated strongly in the patients with VZV CNS infection. Encephalitis was associated with significantly higher levels of NFL in both serum and CSF compared with meningitis and Ramsay Hunt syndrome. Surprisingly, herpes zoster controls had very high serum NFL levels, comparable with those shown in encephalitis patients. We show that analysis of serum NFL can be used instead of CSF NFL for estimation of neuronal injury in patients with VZV CNS infection. However, high levels of serum NFL also in patients with herpes zoster, without signs of CNS involvement, may complicate the interpretation.
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64.
  • Wirestam, Lina, 1986- (författare)
  • Biomarkers of disease activity and organ damage in systemic lupus erythematosus
  • 2017
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • Systemic lupus erythematosus (SLE) is a systemic inflammatory disease. Clinically, the distinction between ongoing inflammation attributed to SLE, and organ damage due to medication or co-morbidities remains challenging. In addition, SLE is a heterogeneous disease where the various disease phenotypes complicate the search for biomarkers that adequately reflect disease activity and/or signs of increasing organ damage. The aim of the thesis was to investigate and evaluate potential new biomarkers of disease activity and/or organ damage in SLE patients.High mobility group box protein-1 (HMGB1) is a nuclear non-histone protein that can shuttle to the cytoplasm, become secreted extracellularly, and participate in systemic inflammation. Administration of monoclonal anti-HMGB1 antibodies has been reported both to attenuate and intensify disease in animal models of arthritis and lupus. In Paper I of the thesis, circulating anti-HMGB1 was found in 23% of the SLE patients and correlated with disease activity variables. The biological role of these autoantibodies remains to be elucidated.As a consequence of massive circulating levels of cellular debris and immune complexes, SLE patients have insufficient capacity to remove such material via the reticuloendothelial system. Pentraxin 3 (PTX3) may possibly protect against lupus flares due to classical complement activation, opsonization of apoptotic cells, and cytokine induction. In Paper II, circulating PTX3 was found to be inhibited or exhausted by interferon (IFN)-α, a key cytokine of SLE pathogenesis, and serum levels of PTX3 in SLE patients were inversely related to IFN-α levels. Suppressed PTX3 levels may contribute to a vicious circle resulting in impaired waste clearance, autoantigen exposure and autoantibody production, and sustained disease activity.Osteopontin (OPN), a protein known to influence cell signaling and apoptosis, has been proposed as a marker of organ damage in pediatric lupus. In a Swedish cross-sectional study, circulating OPN levels were found to be raised in SLE (Paper III). In patients with recent-onset disease, OPN reflected disease activity, while in established disease, OPN appeared to mirror damage accrual and cardiovascular damage. In Paper IV, OPN was instead analyzed in an international longitudinal multi-center study based on patients with recent-onset SLE and follow-up data. OPN turned out to be a poor predictor of organ damage, but significant associations were observed between OPN and disease activity both at disease onset, as well as over 5 years of follow-up.In conclusion, increased anti-HMGB1 antibody and decreased PTX3 levels could potentially sustain the impaired waste-disposal. Of the molecules analyzed in this thesis, OPN seems to be the best marker of disease activity. Further studies of these proteins may help to better understand SLE pathogenesis and to optimize treatment of patients.
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65.
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66.
  • Yilmaz, Aylin, et al. (författare)
  • Upper Respiratory Tract Levels of Severe Acute Respiratory Syndrome Coronavirus 2 RNA and Duration of Viral RNA Shedding Do Not Differ Between Patients With Mild and Severe/Critical Coronavirus Disease 2019
  • 2021
  • Ingår i: Journal of Infectious Diseases. - : Oxford University Press (OUP). - 1537-6613 .- 0022-1899. ; 223:1, s. 15-18
  • Tidskriftsartikel (refereegranskat)abstract
    • This study reports longitudinal viral RNA loads from the nasopharynx/throat in patients with mild and severe/critical coronavirus disease 2019 (COVID-19). We also investigated whether the duration of symptoms correlated with the duration of viral RNA shedding. A total of 56 patients were included. The highest viral loads occurred early after onset of symptoms. Neither the viral RNA loads in the upper respiratory tract nor the time to viral RNA clearance differed between patients with mild or severe/critical disease. There was a moderate correlation between number of days with symptoms and number of days with viral RNA shedding in patients with mild COVID-19.
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67.
  • Östman-Smith, Ingegerd, 1947, et al. (författare)
  • Sudden cardiac death in childhood hypertrophic cardiomyopathy is best predicted by a combination of electrocardiogram risk-score and HCMRisk-Kids score
  • 2021
  • Ingår i: Acta Paediatrica. - : Wiley. - 0803-5253 .- 1651-2227. ; 110:11, s. 3105-3115
  • Tidskriftsartikel (refereegranskat)abstract
    • Aim To compare risk algorithms (HCMRisk-Kids, ECG Risk-score) in hypertrophic cardiomyopathy (HCM) without syndrome association (ns-HCM) and with Noonan-like syndromes (RAS-HCM). Methods A national paediatric HCM cohort (n = 151), presenting <19 years of age, mean follow-up 13.3 years, from all Swedish centres of Paediatric Cardiology (presenting 1972-2015), with 41 RAS-HCM patients (61% males), and 110 ns-HCM patients (68% familial; 65% males). The end-point was a composite of sudden cardiac death and resuscitated cardiac arrest (SCD/CA). Risk-factors were studied with Cox-hazard regression, and receiver operating characteristic curve analysis (C-statistic). Results There were 33 SCD/CA, 27/110 in ns-HCM and 6/41 in RAS-HCM (p = 0.27). In ns-HCM HCMRisk-Kids >= 6% at diagnosis had C-statistic of 0.69 for predicting SCD/CA during first 5 years of follow-up and positive predictive value (PPV) of 22%. After 7 years of age (HCMRisk-Kids7plus), C-statistic was 0.76. ECG Risk-score >= 6 at diagnosis had C-statistic 0.87 and PPV of 31%. Independent risk factors for SCD/CA were HCMRisk-Kids7plus score (p = 0.005) and ECG risk-score (p < 0.001), whereas early beta-blocker dose (p = 0.001) and myectomy (p = 0.004) reduced risk. The sum of HCMRisk-Kids7yplus and ECG Risk-score7yplus >= 14 best predicted SCD/CA within 5 years in ns-HCM with C-statistic of 0.90 [0.83-0.96], sensitivity 100% and PPV 38%. Conclusion Combining the ECG Risk-score with HCMRisk-Kids improves risk stratification in ns-HCM and shows promise in RAS-HCM.
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68.
  • Andersson, Ingemar, 1950- (författare)
  • Långvarig smärta - en introduktion
  • 2010. - 2
  • Ingår i: Smärta och smärtbehandling. - Stockholm : Liber. - 9789147084135 ; , s. 387-400
  • Bokkapitel (övrigt vetenskapligt/konstnärligt)
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69.
  • Andersson, Ingemar, 1950- (författare)
  • Rehabilitering vid långvarig smärta
  • 2010. - 2
  • Ingår i: Smärta och smärtbehandling. - Stockholm : Liber. - 9789147084135 ; , s. 401-409
  • Bokkapitel (övrigt vetenskapligt/konstnärligt)
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70.
  • Askling, Johan, et al. (författare)
  • Cancer risk in patients with rheumatoid arthritis treated with anti-tumor necrosis factor alpha therapies : does the risk change with the time since start of treatment?
  • 2009
  • Ingår i: Arthritis and Rheumatism. - : Wiley. - 0004-3591 .- 1529-0131. ; 60:11, s. 3180-3189
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE:To determine the short-term and medium-term risks of cancer in patients receiving anti-tumor necrosis factor alpha (anti-TNFalpha) therapies that have proven effective in the treatment of chronic inflammatory conditions.METHODS:By linking together data from the Swedish Biologics Register, Swedish registers of RA, and the Swedish Cancer Register, we identified and analyzed for cancer occurrence a national cohort of 6,366 patients with RA who first started anti-TNF therapy between January 1999 and July 2006. As comparators, we used a national biologics-naive RA cohort (n = 61,160), a cohort of RA patients newly starting methotrexate (n = 5,989), a cohort of RA patients newly starting disease-modifying antirheumatic drug combination therapy (n = 1,838), and the general population of Sweden. Relative risks (RRs) were estimated using Cox regression analyses, examining overall RR as well as RR by time since the first start of anti-TNF therapy, by the duration of active anti-TNF therapy, and by the anti-TNF agent received.RESULTS:During 25,693 person-years of followup in 6,366 patients newly starting anti-TNF, 240 first cancers occurred, yielding an RR of 1.00 (95% confidence interval 0.86-1.15) versus the biologics-naive RA cohort, and similar RRs versus the other 2 RA comparators. RRs did not increase with increasing time since the start of anti-TNF therapy, nor with the cumulative duration of active anti-TNF therapy. During the first year following the first treatment start, but not thereafter, dissimilar cancer risks for adalimumab, etanercept, and infliximab were observed.CONCLUSION:During the first 6 years after the start of anti-TNF therapy in routine care, no overall elevation of cancer risk and no increase with followup time were observed.
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