共查询到20条相似文献，搜索用时 570 毫秒
1.
Chunhua Yang Jieruo Gu Markus Rihl Dominique Baeten Feng Huang Miansong Zhao Hanwei Zhang Walter P. Maksymowych Filip De Keyser Eric M. Veys David T. Y. Yu 《Arthritis care & research》2004,51(5):691-699
Objective
To assess the usefulness of measuring serum matrix metalloproteinase 3 (MMP‐3) and macrophage colony‐stimulating factor (M‐CSF) in patients with ankylosing spondylitis (AS).Methods
Serum levels of MMP‐3 and M‐CSF were measured in AS patients who did and did not receive infliximab treatment. These were compared with those of 28 healthy subjects.Results
In the group of AS patients not treated with biologics, both M‐CSF and MMP‐3 correlated with the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) values, but not with each other. Logistic regression analysis showed that MMP‐3 values were high in those with severely active disease. Infusions of infliximab in AS patients led to a significant decrease in the values of the BASDAI as well as the serum MMP‐3, but no change in the serum M‐CSF values.Conclusion
MMP‐3 and M‐CSF are potentially useful markers of AS disease activity.2.
Nicola Locuratolo Giuseppe Pugliese Flavia Pricci Giulio Romeo Paolo Mariani Oscar Diaz‐Horta Luisa Calvani Monica Montuori Elsa Cipolletta Umberto Di Mario Margherita Bonamico 《Diabetes/metabolism research and reviews》1999,15(4):254-260
Background
Chronic undernutrition resulting from coeliac disease (CD) could be associated with changes in the circulating insulin‐like growth factor (IGF) system, which may participate in the pathogenesis of growth retardation occurring in these patients.Methods
We performed a cross‐sectional study in CD subjects attempting to (1) document the pattern of serum IGF‐I and IGF binding protein (IGFBP) 1 and 3 at diagnosis and (2) assess the response of circulating IGF system to dietary treatments, in comparison with the response of clinical and laboratory findings utilized for the diagnosis of CD. Thirty‐two prepubertal CD children were divided into three groups based on the dietetic treatment: at diagnosis (D, n=18); on gluten‐free diet for at least 6 months (GFD, n=7); and on gluten challenge for at least 3 months (CH, n=7). Six postpubertal CD patients were also studied at diagnosis.Results
In prepubertal children IGF‐I levels were significantly reduced (by 29%) in D vs sex‐ and age‐matched normal control (NC) subjects, with reductions being more pronounced before 3 years of age. Likewise, serum IGFBP‐3 concentrations were decreased by 22%, whereas circulating IGFBP‐1 levels were increased by 60%, compared with NC, with more marked IGFBP changes in older children. Similar alterations were observed in postpubertal patients. Changes in the circulating IGF system disappeared in GFD subjects and reappeared in CH children, as positivity of disease‐specific antibodies. Body mass index (BMI) also improved in GFD subjects, but did not decrease in CH children. Changes in IGF‐I and IGFBPs did not correlate with each other. Levels of IGF‐I, but not of IGFBPs, maintained the relation with age and correlated significantly with BMI and positivity of antibodies.Conclusions
These results demonstrate that CD patients show significant changes in serum IGF‐I, in younger children, and IGFBPs (particularly IGFBP‐1), in older children and adolescents, correlating with clinical course and response to dietary treatments. The alteration in the circulating IGF system could be implicated in the pathogenesis of growth retardation occurring in CD and may provide an additional tool in monitoring of the disease. Copyright © 1999 John Wiley & Sons, Ltd.3.
Carle Ryckman Shaun R. McColl Karen Vandal Rinaldo de Mdicis Andr Lussier Patrice E. Poubelle Philippe A. Tessier 《Arthritis \u0026amp; Rheumatology》2003,48(8):2310-2320
Objective
To examine the role of chemokines, S100A8, and S100A9 in neutrophil accumulation induced by the causative agent of gout, monosodium urate monohydrate (MSU) crystals.Methods
MSU crystal–induced neutrophil migration was studied in the murine air‐pouch model. Release of chemokines, S100A8, S100A9, and S100A8/A9 in response to MSU crystals was quantified by enzyme‐linked immunosorbent assays. Recruited cells were counted following acetic blue staining, and the subpopulations were characterized by Wright‐Giemsa staining of cytospins.Results
MSU crystals induced the accumulation of neutrophils following injection in the air pouch, which correlated with the release of the chemokines CXCL1, CXCL2, CCL2, and CCL3. However, none of these was found to play an important role in neutrophil migration induced by MSU crystals by passive immunization with antibodies directed against each chemokine. S100A8, S100A9, and S100A8/A9 were also found at high levels in the pouch exudates following injection of MSU crystals. In addition, injection of S100A8, S100A9, or S100A8/A9 led to the accumulation of neutrophils in the murine air pouch, demonstrating their proinflammatory activities in vivo. Passive immunization with anti‐S100A8 and anti‐S100A9 led to a total inhibition of the accumulation of neutrophils. Finally, S100A8/A9 was found at high concentrations in the synovial fluid of patients with gout.Conclusion
S100A8 and S100A8/A9 are essential to neutrophil migration induced by MSU crystals. These results suggest that they might be involved in the pathogenesis of gout.4.
Karl Egerer Julia Hertzer Eugen Feist Anja Albrecht Paul Eberhard Rudolph Thomas Drner Gerd‐Rüdiger Burmester 《Arthritis care & research》2003,49(4):546-548
Objectives
To determine the usefulness of sE‐selectin as a marker for early diagnosis and stratification of rheumatoid arthritis.Methods
We investigated several markers of disease activity, including circulating adhesion molecules and other standard laboratory tests, in a 2–3 year followup analysis of patients with rheumatoid arthritis.Results
The mean ± SD levels of sE‐selectin (91.68 ± 31.8 ng/ml versus 49.83 ± 14.76 ng/ml) and rheumatoid factor (375.7 ± 394.4 U versus 44.66 ± 37.63 U) were strongly elevated in severe (n = 15) versus mild (n = 7) courses of disease. Statistical calculation of mean and standard deviation revealed that sE‐selectin represents a highly significant marker for the presence of persistent and aggressive disease over time, regardless of therapeutic intervention and observation time points (P = 0.0004). Notably, regression analysis identified constant values for all parameters analyzed and, therefore, a stable course of the disease could be predicted from the beginning.Conclusion
sE‐selectin appears to be a powerful marker to predict the severity of rheumatoid arthritis.5.
Background:
Serum total bilirubin has been suggested to have potential anti‐inflammatory and antioxidant effects on the vasculature, acting against plaque formation and subsequent atherosclerosis. This study was designed to assess the association of serum total bilirubin with coronary artery calcification (CAC).Hypothesis:
Individuals with higher bilirubin level would be less likely to develop CAC.Methods:
Male subjects (N = 3408) underwent evaluation of CAC by cardiac computed tomography. Correlation and logistic regression analysis were performed to assess the relationships between CAC score and other variables.Results:
Subjects with a higher CAC score had significantly lower total bilirubin level (P = 0.001). Total bilirubin level was negatively correlated with CAC score (r = ?0.052, P = 0.002). A 0.1‐mg/dL increase in bilirubin was associated with a reduced odds ratio (OR) of the risk by 29.2% for a CAC score above 100 (OR: 0.708, 95% confidence interval: 0.542‐0.927, P = 0.012) after adjustment for several variables. Bilirubin was inversely correlated with high‐sensitivity C‐reactive protein (hsCRP) (r = ?0.117, P < 0.001).Conclusions:
This study demonstrated an independent inverse association between serum total bilirubin and CAC score in males. Low serum bilirubin concentration would be useful as a potential risk factor for CAC in males. Additionally, reduced hsCRP may be 1 of the mechanisms for how bilirubin reduces CAC. © 2012 Wiley Periodicals, Inc. Additional Supporting Information may be found in the online version of this article. Zheng‐Yun Zhang, MD, and Lu‐Qin Bian, MD, contributed equally to this work. The authors have no funding, financial relationships, or conflicts of interest to disclose.6.
J.‐E. Gottenberg P. Ravaud T. Bardin P. Cacoub A. Cantagrel B. Combe M. Dougados R. M. Flipo B. Godeau L. Guillevin X. Le Loët E. Hachulla T. Schaeverbeke J. Sibilia G. Baron X. Mariette 《Arthritis \u0026amp; Rheumatology》2010,62(9):2625-2632
Objective
The risk of severe infection is a crucial factor in the assessment of the short‐term risk:benefit ratio of biologic drugs in rheumatoid arthritis (RA). There is no increase in severe infections in RA patients treated with rituximab (RTX) in controlled trials, but this has not yet been assessed in daily practice. We undertook this study to investigate the occurrence of and risk factors for severe infections in off‐trial patients using data from the AutoImmunity and Rituximab (AIR) registry.Methods
The AIR registry was set up by the French Society of Rheumatology. The charts of patients with severe infections were reviewed.Results
Of the enrolled patients, 1,303 had at least 1 followup visit at 3 months or later, with a mean ± SD followup period of 1.2 ± 0.8 years (1,629 patient‐years). Eighty‐two severe infections occurred in 78 patients (5.0 severe infections per 100 patient‐years), half of them in the 3 months following the last RTX infusion. Multivariate analysis showed that chronic lung disease and/or cardiac insufficiency (odds ratio 3.0 [95% confidence interval 1.3–7.3], P = 0.01), extraarticular involvement (odds ratio 2.9 [95% confidence interval 1.3–6.7], P = 0.009), and low IgG level (<6 gm/liter) before initiation of RTX treatment (odds ratio 4.9 [95% confidence interval 1.6–15.2], P = 0.005) were significantly associated with increased risk of a severe infection.Conclusion
The rate of severe infections in current practice is similar to that reported in clinical trials. The risk factors for severe infections include chronic lung and/or cardiac disease, extraarticular involvement, and low IgG before RTX treatment. This suggests that serum IgG should be checked and the risk:benefit ratio of RTX discussed for patients found to have low levels of IgG.7.
Objectives
While highly active antiretroviral therapy (HAART) decreases long‐term morbidity and mortality, its short‐term effect on hospitalization rates is unknown. The primary objective of this study was to determine hospitalization rates over time in the year after HAART initiation for virological responders and nonresponders.Methods
Hospitalizations among 1327 HAART‐naïve subjects in an urban HIV clinic in 1997–2007 were examined before and after HAART initiation. Hospitalization rates were stratified by virological responders (≥1 log10 decrease in HIV‐1 RNA within 6 months after HAART initiation) and nonresponders. Causes were determined through International Classification of Diseases, 9th Revision (ICD‐9) codes and chart review. Multivariate negative binomial regression was used to assess factors associated with hospitalization.Results
During the first 45 days after HAART initiation, the hospitalization rate of responders was similar to their pre‐HAART baseline rate [75.1 vs. 78.8/100 person‐years (PY)] and to the hospitalization rate of nonresponders during the first 45 days (79.4/100 PY). The hospitalization rate of responders fell significantly between 45 and 90 days after HAART initiation and reached a plateau at approximately 45/100 PY from 91 to 365 days after HAART initiation. Significant decreases were seen in hospitalizations for opportunistic and nonopportunistic infections.Conclusions
The first substantial clinical benefit from HAART may be realized by 90 days after HAART initiation; providers should keep close vigilance at least until this time.8.
A. Lindgren A. Lindgren G. Lindstedt & A. F. Kilander 《Journal of internal medicine》1998,244(4):341-349
Objectives
Since there is a significant overlap in serum cobalamin concentrations between healthy and cobalamin-deficient individuals, we wanted to compare two different principles for use as supplementary tests to serum cobalamin concentration in patients with suspected cobalamin malabsorption and deficiency.Design
Clinical study of consecutive patients.Setting
The catchment area of Sahlgrenska University Hospital, Göteborg.Subjects
A total of 112 patients with suspected cobalamin deficiency who had not previously undergone gastrointestinal surgery.Interventions
Gastroduodenoscopy with biopsies taken from the gastric body and the duodenum, Schilling test, and measurement of serum methylmalonic acid (MMA), total homocysteine (Hcy), pepsinogens A and C, and gastrin.Main outcome measures
Number of patients with gastric body atrophy identified with the combination of MMA and Hcy, and pepsinogen A combined with pepsinogen C or gastrin.Results
About 95% of the patients with severe gastric body atrophy had abnormal concentrations of serum pepsinogen A and/or gastrin or pepsinogen A/C ratio, whereas 65% had abnormal metabolite concentrations. Serum pepsinogen A combined with pepsinogen C identified 100%, and combined with gastrin 88%, of the patients with gastric body atrophy and elevated metabolite tests, and 67 and 75%, respectively, of those who had not yet developed elevated metabolite tests.Conclusions
Pepsinogen A, combined with pepsinogen C or gastrin, should be the first option in evaluating patients with suspected cobalamin deficiency who have not previously undergone gastrointestinal surgery.9.
E. William St.Clair Carrie L. Wagner Adedigbo A. Fasanmade Benjamin Wang Thomas Schaible Arthur Kavanaugh Edward C. Keystone 《Arthritis \u0026amp; Rheumatology》2002,46(6):1451-1459
Objective
To investigate the relationship between serum concentrations of infliximab, a monoclonal anti–tumor necrosis factor α antibody, and clinical improvement from infliximab therapy for rheumatoid arthritis (RA).Methods
Multiple blood samples were obtained from each of 428 subjects with active RA who were enrolled in a multicenter, randomized, double‐blind, placebo‐controlled trial (ATTRACT [Anti–Tumor Necrosis Factor Trial in Rheumatoid Arthritis with Concomitant Therapy]) evaluating the clinical efficacy and safety of infliximab therapy. Serum levels of infliximab were measured by enzyme‐linked immunosorbent assay. Dose‐response trends were analyzed using generalized logistic regression techniques. Pharmacokinetic modeling was used to predict the serum concentrations of infliximab after simulated infusions using doses and dosing intervals not evaluated in the trial.Results
At week 54, 26% of the subjects receiving 3 mg/kg infliximab every 8 weeks had undetectable trough serum levels of infliximab, a significantly greater proportion than in the other 3 treatment groups (P < 0.001). Increased magnitude of American College of Rheumatology (ACR) response (measured by the ACR‐N, a continuous measure of clinical improvement derived from the ACR 20% response criteria) and greater reduction from baseline in serum C‐reactive protein level were both associated with higher trough serum concentrations of infliximab (P < 0.001), as was less progression of radiographic joint damage (P = 0.004), providing support for a dose‐response relationship. Pharmacokinetic models predicted that decreasing the dosing interval from 8 weeks to 6 weeks would yield higher trough serum levels of infliximab than increasing the dose by 100 mg.Conclusion
These results suggest that some patients with RA may benefit from infliximab given at higher doses than 3 mg/kg or more frequently than every 8 weeks.10.
11.
Objectives
This study aims to correlate clinical, biochemical and immunological factors seen at diagnosis of thyrotoxicosis with subsequent relapse within 5 years.Design
Retrospective review of case notes, and biochemical assessment at least 5 years after cessation of treatment.Setting
A large general hospital endocrine clinic.Subjects
Patients presenting with a first episode of thyrotoxicosis between 1988 and 1991 who were treated with antithyroid drugs for at least 18 months. Main outcome measures. Relapse was determined by examination of hospital records, general practice records, patient questionnaire and thyroid function tests.Results
A total of 216 subjects presented for the first time with thyrotoxicosis, of whom 89 (41.2%) suffered a relapse of the disease. On univariate analysis, clinical factors associated with increased relapse include younger age at diagnosis, goitre, marked tachycardia, requirement for higher maintenance dose of carbimazole, higher FT4 levels at diagnosis and smoking. Factors not predictive of relapse include presence of thyroid eye signs, positive family history, atrial fibrillation or congestive cardiac failure, acropachy or pretibial myxoedema, and presence or absence of thyroid autoantibodies. Logistic regression analysis showed relapse was predominantly determined by an FT4 > 56.2 nmol L?1, pulse rate > 110, presence of goitre and a positive smoking history (R2= 0.36, P < 0.001). Presence of these four factors predicted relapse in 76 (85.4%) of the 89 patients who relapsed.Conclusions
Increased ‘toxicity’ of thyrotoxicosis, goitre and smoking are associated with relapse of thyrotoxicosis, and this may be helpful in determining which patients may be better managed with early ablative therapy.12.
Gianluca Fossati Robert J. Moots Roger C. Bucknall Steven W. Edwards 《Arthritis \u0026amp; Rheumatology》2002,46(5):1351-1361
Objective
To determine the roles played by the neutrophil Fcγ receptor type II (FcγRII) (CD32) and FcγRIIIb (CD16) in phagocytosis, bacterial killing, and activation by immune complexes (ICs) and to test the hypothesis that inhibition of pathologic effector neutrophil function is possible without compromising host defense.Methods
Receptor function was probed by enzymic removal of FcγRIIIb from the cell surface and by use of Fab/F(ab‘)2 fragments of monoclonal antibodies to block receptor‐ligand binding. Cells were challenged with (a) serum‐opsonized Staphylococcus aureus, (b) serum‐ and IgG‐opsonized latex particles, and (c) synthetic soluble and insoluble ICs to mimic bacterial and inflammatory stimuli.Results
Phosphatidylinositol‐phospholipase C treatment removed >97% of surface FcγRIIIb from neutrophils previously treated with tumor necrosis factor α to mobilize intracellular stores of receptor. This treatment profoundly inhibited activation of primed neutrophils by soluble ICs of the type found in diseased rheumatoid joints, but had no effect on phagocytosis and killing of serum‐opsonized S aureus.Conclusion
FcγRIIIb plays a major role in the secretion of toxic products in response to ICs, but little or no role in the phagocytosis and killing of serum‐opsonized bacteria. The selective suppression of effector neutrophil function is therefore possible. FcγRIIIb, or its intracellular signaling pathway, is a potential therapeutic target in inflammatory diseases such as rheumatoid arthritis, because disruption of its function should decrease inflammatory tissue damage, but not jeopardize host protection against infection.13.
LA Szczech P Menezes E Byrd Quinlivan C Van Der Horst JA Bartlett LP Svetkey 《HIV medicine》2010,11(7):419-426
Background
This study examines the association between microalbuminuria and the development of proteinuria among HIV‐infected persons.Methods
A total of 948 subjects provided urine samples for albumin, protein and creatinine measurements semiannually. Microalbuminuria was defined as an albumin‐to‐creatinine ratio of >30 mg/g. Proteinuria was defined as a protein‐to‐creatinine ratio of ≥0.350 mg/mg. The progression from microalbuminuria to proteinuria was described.Results
At baseline, 69.4% of the subjects had no detectable proteinuria, 20.2% had microalbuminuria, and 10.4% had proteinuria. Subjects with microalbuminuria and proteinuria were more likely to be black (P=0.02), have lower CD4 cell counts (P=0.02 comparing subjects without abnormal urine protein excretion to subjects with microalbuminuria; P=0.0001 comparing subjects with microalbuminuria to subjects with proteinuria), and have a higher HIV RNA level (P=0.08 and 0.04, respectively). Among 658 subjects with normal urine protein, 82.7% continued to have no abnormality, 14.3% developed microalbuminuria, and 3.0% developed proteinuria. Subjects without baseline proteinuria (i.e. either normal protein excretion or microalbuminuria) who developed proteinuria were more likely to have microalbuminuria (P=0.001), a lower CD4 cell count (P=0.06), and a higher plasma HIV RNA (P=0.03) than those who did not progress to proteinuria. In multivariate analysis, only microalbuminuria remained associated with the development of proteinuria (odds ratio 2.9; 95% confidence interval 1.5, 5.5; P=0.001).Conclusion
Microalbuminuria predicts the development of proteinuria among HIV‐infected persons. Because proteinuria has been linked to poorer outcomes, strategies to affect microalbuminuria should be tested.14.
Objectives
.To investigate hypercalcaemia (serum ionized calcium (S-Ca2+) > 1.35 mmol L?1) in breast cancer patients before and after the introduction of bisphosphonates and the effect of disease- and treatment-related factors on survival.Design
.Prospective and retrospective registration of covariates.Setting
.A department of oncology in a university hospital.Subjects
.A consecutive cohort of 212 hypercalcaemic patients never treated with bisphosphonate was identified prospectively (period 1) and 193 patients with metastases were classified into three groups: mild (S-Ca2+ < 1.48; n= 102), moderate (1.48 ≤ S-Ca2+≤ 1.60; n= 41), and severe hypercalcaemia (S-Ca2+ > 1.60 mmol L?1; n= 50). Fifty-one patients with severe hypercalcaemia all treated with bisphosphonate except one were identified retrospectively (period 2).Results
.For period 1 median survival was 6.7 months. Survival was significantly decreased in the two groups with the highest initial S-Ca2+ (P < 0.0001). Median survival times in severely hypercalcaemic patients from periods 1 and 2 were 1.4 (95% confidence interval 0.8–2.1) and 2.2 (95% confidence interval 1.3–3.1) months, respectively. In a Cox model for period 1 significant covariates were: WHO performance, extent of metastases, whether systemic anticancer treatment could be given, and haemoglobin, but not S-Ca2+.Conclusion
.Prognosis is poor in hypercalcaemic breast cancer patients with WHO performance 3–4 and advanced metastatic disease when effective systemic treatment can no longer be offered. Bisphosphonate treatment does not seem to improve survival in severe hypercalcaemia. Antihypercalcaemic treatment of mild malignancy-associated hypercalcaemia appears not to be vital. Therapeutic efforts should be aiming at patients with moderate hypercalcaemia.15.
Dimitrios Daoussis Stamatis‐Nick C. Liossis Elena E. Solomou Anastasia Tsanaktsi Konstadina Bounia Maria Karampetsou Georgios Yiannopoulos Andrew P. Andonopoulos 《Arthritis \u0026amp; Rheumatology》2010,62(1):150-158
Objective
Dkk‐1 is an inhibitory molecule that regulates the Wnt pathway, which controls osteoblastogenesis. This study was undertaken to explore the potential role of Dkk‐1 in ankylosing spondylitis (AS), a prototypical bone‐forming disease.Methods
Serum Dkk‐1 levels were measured in 45 patients with AS, 45 patients with rheumatoid arthritis (RA), 15 patients with psoriatic arthritis (PsA), and 50 healthy subjects by sandwich enzyme‐linked immunosorbent assay (ELISA). A functional ELISA was used to assess the binding of Dkk‐1 to its receptor (low‐density lipoprotein receptor–related protein 6). Furthermore, we studied the effect of sera from patients with AS and healthy subjects on the activity of the Wnt pathway in the Jurkat T cell model, with and without a neutralizing anti–Dkk‐1 monoclonal antibody, by Western immunoblotting.Results
Serum Dkk‐1 levels were significantly increased in patients with AS (mean ± SEM 2,730 ± 135.1 pg/ml) as compared with normal subjects (P = 0.040), patients with RA (P = 0.020), and patients with PsA (P = 0.049). Patients with AS receiving anti–tumor necrosis factor α (anti‐TNFα) treatment had significantly higher serum Dkk‐1 levels than patients with AS not receiving such treatment (P = 0.007). Patients with AS studied serially prior to and following anti‐TNFα administration exhibited a significant increase in serum Dkk‐1 levels (P = 0.020), in contrast to patients with RA, who exhibited a dramatic decrease (P < 0.001). Jurkat cells treated with serum from AS patients exhibited increased Wnt signaling compared with cells treated with control serum. In that system, Dkk‐1 blockade significantly enhanced Wnt signaling in control serum–treated, but not AS serum–treated, Jurkat T cells.Conclusion
Our findings indicate that in patients with AS, circulating bone formation–promoting factors functionally prevail. This can be at least partially attributed to decreased Dkk‐1–mediated inhibition.16.
Nancy C. Gyurcsik Paul A. Estabrooks Melissa J. Frahm‐Templar 《Arthritis care & research》2003,49(3):306-313
Objective
To examine whether aquatic exercise–related goals, task self‐efficacy, and scheduling self‐efficacy are predictive of aquatic exercise attendance in individuals with arthritis. A secondary objective was to determine whether high attendees differed from low attendees on goals and self‐efficacy.Methods
The sample comprised 216 adults with arthritis (mean age 69.21 years). Measures included exercise‐related goal difficulty and specificity, task and scheduling self‐efficacy, and 8‐week aquatic exercise attendance.Results
Results of a multiple hierarchical regression analysis were significant (P < 0.01). Goal difficulty, specificity, and task self‐efficacy were independent predictors of attendance (P < 0.05). A significant multivariate analysis of variance (P < 0.01) indicated that high attendees had higher task and scheduling self‐efficacy and lower goal difficulty than did low attendees (P < 0.05).Conclusion
Support for the importance of exercise‐related goal setting and self‐efficacy was demonstrated. Implications pertain to the design of interventions to impact aquatic exercise.17.
Background:
The purpose of this study was to investigate the relationship between left atrial (LA) myocardial function and left ventricular (LV) diastolic dysfunction in subjects with preserved LV ejection fraction (LVEF).Methods:
The study included a group of 118 hypertensive patients and normal subjects. LV diastolic dysfunction was classified into 4 groups: none, mild, moderate, and severe. Peak strain rates in systole (S‐Sr), early diastole (E‐Sr), and late diastole (A‐Sr) were obtained from Doppler‐derived strain rate imaging to evaluate LA myocardial deformation.Results:
No significant difference in LA dimension was observed in subjects with different degrees of LV diastolic dysfunction, although LA myocardial strain rate parameters were all significantly different across the 4 groups (all with P < 0.001). Compared with patients of normal diastolic function, the mild diastolic dysfunction group had significantly lower E‐Sr (0.62 ± 0.18 s?1 vs 1.20 ± 0.38 s?1, P < 0.001) and S‐Sr (0.78 ± 0.16 s?1 vs 0.94 ± 0.22 s?1, P < 0.001) but increased A‐Sr (1.14 ± 0.29 s?1 vs 1.00 ± 0.23 s?1, P = 0.05).Conclusions:
By using strain rate imaging, significant changes of LA deformation in response to different stages of LV diastolic dysfunction were detected in subjects with preserved LVEF. Quantification of LA myocardial function rather than LA size may have the potential to predict early LV diastolic dysfunction in subjects with preserved LVEF. Copyright © 2010 Wiley Periodicals, Inc. The authors have no funding, financial relationships, or conflicts of interest to disclose.18.
Heike A. Bischoff‐Ferrari Yuqing Zhang Douglas P. Kiel David T. Felson 《Arthritis care & research》2005,53(6):821-826
Objective
To describe the association between serum 25‐hydroxyvitamin D (25[OH]D) level and bone mineral density (BMD) in persons with primary knee osteoarthritis (OA).Methods
We conducted a population‐based survey of the Framingham Study. A total of 228 subjects with primary radiographic knee OA were identified. For vitamin D status, 25(OH)D levels ≤15 ng/ml were classified as vitamin D deficient, 25(OH)D levels 16–32 ng/ml were classified as hypovitaminosis D, and 25(OH)D levels >32 ng/ml were classified as vitamin D replete. We compared average BMD between categories of 25(OH)D levels in subjects with OA using a linear regression model while adjusting for sex, age, body mass index (BMI), knee pain, physical activity, cohort, and disease severity.Results
Mean age was 74.4 years and 36% were men. Of 228 individuals, 15% were vitamin D deficient, 51% had hypovitaminosis D, and 34% were vitamin D replete. Compared with subjects with vitamin D deficiency, those with hypovitaminosis D had a 7.3% higher BMD (adjusted percent difference; P = 0.02) and vitamin D replete subjects had an 8.5% higher BMD (adjusted percent difference; P = 0.02; test for trend across categories: P = 0.04).Conclusion
We observed a significant positive association between serum 25(OH)D and BMD in individuals with primary knee OA, independent of sex, age, BMI, knee pain, physical activity, and disease severity. Given the high prevalence of low 25(OH)D status in persons with knee OA and the positive association between 25(OH)D and BMD, vitamin D supplementation may enhance BMD in individuals with OA.19.