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Annals of the Rheumatic Diseases | 2014
M. Bernardes; J.C. Machado; T. Vieira; D. Gonçalves; R. Vieira; R. Fonseca; P. Madureira; J. Abelha-Aleixo; A. Bernardo; J.G. Pereira; M.J. Martins; L. Costa; F. Simões-Ventura
Background Rheumatoid arthritis (RA) is characterized by a localized bone resorption at the hands, namely, as well as a generalized osteoporosis. BsmI vitamin D receptor (VDR) gene polymorphism is a well known genetic determinant of bone mineral density (BMD) in healthy populations. Objectives Determine the degree of association of BsmI VDR gene polymorphism with BMD and bone metabolism in patients with established RA. Methods Clinical features and peripheral blood samples were collected from a monitoring visit. HAQ and DAS28 (4v) were obtained. We measured the following laboratory parameters: ESR, CRP, serum β-CTX1, osteocalcin, Dkk-1, sclerostin, RANKL and OPG. Genomic DNA was extracted from blood and genotyped for the BsmI (A/G) (rs1544410) SNP by PCR-RFLPs analysis. BMD was assessed by Dual energy X-ray Absorptiometry (Lunar Expert ® 1320) at the lumbar spine, total hip, femoral neck, hands and second proximal phalanges. A multivariate analysis model was used for statistical analysis (IBM SPSS Statistics 21). Results We evaluated 208 RA patients, 166 (80%) women, 65 (31%) premenopausal women, age 54±12 years, disease duration 14±10 years, mean DAS28 (4v) of 4.25±1.33 and a mean HAQ of 1.254±0.709. In our sample, 107 (51%) were under biologics, 87 (42%) under anti-TNFalpha agents, 69 (33%) under bisphosphonates and 42 (20%) under vitamin D supplements, Genotype frequencies were determined for BsmI VDR gene polymorphism: GG 37%, AG 44%, AA 19%. AA genotype was associated with higher BMD at femoral neck, lumbar spine, hands and second proximal phalanges (p<0.001). In the subgroup of patients without vitamin D supplements, AA genotype was also associated with higher BMD at the hip (p<0.001). These associations were found after adjusting for age, disease duration, body mass index, DAS28 (4v), current HAQ, time under DMARDs therapy, years of corticosteroid use and years of bisphosphonates use. In terms of bone metabolism, AA genotype was associated with higher values of Dkk-1 (p<0.05) and sclerostin (p<0.001). The presence of A allele was associated with higher RANKL levels (p<0.05). In the subgroup of patients without vitamin D supplements, AA genotype was only associated with higher sclerostin levels (p<0.001). These later associations were found after adjusting for age, age at diagnosis, disease duration, body mass index, DAS28 (4v), current HAQ, current average daily dose of prednisolone and years of bisphosphonates use. Conclusions BsmI VDR gene polymorphism may serve as a genetic marker of both, localized and generalized, bone loss in RA population since it is associated with BMD in several anatomic sites. The link of this polymorphism to high serum levels of sclerostin reinforce a possible role for this bone marker in coupling bone resorption to bone formation. There is recent evidence that zoledronic acid increases sclerostin serum levels in treated postmenopausal women and that sclerostin serum levels correlate positively with BMD in haemodialysis patients. Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.3868
Annals of the Rheumatic Diseases | 2014
R. Fonseca; G. Terroso; D. Gonçalves; J. Abelha-Aleixo; F. Aguiar; P. Madureira; R. Vieira; M. Bernardes; L. Costa
Background Low bone mineral density (BMD) is highly prevalent in patients with systemic lupus erythematosus (SLE). However, determinants of BMD changes in SLE are still largely unknown. Objectives The aim of this study was to describe the clinical characteristics of SLE patients submitted to a dual energy X-ray absorptiometry (DEXA), evaluating the prevalence of osteopenia/osteoporosis and searching for possible predictors of bone loss in these patients. Methods Retrospective observational study of 160 SLE patients of our Rheumatology department, was performed. Demographic, clinical data and BMD measurements (g/cm2) of the lumbar spine (LS) and total hip (TH) were collected. The DEXA results were classified according to WHO criteria for osteoporosis. Statistical analyses was performed using t-test, Mann-Whitney U-test, and Spearman correlation (SPSS 21.0). Results Out of 160 SLE patients, 148 (92,5%) were female with a mean age 44,23±12,5 years. The median SLEDAI was 2 [0-23], median SLICC was 0,2 [0-5]. 74 (56%) patients were taking vitamin D supplements, 56 (35%) were taking calcium supplements and 24 (15%) received bisphosphonate therapy. Only 81 (50,6%) had a DEXA done. Patients with DEXA were older (47.28±12.7 vs 41.09±11.8 years, p<0.01), had a longer disease duration (13.8±9 vs. 10.6±8 years, p=0.02), high SLICC score (2,0 vs 0,0 p=0,04) and were taking a higher dose of steroids (7 vs 5; p=0,01). No significant differences were found between gender, SLEDAI, serum vitamin D, complement levels, erythrocyte sedimentation rate or c-reactive protein. Of the 81 patients with DEXA, 34 (42%) had osteopenia, 13 (16%) had osteoporosis and 34 (42%) had normal BMD. The mean lumbar spine BMD was 0.96±0.12 g/cm2 and the mean total hip BMD was 0.87±0.13 g/cm2. Statistically significantly correlation was found between age and lumbar spine BMD (r=-0,256; p=0,02), age and total hip BMD (r=-0,262; p=0,02), SLICC score and lumbar spine DMO (r=-0,230; p=0,04) and SLICC score and total hip BMD (r=-0,279; p=0,04). Conclusions In our cohort, SLE patients referred for a DEXA have more traditional risk factors, take a higher dose of corticosteroids and have a higher disease damage access by SLICC score. The prevalence of osteopenia and osteoporosis in our SLE-patients was greater than in general population. In addition to age, disease damage access by SLICC score was associated with low BMD. Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.4635
Annals of the Rheumatic Diseases | 2016
D. Gonçalves; R. Fonseca; F. Aguiar; T. Martins-Rocha; M. Bernardes; L. Costa
Background Interstitial lung disease (ILD) is one of the major types of lung involvement in systemic sclerosis (SSc). Affected patients have a worse prognosis than patients with SSc who are free of pulmonary involvement. Therefore, it is important to explore determinants of this organ complication. Objectives To found possible determinants of ILD in SSc patients. Methods A cross-sectional study was conducted in 104 SSc patients (2013 ACR/EULAR criteria) from a university hospital of Portugal. The analyzed variables were: age, sex, age at disease onset, disease duration, antinuclear antibodies (ANA), topoisomerase I DNA (Scl70) and anticentromere antibodies (ACAs) status, Raynaud phenomenon, areas of skin sclerosis (limited was divided into sclerodactyly or proximal to the metacarpophalangeal (MCP) joints), digital ulcers (DU), digital pitting scar and telangiectasia status, diffusion capacity of carbon monoxide transfer/alveolar volume (DLCO/VA, % of the predicted value) at diagnosis and esophagus involvement. Descriptive statistics were calculated for several demographic and clinical characteristics. Pearson or Spearman correlation and chi-square or Fishers exact test was used for the assessment of the correlation between ILD and the different continuous and categorical variables. Subsequently, binary logistic regression analysis (method enter) was carried out using the ILD as the dependent variable. As independent variables, were included variables that had clinical or statistical significance. Results Most (89.4%) of patients were women; mean (SD) age was 59 (±13) years. Mean age at diagnosis was 51 (±13) years with disease duration median (min;max) of 6 (0;38) years. Ninety-three (89.4%) patients had limited (lcSSc) scleroderma. Most (98.1%) patients had ANA positive (mainly centromere (n=61) followed by nucleolar pattern (n=15)), 61 (58.7%) patients were ACAs positive and 21 (20.2%) positive for Scl70 antibodies. DLCO/VA mean at SSc diagnosis was 74.8% (±13.6). Twenty-three (22.1%) patients had ILD (most NSIP pattern) and 64 (61.5%) had esophagus involvement. Correlation coefficients with statistical significance were noted for disease duration and age however, these were weak (rô=0.22, p=0.03 and r=0.29, p=0.004; respectively). For categorical variables we observed statistical significance for SSc subgroups (ILD prevalence of 15.1% in lcSSc vs 72.7% in diffuse SSc; p<0.001), ACAs and Scl70 serology (6.6% in ACAs vs 57.1% in Scl70 positive patients; p<0.001) and DU (33.3% if history vs 15.5% if without history of DU, p=0.02). Correlation of ILD with DLCO/VA at SSc diagnosis and sex had not statistical significance (p=0.064). In logistic regression the following variables were introduced: age, disease duration, SSc subgroups, ACAs and Scl70 serology, skin sclerosis proximal to the MCP joints, DU status and DLCO/VA at SSc diagnosis. The analysis showed that the age (OR=1.13,p=0.003), SSc subgroups (OR=22.95,p<0.001) and ACAs status (OR=0.08,p=0.001) influence the ILD in the model. Conclusions Our results suggest that higher age and diffuse sclerosis increased ILD risk and ACAs decreases. A prospective longitudinal study with a larger sample is desirable to confirm these results. Disclosure of Interest None declared
Annals of the Rheumatic Diseases | 2016
D. Gonçalves; R. Fonseca; F. Aguiar; T. Martins-Rocha; M. Bernardes; L. Costa
Background Dissociation between the responses of a number of acute-phase proteins (APP) is well known. C reactive protein (CRP) levels have been used extensively to model disease activity in rheumatoid arthritis (RA). However, biologic therapy reduce CRP levels, even without associated reductions in RA disease activity. Serum amyloid A (SAA) also models RA disease activity and has been suggested as a better biomarker for RA disease activity. Objectives To determine if SAA levels had better correlation with conventional clinical and serological assessments in RA than CRP and ESR. Methods A cross-sectional study was performed. Samples were analyzed from RA patients under biologic therapy of a reference hospital in northern Portugal. We compared the correlation between SAA, CRP and ESR levels with swollen and tender joints counts (SJC and TJC), DAS28-4v, SDAI, CDAI, HAQ and visual analogue scale for pain (VAS-P). Correlation was calculated using the Spearman rank correlation (r). P-values <0.05 were regarded as significant. Results 173 patients were evaluated, 86.7% (n=150) were women. The mean (SD) age was 56 years (10.75). Mean disease duration was 16.31 years (8.87). Most of patients had positive serology (rheumatoid factor and/or anti-CCP antibody) (n=146, 84.4%). Ninety eight patients (56.6%) were under TNF antagonists, 23.7% (n=41) were under rituximab and the remaining under tocilizumab (TCZ). SAA levels were moderately correlated with CRP levels (r=0.49, p<0.001) but there was no statistically significant correlation with ESR (r=0.03, p=0.75). Correlation analysis of SAA and CRP levels with several conventional assessments showed (SAA and CRP, respectively): SJC - 0.17 vs 0.08, TJC - 0.18 vs 0.09, DAS28-4v - 0.32 vs 0.41, SDAI - 0.23 vs 0.18, CDAI - 0.18 vs 0.11, ESR – 0.32 vs 0.55; all p values <0.05 except SJC, TJC and SDAI for CRP values. There was no statistically significant correlation of these acute-phase protein with HAQ and VAS-P. ESR levels showed very weak correlation with all parameters (p>0.05), except with DAS28-4v (r=0.58, p<0.001). We also noted that SAA levels were raised (>6.4mg/L) in 37.6% (n=65) of patients in which the CRP concentration was normal (<0.3mg/dL). However, only 6% (n=11) with normal SAA levels had raised concentrations of CRP. When evaluated SAA and CRP levels in patients with active disease (DAS28-4v 32.6, SDAI>3.3 and CDAI>2.8) we found more patients with normal CRP values than SAA (62 vs 26, 82 vs 32, 84 vs 33, respectively). Interestingly, when comparing the effects of biological therapy on APP we noted that in TCZ group the CRP, ESR and SAA levels were lower than in group under TNF antagonists and rituximab (p<0.001 for all, Mann-Whitney test). Conclusions The lack of a strong correlation between SAA and CRP or ESR levels coupled with their better correlation with markers of RA activity suggests that changes in their levels may provide a more sensitive indicator of disease activity, especially during treatment with biologic therapy. Disclosure of Interest None declared
Annals of the Rheumatic Diseases | 2015
P. Madureira; S. Pimenta; R. Vieira; R. Fonseca; D. Gonçalves; F. Aguiar; T. Rocha; A. Bernardo; M. Bernardes; L. Costa
Background Smoking is a known environmental risk factor for developing rheumatoid arthritis (RA), and is also a marker of a worst clinical and radiological prognosis. Despite this relation, the effect of smoking on RA treatment effectiveness is still controversial, with the available reports suggesting a deleterious effect. Objectives To analyse the effect of smoking on treatment response in RA patients under biologics, addressing possible differences in the degree of response between those being treated with anti-TNF alpha agents and those under other biologics. Methods A retrospective analysis of all patients with RA receiving biologic therapy of a rheumatology department of a Portuguese University Hospital. Were excluded from the analysis all the patients without data on smoking history. For this analysis, were considered “smokers” all patients with current or past smoking habits. The demographic and clinic baseline data, disease activity at baseline, 6, 12 and 18 months of therapy (DAS28 and EULAR response) and HAQ at baseline were collected. The variations in DAS28 and EULAR response were determined, as well as their difference according to current exposure to anti-TNF alpha agents or to other biologics (Rituximab, Tocilizumab, Abatacept). The effect of smoking on DAS28 was adjusted to age and gender. Statistical analysis was done using SPSS® 22. Results In January 2015, 145 patients met the inclusion criteria; 88.3% were women, with median disease duration of 16.5 years. Rheumatoid factor and/ or anti-cyclic citrullinated peptide (anti-CCP) antibodies were positive in 82.8% of patients. Median baseline DAS28 was 6.09 and median baseline HAQ was 1.86. There were 35 patients with past or current smoking history. Smoker patients were younger than non-smoker patients (median age 52.4 vs. 57.2, p=0.047), and have a lower proportion of women (62.6% vs. 94.5%, p<0.001). The median DAS28 reduction at 6 months was significant different between smokers and non-smokers, favouring the latter (-1.41 vs. -1.68, p=0.029), even after adjusting for age; after adjusting for gender the relation lost significance. It was observed a tendency for a smaller proportion of patients achieving EULAR response (moderate or good) among smokers at 6 months (56.5% vs. 75.3%, p=0.083). At 12 and 18 months of treatment was also observed the same trend to a smaller reduction of DAS28 among smokers (-1.79 vs. -1.84, p=0.892 and -1.98 vs. -2.21, p=0.140 respectively). Amongst smoking patients, those treated with anti-TNF agents seem to have worse response when compared with patients under biologics with other mechanism of action after 6 months (-0.75 vs. -1.43, p=0.220), 12 months (-1.63 vs. -2.16, p=0.790) and 18 months of treatment (-1.40 vs. -2.30), p=0.159). The same trend was observed in those achieving a moderate or good EULAR response. Conclusions This analysis suggests a negative effect of smoking on therapeutic response in Rheumatoid Arthritis patients under Biologics, and that other biologics than anti-TNF alpha agents may be better choices for smoker rheumatoid arthritis patients. Disclosure of Interest None declared
Annals of the Rheumatic Diseases | 2015
P. Madureira; S. Pimenta; R. Vieira; R. Fonseca; D. Gonçalves; F. Aguiar; T. Rocha; A. Bernardo; M. Bernardes; L. Costa
Background Corticosteroids (CS) are used on rheumatoid arthritis (RA) treatment for decades, due to their rapid and efficacious improvement of arthritis. With the recent advances in RA treatment and the increasing awareness given to CS side effects it should be expected that these drugs started being used scarcely and for shorter periods of time. Objectives Analyse the variations in CS dose in patients with RA after the start of biologic therapy. Analyse the existence of differences between biologics regarding CS therapy. Methods A retrospective analysis of all patients with RA receiving biologic therapy of a rheumatology department of a Portuguese University Hospital. The demographic and clinic baseline data was collected. The variations in CS dose between baseline and 12 and 24 months were determined, as well as their difference according to the biologic agent: anti-TNF, Rituximab and Tocilizumab. Other biologics were excluded due to the small number of patients assigned to them. The proportion of patients steroid-free was determined as well as the differences according to the current biologic. All CS dose are displayed as the equivalent prednisolone doses. Results In January 2015, 176 patients met the inclusion criteria; 88.3% were women, with mean age of 57.2 (±10.9) years, and disease duration of 19.8 (±9.8) years. Rheumatoid factor and/ or anti-cyclic citrullinated peptide (anti-CCP) were positive in 77.8% of patients. Mean baseline DAS28 was 6.02 (±1.41) and mean baseline HAQ was 1.80 (±0.56). Most of the patients (n=98) were treated with anti-TNF agents; 48 patients received rituximab and 30 tocilizumab. Mean CS dose at baseline was 7.02 (±4.33) mg/day; after 12 months of biologic therapy reduced to 6.29 (±3.93) mg/day (p<0.001) and after 24 months to 5.65 (±3.90) mg/day (p<0.001). With all the biologics analysed it was seen a significant reduction in steroids dose: in patients receiving anti-TNF agents mean CS dose reduced from 6.44 (±4.20) to 5.81 (±3.91) mg/day at 12 months (p=0.015) and to 5.48 (±4.01) mg/day at 24 months (p=0.002). With Rituximab it reduced from 7.74 (±4.42) to 6.55 (±3.54) at 12 months (p=0.032) and to 5.68 (±3.73) mg/day at 24 months (p=0.005); with Tocilizumab from 7.20 (±3.11) to 6.76 (±2.83) (p=0.136) and to 5.91 (±2.56) mg/day (p=0.043), respectively. We found a significant higher CS dose at 12 months of treatment in patients that switched biologic 2 or more times (7.50±4.59 mg/day) vs. patients that switched 1 time (6.23±2.65 mg/day) vs. patients that were being treated with their first biologic (6.14±4.19 mg/day) (p<0.001). The results were also significant different at 24 months. While at baseline only 8.9% of patients were steroid-free, this number increased to 10.7% at 12 months (p<0.001) and to 15.8% at 24 months (p<0.001). This effect was similar in anti-TNF agents (10.2%, 12.4% (p<0.001), 15.1% (p<0.001), respectively), Rituximab (8.3%, 10.4% (p=0.002), 20.0% (p<0.001), respectively). In tocilizumab this effect was less pronounced. Conclusions This analysis suggests that RA patients can be maintained with low dose CS therapy for long periods, and that biologic therapies can contribute to decrease the dose of CS in these patients, and even allow a greater proportion of them to stop CS therapy. Disclosure of Interest None declared
Annals of the Rheumatic Diseases | 2015
R. Fonseca; D. Gonçalves; R. Vieira; J. Abelha-Aleixo; G. Terroso; M. Bernardes; L. Costa
Background Biochemical markers of bone turnover levels have been suggested as predictors of long-term response in bone mass density (BMD) to teriparatide. However, its usefulness in clinical practice is unknown. Objectives To identify the patients that will have significant increases in BMD after teriparatide using osteocalcin (OC) levels. Methods Prospective observational study was performed. OC was measured at baseline, 3 months (M) and 18 M and BMD at baseline and 18 M (LUNAR Expert 1320R). Correlation between OC levels and BMD changes was evaluated by Spearman rank correlation analysis. Discriminant cut-off values for OC (baseline and 3M changes) in predicting “threshold” BMD increases >15% were determined using receiver operating characteristics curve (ROC). Kappa coefficient was calculated to identify the agreement between patients identified as good responders by their OC levels. Results 57 patients (91.2% female) with mean age of 67.65±8.8 years were included. After treatment, median BMD change in lumbar spine (LS) was 0.088 g/cm2 (10.65%). Median baseline OC level was 18.9 ng/mL [4.2 – 71.3] and median 3M OC change was 27.5 ng/mL [0.30 – 93.50]. LS BMD gains after treatment correlated significantly with baseline OC (r=0.324; p=0.036) as well with 3M OC changes (r=0.336; p=0.049). Baseline OC and 3M OC changes showed a good accuracy in predicting >15% LS BMD change (area under the curve AUC 0.694, p=0.03 and AUC 0.748, p=0.017, respectively). Baseline OC of 26.75 ng/mL predict 15% improvement in BMD with sensitivity (S) 40%, specificity (E) 92.6%, positive predictive value (PPV) 74.84%, negative predictive value (NPV) 74%, positive likelihood ratio (LR) 5.4 and negative LR 0.65. 39.3 ng/mL in 3M OC changes predict 15% improvement in BMD with: S 50%, E 91.3%, PPV 74.89%, NPV 41.67%, positive LR 5.74 and negative LR 0.55. We found a good agreement (Kappa 0.697; p=0.01) between patients identified as good responders (baseline OC ≥26.75 ng/mL and 3M OC changes≥39.3 ng/mL). Conclusions 26.75 ng/mL in baseline OC and 39.3 ng/mL increases in OC were the most convenient predictors of BMD response in clinical practice. These values can be used either to select patients (that will probably have good results) as well for assessing adherence and treatment response at 3 months. Disclosure of Interest None declared
Annals of the Rheumatic Diseases | 2014
M. Bernardes; J.C. Machado; D. Gonçalves; J. Abelha-Aleixo; R. Fonseca; P. Madureira; R. Vieira; A. Bernardo; M.J. Martins; L. Costa; F. Simões-Ventura
Background Vitamin D has been shown to have significant immunomodulatory effects. Its actions are mediated by the ubiquitous vitamin D receptor (VDR). In one study, BsmI VDR gene polymorphism was associated with an early onset of rheumatoid arthritis (RA). Additionally, TT genotype of the FokI VDR gene polymorphism was established as a genetic susceptibility marker for RA in French and Tunisian populations. Objectives To determine the degree of association of BsmI and FokI VDR gene polymorphisms with disease activity in patients with established RA. Methods Clinical features and peripheral blood samples were collected from a monitoring visit. The Portuguese version of HAQ and the disease activity scores (DAS28 (4v; ESR), DAS28 (3v; ESR), DAS 28 (4v; CRP), DAS28 (3v; CRP)) were obtained. We measured the following acute phase reactants: ESR and CRP. Genomic DNA was extracted from blood and genotyped for the BsmI (A/G) (rs1544410) and FokI (T/C) (rs 2228570) SNPs by PCR-RFLPs analysis. A multivariate analysis model was used for statistical analysis (IBM SPSS Statistics 21). Results We evaluated 208 RA patients, 166 (80%) women, 65 (31%) premenopausal women, age 54±12 years, disease duration 14±10 years, mean DAS28 (4v) of 4.25±1.33 and a mean HAQ of 1.254±0.709. In our sample, 107 (51%) were under biologics, 87 (42%) under anti-TNFalpha agents and 42 (20%) under vitamin D supplements. Genotype frequencies were determined for the two distinct VDR polymorphisms: BsmI (GG 37%, 44% AG, AA 19%) and FoKI (CC 42%, TC 46%, TT 12%). GG genotype of the BsmI VDR gene polymorphism was associated with higher DAS28 (4v; ESR), DAS28 (3v; ESR), DAS 28 (4v; CRP) and DAS28 (3v; CRP) scores (p<0.001). Additionally, TT genotype of the FokI VDR gene polymorphism was associated with higher DAS28 (4v; ESR), DAS28 (3v; ESR), DAS 28 (4v; CRP) and DAS28 (3v; CRP) scores (p<0.001). In the subgroup of patients without vitamin D supplements, the previously observed associations remained significant (p<0.001). All these associations were found after adjusting for age, disease duration, current HAQ, time under DMARDs therapy, current average daily dose of prednisone and years of corticosteroid use. Conclusions In our RA population, the BsmI GG and the FokI TT genotypes of the VDR gene were related with disease severity. In the future, VDR gene polymorphisms could be useful in establishing RA prognosis. Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.3913
Annals of the Rheumatic Diseases | 2014
J. Abelha-Aleixo; R. Fonseca; D. Gonçalves; R. Vieira; G. Terroso; P. Madureira; A. Bernardo; M. Bernardes; L. Costa
Background Teriparatide is an anabolic agent that has been shown to increase bone mineral density (BMD) and reduce the risk of fracture. Despite its unique mechanism, there are still few reviews respecting any differences on treatment efficacy in the different types of osteoporosis. Objectives To evaluate if there are differences between primary (OP1) and secondary (OP2) osteoporosis (glucocorticoid-induced osteoporosis and/or secondary to chronic inflammatory diseases), and the several initial indications for treatment, concerning the markers of bone turnover (MBT) and bone mineral density changes, on patients under teriparatide treatment. Methods All patients treated with teriparatide for osteoporosis at our centre were retrospectively evaluated. The indications for treatment were listed as: lumbar spine T-score ≤-4 (13 patients); lumbar spine T-score ≤-3 and presence of radiographic vertebral fractures (32 patients); and others (18 patients). BMD values at baseline and 18 months were obtained by DEXA with a LUNAR Expert 1320. The MBT measured at baseline, 3 and 18 months were: β-C-telopeptide of collagen 1 crosslinks, osteocalcin, alkaline phosphatase and 25(OH) vitamin D3. MBT and BMD variations between baseline and 18 months were tested according to the presence of OP1 or OP2, and indications for treatment, using non-parametric tests (SPSS 21.0 for statistical data analysis). Results Sixty three patients were evaluated (58 women), 25 (39,7%) with OP1, and 38 (60,3%) with OP2. Comparing to OP2, OP1 was significantly associated (p<0,050) with higher gains of BMD at Wards triangle (5,5% vs 1,3%), total hip (3,5% vs 0,3%) and lumbar spine (21,65% vs 9,9%). There were no differences concerning MBT in OP1 vs OP2. Regarding the several treatment indications, there were no differences in terms of MBT. Concerning BMD variations, the group with lumbar spine T-score <-4 was the only that showed higher gains in bone mass, namely at the lumbar spine BMD (22,8% vs 8,9% g/cm2). Conclusions OP1 seems to have better response than OP2 to teriparatide treatment at total hip, lumbar spine and Wards triangle in terms of BMD gains. The indication for treatment does not appear to influence the results, both in terms of BMD gains and MBT changes, with the exception of those patients with lumbar spine T-score<-4, who exhibited greater gains at lumbar spine BMD. Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.4267
Annals of the Rheumatic Diseases | 2014
R. Fonseca; D. Gonçalves; J. Abelha-Aleixo; F. Aguiar; P. Madureira; R. Vieira; G. Terroso; M. Bernardes; L. Costa
Background Short-term changes in biochemical markers of bone turnover have been suggested as predictors of long-term response in bone mass density (BMD) during teriparatide treatment. However, few data are available, particularly regarding increases in hip BMD. Objectives The aim of this study was to examine whether early changes in biochemical markers of bone turnover predict long-term changes of BMD in patients treated with teriparatide. Methods BMD values at baseline and 18 months were obtained with a LUNAR Expert 1320 R. β-C-telopeptide of collagen 1 crosslinks (β-CTX1), osteocalcin (OC), alkaline phosphatase and 25 (OH) vitamin D3 were measured at baseline, 3 and at 18 months. The association between baseline and 3 months markers levels and BMD changes at the end of treatment was evaluated using Spearman correlation analysis (SPSS 21.0). Results Sixty three patients were evaluated. 92,1% (58) were female and the mean age was 67,65±8,8 years. 60,3% (38) had glucocorticoid-induced osteoporosis and/or secondary to chronic inflammatory diseases. After treatment median DMD changes were: 0,088 g/cm2 in lumbar spine (gain of 10,65%), 0,024 g/cm2 in femoral neck (gain of 4,16%), 0,03g/cm2 in wards triangle (gain of 7,7%) and 0,011g/cm2 in total hip (gain of 1,1%). At baseline, β-CTX1 and OC levels correlated positively with the variation of BMD in lumbar spine at 18 months (r =0,452; p=0,01 and r=0,305; p=0,04, respectively). Baseline OC levels also correlated significantly with BMD variation in femoral neck (r=0,524; p<0,01), wards triangle (r=0,442; p=0,02) and total hip (r=0,364; p=0,01). Statistically significant correlation was found between β-CTX1 level at 3 months and BMD variation in femoral neck (r=0,389; p=0,01) and wards triangle (r=0,402; p=0,03). 3 months OC levels correlated significantly with femoral neck DMO variation (r=0,517; p<0,01) and wards triangle DMO variation (r=0,501; p<0,01). No association was found between alkaline phosphatase and 25 (OH) vitamin D3 values at baseline and 3 months and BMD changes. Conclusions In our study, we found an association between bone turnover markers levels at baseline and 3 months and final changes in BMD at the lumbar spine and total hip. The early measurement of bone turnover markers may be a useful tool to predict BMD response to this anabolic therapy. Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.4623