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In: The Lancet, Elsevier BV, Vol. 400, No. 10363 ( 2022-11), p. 1607-1617

Type of Medium: Online Resource

ISSN: 0140-6736

URL: Article

DOI: 10.1016/S0140-6736(22)01846-3

Language: English

Publisher: Elsevier BV

Publication Date: 2022

detail.hit.zdb_id: 2067452-1

detail.hit.zdb_id: 3306-6

detail.hit.zdb_id: 1476593-7

SSG: 5,21

In: American Journal of Infection Control, Elsevier BV, Vol. 48, No. 4 ( 2020-04), p. 423-432

Type of Medium: Online Resource

ISSN: 0196-6553

URL: Article

DOI: 10.1016/j.ajic.2019.08.023

Language: English

Publisher: Elsevier BV

Publication Date: 2020

detail.hit.zdb_id: 2011724-3

In: Lupus, SAGE Publications, Vol. 30, No. 4 ( 2021-04), p. 630-640

Abstract: Introduction: After more than 20 years of sustained work, the Latin American Group for the Study of Lupus (GLADEL) has made a significant number of contributions to the field of lupus, not only in the differential role that race/ethnicity plays in its course and outcome but also in several other studies including the beneficial effects of using antimalarials in lupus patients and the development of consensus guidelines for the treatment of lupus in our region. Methods: A new generation of “Lupus Investigators” in more than 40 centers throughout Latin America has been constituted in order to continue the legacy of the investigators of the original cohort and to launch a novel study of serum and urinary biomarkers in patients with systemic lupus erythematosus. Results: So far, we have recruited 807 patients and 631 controls from 42 Latin-American centers including 339 patients with SLE without renal involvement, 202 patients with SLE with prevalent but inactive renal disease, 176 patients with prevalent and active renal disease and 90 patients with incident lupus nephritis. Conclusions: The different methodological aspects of the GLADEL 2.0 cohort are discussed in this manuscript, including the challenges and difficulties of conducting such an ambitious project.

Type of Medium: Online Resource

ISSN: 0961-2033 , 1477-0962

URL: Article

DOI: 10.1177/0961203320988586

Language: English

Publisher: SAGE Publications

Publication Date: 2021

detail.hit.zdb_id: 2008035-9

In: Rheumatology, Oxford University Press (OUP), Vol. 49, No. Supplement 1 ( 2010-04-01), p. i89-i111

Type of Medium: Online Resource

ISSN: 1462-0324 , 1462-0332

URL: Article

DOI: 10.1093/rheumatology/keq725

Language: English

Publisher: Oxford University Press (OUP)

Publication Date: 2010

detail.hit.zdb_id: 1474143-X

In: The Lancet, Elsevier BV, Vol. 390, No. 10093 ( 2017-07), p. 457-468

Type of Medium: Online Resource

ISSN: 0140-6736

URL: Article

DOI: 10.1016/S0140-6736(17)31618-5

Language: English

Publisher: Elsevier BV

Publication Date: 2017

detail.hit.zdb_id: 2067452-1

detail.hit.zdb_id: 3306-6

detail.hit.zdb_id: 1476593-7

SSG: 5,21

In: Annals of the Rheumatic Diseases, BMJ, Vol. 81, No. Suppl 1 ( 2022-06), p. 637-638

Abstract: Belimumab (BEL) is an approved systemic lupus erythematosus (SLE) treatment. Despite BEL clinical studies demonstrating a favourable benefit–risk profile, varying incidence rates of mortality and adverse events of special interest, including malignancies, require further evaluation. Objectives To assess long-term safety following BEL therapy. Methods This was a Year (Yr)-4 post-treatment follow-up of the Phase 4, double-blind, placebo (PBO)-controlled Belimumab Assessment of Safety in SLE (BASE) study (GSK Study BEL115467; NCT01705977 ). 1 Overall, 4003 adults with active, autoantibody-positive SLE received BEL (10 mg/kg IV) or PBO, plus standard therapy (ST), for 48 weeks. Patients (pts) then entered a Yr 2–5 follow-up period in which they received physician-directed ST. All pts were contacted annually by telephone, including pts who discontinued treatment. Mortality and new malignancies (including nonmelanoma skin cancer) were the endpoints collected, and rates summarised. We present Yr-4 follow-up data by Yr-1 treatment received. Results Baseline characteristics for the Yr-4 follow-up population (N=3204) were similar to the Yr-1 double-blind study population (N=4003). By the Yr-4 follow-up, cumulatively 12.7% and 11.0% of pts in the BEL and PBO Yr-1 groups had received BEL as part of physician-directed care, respectively (data not shown). As shown in the Table 1, cumulative follow-up adjusted mortality rates were lower in the BEL vs PBO Yr-1 treatment group for Yrs 2 to 4. Cumulative follow-up adjusted new primary malignancy rates were lower in the BEL vs PBO Yr-1 treatment group for Yrs 2 and 3, but similar in Yr 4. Table 1. Yr 1 plus Yrs 2–4 post-treatment* follow-up mortality and new primary malignancy rates by Yr-1 study treatment Pts with events per yr, n (%) Pt incidence rate per 100 pt-yrs (Cumulative rate, %) BEL PBO Total BEL PBO Total Yr-1 (as-treated) population N=2002 N=2001 N=4003 Deaths 13 (0.65) 22 (1.10) 35 (0.87) 0.66 (0.65) 1.11 (1.10) 0.87 New primary malignancies† 9 (0.45) 10 (0.50) 19 (0.47) 0.45 0.50 0.47 Yr-2 (as-treated in Yr-1) population N=1695 N=1670 N=3365 Deaths 9 (0.53) 21 (1.26) 30 (0.89) 0.60 (1.10) 1.18 (2.15) 0.89 (1.62) New primary malignancies 3 (0.18) 7 (0.42) 10 (0.30) 0.34 (0.60) 0.48 (0.85) 0.41 (0.72) Yr-3 (as-treated in Yr-1) population N=1659 N=1630 N=3289 Deaths 9 (0.54) 17 (1.04) 26 (0.79) 0.58 (1.55) 1.14 (3.00) 0.86 (2.27) New primary malignancies, n (%) 7 (0.42) 9 (0.55) 16 (0.49) 0.37 (0.95) 0.49 (1.25) 0.43 (1.10) Yr-4 (as-treated in Yr-1) population N=1622 N=1582 N=3204 Deaths by MedDRA SOC 14 (0.86) 13 (0.82) 27 (0.84) 0.65 (2.25) 1.07 (3.65) 0.86 (2.95) Infections/infestations 4 (0.25) 5 (0.32) 9 (0.28) Cardiac disorders 2 (0.12) 1 (0.06) 3 (0.09) General disorders/ administration site conditions 2 (0.12) 2 (0.13) 4 (0.12) Respiratory/thoracic/ mediastinal disorders 2 (0.12) 1 (0.06) 3 (0.09) Nervous system disorders 2 (0.12) 1 (0.06) 3 (0.09) Other‡ 2 (0.12) 3 (0.18) 5 (0.15) New primary malignancies 10 (0.62) 5 (0.32) 15 (0.47) 0.43 (1.45) 0.44 (1.45) 0.43 (1.45) *Pts in the post-treatment follow-up period are no longer receiving study treatment. †Includes nonmelanoma skin cancer. ‡Contains 1 event for 5 distinct pts of each of renal/urinary disorders, and neoplasms (BEL); musculoskeletal/connective tissue disorders, injury/poisoning/procedural complications, and vascular disorders (PBO). MedDRA, Medical Dictionary for Regulatory Activities; SOC, system organ class Conclusion Post-treatment Yr-4 follow-up results in BASE, the largest double-blind trial in pts with SLE to date, support the safety of BEL therapy, with no new BEL safety concerns identified in this analysis. References [1]Sheikh SZ, et al . Lancet Rheumatol 2020;3:e122–30 Acknowledgements This analysis was funded by GlaxoSmithKline (GSK). Medical writing support was provided by Lulu Hill, MPharmacol, Fishawack Indicia Ltd. UK, part of Fishawack Health, and was funded by GSK. Disclosure of Interests Saira Sheikh Consultant of: GSK, Grant/research support from: Pfizer, Morton Scheinberg Consultant of: GSK, Pfizer, Alnylam, AbbVie, PTC Therapeutics, James Cheng-Chung Wei Consultant of: TSH Biopharm, AbbVie, BMS, Celgene, Chugai, Eisai, Janssen, Novartis, Pfizer, Sanofi-Aventis, and UCB Pharma, Grant/research support from: AbbVie, Amgen, Astellas, BMS, Celgene, Eli Lilly, Gilead, Janssen, Novartis, Pfizer, Sun and UCB Pharma, Dana Tegzová: None declared, William Stohl Consultant of: GSK, Grant/research support from: GSK, Pfizer, Gilead, RICARDO ACAYABA DE TOLEDO Speakers bureau: AbbVie, Janssen, UCB, Novartis, Celltrion, Consultant of: AbbVie, Janssen, Novartis, UCB, Grant/research support from: Pfizer, AbbVie, Novartis, GSK, Tamara Mucenic Speakers bureau: Novartis, Janssen, BMS, AbbVie, Pfizer, Roche, Grant/research support from: GSK, Janssen, Roche, Eli Lilly, Gilead, UCB, Mauricio R Abello Banfi: None declared, Kathleen Maksimowicz-McKinnon Grant/research support from: Chemocentryx, Carlos Abud-Mendoza Speakers bureau: GSK, Lilly, Pfizer, Sandra Navarra Speakers bureau: Pfizer, Novartis, Johnson & Johnson, Consultant of: Biogen, Boehringer Ingelheim, Grant/research support from: Astellas, Mercedes García Speakers bureau: GSK, Janssen, Pfizer, Ignacio Garcia-De La Torre: None declared, Andrew Liu Shareholder of: GSK, Employee of: GSK, Abhishek Roy Employee of: GSK, Paul Wilde Shareholder of: GSK, Employee of: GSK, Sofia Fernandes Shareholder of: GSK, Employee of: GSK, Julia Harris Shareholder of: GSK, Employee of: GSK, David Roth Shareholder of: GSK, Employee of: GSK

Type of Medium: Online Resource

ISSN: 0003-4967 , 1468-2060

URL: Article

DOI: 10.1136/annrheumdis-2022-eular.1993

Language: English

Publisher: BMJ

Publication Date: 2022

detail.hit.zdb_id: 1481557-6

In: Annals of the Rheumatic Diseases, BMJ, Vol. 79, No. Suppl 1 ( 2020-06), p. 600.1-601

Abstract: Patients with rheumatoid arthritis (RA) have been associated to higher morbidity and mortality due to cardiovascular events. The impact of atorvastatin and colchicine in reducing these complications has been evaluated without comparative studies of these drugs in RA patients. We assess whether atorvastatin is superior to colchicine in cardiovascular risk markers (high-sensitivity troponin I (hs-cTnI), echocardiographic abnormalities and inflammatory cytokine) in patients with RA Objectives: The primary objective was to compare the initial and final levels of hs-cTnI with both treatments. Secondary objectives: Describe initial echocardiographic abnormalities, compare changes in these alterations with treatment, evaluate factors associated with a higher level of hs-cTnI and echocardiographic abnormalities, compare changes in serum levels of inflammatory cytokines (TNF, IL 8, IL 1β, IL 6, IL 10, IL 12p70) and values of lipid profile Methods: Prospective randomized pilot study, blinded for cardiologist and rheumatologist, with patients with RA and severe disease activity (DAS 28 〉 5.1), without known heart disease, kidney disease or previous use of atorvastatin and / or colchicine. Patients were assigned according to randomization in two groups: atorvastatin 40 mg/day or colchicine with an initial dose of 0.75 mg/day titled according to tolerance up to a maximum dose of 1.5 mg/day, both were received for four weeks. NCT04056039 Results: Recruitment of September 2018 to August 2019, 60 participants had undergone randomization (30 in each group) with a median age 48. The duration of follow-up from randomization was 28 days in each group. Participants were followed by weekly telephone contact to assess of adherence treatment. A detected value of hs-cTnI was found in all patients, initial value in the atorvastatin group: Median 1ng /L, IQR 1-2 and final: Median 1ng /L, IQR 1-3 vs initial value in the colchicine group: 1ng /L, IQR 1-2 and final: 1ng /L, IQR1-2 p = 0.67. Echocardiographic abnormalities in 46 patients (76.66%); 63.33% diastolic dysfunction, 15% tricuspid regurgitation and 11.66% left ventricular hypertrophy. There were changes in initial and final diastolic dysfunction in the atorvastatin group from 19 to 9 vs colchicine 19 to 12 p = 0.05, 95% CI 0.49-0.82. Correlation of initial hs-cTnI with age p 〈 0.001 and rheumatoid factor p = 0.02; correlation of diastolic dysfunction and age p 〈 0.001. There was a greater decrease in the level of tumor necrosis factor (TNF) and IL 1β in the atorvastatin group, however, decrease was higher in IL6 and IL12p70 in the colchicine group. Mild diarrhea was reported as the most frequent adverse effect in the atorvastatin group of 3.33% and colchicine of 23.33% p = 0.010. There was a statistically significant decrease in cholesterol and LDL-cholesterol levels in favor of treatment with atorvastatin Conclusion: We do not observe substantial differences in decrease in hs-cTnI with atorvastatin and colchicine, a prospective study of 222 patients is required to avoid β-type error. Echocardiographic abnormalities in 76% of patients showed a greater decrease in diastolic dysfunction in the atorvastatin group, as well as lower cholesterol and LDL-cholesterol levels, thus, as a tendency to falling of TNF and IL 1β in this group References: [1]Liao KP, Solomon DH. Traditional cardiovascular risk factors, inflammation and cardiovascular risk in rheumatoid arthritis Rheumatol 2013;52(1):45–52 [2]Papageorgiou N, Briasoulis A, Lazaros G. Colchicine for prevention and treatment of cardiac diseases: A meta-analysis Cardiovasc Ther 2017;35(1):10–8 [3]Li G min, Zhao J, Li B, et al. The anti-inflammatory effects of statins on patients with rheumatoid arthritis: A systemic review and meta-analysis of 15 randomized controlled trials Autoimmun Rev 2018;17(3):215–25 Disclosure of Interests: Jose Alfredo Alvarado: None declared, Juan Manuel Lopez: None declared, Ana Cecilia Bardan: None declared, Carlos Abud-Mendoza Speakers bureau: Eli Lilly, Pfizer Inc

Type of Medium: Online Resource

ISSN: 0003-4967 , 1468-2060

URL: Article

DOI: 10.1136/annrheumdis-2020-eular.2513

Language: English

Publisher: BMJ

Publication Date: 2020

detail.hit.zdb_id: 1481557-6

In: Annals of the Rheumatic Diseases, BMJ, Vol. 79, No. Suppl 1 ( 2020-06), p. 180.2-181

Abstract: Tofacitinib is an oral JAK inhibitor that is being investigated for JIA. Objectives: To assess tofacitinib efficacy and safety in JIA patients (pts). Methods: This was a Phase 3, randomised, double-blind (DB), placebo (PBO)-controlled withdrawal study in pts aged 2− 〈 18 years with polyarticular course JIA (pcJIA), PsA or ERA ( NCT02592434 ). In the 18-week open-label Part 1, pts received weight-based tofacitinib doses (5 mg BID or lower). Pts with ≥JIA ACR30 response at Week (W)18 were randomised 1:1 in the DB Part 2 (W18−44) to continue tofacitinib or switch to PBO. Primary endpoint: disease flare rate by W44. Key secondary endpoints: JIA ACR50/30/70 response rates; change from Part 2 baseline (Δ) in CHAQ-DI at W44. Other efficacy endpoints: time to disease flare in Part 2; JADAS27-CRP in Parts 1 and 2. PsA/ERA pts were excluded from these efficacy analyses. Safety was evaluated in all pts up to W44. Results: 225 enrolled pts with pcJIA (n=184), PsA (n=20) or ERA (n=21) received tofacitinib in Part 1. At W18, 173/225 (76.9%) pts entered Part 2 (pcJIA n=142, PsA n=15, ERA n=16). In pcJIA pts, disease flare rate in Part 2 was significantly lower with tofacitinib vs PBO by W44 (p=0.0031; Fig 1a). JIA ACR50/30/70 response rates (Fig 1b) and ΔCHAQ-DI (Fig 1c) at W44, and time to disease flare in Part 2 (Fig 2a), were improved with tofacitinib vs PBO. Tofacitinib reduced JADAS27-CRP in Part 1; this effect was sustained in Part 2 (Fig 2b). Overall, safety was similar with tofacitinib or PBO (Table): 77.3% and 74.1% had adverse events (AEs); 1.1% and 2.4% had serious AEs. In Part 1, 2 pts had herpes zoster (non-serious) and 3 pts had serious infections (SIs). In Part 2, SIs occurred in 1 tofacitinib pt and 1 PBO pt. No pts died. Conclusion: In pcJIA pts, tofacitinib vs PBO resulted in significantly fewer disease flares, and improved time to flare, disease activity and physical functioning. Tofacitinib safety was consistent with that in RA pts. Table. Safety in all pts Part 1 Part 2 Tofacitinib a N=225 Tofacitinib a N=88 PBO N=85 Pts with events, n (%) AEs 153 (68.0) 68 (77.3) 63 (74.1) SAEs 7 (3.1) 1 (1.1) 2 (2.4) Permanent discontinuations due to AEs 26 (11.6) 16 (18.2) 29 (34.1) AEs of special interest  Death 0 0 0  Gastrointestinal perforation b 0 0 0  Hepatic event b 3 (1.3) 0 0  Herpes zoster (non-serious and serious) 2 (0.9) c 0 0  Interstitial lung disease b 0 0 0  Major adverse cardiovascular events b 0 0 0  Malignancy (including non-melanoma skin cancer) b 0 0 0  Macrophage activation syndrome b 0 0 0  Opportunistic infection b 0 0 0  SI 3 (1.3) 1 (1.1) d 1 (1.2)  Thrombotic event (deep vein thrombosis, pulmonary embolism b or arterial thromboembolism) 0 0 0  Tuberculosis b 0 0 0 a 5 mg BID or equivalent weight-based lower dose in pts 〈 40 kg b Adjudicated events c Both non-serious d One SAE of pilonidal cyst repair was coded to surgical procedures instead of infections, and was inadvertently not identified as an SI. Following adjudication, the SAE did not meet opportunistic infection criteria; it is also included in the table as an SI AE, adverse event; BID, twice daily; PBO, placebo; pts, patients; SAE, serious AE; SI, serious infection Acknowledgments: Study sponsored by Pfizer Inc. Medical writing support was provided by Sarah Piggott of CMC Connect and funded by Pfizer Inc. Disclosure of Interests: Nicolino Ruperto Grant/research support from: Bristol-Myers Squibb, Eli Lily, F Hoffmann-La Roche, GlaxoSmithKline, Janssen, Novartis, Pfizer, Sobi (paid to institution), Consultant of: Ablynx, AbbVie, AstraZeneca-Medimmune, Biogen, Boehringer Ingelheim, Bristol-Myers Squibb, Eli Lily, EMD Serono, GlaxoSmithKline, Hoffmann-La Roche, Janssen, Merck, Novartis, Pfizer, R-Pharma, Sanofi, Servier, Sinergie, Sobi, Takeda, Speakers bureau: Ablynx, AbbVie, AstraZeneca-Medimmune, Biogen, Boehringer Ingelheim, Bristol-Myers Squibb, Eli Lily, EMD Serono, GlaxoSmithKline, Hoffmann-La Roche, Janssen, Merck, Novartis, Pfizer, R-Pharma, Sanofi, Servier, Sinergie, Sobi, Takeda, Olga Synoverska Speakers bureau: Sanofi, Tracy Ting: None declared, Carlos Abud-Mendoza Speakers bureau: Eli Lilly, Pfizer Inc, Alberto Spindler Speakers bureau: Eli Lilly, Yulia Vyzhga Grant/research support from: Pfizer Inc, Katherine Marzan Grant/research support from: Novartis, Vladimir Keltsev: None declared, Irit Tirosh: None declared, Lisa Imundo: None declared, Rita Jerath: None declared, Daniel Kingsbury: None declared, Betül Sözeri: None declared, Sheetal Vora: None declared, Sampath Prahalad Grant/research support from: Novartis, Elena Zholobova Grant/research support from: Novartis and Pfizer Inc, Speakers bureau: AbbVie, Novartis, Pfizer Inc and Roche, Yonatan Butbul Aviel: None declared, Vyacheslav Chasnyk: None declared, Melissa Lerman Grant/research support from: Amgen, Kabita Nanda Grant/research support from: Abbott, AbbVie, Amgen and Roche, Heinrike Schmeling Grant/research support from: Janssen, Pfizer Inc, Roche and USB Bioscience, Heather Tory: None declared, Yosef Uziel Speakers bureau: Pfizer Inc, Diego O Viola Grant/research support from: Bristol-Myers Squibb, GSK, Janssen and Pfizer Inc, Speakers bureau: AbbVie and Bristol-Myers Squibb, Holly Posner Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, Keith Kanik Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, Ann Wouters Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, Cheng Chang Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, Richard Zhang Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, Irina Lazariciu Consultant of: Pfizer Inc, Employee of: IQVIA, Ming-Ann Hsu Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, Ricardo Suehiro Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, Alberto Martini Consultant of: AbbVie, Eli Lily, EMD Serono, Janssen, Novartis, Pfizer, UCB, Daniel J Lovell Consultant of: Abbott (consulting and PI), AbbVie (PI), Amgen (consultant and DSMC Chairperson), AstraZeneca, Boehringer Ingelheim, Bristol-Myers Squibb (PI), Celgene, Forest Research (DSMB Chairman), GlaxoSmithKline, Hoffman-La Roche, Janssen (co-PI), Novartis (consultant and PI), Pfizer (consultant and PI), Roche (PI), Takeda, UBC (consultant and PI), Wyeth, Employee of: Cincinnati Children’s Hospital Medical Center, Speakers bureau: Wyeth, Hermine Brunner Consultant of: Hoffman-La Roche, Novartis, Pfizer, Sanofi Aventis, Merck Serono, AbbVie, Amgen, Alter, AstraZeneca, Baxalta Biosimilars, Biogen Idec, Boehringer, Bristol-Myers Squibb, Celgene, EMD Serono, Janssen, MedImmune, Novartis, Pfizer, and UCB Biosciences, Speakers bureau: GSK, Roche, and Novartis

Type of Medium: Online Resource

ISSN: 0003-4967 , 1468-2060

URL: Article

DOI: 10.1136/annrheumdis-2020-eular.396

Language: English

Publisher: BMJ

Publication Date: 2020

detail.hit.zdb_id: 1481557-6

In: Annals of the Rheumatic Diseases, BMJ, Vol. 72, No. Suppl 3 ( 2013-06), p. A516.2-A517

Type of Medium: Online Resource

ISSN: 0003-4967 , 1468-2060

URL: Article

DOI: 10.1136/annrheumdis-2013-eular.1548

Language: English

Publisher: BMJ

Publication Date: 2013

detail.hit.zdb_id: 1481557-6

In: Lupus, SAGE Publications, Vol. 25, No. 12 ( 2016-10), p. 1349-1356

Abstract: The objective of this study was to determine dental caries frequency and to analyze salivary and bacterial factors associated with active and inactive systemic lupus erythematous (SLE) patients. Also, a proposal to identify dental caries by a surface, teeth, and the patient was developed. Material and methods A cross-sectional, blinded study that included 60 SLE patients divided into two groups of 30 subjects each, according to the Activity Index for Diagnosis of Systemic Lupus Erythematous (SLEDAI). The decayed, missing, and filled teeth (DMFT) index and Integrative Dental Caries Index (IDCI) were used for analyzing dental caries. The saliva variables recorded were: flow, pH, and buffer capacity. The DNA copies of Streptococcus mutans and Streptococcus sobrinus were estimated by real-time PCR. Results The caries frequency was 85% for SLE subjects (73.3% for inactive systemic lupus erythematous (ISLE) and 100% for active systemic lupus erythematous (ASLE)); DMFT for the SLE group was 12.6 ± 5.7 and the IDCI was (9.8 ± 5.9). The ASLE group showed a salivary flow of 0.65 compared with 0.97 ml/1 min from the ISLE group; all variables mentioned above showed a statistical difference ( p  〈  0.05). The salivary pH was 4.6 (6.06 for ISLE and 3.9 for ASLE). The DNA copies of S. mutans and S. sobrinus were high; all variables mentioned above show a significant statistical difference ( p  〈  0.05) between groups. Conclusion SLE patients had high DMFT and IDCI scores that were associated with a decrease in salivary flow, pH, and buffer capacity. There were high counts of S. sobrinus and S. mutans species, and IDCI is a useful tool to provide more detail about dental caries in epidemiological studies.

Type of Medium: Online Resource

ISSN: 0961-2033 , 1477-0962

URL: Article

DOI: 10.1177/0961203316640909

Language: English

Publisher: SAGE Publications

Publication Date: 2016

detail.hit.zdb_id: 2008035-9