Publications by authors named "Muhammad S Soyfoo"

24 Publications

  • Page 1 of 1

Soluble ST2 is increased in systemic lupus erythematous and is a potential marker of lupus nephritis.

Clin Exp Rheumatol 2021 Jun 8. Epub 2021 Jun 8.

Department of Rheumatology, Hôpital Erasme, Université Libre de Bruxelles, Belgium.

Objectives: To investigate the role of the interleukin IL-33/ST2 axis in systemic lupus erythematosus (SLE).

Methods: Serum concentrations of IL-33 and sST2 were measured by sandwich ELISA in SLE patients (n=111) compared to sex- and age-matched healthy controls (n=36). The serum concentrations of IL-33 and sST2 were correlated with various clinical and biological parameters. The expressions of IL-33 and ST2L were investigated in kidney sections by immunohistochemistry in lupus nephritis patients (n=23) and controls (n=10).

Results: Serum levels of IL-33 were significantly higher in SLE patients (11.64±3.141 pg/mL) than in controls (1.043±0.8526 pg/mL) (p<0.0001). Similarly, the serum concentrations of sST2 were significantly higher in SLE patients (34.013±2.043 pg/mL) than in controls (25.278±2.258 pg/mL) (p=0.046). sST2, but not IL-33, correlated significantly with disease activity index (SLEDAI). In addition, serum levels of sST2 were significantly higher in patients with lupus nephritis (45.438±5.661 pg/mL) that in SLE patients without renal involvement (30.691±1.941 pg/mL) (p=0.016). The immunoreactivity of IL-33 in renal biopsies of patients with lupus nephritis was not increased compared to controls, while the glomerular expression of ST2L was significantly higher in nephritis patients compared to controls.

Conclusions: Although IL-33 and sST2 levels are both increased in SLE, sST2 represents a surrogate marker of disease activity and complications of nephritis.
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June 2021

Pathophysiologic role of Interleukin-33/ST2 in Sjögren's syndrome.

Autoimmun Rev 2021 Mar 18;20(3):102756. Epub 2021 Jan 18.

URPhyM - NARILIS, Université de Namur, Belgium.

Interleukin-33 (IL-33) is a member of the IL-1 family and has dual functions as a nuclear factor as well as a cytokine. The pivotal role of IL-33 as an active player contributing to aberrant local and systemic damage has been highlighted in several inflammatory and autoimmune diseases. Primary Sjögren's syndrome (pSS) is an autoimmune disease characterized by dry eyes and mouth syndrome due to local dysfunctions of exocrine glands, but also accompanied with systemic manifestations. The pathophysiology of pSS has been advocated as a conjecture of activated B and T cells as well as the production of inflammatory cytokines and autoantibodies, driving epithelial tissue damage and disease progression. In pSS, IL-33 is released in the extracellular space from damaged salivary cells upon pro-inflammatory stimuli and/or dysfunction of epithelial barrier. Counter-regulatory mechanisms are initiated to limit the pro-inflammatory actions of IL-33 as portrayed by an increase in the decoy receptor for IL-33, the soluble form of ST2 (sST2). In pSS and associated diseases, the levels of IL-33 are significantly elevated in the serum or tears of patients. Mechanistically, IL-33 acts in synergy with IL-12 and IL-23 on NK and NKT cells to boost the production of IFN-γ contributing to inflammation. TNF-α, IL-1β and IFN-γ in turn further increase the activation of IL-33/ST2 pathway, thereby constituting a vicious inflammatory loop leading to disease exacerbation. IL-33/ST2 axis is involved in Sjögren's syndrome and opens new perspectives as therapeutic target of one of the culprits in the inflammatory perpetuation.
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http://dx.doi.org/10.1016/j.autrev.2021.102756DOI Listing
March 2021

Clinical course of COVID-19 infection in inflammatory rheumatological patients: a monocentric Belgian experience.

Rheumatol Adv Pract 2020 5;4(2):rkaa055. Epub 2020 Nov 5.

Service de rhumatologie, Cliniques universitaires de Bruxelles - HÔpital Erasme, Université libre de Bruxelles (ULB), Brussels, Belgium.

Objective: Little is known about the incidence and consequences of coronavirus disease 2019 (COVID-19) infection in patients with rheumatic diseases. To improve our knowledge in this field, we collected data from patients with inflammatory rheumatic diseases who developed COVID-19 infection.

Methods: We performed a monocentric observational longitudinal study and collected data retrospectively from patients with inflammatory rheumatic diseases who developed a confirmed or suspected COVID-19 infection between 3 March and 10 June 2020.

Results: A total of 23 patients developed COVID-19 infection. Seven patients needed hospitalization [female 57%, mean age 59 +/- 9 years], and 16 patients were followed as outpatients [female 80%, mean age 50  +/- 14 years]. All hospitalized patients had more than one co-morbidity. At the time of infection, all patients were on immunosuppressive therapy consisting of either conventional synthetic DMARDs and/or biotherapy, with or without CSs. A minority received Corticoids (CSs) only. The most common symptoms of COVID-19-infected patients were fever, dyspnoea, cough and fatigue. PCR and chest CT were performed in all hospitalized patients to confirm the diagnosis (100% positive PCR, 71% positive CT). All outclinic patients were diagnosed clinically (confirmed by PCR in only one). The mean length of hospital stay was 21 +/- 19 days. Three patients developed an ARDS, including one who died.

Conclusion: A limited number of patients with inflammatory rheumatic diseases suffered from COVID-19 infection. Two patients needed mechanical ventilation and survived, whereas one patient died. All patients with a severe form of infection had at least one co-morbidity.
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http://dx.doi.org/10.1093/rap/rkaa055DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7661841PMC
November 2020

A Training Tool to support the management and diagnosis of Sjögren's syndrome.

Clin Exp Rheumatol 2020 Jul-Aug;38 Suppl 126(4):174-179. Epub 2020 Oct 23.

Biomedical Informatics & eHealth Laboratory, Department of Electrical and Computer Engineering, School of Engineering, Hellenic Mediterranean University, Crete, and Computational BioMedicine Laboratory (CBML), Institute of Computer Science (ICS), Foundation for Research and Technology Hellas (FORTH), Greece.

Objectives: The objective of this work is to present a Training Tool designed to support healthcare professionals involved in the diagnosis and management of Sjögren's syndrome.

Methods: The Training Tool aims to fulfil the gap of targeted education by providing a structured protocol of training including state of the art guidelines and practices. For the development of the Training Tool, latest relevant technologies have been used to assure efficiency and usability. Core functionalities include training by a series of multimedia courses, testing during the learning process, and profiling for monitoring the progress. An iterative requirement analysis process was established involving a large number of clinical experts, with the objective to identify user's training needs.

Results: Comprehensive usability evaluation was performed by applying, an Unmoderated Remote Usability Test resulting to 97.2% Success Rate; and the well-established System Usability Scale, reaching a score of 90.4 which classifies the Training Tool as "A" graded-excellent.

Conclusions: The Training Tool offers open-online training of healthcare professionals involved in the diagnosis and management of Sjögren's syndrome, using a well-designed training protocol in highly usable manner. To our knowledge, this is the first such tool for Sjögren's syndrome.
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October 2020

Non traumatic osteonecrosis of the femoral head is associated with low bone mass.

Bone 2018 02 14;107:88-92. Epub 2017 Nov 14.

Department of Rheumatology, CHU Sart Tilman, Université de Liège (Ulg) and Hôpital de Braine l'Alleud, CHIREC, Belgium.

Objective: Osteoporosis (OP) and osteonecrosis of the femoral head (ONFH) share common clinical and pathophysiological features we sought to determine whether ONFH was associated with an increased prevalence of OP and whether the increased prevalence of OP was related to the stage of ONFH at diagnosis.

Methods: We included 243 patients with ONFH and 399 age and sex-matched healthy controls. Data was gathered including demography, risk factors, ARCO staging of ONFH and bone mineral density (BMD).

Results: Overall, BMD (defined by the T-score) was significantly lower in the ONFH group at both the femoral head (-0.96±1.11) and the lumbar spine (-1.22±1.47) compared to the control group (-0.55±0.97 and -0.73±1.31) (p<0.01). The ONFH group depicted a significantly higher proportion of osteopenia (50.39% vs 40.87%, p=0.027) and of OP (18.78% vs 7.33%, p<0.001) relative to the control group. Stage 1 and 2 ONFH patients (53.86%, p=0.0203; OR=1.54 (95% CI: [1.04; 2.29])) were at a higher risk of osteopenia than the control group (40.88%), but not stages 3 or 4 (48.47%, p=0.2569; OR=1.27 (95% CI: [0.78; 2.06]). Patients with stage 3 or 4 ONFH (25.31%, p<0.001; OR=3.93 (95% CI: [1.63; 10.96])) were at a higher risk of osteoporosis than patients in the stage 1 and 2 ONFH (7.24%), and compared to the control group (7.33%, adj. p-value<0.001; OR=4.89 (95% CI: [2.77; 8.76]).

Conclusions: Non-traumatic osteonecrosis of the femoral heads is associated with low bone mineral density. This study showed that fractural stages ONFH were associated with a 5-fold risk of osteoporosis.
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http://dx.doi.org/10.1016/j.bone.2017.11.005DOI Listing
February 2018

Efficacy of golimumab in Belgian patients with active rheumatoid arthritis despite treatment with non-biologic disease-modifying anti-rheumatic drugs: sub-analysis of the GO-MORE study.

Acta Clin Belg 2017 12 21;72(6):424-428. Epub 2017 Apr 21.

f UH & MUMC & ReumaClinic , Genk , Belgium.

Objectives: The GO-MORE trial (NCT00975130) was a phase 3 study in 40 countries evaluating the efficacy and safety of golimumab as add-on therapy in biologic-naïve adults with active rheumatoid arthritis despite stable treatment with disease-modifying anti-rheumatic drugs. To inform local practice in Belgium and examine the role of baseline disease activity in treatment response, we compared the efficacy of golimumab in the Belgian subpopulation and the rest of the world.

Methods: Baseline disease activity and six-month efficacy rates in the GO-MORE trial were compared for the Belgian subpopulation and the rest of the world by t-tests and chi-squared tests.

Results: Except for functional impairment, all measures of baseline disease activity were significantly lower (p < 0.0001) in the Belgian population (n = 123) than in the rest of the world (n = 3157). At month six, the rate of good/moderate EULAR response was similar in Belgium and the rest of the world (78.9% vs. 82.2%; p = 0.34), but remission rates were higher in Belgium according to the DAS28-ESR (43.1% vs. 23.2%; p < 0.0001) and Simplified Disease Activity Index (22.0% vs. 13.8%; p = 0.01). Rates of low DAS28-ESR disease activity were also higher in Belgium (54.5% vs. 36.8%; p < 0.0001). Within the Belgian subpopulation, efficacy measures were not significantly different between patients with moderate (n = 73) and high baseline activity (n = 49). Rates of functional impairment at month six did not differ between the two populations.

Conclusion: In the Belgian population of the GO-MORE trial, baseline disease activity was lower and six-month remission rates were higher than in the rest of the world.
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http://dx.doi.org/10.1080/17843286.2017.1314079DOI Listing
December 2017

Value of non-identified ANCA (non-PR3, non-MPO) in the diagnosis of granulomatosis with polyangiitis (Wegener's granulomatosis).

Acta Clin Belg 2017 Oct 9;72(5):313-317. Epub 2017 Jan 9.

a Department of Rheumatology , Hôpital Erasme, Université Libre de Bruxelles , Bruxelles , Belgium.

Objective: Determine the frequency of granulomatosis with polyangiitis (GPA) associated with non-identified ANCA (non-MPO, non-PR3 ANCA) and secondarily compare their clinic with GPA associated with MPO-positive or PR3-positive ANCA.

Methods: In a monocentric retrospective observational study, clinical data of 398 patients with non-identified ANCA (titer of ANCA at least 1/80 by immunofluorescence on ethanol fixed PMN) was gathered over a period of 6 years. GPA patients from this population were compared with GPA patients with identified ANCA on the basis of clinical, biological, immunological and histological features.

Results: The most common diseases associated with non-identified ANCA were inflammatory bowel diseases accounting for 17% of diseases. GPA accounted for only 1.8% of cases. There were no significant differences in terms of clinical and histological characteristics between GPA with non-identified ANCA and GPA with identified ANCA, but significantly higher CRP levels were observed in GPA patients with identified ANCA (p = 0.005). Localized disease (ear, nose and throat and/or lung involvement without any other systemic involvement) was more frequent in the group of GPA with nonidentified ANCA (p = 0.047) as compared to GPA with identified ANCA. This explains that the former group of patients was less frequently treated by cyclophosphamide than the latter (p = 0.016).

Conclusion: GPA with non-MPO, non-PR3 ANCAs is relatively rare. Our study suggests that GPA with nonidentified ANCA differs from GPA with identified ANCA by the frequency of localized forms.
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http://dx.doi.org/10.1080/17843286.2016.1275374DOI Listing
October 2017

Phagocyte-specific S100A8/A9 is upregulated in primary Sjögren's syndrome and triggers the secretion of pro-inflammatory cytokines in vitro.

Clin Exp Rheumatol 2017 Jan-Feb;35(1):129-136. Epub 2016 Oct 7.

Department of Rheumatology, Hôpital Erasme and Laboratory of Bone and Metabolic Biochemistry, Faculty of Medicine, Université Libre de Bruxelles, Belgium.

Objectives: To determine the role of S100A8/A9 in the pathogenesis of primary Sjögren's syndrome (pSS).

Methods: The serum levels of S100A8/A9 were determined in pSS patients and healthy controls by ELISA. The expression of S100A8/A9 in salivary glands was assessed by immunohistochemistry. The phenotype of S100A8+ and S100A9+ cells was identified using double immunofluorescence. The effects of S100A8/A9 on cytokine production by peripheral blood mononuclear cells (PBMCs) from pSS patients were determined in vitro by flow cytometry. The effects of pro-inflammatory cytokines on S100A8/A9 secretion were additionally investigated in vitro by ELISA in PBMCs from pSS patients and control subjects.

Results: Serum levels of S100A8/A9 were significantly increased in pSS patients compared to healthy controls. The tissular expression of S100A8 and S100A9, identified in professional phagocytes (neutrophils, monocytes and plasmacytoid dendritic cells), was increased in the salivary glands of pSS patients and correlated with focus score. In vitro, recombinant S100A8/A9 increased the production of IL-1β, IL-6, TNF-α, IFN-γ, IL-10, IL-17A and IL-22 by PBMCs. The S100A8/A9-induced increase in TNF-α production in pSS patients was significant relative to controls. Furthermore, IL-1β, TNF-α, IL-6, and IL-17A stimulated release of S100A8/A9 from PBMCs in pSS patients.

Conclusions: S100A8/A9 is increased in pSS patients contributing to the in vitro increased production of pro-inflammatory cytokines. As such, S100A8/A9 in concert with other cytokines might contribute to the pathogenesis of pSS.
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June 2017

Successful treatment of tumor necrosis factor receptor-associated periodic syndrome (TRAPS) with tocilizumab: A case report.

Eur J Rheumatol 2015 Mar 1;2(1):35-36. Epub 2015 Mar 1.

Department of Rheumatology, Hôpital Erasme, Université Libre de Bruxelles, Brussels, Belgium.

Tumor necrosis factor receptor-associated periodic syndrome (TRAPS) is an autosomal dominant autoinflammatory disease linked to chromosome 12p13 and, more specifically, with mutations within the tumor necrosis factor receptor superfamily, member 1A gene (TNFRSF1A gene). It is characterized by the presence of fever, abdominal pain, myalgia, arthralgia or arthritis, and skin rash. In this report, we describe the case of a patient with tumor necrosis factor receptor-associated periodic syndrome (TRAPS) treated successfully with the anti-interleukin-6 (anti-IL-6) receptor monoclonal antibody tocilizumab, while treatment with anti-TNF α etanercept and infliximab had both failed.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5047242PMC
http://dx.doi.org/10.5152/eurjrheumatol.2014.14053DOI Listing
March 2015

Adenosine triphosphate prevents serum deprivation-induced apoptosis in human mesenchymal stem cells via activation of the MAPK signaling pathways.

Stem Cells 2015 Jan;33(1):211-8

Laboratory of Bone and Metabolic Biochemistry, Faculty of Medicine, Université libre de Bruxelles, Brussels, Belgium.

Human mesenchymal stem cells (hMSC) are multipotent cells derived from various sources including adipose and placental tissues as well as bone marrow. Owing to their regenerative and immunomodulatory properties, their use as a potential therapeutic tool is being extensively tested. However, one of the major hurdles in using cell-based therapy is the use of fetal bovine serum that can trigger immune responses, viral and prion diseases. The development of a culture medium devoid of serum while preserving cell viability is therefore a major challenge. In this study, we demonstrated that adenosine triphosphate (ATP) restrained serum deprivation-induced cell death in hMSC by preventing caspases 3/7 activation and modulating ERK1/2 and p38 MAPK signaling pathways. We also showed that serum deprivation conditions triggered dephosphorylation of the proapoptotic protein Bad leading to cell death. Adjunction of ATP restored the phosphorylation state of Bad. Furthermore, ATP significantly modulated the expression of proapoptopic and antiapoptotic genes, in favor of an antiapoptotic profile expression. Finally, we established that hMSC released a high amount of ATP in the extracellular medium when cultured in a serum-free medium. Collectively, our results demonstrate that ATP favors hMSC viability in serum deprivation conditions. Moreover, they shed light on the cardinal role of the MAPK pathways, ERK1/2 and p38 MAPK, in promoting hMSC survival.
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http://dx.doi.org/10.1002/stem.1831DOI Listing
January 2015

Potential involvement of the IL-33-ST2 axis in the pathogenesis of primary Sjogren's syndrome.

Ann Rheum Dis 2014 Jun 2;73(6):1259-63. Epub 2014 Jan 2.

Department of Rheumatology and Physical Medicine, Hôpital Erasme, Université Libre de Bruxelles, , Brussels, Belgium.

Objectives: To investigate the role of the interleukin (IL)-33-ST2 axis in the pathophysiology of primary Sjögren's syndrome (pSS).

Methods: Serum levels of IL-33 and sST2 were determined by ELISA. The expression of IL-33 and ST2 was investigated in salivary glands (SG) by immunohistochemistry. PBMC were isolated and stimulated with IL-33, IL-12 and IL-23 and the cytokine profile response was examined by flow cytometry. Intracellular cytokine detection of IFNγ and IL-17 was performed by flow cytometry.

Results: Serum IL-33 and sST2 levels were increased in pSS patients compared with controls and patients with systemic lupus erythematosus. Expression of IL-33 was upregulated in SG with Chisholm scores of 2 and 3 of pSS patients but comparable with controls for SG with Chisholm score of 4. ST2 expression in SG was downregulated in pSS patients. IL-33 at different concentrations did not increase the secretion of pro-inflammatory cytokines but acted synergistically with IL-12 and IL-23 to promote IFNγ production. NK and NKT cells were identified as main producers of IFNγ in vitro and were found in SG of pSS patients.

Conclusions: IL-33 is released in pSS, and acts with IL-12 and IL-23 to favour the secretion of IFNγ by NK and NKT cells.
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http://dx.doi.org/10.1136/annrheumdis-2012-203187DOI Listing
June 2014

Cryofibrinogen levels are increased in non-traumatic osteonecrosis: a new pathogenic clue to osteonecrosis?

Rheumatology (Oxford) 2013 Sep 17;52(9):1694-700. Epub 2013 Jun 17.

Department of Rheumatology, Hôpital Erasme, Université Libre de Bruxelles, Brussels, Belgium.

Objective: To determine whether levels of cryofibrinogen are increased in non-traumatic osteonecrosis (ON) and could correlate with disease staging.

Methods: We prospectively analysed cryofibrinogen levels by immunofixation electrophoresis in 50 patients with non-traumatic ON, 50 healthy volunteers and 8 patients with traumatic ON. Staging of disease involving the femoral heads and the size of necrotic lesions were assessed by the Association Research Circulation Osseous (ARCO) classification system.

Results: Mean cryofibrinogen levels in patients with non-traumatic ON were significantly increased relative to healthy controls and to patients with traumatic ON (222.1 ± 20.6, 59.9 ± 5.6 and 52.3 ± 14.9 mg/dl, respectively, P < 0.001). In the non-traumatic ON group, mean cryofibrinogen levels were significantly increased in patients with multifocal ON compared with patients with mono/bifocal ON (276.5 ± 56.5 and 149.3 ± 15.4 mg/dl, respectively, P = 0.03). There were no significant differences in cryofibrinogen levels observed with respect to the size of the necrotic lesions involving the femoral heads. Moreover, cryofibrinogen levels in patients with ON of the femoral heads classified according to the stage of disease were not significantly different between patients with stage 1/2 and patients with stage 3 ON (179.2 ± 31.3 vs 204.1 ± 29.0 mg/dl, respectively; P = 0.813).

Conclusion: Cryofibrinogen levels are increased in non-traumatic ON and, more importantly, in multifocal ON. The fact that cryofibrinogen levels are not correlated with the size of lesions and the stage of disease could imply systemic rather than local involvement characterizing the pathogenesis of ON.
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http://dx.doi.org/10.1093/rheumatology/ket208DOI Listing
September 2013

Diffuse Muscular Pain, Skin Tightening, and Nodular Regenerative Hyperplasia Revealing Paraneoplastic Amyopathic Dermatomyositis due to Testicular Cancer.

Case Rep Rheumatol 2012 17;2012:534236. Epub 2012 Dec 17.

Department of Dermatology, Hôpital Erasme, Université Libre de Bruxelles, 1070 Bruxelles, Belgium.

Paraneoplastic dermatomyositis (DM) associated with testicular cancer is extremely rare. We report the case of a patient with skin tightening, polymyalgia, hypereosinophilia, and nodular regenerative hyperplasia revealing seminoma and associated paraneoplastic DM.
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http://dx.doi.org/10.1155/2012/534236DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3534208PMC
January 2013

Clinical significance of Cryofibrinogenemia: possible pathophysiological link with Raynaud's phenomenon.

J Rheumatol 2012 Jan 15;39(1):119-24. Epub 2011 Nov 15.

Department of Rheumatology, Erasme Hospital, Université Libre de Bruxelles, 808 Route de Lennik, 1070 Brussels, Belgium.

Objective: To describe the clinical findings and prevalence of patients with cryofibrinogenemia (CF) and to determine whether CF is associated with primary Raynaud's phenomenon.

Methods: Between June 2006 and December 2009, 227 patients were tested for CF in a single university hospital. Forty-five patients with primary Raynaud's phenomenon were tested for CF.

Results: A total of 117 patients with CF without cryoglobulinemia were included. The main clinical manifestations included skin manifestations (50%) and arthralgia (35%). There were 67 patients with primary CF and 50 patients with secondary CF. There was no significant difference in the mean concentration of the cryoprecipitate in primary CF as compared to the secondary form (172 ± 18.6 vs 192 ± 20.9 mg/dl, respectively; p = 0.41). Highest concentrations of cryoprecipitate were observed in those containing fibrinogen only as compared to cryoprecipitates containing fibrinogen and fibronectin (301 ± 43.5 vs 125 ± 10.6 mg/dl; p < 0.001). Patients having skin necrosis (n = 3) had significantly higher values of cryofibrinogen compared to those without necrosis (638 ± 105 vs 160 ± 10.2 mg/dl; p = 0.0046). Among the 45 patients with primary Raynaud's phenomenon, 36 had associated CF. There was no significant difference in the mean concentration of the cryoprecipitate in these patients compared to those with primary CF.

Conclusion: There seems to be a significant correlation between cryofibrinogen concentration and the severity of the clinical signs, particularly when cryoprecipitate is composed of fibrinogen alone. CF might have a possible pathophysiological role in primary Raynaud's phenomenon.
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http://dx.doi.org/10.3899/jrheum.110793DOI Listing
January 2012

Parotid Gland Biopsy as an Additional Diagnostic Tool for Supporting the Diagnosis of Sjögren's Syndrome.

Int J Rheumatol 2011 7;2011:302527. Epub 2011 Aug 7.

Department of Rheumatology, Erasme Hospital, 808 Route de Lennik, 1070 Brussels, Belgium.

Sjögren's syndrome (SS) is an autoimmune disease characterized by keratoconjunctivitis sicca and xerostomia. There are actually no diagnostic criteria for SS, but classification criteria based on the revised American-European criteria have been elaborated. These include subjective criteria: ocular and oral symptoms, and objective criteria: ocular, histopathological, oral, and serological signs. SS is considered if 4 of the 6 criteria are present, when histopathology or serology is positive, or if 3 of any 4 objective criteria are present. A patient presented with both ocular and oral symptoms and signs but did not meet the SS classification criteria. Indeed, no anti-SSA or anti-SSB antibodies were detected, and minor salivary gland biopsy was normal. To further understand the origin of the sicca symptoms, a parotid gland biopsy was performed and showed important lymphocytic infiltrates. This could account for the sicca symptoms and signs since parotid glands are one the major contributors to salivary flow. Therefore, parotid gland biopsy could be a useful asset for the diagnosis of SS.
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http://dx.doi.org/10.1155/2011/302527DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3154392PMC
November 2011

Cricoarytenoiditis as an initial manifestation of systemic lupus erythematosus.

Case Rep Rheumatol 2011 7;2011:317379. Epub 2011 Sep 7.

Department of Internal Medicine, Erasme Hospital, Université Libre de Bruxelles, 1070 Brussels, Belgium.

Systemic lupus erythematosus (SLE) is a chronic inflammatory disease encompassing a broadened spectrum of clinical manifestations. Vocal cords involvement in SLE is not a frequent entity but can be life threatening if not treated. We hereby report the case of a patient presenting with cricoarytenoiditis and vocal cord dysfunction revealing SLE.
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http://dx.doi.org/10.1155/2011/317379DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3420570PMC
August 2012

Disseminated tuberculosis mimicking ankylosing spondylitis.

Case Rep Rheumatol 2011 6;2011:195085. Epub 2011 Sep 6.

Department of Nuclear Medicine, Hôpital Erasme, Université Libre de Bruxelles (ULB), 1070 Brussels, Belgium.

Ankylosing spondylitis is a chronic inflammatory disorder affecting mainly the axial skeleton. Here we report a case of a man with a clinical suspicion of ankylosing spondylitis but with a persistence of increased inflammatory markers. In this case, (18)F-FDG-PET/CT revealed multiple hypermetabolic lesions in axial skeleton, lymph nodes, and the lung, suggestive of either disseminated tuberculosis or lymphoma. Histological analysis of the pulmonary lesion revealed mycobacterium tuberculosis. This case highlights, firstly, the importance of excluding other diagnoses in the presence of clinical picture of ankylosing spondylitis and high inflammatory markers and, secondly, the determining role of PET/CT.
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http://dx.doi.org/10.1155/2011/195085DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3420786PMC
August 2012

Pericarditis revealing large vessel vasculitis.

ISRN Rheumatol 2011 22;2011:648703. Epub 2011 Jun 22.

Department of Internal Medicine, Erasme Hospital, Université Libre de Bruxelles, 1070 Bruxelles, Belgium.

Large vessels vasculitis and more specifically, Giant cell arteritis, is characterized by increased inflammatory markers, headaches and altered clinical status. Diagnosis is confirmed by biopsy of temporal arteries showing the presence of granuloma and vasculitis. We hereby report the case of a patient presenting initially as pericarditis and revealing large vessel vasculitis using FDG-PET.
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http://dx.doi.org/10.5402/2011/648703DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3263740PMC
August 2012

Phagocyte-specific S100A8/A9 protein levels during disease exacerbations and infections in systemic lupus erythematosus.

J Rheumatol 2009 Oct 15;36(10):2190-4. Epub 2009 Sep 15.

Department of Rheumatology, Erasme Hospital, Université Libre de Bruxelles, 808 route de Lennik, 1070, Bruxelles, Belgium.

Objective: S100A8 and S100A9 are calcium binding proteins of the S100 family highly expressed in neutrophils and monocytes. S100 proteins are novel ligands of TLR4 important in modulating inflammation. High levels of S100A8/A9 found in human inflammatory diseases are a marker of disease activity in rheumatoid arthritis (RA) and juvenile rheumatoid arthritis (JRA). We determined levels of S100A8/A9 in sera of patients with systemic lupus erythematosus (SLE) and analyzed their relation to clinical variables of disease activity.

Methods: A group of 93 patients with SLE were studied over a period of 3 years, and 143 serum samples were analyzed. S100A8/A9 serum concentrations were determined by a sandwich ELISA. Sera from 10 primary Sjögren's syndrome (pSS) patients and 50 healthy volunteers were used as controls. Correlations to SLEDAI, ANA, anti-dsDNA, WBC, CH50, C4, and CRP were made. In addition, infections were recorded in all SLE patients.

Results: Serum levels of S100A8/A9 were significantly (p = 0.04) higher in SLE patients (1412 +/- 664 ng/ml) versus healthy controls (339 +/- 35 ng/ml) and pSS patients (400 +/- 85 ng/ml). The only significant correlation (r = 0.219; p = 0.015) was found was between S100A8/A9 and SLEDAI. Further, SLE patients with concomitant infections had higher serum levels of S100A8/A9 (39300 +/- 13375 ng/ml) than those without infections (1150 +/- 422 ng/ml).

Conclusion: Serum levels of S100A8/A9 are significantly raised in SLE versus pSS patients and healthy controls and can be correlated to a disease activity index. S100A8/A9 is a more relevant marker of infection in SLE patients.
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http://dx.doi.org/10.3899/jrheum.081302DOI Listing
October 2009

Expression of the electrogenic Na+-HCO3--cotransporters NBCe1-A and NBCe1-B in rat pancreatic islet cells.

Endocrine 2009 Jun 18;35(3):449-58. Epub 2009 Apr 18.

Laboratory of Biological Chemistry and Nutrition, Université Libre de Bruxelles, Brussels, Belgium.

It was recently proposed that, in rat pancreatic islets, the production of bicarbonate accounts for the major fraction of the carbon dioxide generated by the oxidative catabolism of nutrient insulin secretagogues. In search of the mechanism(s) supporting the membrane transport of bicarbonate, the possible role of the electrogenic Na(+)-HCO(3) (-)-cotransporters NBCe1-A and NBCe1-B in rat pancreatic islet cells was investigated. Expression of NBCe1-A and NBCe1-B in rat pancreatic islet cells was documented by RT-PCR, western blotting, and immunocytochemistry. The latter procedure suggested a preferential localization of NBCe1-B in insulin-producing cells. Tenidap (3-100 microM), previously proposed as an inhibitor of NBCe1-A-mediated cotransport in proximal tubule kidney cells, caused a concentration-related inhibition of glucose-stimulated insulin secretion. It also inhibited 2-ketoisocaproate-induced insulin release and to a relatively lesser extent, the secretory response to L: -leucine. Tenidap (50-100 microM) also inhibited the metabolism of D: -glucose in isolated islets, increased (22)Na net uptake by dispersed islet cells, lowered intracellular pH and provoked hyperpolarization of plasma membrane in insulin-producing cells. This study thus reveals the expression of the electrogenic Na(+)-HCO(3) (-)-cotransporters NBCe1-A and NBCe1-B in rat pancreatic islet cells, and is consistent with the participation of such transporters in the process of nutrient-stimulated insulin secretion.
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http://dx.doi.org/10.1007/s12020-009-9175-1DOI Listing
June 2009

Modified aquaporin 5 expression and distribution in submandibular glands from NOD mice displaying autoimmune exocrinopathy.

Arthritis Rheum 2007 Aug;56(8):2566-74

Laboratory of Biochemistry, Université Libre de Bruxelles, Route de Lennik 808, B-1070 Brussels, Belgium.

Objective: To investigate the expression and localization of aquaporin 5 (AQP5) in salivary glands and salivary gland function in the NOD mouse.

Methods: All experiments were performed using NOD and BALB/c mice (ages 8 weeks and 24 weeks). Real-time reverse transcription-polymerase chain reaction, Western blotting, and immunohistochemical analysis were used to study the expression and distribution of AQP5 in salivary glands. In addition, salivary gland function was determined.

Results: Compared with the levels in BALB/c mice, relative AQP5 messenger RNA levels were not significantly modified in the parotid glands from NOD mice of both ages but were significantly increased in the submandibular glands from NOD mice of both ages. Western blot analyses of both salivary gland membranes revealed that the level of AQP5 protein was increased in 24-week-old NOD mice. Important inflammatory infiltrates were observed in the submandibular glands, but not in the parotid glands, from 24-week-old NOD mice. The 8-week-old and 24-week-old BALB/c mice and the 8-week-old NOD mice showed AQP5 primarily at the apical membrane of the salivary gland acinus. In contrast, in acini from the submandibular glands (but not the parotid glands) from 24-week-old NOD mice, AQP5 staining was reduced at the apical membrane but was increased at the basal membrane. A moderately statistically significant decrease in pilocarpine-stimulated salivary flow was observed in 24-week-old NOD mice compared with that in age-matched BALB/c mice.

Conclusion: Submandibular glands from 24-week-old NOD mice displayed inflammatory infiltrates, increased AQP5 protein expression, and impaired AQP5 distribution. However, the moderately statistically significant decrease in the salivary flow rate in these mice did not match the extent of AQP5 misdistribution.
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http://dx.doi.org/10.1002/art.22826DOI Listing
August 2007
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