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ID PMID Title PublicationDate abstract
18757116 [Orofacial manifestations of systemic sclerosis: a study of 30 consecutive patients]. 2009 Jan INTRODUCTION: The face is frequently involved in systemic sclerosis. The main stomatologic manifestations include limited mouth opening, xerostomia, skin atrophy, trigeminal neuralgia. The objective of this study was to describe oral and facial manifestations observed in scleroderma patients from our cohort. METHODS: Between March and October 2006, a stomatologic consultation was included in the follow-up of scleroderma patients seen during consultation or daily hospital in internal medicine or dermatology units. Demographic, clinical and biological data were collected. Stomatologic examination comprised measure of the mouth opening, sugar's and Schirmer's tests, orthopantomogram analysis, and evaluation of the repercussion of symptoms on quality of life using a visual analogical scale (VAS between 0 and 10). RESULTS: This study included 30 patients (women 87%, mean age 58.6+/-13.6 years). Mean duration of systemic sclerosis (n=20 limited cutaneous form, n=10 diffuse form) was eight years. Stomatologic manifestations were: skin atrophy (n=28), peribuccal rhagades (n=25), telangiectasia (n=21), decreased mouth opening (n=20), xerostomia (n=20), xerophtalmia (n=16), periodontal ligament space widening (n=10), bone resorptions (n=2), trigeminal neuralgia (n=1). Xerostomia was considered more discomforting (mean VAS=3.8) than decreased mouth opening (mean VAS=2.6). Xerostomia was the second more discomforting sign of scleroderma and was significantly associated to the limited cutaneous form (p=0.045) and to anticentromeres antibodies expression (p=0.002). Decreased mouth opening was correlated to oesophageal involvement (p=0.025). CONCLUSION: Oral and facial manifestations are frequently observed in scleroderma patients. These manifestations lead to major functional discomfort, mainly due to decreased mouth opening that seems to be frequently associated to oesophageal involvement. Xerostomia is also frequent and is commonly observed in anticentromere antibodies positive cutaneous limited forms of systemic sclerosis. Evolution of radiographic abnormalities like periodontal ligament space widening (33% of cases), or osteolytic lesions (7%) is poorly known.
18677232 Tear lipocalin and lysozyme in Sjögren and non-Sjögren dry eye. 2008 Aug PURPOSE: To evaluate the concentration of tear lipocalin, lysozyme, and total protein in Sjögren's Syndrome (SS), non-Sjögren's keratoconjunctivitis sicca (KCS), and non-dry-eyed (NDE) individuals. METHODS: Seventy-six subjects were recruited for this study: 25 SS subjects; 25 KCS subjects, and 26 NDE individuals. Symptoms were measured with a visual analogue scale. Tear flow was measured by the Schirmer I test without anesthesia. Tears were collected using an eye wash technique. Total tear protein was quantified using the DC Protein Assay Kit. Tear lipocalin and lysozyme were quantified via Western blotting performed on a Phast System. RESULTS: By definition, the SS and KCS groups both had significantly lower mean Schirmer scores (5.12 +/- 5.96 mm and 7.84 +/- 7.35 mm) compared with the NDE group (23.83 +/- 7.85 mm; p < 0.0001). There was no difference in mean Schirmer scores between SS and KCS groups (p = 0.19). The tear film of the SS group was characterized by significantly reduced (p < 0.0001) total protein and lipocalin concentrations compared with both KCS and NDE groups. No difference between the KCS and NDE groups was found in total protein (p = 0.92) or lipocalin (p = 0.19) concentration. In contrast, the concentration of tear film lysozyme was found to be statistically similar in all three groups examined. No statistically significant correlation was found in any group between mean Schirmer values compared with total protein, lipocalin or lysozyme concentration. CONCLUSION: Our data demonstrate a biochemical distinction between the Sjögren's group compared with both KCS and control groups, in that both tear lipocalin and total tear protein were significantly reduced. Although correlations were not found between protein measurements and tear flow, a combination of tests including Schirmer I and quantitation of tear film biomarkers may allow for the identification of SS patients without the need for invasive testing.
17599665 Amicrobial pustulosis associated with IgA nephropathy and Sjögren's syndrome. 2007 Sep Amicrobial pustulosis is a rare clinical entity characterized by a relapsing pustular eruption, primarily involving the skin folds. We describe a case of amicrobial pustulosis associated with autoimmune diseases (APAD). The patient suffered from IgA nephropathy and Sjögren's syndrome. Skin symptoms were alleviated dramatically after corticosteroid pulse therapy and tonsillectomy.
19032812 Acinar epithelial cell laminin-receptors in labial salivary glands in Sjögren's syndrome. 2008 Sep OBJECTIVE: To analyze the epithelial cell-basement membrane attachment, in particular in the secretory end pieces (responsible for secretion of saliva) and in Sjögren's syndrome (SS) characterized by acinar cell failure. METHOD: Immunohistochemistry with laminin receptor chain-specific monoclonal antibodies to integrin (Int) subunits, Lutheran blood group antigen and alpha-dystroglycan. RESULTS: Only acinar cells contained Int alpha1 and alpha2 subunits. This staining was interrupted but strong in controls, but very weak in SS. Both acinar and ductal cells contained Int alpha3, alpha6, b1 and b4 and Lutheran blood group antigen and ductal cells also contained alpha-dystroglycan. These staining patterns were similar in SS and controls. CONCLUSIONS: Binding of the acinar and ductal cells to the basement membrane laminins seems to be mediated by Int alpha3b1, alpha6b1 and alpha6b4 integrin-receptors and Lutheran blood group antigen and alpha-dystroglycan non-integrin receptors. This structure-supporting system is intact in SS, compatible with the maintenance of the tubuloalveolar architecture of the SS glands. The irregular staining pattern of the acinus-specific Int alpha1b1 and alpha2b1 was compatible with a regulated signaling role, which was apparently impaired in SS. Indeed, their laminin counterparts (Lm -1/111 and -2/211) are also aberrant in SS revealing this as the central cell-matrix defect in the syndrome.
18612929 Fatigue and blood pressure in primary Sjogren's syndrome. 2008 Jul OBJECTIVE: Primary Sjogren's syndrome (SS) is an autoimmune disease characterized by fatigue. Little is known about the genesis of fatigue. Fatigue is thought to represent a multidimensional concept and it is important to be able to measure it confidently. The aims were to evaluate the reliability and validity of the 20-item Multidimensional Fatigue Inventory (MFI-20) in SS and to search for factors associated with this disabling symptom. METHODS: Forty-eight women with primary SS completed the MFI-20 questionnaire. The results were compared with age-matched women with fibromyalgia (FM) and healthy controls. Convergent construct validity was assessed by correlations to a Visual Analogue Scale (VAS) for global fatigue by Spearman's correlation (r(s)). Test-retest reliability was analysed by the intraclass correlation coefficient (ICC) in 28 women. Associations between clinical variables and subscales of the MFI-20 were analysed. RESULTS: The SS women scored significantly higher in all subscales of the MFI-20 compared to controls but similar to FM. The ICCs were satisfactory, ranging from 0.66 for general fatigue to 0.85 for the total score of MFI-20. All subscales correlated significantly to VAS for global fatigue, general fatigue showing the highest correlation (r(s) = 0.70). The estimated number of hours of sleep/day was significantly associated with many of the fatigue dimensions. All five subscales of the MFI-20 were inversely associated with diastolic blood pressure (BP) and two with systolic BP. CONCLUSIONS: The MFI-20 was found to be a reliable and valid tool for the measurement of fatigue in primary SS. High levels of fatigue were correlated with low BP, suggesting an associated involvement of the autonomic nervous system.
18325192 Hypokalaemic paralysis precipitated by distal renal tubular acidosis secondary to Sjögren 2008 Mar A 43-year-old woman presented with a sudden onset of hypokalaemic paralysis requiring intubation and ventilatory support. Subsequent biochemical and clinical assessments established a diagnosis of distal renal tubular acidosis (RTA) in association with underlying Sjögren's syndrome as the aetiology of her profound hypokalaemia. Distal RTA is rare, but Sjögren's syndrome is one of the more common causes in adults and should be considered in the differential diagnosis of patients who present with hypokalaemic muscular paralysis.
17992590 A conspicuous role for B cells In Sjögren's syndrome. 2007 Jun Although the relative contributions of T cells and B cells in Sjögren's syndrome (SS) are far from being settled, recent studies have suggested a crucial role for B cells in its pathophysiology. Early investigations have focused on the ability of B cells to produce autoantibodies, and new studies have enlarged the range of their functions. For example, beyond the paradigm that T lymphocytes maintain strict control over B cells, the latter cells are now acknowledged to solicit their own help from the former cells and release a flurry of cytokines. Further, some of these B cells act as antigen-presenting cells. Increased levels of the B cell activating factor (BAFF) found in SS may be responsible for high numbers of circulating Bm2/Bm2' cells and associated functional abnormalities of B cells, such as a BAFF-induced increased expression of CD19, which decreases the required strength generated by antigen binding for transmitting its signal. This review reports compelling evidence that B cells are involved in the pathophysiology of SS. As this brings novel prospects for the treatment of the disease, it is no surprise that B cell ablative treatment has proven to be relatively efficacious in SS.
17430794 [Shared and distinctive characteristics of systemic autoimmune disorders]. 2007 Apr 8 Systemic autoimmune disorders constitute a well-characterized and separate group of diseases in the field of clinical immunology and rheumatology. Despite their shared characteristics, these diseases have several distinctive features. The similarity and the difference are manifested both in etiology (i.e. the importance and ratio of genetic and environmental factors), in pathomechanism (i.e. the dominance of cellular or humoral immune response), in the disease outcome (fluctuating or chronic progressive) and in the diversity of clinical manifestations (i.e. multiple organ involvements or some dominant target organs/tissues). In the present work the authors describe the features of four prototypic autoimmune disorders - systemic lupus erythematosus, Sjogren's disease, dermato-polymyositis and systemic sclerosis - and characterise in general the common and particular specific points of systemic autoimmune disorders focusing on the variability and subgroups which can be observed even within certain diseases.
17233405 [A human T-cell lymphotropic virus type 1 carrier presenting with Sjögren's syndrome and 2006 Dec A 77-year-old asymptomatic woman was found to have a coin lesion on a chest radiograph. Chest computed tomography scans showed the coin lesion, bronchiectasis, tree-in-bud appearance, and ground glass opacity. The histopathology of the lung by video-assisted thoracic surgery showed organizing pneumonia, follicular bronchiolitis, and non-specific interstitial pneumonitis patterns, all of which consisted of mainly mature lymphocytes and plasma cells. She suffered from dry eyes and had a high level of serum anti-SS-A antibody. Examination of her eyes and mouth revealed Sjögren's syndrome. The patient herself and her parents were born in Nagasaki prefecture, an area where human T-cell lymphotropic virus type 1 (HTLV-1) is endemic, and her sister suffered from a hematological malignancy. She was found to be an HTLV-1 carrier. We finally made a diagnosis of an HTLV-1 carrier presenting with Sjögren's syndrome and bronchopneumopathy. This combination (HTLV-1, Sjögren's syndrome, and bronchopneumopathy) is rarely reported.
16540551 Reactive haemophagocytic syndrome in adult-onset Still's disease: a report of six patients 2006 Dec OBJECTIVE: To examine the prevalence and characteristics of patients with reactive haemophagocytic syndrome (RHS) complicating adult-onset Still's disease (AOSD). METHODS: Of 50 patients with AOSD fulfilling Yamaguchi and Fautrel criteria followed in our department, clinical and laboratory data, course and treatment of six patients with histologically proven RHS and without any obvious cause other than AOSD were retrospectively recorded. RESULTS: RHS led to AOSD in two cases, whereas it appeared after a mean duration of 3.5 years from onset of AOSD in the other cases. The main symptoms were fever (n = 6), polyarthralgias or myalgias (n = 4), lymphadenopathy or splenomegaly (n = 3), pharyngitis (n = 3), rash (n = 3), pleuritis (n = 3), hepatomegaly (n = 1), normal or low leucocyte count (n = 4), anaemia (n = 6), lymphocytopenia (n = 6), thrombocytopenia (n = 4), hyperbasophilic lymphocytes (n = 2), abnormal liver function tests (n = 6) and increased serum triglyceride level (n = 6). Serum ferritin concentration was constantly increased (>10,000 microg/l in five cases, with <5-35% in glycosylated form). Two patients presented with coagulopathy. Treatment comprised corticosteroids (n = 4) and intravenous immunoglobulins (n = 3), whereas prednisone was unchanged in one case. One death due to pneumonia occurred 15 days after RHS. With a follow-up ranging from 2 to 7.5 years, the other patients were in remission with prednisone plus etanercept (n = 1), prednisone plus methotrexate (n = 1), low-dose prednisone (n = 2) or without treatment (n = 1). CONCLUSION: RHS is not uncommon in AOSD. It should be evoked in a patient with AOSD in the absence of hyperleucocytosis, thrombocytopenia, lymphopenia and coagulopathy, or in the presence of high serum ferritin and triglyceride levels.
18509714 Occurrence of organ-specific and systemic autoimmune diseases among the first- and second- 2008 Aug Studies have demonstrated a familial aggregation of systemic and organ-specific autoimmune diseases. The aim of the present survey was to obtain, by patient interviews, a preliminary estimate of the prevalence of systemic and organ-specific autoimmune diseases among the first- and second-degree relatives of Caucasian patients with connective tissue diseases (CTD) or inflammatory arthritis followed at our unit. Between June 2007 and January 2008, 626 patients and 85 controls (patients with osteoarthritis, osteoporosis, or fibromyalgia) were interviewed. Three hundred ten patients (50%) versus 21 controls (25%) were found to have at least one relative affected with an autoimmune condition (p < 0.0001). The most common conditions were organ-specific autoimmune diseases: 160 (34%) autoimmune thyroid (AT) disease, 112 (24%) psoriasis, 21 vitiligo, and 19 insulin-dependent diabetes mellitus. Systemic autoimmune diseases were reported in 126 relatives: rheumatoid arthritis (66 cases, 14%), 16 sacroileitis, and CTD (43 cases). A significant difference was observed in the prevalence of AT disease between the relatives of the patients and controls (3% versus 0.5%). In conclusion, these data confirm the high prevalence of autoimmune conditions, particularly of AT disease, among the relatives of patients.
18040689 Suppression of human macrophage interleukin-6 by a nonpsychoactive cannabinoid acid. 2008 May Interleukin-6 (IL-6) is a multifunctional cytokine which contributes to inflammation and tissue injury in several diseases. Thus, inhibition of IL-6 production may be a useful strategy for treatment of patients with diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). A synthetic nonpsychoactive cannabinoid, ajulemic acid (AjA), prevents joint damage in experimental arthritis. Results of experiments presented here indicate that addition of AjA (3-30 microM) to human monocyte derived macrophages in vitro reduces steady state levels of IL-6 mRNA and the subsequent secretion of IL-6 from LPS stimulated cells. Although AjA binds to and activates PPARgamma, its anti IL-6 effects are PPARgamma independent. These studies provide evidence to support the view that AjA may prove to be an effective, safe antiinflammatory agent.
17929127 Clinical characteristics of polymyalgia rheumatica in Japanese patients: evidence of synov 2007 Polymyalgia rheumatica (PMR) is an inflammatory condition of unknown etiology characterized by diffuse pain and morning stiffness involving neck, shoulder, and pelvic girdles. To facilitate an understanding of PMR and its proper diagnosis, we evaluated clinical symptoms, laboratory data, and radiographic findings of 32 Japanese patients with it. Distal musculoskeletal manifestations were more frequently observed than had been thought before (81% of the patients), and peripheral arthritis was most common (75%). The joints most often affected were knees and wrists, and most episodes were presented as bilateral oligo- or polyarthritis. A swelling of hands was observed in 34% of the patients. Using contrast-enhanced fat suppression magnetic resonance imaging (MRI) of the shoulder, we found the evidence of subacromial and subdeltoid bursitis (100%), glenohumeral joint synovitis (93%), and biceps tenosynovitis (57%) in the PMR patients examined. Inflammatory changes in soft tissues around the joint capsule were prominent. By knee MRI, suprapatellar bursitis and joint synovitis were visualized in all cases examined, and extracapsular abnormalities were also prominent in 90% of the patients. Serum matrix metalloproteinase-3, a parameter of synovial inflammation, was significantly increased in PMR patients. Anticyclic citrullinated peptide antibody was useful for differential diagnosis between PMR and elderly onset rheumatoid arthritis. In conclusion, joint and periarticular synovitis seems to be commonly and primarily responsible for the proximal and distal musculoskeletal symptoms of PMR. The presence of the extracapsular change, probably a nonspecific extension of synovitis, can explain the severe discomfort that radiates toward the periphery. To avoid making a wrong diagnosis, we should be aware that peripheral synovitis is one of the hallmarks of PMR.
17349557 Complications and adverse reactions in the use of newer biologic agents. 2007 Mar New developments in genetic engineering and biotechnology have allowed the creation of bioengineered molecules that target specific steps in the pathogenesis of several immune-mediated disorders, including Crohn's disease, rheumatoid arthritis, psoriasis and psoriatic arthritis, ankylosing spondylitis, pemphigus, and B-cell lymphoma. These drugs work by eliminating pathogenic T cells (alefacept), blocking T-cell activation and/or inhibiting the trafficking of T cells (efalizumab), changing the immune profile from Th1 to Th2, blocking cytokines (eg, tumor necrosis factor alpha antagonists including etanercept, infliximab and adalimumab, or interleukin-1-receptor antagonists [anakinra]), or eliminating pathogenic B cells (rituximab). This article reviews the complications and adverse reactions associated with these medications.
17214581 Therapeutic targeting of B lymphocyte stimulator (BLyS) in the rheumatic diseases. 2006 Dec B lymphocyte stimulator (BLyS) is a vital B cell survival factor. Overexpression of BLyS in mice can lead to clinical and serological features of systemic lupus erythematosus (SLE) and Sjögren's syndrome (SS). Treatment with BLyS antagonists of mice with established SLE ameliorates disease progression and enhances survival. Moreover, similar treatment of mice with inflammatory arthritis ameliorates the ongoing inflammation and subsequent joint destruction. In humans, BLyS overexpression is common in patients with several rheumatic diseases, including SLE, rheumatoid arthritis (RA), Sjögren's syndrome, scleroderma, Wegener's granulomatosis, and ANCA-associated vasculitis. Results from phase-II clinical trials with a BLyS antagonist in human SLE and RA have shown the antagonist to have biological and clinical activity along with a favorable safety profile. These features collectively point to BLyS as an attractive therapeutic target in human rheumatic diseases.
21794394 [How do we evaluate an inadequate response in a patient with rheumaoid arthritis in the cl 2007 Jan Rheumatoid arthritis (RA) is a chronic disease that particularly affects the joints, causing their destruction, changes in its functional capacity and considerably compromising the quality of life. It is known that early treatment can reduce structural damage and improve the disability in the long term, but the optimal therapeutic strategies are still not universally accepted. As with diabetes and hypertension, strict control of the disease is required, with the objective of achieving no disease activity, which may be seen as a remission, or if this is not possible, to keep the inflammatory activity as low as possible so that the unfavourable consequences, such as the articular damage process and the risks that the patients assume deriving from treatment, do not occur. The improvement criteria of the American College of Rheumatology (ACR) are useful for comparing the efficacy of treatment in clinical trials, but they must not be used as a therapeutic objective, since they do not evaluate the final activity, which can be as important as having an improvement. To evaluate the response, the most logical and convenient for the doctor is to use the same tools that are used to evaluate the activity of the disease in clinical practice, such as the DAS and SDAI activity scores. Some limits which separate the different levels of activity have been proposed to improve their interpretation and establish therapeutic objectives. The categorisation into classes according to activity is important for starting or changing treatment (when it is moderate or high) and to define stages of conceptually different activity (activity or remission). The cut-off points that separate these categories were proposed years ago when the therapeutic possibilities of RA were limited and their long term consequences were not known. The therapeutic objective of remission or lower activity is much easier to achieve these days, therefore the therapeutic categories need to be reconsidered and the definition of lower activity levels as a potential objective. Nowadays, to assume moderate or high activity as a result of treatment is unacceptable, particularly when our therapeutic arsenal is already considerable and strategies and therapeutic combinations have been proposed which have demonstrated higher efficacy with tolerable risks. Although changes happen gradually in all aspects of life, there is no reason not to accept remission of RA as not only a desirable objective, but also an achievable one.
17100629 Immunomodulating effects of flavonoids on acute and chronic inflammatory responses caused 2006 Flavonoids have beneficial activities which modulate oxidative stress, allergy, tumor growth and viral infection, and which stimulate apoptosis of tumor cells. In addition to these activities, dietary flavonoids are able to regulate acute and chronic inflammatory responses. Here we describe new aspects of regulatory mechanisms by which flavonoids suppress production of tumor necrosis factor-alpha (TNF-alpha) by macrophages, microglial cells and mast cells stimulated with lipopolysaccharide (LPS) and others via toll-like receptors (TLRs), and TNF-alpha-mediated acute and chronic inflammatory responses. Treatment with flavonoids such as luteolin, apigenin, quercetin, genistein, (-)-epigallocatechin gallate, and anthocyanidin resulted in significant downregulation of LPS-elicited TNF-alpha and nitric oxide (NO) production and diminished lethal shock. In chronic diseases, pathogenesis of collagen-induced arthritis (CIA), a mouse model of rheumatoid arthritis which is triggered by TNF-alpha, was improved by the oral administration of flavonoids after the onset of CIA. Here, we discuss that inhibitory effects of flavonoids on acute and chronic inflammation are due to regulation of signaling pathways, including the nuclear factor kappaB (NF-kappaB) activation and mitogen-activated protein (MAP) kinase family phosphorylation. FcetaRI expression by NF-kappaB activation was also reduced by flavonoids; while accumulation of lipid rafts, which is the critical step for signaling, was blocked by flavonoids. The intake of dietary flavonoids reduces acute and chronic inflammation due to blocking receptor accumulation and signaling cascades, and would assist individuals at high-risk from life-style related diseases.
16863987 Oxidatively modified autoantigens in autoimmune diseases. 2006 Aug 15 Free radical-mediated oxidative damage and consequent protein modification by the end products of oxidative damage are important mediators of cell toxicity and disease pathogenesis. Aldehydic products, mainly the 4-hydroxy-2-alkenals, form adducts with proteins and make them highly immunogenic. Oxidative modification of proteins has been shown to elicit antibodies in a variety of diseases including systemic lupus erythematosus (SLE), alcoholic liver disease, diabetes mellitus (DM), and rheumatoid arthritis (RA). Oxidatively modified DNA (8-oxodeoxyguanine) and low-density lipoproteins (LDL) occur in SLE, a disease in which premature atherosclerosis is a serious problem. In addition, immunization with 4-hydroxy-2-nonenal (HNE)-modified 60-kDa Ro autoantigen elicits an accelerated epitope spreading in an animal model of SLE. Advanced glycation end product (AGE) pentosidine and AGE-modified IgG have been shown to correlate with RA disease activity. Oxidatively modified glutamic acid decarboxylase is important in type 1 DM, while autoantibodies against oxidized LDL are prevalent in Behcet's disease. The fragmentation of scleroderma-specific autoantigens occurs as a result of oxidative modification and is thought to be responsible for the production of autoantibodies through the release of cryptic epitopes. In the face of overwhelming evidence for the involvement of oxidative damage in autoimmunity the administration of antioxidants is a viable untried alternative for preventing or ameliorating autoimmune disease, although results in cardiovascular disease are disappointing.
16646041 Brachio-cervical inflammatory myopathies: clinical, immune, and myopathologic features. 2006 May OBJECTIVE: To characterize patients with inflammatory myopathies who present with weakness in the proximal regions of the arms. METHODS: Clinical, laboratory, and myopathologic features were evaluated in 10 patients, identified consecutively over 12 years, with inflammatory myopathies and weakness that was most severe in the proximal regions of the arms. The features of these brachio-cervical inflammatory myopathy (BCIM) syndromes were compared with those of other inflammatory and immune-mediated myopathies evaluated during the same period. RESULTS: Patients with BCIM developed progressive weakness at ages 24-82 years (mean +/- SD age 55 +/- 9 years). Posterior neck weakness occurred in 60% of patients, while motor neuron disease was the referring diagnosis in 30%. All patients had other systemic autoimmune disorders, including myasthenia gravis (40%) and rheumatoid arthritis (20%). Antinuclear antibodies were present in all patients. Serum creatine kinase levels were usually moderately high (mean 910 IU/liter). Active myopathy was identified in muscle biopsy samples from the patients. Focal collections of mononuclear cells, some predominantly B cells, were present in perivascular and perimysial regions. MxA- and CD123-positive dendritic cells were present in the endomysium. C5b-9 components of complement were present diffusely in endomysial connective tissue. Most patients improved in strength after receiving corticosteroids. CONCLUSION: Patients with BCIM syndromes have progressive weakness in the proximal regions of the arms and neck. The predominant myopathologic findings are active myopathy, C5b-9 staining of endomysium, focal perivascular and perimysial inflammation, often with a prominent B cell component, and endomysial dendritic cells. Corticosteroid treatment of BCIM is often followed by improvement in strength.
16393277 Systematic review: coxibs, non-steroidal anti-inflammatory drugs or no cyclooxygenase inhi 2006 Jan 1 Selective cyclooxygenase-2 inhibitors have been marketed as alternatives of conventional, non-steroidal anti-inflammatory drugs with the purpose of reducing/eliminating the risk of ulcer complications. Unexpectedly, randomized-controlled trials revealed that long-term use of coxibs, such as rofecoxib, significantly increased the risk of myocardial infarction and stroke, while the use of valdecoxib was associated with potentially life-threatening skin reactions. Subsequently, rofecoxib and valdecoxib were withdrawn from the market. Although more strict precautions for other coxibs, such as celecoxib, etoricoxib, lumiracoxib and parecoxib, may be accepted/recommended by regulatory agencies, a critical review of published data suggests that their use may not be justified - even in high-risk patients - taking benefits, costs and risks into consideration. Clinicians should, therefore, never prescribe coxibs to patients with cardiovascular risk factors, and should only reluctantly prescribe coxibs to patients with a history of ulcer disease or dyspepsia to overcome persistent pain due to, e.g. rheumatoid arthritis or osteoarthritis. Instead, they should consider using conventional non-steroidal anti-inflammatory drugs in combination with a proton pump inhibitor or a prostaglandin analogue, especially for patients with increased cardiovascular risks, i.e. established ischaemic heart disease, cerebrovascular disease and/or peripheral arterial disease, or alternatively acetaminophen. An evidence-based algorithm for treatment of a chronic arthritis patient with one or more gastrointestinal risk factors is presented.