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ID PMID Title PublicationDate abstract
12230633 The liver is a common non-exocrine target in primary Sjögren's syndrome: a retrospective 2002 Sep 13 BACKGROUND: The autoimmune destruction of exocrine glands that defines primary Sjögren's syndrome (1 degrees SS) often extends to non-exocrine organs including the liver. We aimed to determine the prevalence of liver disease in patients with 1 degrees SS and to evaluate the association of this complication with other non-exocrine features and serologic markers of autoimmunity and systemic inflammation. METHODS: We reviewed 115 charts of patients with 1 degrees SS and further analyzed the 73 cases that fulfilled the European Epidemiology Center Criteria, seeking evidence for clinical and subclinical liver disease. RESULTS: Liver function tests had been determined in 59 of the 73 patients. Of those, 29 patients (49.1%) had abnormal liver function tests including 20.3% with clinically overt hepatic disease. Liver disease was the most common non-exocrine feature in this cohort. Risk factors for abnormal liver function tests were distributed similarly between the patients with and without liver disease. In 60% of patients with abnormal liver function tests no explanation for this complication was found except for 1 degrees SS. Liver involvement was significantly more common in 1 degrees SS patients who also had evidence of lung, kidney and hematological abnormalities. Patients with abnormal liver function tests were also more likely to have an elevated sedimentation rate and a positive anti-ENA during the course of their disease. CONCLUSION: Liver involvement is a common complication in 1 degrees SS. Its presence correlates with systemic disease. We consider that this complication should be routinely sought in patients with 1 degrees SS, especially when a positive anti-ENA or evidence of systemic inflammation is found.
12038948 Cevimeline for the treatment of xerostomia in patients with Sjögren syndrome: a randomize 2002 Jun 10 BACKGROUND: Cevimeline hydrochloride is a cholinergic agent with muscarinic agonist activity prominently affecting the M1 and M3 receptors prevalent in exocrine glands. We evaluated the safety and efficacy of cevimeline in the treatment of xerostomia in patients with Sjögren syndrome. METHODS: Seventy-five patients with Sjögren syndrome and associated salivary gland dysfunction were enrolled in a double-blind, randomized, placebo-controlled trial at 8 university- and office-based outpatient clinical facilities in the United States. Eligible study participants were randomized to receive 30 mg of cevimeline 3 times daily, 60 mg of cevimeline 3 times daily, or placebo for 6 weeks. Subjective responses were determined using global patient evaluation and visual analog scales. Salivary flow was measured objectively. RESULTS: Sixty-one participants completed the study. Patients in both cevimeline groups had significant improvements in dry mouth, as indicated by symptoms, salivary flow, and use of artificial saliva, compared with the placebo group. The drug was generally well tolerated, with expected adverse events resulting from the drug's muscarinic agonist action. Fourteen patients withdrew from the study because of adverse events, the most frequent being nausea. CONCLUSIONS: Therapy with cevimeline, 30 mg 3 times daily, seems to be well tolerated and to provide substantive relief of xerostomia symptoms. Although both dosages of cevimeline provided symptomatic improvement, 60 mg 3 times daily was associated with an increase in the occurrence of adverse events, particularly gastrointestinal tract disorders. Use of 30 mg of cevimeline provides a new option for the treatment of xerostomia in Sjögren syndrome.
12532204 Autoimmune cholangitis in patients with primary Sjögren's syndrome. A case report. 2002 Dec Sjögren's Syndrome is a very frequent autoimmune disease, characterised by exocrine gland involvement. Immunologic disorders are also responsive for extraglandular manifestations of the disease, mostly for the digestive involvement. We report a case of primary Sjögren's syndrome with multiple extraglandular manifestations: vasculitis, cryoglobulinaemia, hepatic involvement and presumably neurologic involvement. The particularities of the case are the typical pattern of autoimmune cholangitis, hypogammaglobulinaemia, the absence of antinuclear antibodies and the association with vasculitis. To the best of our knowledge, this is the first case report of autoimmune cholangitis in Sjögren's syndrome
11947921 Identification of candidate genes for Sjögren's syndrome using MRL/lpr mouse model of Sjà 2002 May 1 Sjögren's syndrome is a chronic autoimmune disease characterized by focal lymphocytic infiltration of lacrimal and salivary glands, but the precise mechanism of this syndrome is poorly understood. To clarify the mechanism of onset and progression of Sjögren's syndrome, it is necessary to identify Sjögren's syndrome-related genes. For this purpose, we used MLR/MpJ-lpr/lpr (MRL/lpr) mouse as a model of human secondary Sjögren's syndrome and analyzed specific mRNA expression pattern in MRL/lpr mouse salivary glands by in-house cDNA microarray. Among arrayed 2304 genes, 13 genes were isolated as highly expressed genes in MRL/lpr mouse salivary gland in comparison with MRL/MpJ-+/+ (MRL/+) mouse tissue. Subsequently, we performed RT-PCR analysis and confirmed the high expression level of nine genes; caspase3, Ly-6C.2, vimentin, Mel-14 antigen, cathepsin B, mpt1, Laptm5, Gnai2 and UCP2. Five of the nine genes have already been identified in patients with Sjögren's syndrome or mice models of the syndrome, but the remaining four genes; mpt1, Laptm5, Gnai2, and UCP2 have not been reported previously as Sjögren's syndrome-related genes. Although, further experiments are necessary to examine the relationship between these four genes and Sjögren's syndrome, our system of mouse model of Sjögren's syndrome combined with in-house cDNA microarray is suitable for the isolation of Sjögren's syndrome-related genes.
15347330 Multiple dermatofibromas in a patient with systemic lupus erythematosus and Sjögren's syn 2004 Sep Multiple dermatofibromas (DFs) are rare and have been thought to be associated with altered immunity. In this report, we describe a 27-year-old Japanese woman with systemic lupus erythematosus (SLE) and Sjögren's syndrome in whom eight nodules appeared over a period of 4 years. Histopathological findings were consistent with DF. SLE rather than Sjögren's syndrome seemed to have induced the multiple DFs in this patient. We also reviewed the reported cases with multiple DFs associated with SLE and/or Sjögren's syndrome. Review of the previous reports indicates that SLE is the most frequent autoimmune disorder associated with multiple DFs, and that both SLE and immunosuppressive treatments play a part in induction of multiple DFs. Therefore, if multiple DFs are present it is important that the status of the patient be evaluated from the standpoint of autoimmune diseases, particularly SLE, or immunosuppression.
11812420 Impaired functional visual acuity of dry eye patients. 2002 Feb PURPOSE: To report dry eye patients' functional visual acuity, which was measured after sustained eye opening for 10-20 seconds, as a simulation of visual function of daily acts of gazing, which is defined as looking at an object with involuntary blink suppression. METHODS: Interventional clinical nonrandomized comparative trial. We measured ordinary best-corrected visual acuity and functional visual acuity in non-Sjögren's syndrome (non-SS, N = 10) and Sjögren's syndrome (SS, N = 12) patients and in normal controls (N = 8), prospectively. Surface regularity index (SRI) of corneal topography was also measured under routine circumstances and after sustained eye opening. Blink rates while gazing were measured during reading in another 28 dry eye patients and during driving in another 8 normal controls. RESULTS: Functional visual acuity did not change (1.27-1.16) in normal controls, but decreased significantly from 1.18-0.336 in non-SS patients (P = .0007) and from 1.15-0.228 (P < .00001) in SS patients. SRI after sustained eye opening increased in non-SS (P = .032) and SS patients (P = .0007), but not in the normal controls. Blink rates during reading (P < .001) and driving (P = .012) were significantly decreased from baseline blink rates. CONCLUSIONS: This study shows that the visual function of dry eye patients becomes abnormal with ocular surface irregularity when the eye is kept open for 10-20 seconds. Our data indicate impaired visual function in dry eye patients while gazing. Functional visual acuity may be important in daily activities.
12747280 Impaired expression of erythrocyte glycosyl-phosphatidylinositol-anchored membrane CD59 in 2003 Mar OBJECTIVE: Complement-mediated injury is regulated by many factors; among these CD59 has been identified as a widely distributed glycoprotein that inhibits membrane C5b-9 (terminal complement component) formation. The aim of the study was to assess erythrocyte CD59 expression in patients with psoriatic arthritis in order to understand the role of CD59 in the pathogenesis. METHODS: Washed erythrocytes from 50 patients with psoriatic arthritis, 8 with cutaneous psoriasis and 24 healthy subjects were incubated with monoclonal anti-CD59 antibody followed by a second FITC conjugated antibody and fluorescence intensity analysed by FAC-Scan flow cytometer to assess their CD59 membrane expression. SC5b-9 levels were measured in the plasma by ELISA and results compared with CD59 values. Immune complexes, complement C3 and C4 and rheumatoid factor were also determined. RESULTS: Impaired expression of erythrocyte membrane-anchored CD59 was found in patients with psoriatic arthritis; the lowest levels were seen in active patients (p < 0.01). Increased SC5b-9 was seen in the plasma of patients with active disease. An inverse correlation was also found between plasma C5b-9 and the CD59 expression levels (r = -0.81, p < 0.001). CONCLUSION: The low CD59 expression on erythrocytes from patients with psoriatic arthritis may be an index of a low tissue CD59 expression. This impairment could facilitate the activation of complement pathway and increase the risk for arthritis. Membrane attack complex formation in deficient membrane bound CD59 may also exacerbate synovial cell injury and inflammation.
15302639 Three-tiered-copayment drug coverage and use of nonsteroidal anti-inflammatory drugs. 2004 Aug 9 BACKGROUND: Previous studies of 3-tier formularies are rare, although the evidence suggests that their cost-sharing structure reduces overall drug spending. However, it is unclear how incentive-based formularies affect the selection of medications with safety advantages, or restrict the access that high-risk populations have to recommended therapies in the higher tiers. This study was designed to determine whether 3-tier formularies influence the use of nonsteroidal anti-inflammatory drugs (NSAIDs) in a population of patients with arthritis. METHODS: This retrospective study used the 2000 MarketScan Research Database, which contains person-level claims data for employer-sponsored health plans. The sample for this study consisted of 20 868 individuals treated for osteoarthritis or rheumatoid arthritis and using NSAIDs while enrolled in tiered drug plans (n = 32). The likelihood of any use of cyclo-oxygenase (COX-2)-selective inhibitors was determined as a function of tiered drug plan coverage, adjusting for other person-level and plan-level covariates. RESULTS: Use of COX-2-selective inhibitors decreased (63.0% vs 53.6% vs 41.6%, respectively) and use of generic NSAIDs increased (37.7% vs 40.7% vs 55.7%, respectively) as formularies incorporated 1, 2, and 3 tiers. Enrollees in 3-tier plans with arthritis and serious gastrointestinal comorbidities (odds ratio, 0.51; 95% confidence interval, 0.40-0.66) were significantly less likely to use COX-2-selective inhibitors compared with patients in 1-tier plans. CONCLUSIONS: Three-tier formularies appear to reduce the use of COX-2-selective inhibitors among all patients with arthritis, even those at risk of experiencing gastrointestinal complications from using nonselective NSAIDs. These findings are among the first to suggest that tiered-copayment drug plans may be influencing the selection of medications beyond generic and branded products.
17043473 Beaver fever arthritis. 2004 Apr Giardia lamblia, a flagellated protozoan and common cause of gastroenteritis, is a rare but previously reported cause of reactive arthritis (ReA). We report a case of inflammatory oligoarthritis in a young woman after infection with Giardia. Two weeks after being treated, she developed an inflammatory arthritis of her left knee and right elbow that was refractory to nonsteroidal antiinflammatory medication. Antinuclear antibody, rheumatoid factor, and HLA-B27 tests were negative. She had almost immediate relief with intraarticular injection of corticosteroids. We review the previously reported cases of ReA following giardiasis and discuss possible pathogenic mechanisms. Although ReA most commonly occurs after chlamydial urethritis or gastroenteritis associated with typical enteropathic bacteria, important historical clues could point to less common pathogens such as Giardia. Physicians should be aware of these less common causes of ReA, because this could have important diagnostic and therapeutic implications.
12858466 Increased expression of alpha(1,3)-fucosyltransferase-VII and P-selectin binding of synovi 2003 Jul OBJECTIVE: The mechanisms controlling the recruitment of T helper type 1 (Th1) cells to the inflamed synovium are not fully understood. Here, we focus on alpha(1,3)-fucosyltransferase-VII (FucT-VII), an enzyme responsible for the generation of functional P- and E-selectin ligands that is upregulated in Th1 cells. METHODS: Expression of transcripts encoding FucT-VII, interferon-gamma (IFN-gamma), and interleukin 12Rbeta2 (IL-12Rbeta2) were analyzed in T cells purified from synovial fluid (SF) and from peripheral blood (PB) of children with juvenile idiopathic arthritis (JIA) using kinetic reverse transcriptase polymerase chain reaction analysis. Binding of SF and PB T cells to P-selectin was determined by flow cytometry using a soluble P-selectin/IgG1 fusion molecule. Recruitment of T cells to synovial tissue in vivo was studied by analyzing the migration of FucT-VII transfected Jurkat T cells into human rheumatoid synovial tissue grafted into SCID mice. RESULTS: In patients with JIA, the mRNA levels of FucT-VII, as well as of IFN-gamma and IL-12Rbeta2, were up-regulated in SF T cells compared to paired PB T cells. A higher expression of FucT-VII mRNA in SF T cells was associated with increased binding of T cells to P-selectin. Moreover, FucT-VII expression and increased P-selectin binding capacity of T cells were associated with a polyarticular course of oligoarticular JIA. Expression of FucT-VII in Jurkat T cells resulted in an increased accumulation of these cells in human rheumatoid synovial tissue grafted into SCID mice. CONCLUSION: Our data indicate an important role of FucT-VII in the enhanced homing of T cells to the inflamed synovium.
12794164 An inducible nitric oxide synthase-luciferase reporter system for in vivo testing of anti- 2003 Jun 15 The inducible NO synthase gene (iNOS) plays a role in a number of chronic and acute conditions, including septic shock and contact hypersensitivity autoimmune diseases, such as rheumatoid arthritis, gastrointestinal disorders, and myocardial ischemia. The iNOS gene is primarily under transcriptional control and is induced in a variety of conditions. The ability to monitor and quantify iNOS expression in vivo may facilitate a better understanding of the role of iNOS in different diseases. In this study, we describe a transgenic mouse (iNos-luc) in which the luciferase reporter is under control of the murine iNOS promoter. In an acute sepsis model produced by injection of IFN-gamma and LPS, we observed an induction of iNOS-driven luciferase activity in the mouse liver. This transgene induction is dose and time dependent and correlated with an increase of liver iNOS protein and iNOS mRNA levels. With this model, we tested 11 compounds previously shown to inhibit iNOS induction in vitro or in vivo. Administration of dexamethasone, epigallocatechin gallate, alpha-phenyl-N-tert-butyl nitrone, and ebselen significantly suppressed iNOS transgene induction by IFN-gamma and LPS. We further evaluated the use of the iNos-luc transgenic mice in a zymosan-induced arthritis model. Intra-articular injection of zymosan induced iNos-luc expression in the knee joint. The establishment of the iNos-luc transgenic model provides a valuable tool for studying processes in which the iNOS gene is induced and for screening anti-inflammatory compounds in vivo.
15775140 [Seronegative spondyloarthropathies--pathogenesis, diagnosis, treatment-]. 2003 Jun Seronegative spondyloarthropathies (SNSA) include a group of diseases with arthritis that are negative for rheumatoid factor. The borders of the disease are sometimes obscure, and SNSA has its own classification criteria. The investigation on the speciality of HLA-B27 will be important for the understanding of SNSA pathogenesis. Several reports shows that anti-TNF-alpha therapy is powerful measure for the management of SNSA.
14770093 Health outcomes in pediatric rheumatic diseases. 2004 Mar PURPOSE OF REVIEW: Health outcomes in the pediatric rheumatic diseases have been a very active area of research in the past several years, with a significant number of published studies from the United States, Canada, and Europe. Although most studies have been in the area of juvenile idiopathic arthritis, there are increasing numbers of studies in juvenile dermatomyositis and juvenile systemic lupus erythematosus. RECENT FINDINGS: These studies suggest that although there has been an improvement in overall outcomes, active disease persists in significant proportions of individuals into adulthood, causing damage and disability. In juvenile idiopathic arthritis, this is particularly so for patients with systemic arthritis and polyarthritis with rheumatoid factor positivity who overall appear to have a poor prognosis. SUMMARY: With the current approach to treatment of all these diseases being more aggressive, one anticipates an improvement in these outcomes in the future. Better longitudinal outcome studies with larger inception cohorts of new-onset disease are required to ascertain whether this prediction can be upheld. Such studies are now ongoing.
15142274 CD14 mediates the innate immune responses to arthritopathogenic peptidoglycan-polysacchari 2004 Bacterial infections play an important role in the multifactorial etiology of rheumatoid arthritis. The arthropathic properties of Gram-positive bacteria have been associated with peptidoglycan-polysaccharide complexes (PG-PS), which are major structural components of bacterial cell walls. There is little agreement as to the identity of cellular receptors that mediate innate immune responses to PG-PS. A glycosylphosphatidylinositol-linked cell surface protein, CD14, the lipopolysaccharide receptor, has been proposed as a PG-PS receptor, but contradictory data have been reported. Here, we examined the inflammatory and pathogenic responses to PG-PS in CD14 knockout mice in order to examine the role for CD14 in PG-PS-induced signaling. We found that PG-PS-induced responses in vitro, including transient increase in intracellular calcium, activation of nuclear factor-kappaB, and secretion of the cytokines tumor necrosis factor-alpha and interleukin-6, were all strongly inhibited in CD14 knockout macrophages. In vivo, the incidence and severity of PG-PS induced acute polyarthritis were significantly reduced in CD14 knockout mice as compared with their wild-type counterparts. Consistent with these findings, CD14 knockout mice had significantly inhibited inflammatory cell infiltration and synovial hyperplasia, and reduced expression of inflammatory cytokines in PG-PS arthritic joints. These results support an essential role for CD14 in the innate immune responses to PG-PS and indicate an important role for CD14 in PG-PS induced arthropathy.
14709895 The Oriental medicine "Cool-Cool (Cool-X-A)" inhibits inflammatory cytokine production and 2004 Jan Plant medications have been applied to treat pains from various types of arthritis in Korea. Rheumatoid arthritis (RA) is well known to be a chronic autoimmune/inflammatory disease that leads to progressive joint damage and cartilage destruction. Accumulation and activation of mast cells have been demonstrated in rheumatoid synovial tissue. Because infiltrated mast cells and their mediators may contribute to the initiation and progression of the inflammatory process and matrix degradation of RA, we tested the inhibitory effects of "Cool-Cool" (CC, Cool-X-A), an Oriental medication, on the production and migration of major inflammatory cytokines in mast cells. CC was treated in vitro before activation of human mast cell line (HMC-1) with phorbol 12-myristate 13-acetate, and the cytotoxicity of CC was assessed by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazoliumbromide assay. CC had no cytotoxic effects on HMC-1 cell viability. The inhibitory effects on cytokine production were monitored by enzyme-linked immunosorbent assay and reverse transcriptase-polymerase chain reaction (RT-PCR). CC inhibited not only the secretion but also the expression of TNF-alpha and IL-8 in HMC-1 cells. CC also suppressed migration of mast cells induced by stem cell factor. These findings may help in understanding the mechanism of action of this herbal medication, leading to the control of mast cells in inflammatory conditions like RA.
12489321 [Osteoporosis in the aged male]. 2002 Nov 23 A MAJOR PROBLEM: Osteoporosis in elderly men is a public health problem. However, the criteria for its diagnosis remain to be defined. With the aging of the male population, the number of osteoporotic fractures is increasing together with the incidence of fractures per age range. These fractures create handicaps and an excess of mortality and generate great expense for the health budget. VARIOUS PHYSIOPATHOLOGICAL MECHANISMS: In the pathogenesis of osteoporosis of the elderly men, various elements must be taken into account: hormone factors (decreased testicular secretion, vitamin D deficiency), life style (chronic alcoholism, smoking, lack of exercise), certain diseases (rheumatoid arthritis) and certain drugs (corticosteroids, anti-androgenes). THE PROGRESSION OF BONE MINERAL DENSITY (BMD) WITH AGE: Depending on the area measured, the BMD peak is reached before the age of 30 in the hip and in the trabecular bone areas, whilst it is reached around the age of 40 in the cortical bone areas. Bone loss accelerates after the age of 70. After the age of 80, the BMD peak is around 16 to 20% lesser, except for the lumbar spine where the arthrosic calcifications artificially increase the BMD value. Bone formation marker blood levels remain stable in elderly men whereas the urinary excretion of deoxypyridinoline (bone resorption marker) increases after the age of 60. THE DIAGNOSIS OF OSTEOPOROSIS IN ELDERLY MEN: Osteoporosis must be evoked when confronted with a recent fracture, notably of the vertebra, or following moderate trauma and the diagnosis is confirmed by the measurement of a low BMD score (T-score < -2.5). WITH REGARD TO TREATMENT: There are few studies on the treatment of male osteoporosis. In the elderly man, documented hypogonadism justifies testosterone replacement therapy, although its anti-fracture efficacy has not been studied. In elderly men, particularly those living in homes, vitamin D deficiency and the subsequent hyperthyroidism justify treatment with vitamin D and calcium. The new bisphosphonates appear promising. In a randomised study, alendronate increased BMD and reduced the incidence of vertebral fractures. Alendronate and risedronate were also effective in the prevention and treatment of cortisone-induced osteoporosis in men.
14613270 Turnover of type II collagen and aggrecan in cartilage matrix at the onset of inflammatory 2003 Nov OBJECTIVE: To determine in vivo the extent of damage to, and changes in turnover of, articular cartilage type II collagen (CII) and the proteoglycan aggrecan following the onset of inflammatory arthritis in humans, and to examine the hypothesis that there are direct relationships between cartilage biomarkers of damage/turnover and clinical, histologic, and molecular markers of inflammation. METHODS: Synovial fluid (SF) and synovial membrane (SM) were obtained by arthroscopy, and a synovitis score was determined, in 32 patients with rheumatoid arthritis (RA) (13 with early untreated disease, 19 with established disease), 18 with psoriatic arthritis (PsA), and 10 with osteoarthritis (OA). Systemic disease activity markers were recorded, and SM CD3+ T cells, CD4+ T cells, CD68+ macrophages, and lining layer hyperplasia were quantified. SF levels of tumor necrosis factor alpha (TNFalpha), interleukin-10 (IL-10), matrix metalloproteinase 1 (MMP-1), MMP-3, Col2-3/4C(Long mono) neoepitope (C2C) (reflecting collagenase cleavage of cartilage CII), C-propeptide of type II procollagen (PIICP) (a biosynthesis marker), keratan sulfate (KS), and the 846 epitope of aggrecan (turnover) were measured by enzyme-linked immunosorbent assay or radioimmunoassay. RESULTS: Levels of cartilage degradation products in early RA or early PsA were not elevated above levels in OA, although in early inflammatory arthritis, TNFalpha and MMP-1 levels were similar to those observed in late inflammatory disease and higher than those in OA. PIICP was reduced in early RA. Correlations were observed between the SF C2C neoepitope level and the Health Assessment Questionnaire score, C-reactive protein level, plasma viscosity, synovitis score, and SF TNFalpha and MMP-1 levels. KS epitope content was reduced in direct relation to SM macrophage infiltration in the sublining and lining layers and in the presence of elevated SF MMP-3. Both SF MMP-1 and SF MMP-3 levels correlated with CD4+ T cell infiltration and lining layer hyperplasia in the SM, and MMP-1 levels correlated with lining layer CD68 levels, but TNFalpha and IL-10 levels did not. CONCLUSION: Except for CII synthesis, there were no significant changes in extracellular matrix turnover of aggrecan or CII in the early stages of human inflammatory arthritis. However, the direct correlation between the increases in TNFalpha and MMP-1 production and collagen degradation suggests that collagenase cleavage of cartilage collagen is related to the activities of TNFalpha and MMP-1. The reduction in CII synthesis in early RA may contribute to the developing pathology, since a lack of synthesis of this molecule would inhibit maintenance of cartilage matrix.
12148186 [Acetabular bone grafting in primary total hip arthroplasty]. 2002 A group of 108 hips in 102 patients (81 females and 21 males; average age: 66.9 years) operated at our Centre between 1989 and 1998 was evaluated. There were 76 hips with idiopathic arthritis, 21 hips with rheumatoid arthritis, 2 hips with post-traumatic lesions and 9 cases of dysplastic arthritis of the hip. Cemented total hip arthroplasty was performed in all cases (62 Weller prostheses, 28 Charnley prostheses, 12 Ultima-Straight prostheses and 6 Centrament prostheses). In the presented material three different kinds of bone grafting were performed: "impaction bone grafting" with autogenous cancellous bone grafts in cases of bone cysts and cavitary lesions (57 cases); augmentation of thin sclerotic or protrusive acetabulums with autogenous cancellous bone grafts with or without allogenous cancellous bone grafts (26 and 16 cases respectively); and reconstruction of the roof of the acetabulum with autogenic cortico-cancellous bone grafts 9 cases). In 17% cases autogenous and allogenous bone grafts were used simultaneously and in 83% autogenous bone grafts only were employed. Acetabular bone grafting was necessary to create proper bone substrate for endoprostheses implantation. Evaluation of results was based on criteria proposed by a joint committee of The Hip Society, SICOT and AAOS. A mean of 83.5% points were achieved in the Harris Hip Score. Aseptic loosening was observed in 15 sockets and 9 stems. Bone grafts didn't heal in 25 hips, of which 14 had loose sockets. These results are comparable to those in primary total hip arthroplasties without acetabular bone grafting. The results in the presented paper support the opinion that acetabular bone grafting is a useful tool in reconstructive surgery of the hip and allows to achieve good results in technically difficult acetabuli.
15106410 [Comparative efficacy of different therapeutic schemes in gastropathies induced by nonster 2004 AIM: To study efficacy of colloid bismuth subcitrate (de-nol, Yamanuchi) in therapy of gastropathies provoked by nonsteroidal anti-inflammatory drugs (NSAID). MATERIAL AND METHODS: 63 patients (38 women and 25 men, mean age 54.2 +/- 12.8 years) with rheumatoid arthritis (n = 14), osteoarthrosis (n = 47), gouty arthritis (n = 2) regularly taking NSAID were examined. The patients were randomized into two groups. The patients of the control group 1 received therapy with omeprasol (40 mg/day), patients of group 2 were given omeprasol (40 mg/day) and de-nol (480 mg/day). RESULTS: Epithelization of erosive-ulcerous lesions were observed on the treatment day 28 in 93.9% patients of group 1 and all the patients of group 2. Normalization of the level of prostaglandin E1 by the end of the treatment was registered in 57% and 93.3% patients of groups 1 and 2, respectively. CONCLUSION: Colloid bismuth subcitrate (de-nol) effectively improves the condition of NSAID gastropathy patients, stimulates healing of erosive-ulcerous lesions of gastroduodenal zone in elevation of prostaglandins levels.
12672836 Instability after shoulder arthroplasty: results of surgical treatment. 2003 Apr BACKGROUND: Currently, there is little available information regarding the surgical treatment of instability following shoulder arthroplasty. The purpose of the present study was to review the results of revision surgery performed for the treatment of instability after shoulder arthroplasty to better define the causes of instability and the risk factors for an unsatisfactory outcome. METHODS: Between 1985 and 1999, thirty-three shoulders (seven of which had had a hemiarthroplasty and twenty-six of which had had a total shoulder arthroplasty) were treated surgically at our institution for anterior instability (nineteen shoulders) or posterior instability (fourteen shoulders). The primary arthroplasty had been performed for the treatment of degenerative arthritis in sixteen shoulders, arthritis of dislocation in six, acute fracture in four, rheumatoid arthritis in three, and other conditions in four. RESULTS: The instability was attributed to abnormal capsular tension and/or rotator cuff dysfunction in twenty-one shoulders, component malpositioning in one shoulder, and a combination of both in eleven shoulders. One shoulder was treated with removal of the components. In the remaining thirty-two shoulders, each of the elements that was contributing to the instability was specifically addressed at the time of surgery. Revision surgery restored stability in nine of the thirty-two shoulders. Anterior instability was associated with a higher failure rate than posterior instability was (p = 0.04). Although eleven shoulders had additional surgery for the treatment of recurrent instability, only fourteen of the thirty-three shoulders were stable at the time of the final follow-up. According to the Neer rating system, there were four excellent, six satisfactory, and twenty-three unsatisfactory results. CONCLUSIONS: Soft-tissue imbalance is present in most cases of instability following shoulder arthroplasty, and component malpositioning plays an additional role in some cases. More than one-half of the shoulders in the present study remained unstable despite attempts at revision. Surgical treatment of instability following arthroplasty is associated with only a modest success rate.