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ID PMID Title PublicationDate abstract
9212665 [Conversion of chronic necrotizing pulmonary aspergillosis to invasive pulmonary aspergill 1997 Apr An 82-year-old man with rheumatoid arthritis was admitted to the hospital because of bloody sputum, appetite loss, and a chest-radiographic abnormality. He had previously been treated with oral steroid therapy. The chest X-ray film showed an infiltrative shadow with airlucency in the right upper lung field. Sputum culture for fungi was negative, but a test for aspergillus antigen in serum was positive. Other clinical findings were also compatible with conversion of chronic necrotizing pulmonary aspergillosis to invasive pulmonary aspergillosis. The patient was successfully treated with a drip infusion of fulconazole. The patients condition was stable for several months, after which he died due to uncontrollable atrial flutter. Mild immunosuppression due to oral steroid therapy probably caused chronic necrotizing pulmonary aspergillosis in this case. The patient's general condition worsened after admission and invasive pulmonary aspergillosis developed. This case taught us that therapy for chronic necrotizing pulmonary aspergillosis should include management of the patient's general condition as well as treatment of the pulmonary lesions.
9825744 A 36 month comparative trial of methotrexate and gold sodium thiomalate in the treatment o 1998 Oct OBJECTIVE: To compare the safety and efficacy of methotrexate (MTX) and gold sodium thiomalate (GSTM) in patients with active early erosive rheumatoid arthritis (RA) during 3 yr. METHODS: A total of 174 patients from two centres were randomly assigned to receive weekly i.m. injections of either 15 mg MTX or 50 mg GSTM for 1 yr in a double-blind fashion. Thereafter, the study was continued as an open prospective trial for an additional 2 yr with the same dose of MTX and half of the GSTM dose. Clinical and laboratory evaluations were carried out at baseline and at months 6, 12, 18, 24 and 36 in all patients, including withdrawals. RESULTS: An intention-to-treat analysis revealed inactivation ['clinical remission': no swollen/tender joints, erythrocyte sedimentation rate (ESR) of < 20 mm/h in males and < 30 mm in females, no corticosteroids within the last 4 weeks] in 33.3% of MTX patients and 37.9% of GSTM patients. The mean time to inactivation was insignificantly shorter with GSTM (MTX: 12.1 months; GSTM: 9.1 months; P = 0.06). At least marked improvement (> 50% reduction of the number of swollen/tender joints and of the ESR) was found in 78.2% (MTX) and 87.4% (GSTM). Withdrawal from the study due to toxicity was recorded in 16.1% of MTX and 52.9% of GSTM patients after a mean time of 30.6 and 6.1 months, respectively (P = 0.0001). In MTX and GSTM non-completers, inactivation was recorded in 24.2 and 54.7% of all patients. Among completers (54 and 34 patients, respectively), significant improvement compared to baseline was noted in all seven clinical variables (morning stiffness, overall joint pain, count of tender/swollen joints, Lansbury articular score, functional score and grip strength), ESR and C-reactive protein without significant intergroup differences. The steroid-sparing effect appeared more pronounced with GSTM. CONCLUSION: Over 36 months, treatment with MTX or GSTM induces inactivation ('clinical remission') of early and erosive RA in about one-third and at least marked improvement in four-fifths of patients (intention-to-treat analysis). Patients withdrawn from MTX or GSTM due to toxicity develop a clinical remission from the disease; this occurred more often with GSTM. Tolerability is significantly better with MTX.
9706295 Total shoulder arthroplasty versus hemiarthroplasty. Current trends. 1998 Jul Currently, a debate exists regarding the indications for hemiarthroplasty and total shoulder arthroplasty. A number of factors are important in making this decision. The article discusses some of the variables related to choosing the appropriate procedure for every patient. The authors also discuss their approach to various arthritic conditions of the shoulder, the rationale behind their approach, and their results. Future work will be necessary before more definitive recommendations can be made, and they may well be different for each individual surgeon.
9783766 A long-term five-year randomized controlled trial of hydroxychloroquine, sodium aurothioma 1998 Sep OBJECTIVE: To compare the efficacy of hydroxychloroquine, penicillamine, sodium aurothiomalate and auranofin in the treatment of active rheumatoid arthritis over a period of 5 yr. METHOD: Five hundred and forty-one patients with definite or classical rheumatoid arthritis were entered into an open randomized controlled trial with a flexible dose regimen designed to reflect clinical practice. Decisions to stop treatment with any one of the disease-modifying anti-rheumatic drugs (DMARDs) were based on an agreed trial protocol which defined criteria for adverse reactions and therapeutic failure. The managing physicians' decisions were confirmed in a separate monitor clinic. RESULTS: The proportion of patients who remained on their first DMARD or who were in remission at 5 yr was 53% for penicillamine, 34% for sodium aurothiomalate, 31%, for auranofin and 30% for hydroxychloroquine (P < 0.001). In patients who stayed on their first DMARD, all groups showed a 30-50% improvement in C-reactive protein, erythrocyte sedimentation rate, Ritchie Index and joint stiffness, and a deterioration in their Larsen score. There was no evidence of physician bias to explain the larger proportion of patients remaining on penicillamine for 5 yr. CONCLUSION: Despite the increased popularity of sulphasalazine and inmmunosuppressives, the drugs in this study continue to be used worldwide. The natural history of rheumatoid arthritis requires long-term follow up to establish drug efficacy. Evidence is needed as to whether the newer regimens will prove to be more effective and safer in the longer term than the commonly prescribed DMARDs. The data from this trial will provide a reference for comparison with future studies.
9482920 Model studies directed toward the application of boron neutron capture therapy to rheumato 1998 Mar 3 The application of boron neutron capture therapy to rheumatoid arthritis requires the selective delivery of the boron-10 isotope to the synovitic tissue. The use of liposomes as a boron delivery method has been explored through the measurement of the time course biodistribution of boron in rats with collagen-induced arthritis (CIA). Small unilamellar vesicles were composed of a 1:1 mixture of distearoylphosphatidylcholine and cholesterol, incorporated K[nido-7-CH3(CH2)15-7,8-C2B9H11] as an addend in the lipid bilayer and encapsulated Na3[a2-B20H17NH2CH2CH2NH2] in the aqueous core. The tissue concentration of boron delivered by liposomes was determined by inductively coupled plasma-atomic emission spectroscopy after intravenous injection of liposome suspensions into Louvain rats with CIA. With the low injected doses of boron used [13-18 mg of boron per kg (body weight)], the peak boron concentration observed in arthritic synovium was 29 microg of boron per g of tissue. The highest synovium/blood boron ratio observed was 3.0, when the synovial boron concentration was 22 microg of boron per g of tissue. In an attempt to increase the synovium/blood boron ratio by lowering the blood boron concentration, a liposomal formulation characterized by a shorter blood clearance time was examined. Thus, the biodistribution of liposomes with additional K[nido-7-CH3(CH2)15-7, 8-C2B9H11] incorporated in the vesicle membrane not only demonstrated more rapid blood clearance and slightly higher synovium/blood boron ratios but also exhibited reduced boron uptake in synovial tissue. These studies with boron neutron capture therapy for CIA suggest that this form of therapy may be feasible in the treatment of rheumatoid arthritis.
10817568 Stimulation of 92-kd gelatinase (matrix metalloproteinase 9) production by interleukin-17 2000 May OBJECTIVE: To examine the cellular mechanisms by which the proinflammatory cytokine interleukin-17 (IL-17) induces the synthesis of 92-kd gelatinase (matrix metalloproteinase 9 [MMP-9]) by human monocyte/ macrophages in primary culture. METHODS: IL-17-stimulated human monocytes isolated from the peripheral blood of healthy donors were cultured in the presence of antiinflammatory cytokines, neutralizing antibodies against IL-1beta, tumor necrosis factor alpha (TNFalpha), or IL-1 receptor antagonist, and with protein kinase inhibitors of diverse specificity. MMP measurements were performed using specific enzyme-linked immunosorbent assays, while the expression of specific messenger RNA was determined by Northern blotting. Detection of phosphorylated proteins and specific transcriptional factors was performed by Western blotting and by gel retardation experiments, respectively. RESULTS: Biologically active IL-17 was detected in the synovial fluid of patients with rheumatoid arthritis. IL-17-induced MMP-9 production in human monocyte/ macrophages was dependent on endogenous prostaglandin E2 synthesis and related to autocrine stimulation by TNFalpha, but was IL-1beta independent. This activation involves both p42/44 and p38 kinases and nuclear factor kappaB. IL-17-inducible activator protein 1 and signal transducer and activator of transcription 1/3 may transactivate the MMP-9 promoter. CONCLUSION: IL-17 may contribute to an unbalanced production of proinflammatory cytokines and MMP-9 in diseased articular joint tissues by interacting with the macrophages in the rheumatoid synovium.
9632091 Chloroquine related cardiac toxicity. 1998 Jun Chloroquine, an agent used in treatment and prophylaxis of malaria, and also known for its antiinflammatory effects in dermatological, rheumatological, and connective tissue disorders, has been reported to cause toxicity, most commonly in the retina and the cardiovascular system. We describe a 60-year-old woman with longstanding rheumatoid arthritis receiving multidrug treatment, including prolonged administration of chloroquine. She developed complete heart block requiring a permanent pacemaker, congestive heart failure, and progressive myopathy. During hospital investigations for her myopathy, she died of acute pulmonary thromboembolism. Although hypertension and possibly amyloidosis were thought to be the cause of her cardiac disease, cardiac and skeletal muscle changes characteristic of chloroquine toxicity were observed. Chloroquine may be an important unsuspected contributing cause of cardiac dysfunction in patients with rheumatological disease. Endomyocardial biopsy should be considered early in the course of diagnosis and management.
9198366 [Focal segmental glomerulosclerosis presenting nephrotic syndrome and acute renal failure 1997 May A 45-year-old woman with rheumatoid arthritis(RA) who developed nephrotic syndrome and acute renal failure was reported. She first noticed polyarthritis in June 1990, and was diagnosed as RA. Since her RA was not controlled with nonsteroidal anti-inflammatory drugs (NSAID), she started taking prednisolone 10 mg daily and received 100 mg of D-penicillamine from October 1990 with improvement of the RA. In March 1991, she noticed edema of the face and legs, at which time massive proteinuria and hematuria were first noted. Because of her nephrosis, she was referred to our hospital for further evaluation. Laboratory investigations revealed 24-hour urine proteinuria of 37 g, serum creatinine, 2.7 mg/dl, blood urea nitrogen, 43.5 mg/dl, total protein, 4.1 g/dl, albumin, 1.5 mg/dl, and total cholesterol, 600 mg/dl. The rheumatoid factor and anti-nuclear antibody were positive. Renal biopsy showed focal segmental glomerulosclerosis (FSGS). Her nephrotic syndrome and renal dysfunction recovered after the administration of prednisolone at 60 mg/day. The possible pathogenesis of FSGS in patients with RA was discussed.
11641084 [Methotrexate, liver and rheumatoid arthritis in tropical areas]. 2001 Jul Rheumatoid arthritis (RA) is a common disease in tropical areas. Methotrexate which has become the main first-line treatment in western countries is increasingly used in tropics. Well documented liver toxicity of methotrexate led the American College of Rheumatology to provide guidelines about monitoring patients. In endemic areas of hepatitis B and C methotrexate may interfere with the natural history of these infections and exarcerbate liver damage, on the other hand, RA causes extra-articular manifestations which are rare and exceptionnally serious in the liver. The most important hepatic disorders associated with RA are: intrahepatic portal hypertension without cirrhosis, amyloidosis, drug hepato-toxicity and viral interferences. - Intrahepatic portal hypertension Several cases of portal hypertension without cirrhosis have been reported. Most cases were related to Nodural Regenerative Hyperplasia (NRH) which is made of diffuse nodules of hepatocytes without fibrosis. The pathogenesis of this entity is unknown. Distal vascular changes and abnormal perfusion of liver are mentioned. Presentation is cholestasis in one third of cases. Portal hypertension has no particularity and may cause esophageal variceal bleeding. NRH is closely associateed with Felty's syndrome. - Amyloidosis Hepatic amyloidosis is a classical complication of RA even rare. It is a secondary amyloidosis of AA type. Hepatic injury is generally silent and renal symptoms are dominant. - Drug hepatotoxicity Several medications used in the management of RA are potentially hepatotoxic : salicylates, nonsteroidal antiinflammatory drugs (NSAID), corticosteroids, gold, sulfasalazine and methotrexate above all. Methotrexate hepatotoxicity is well documented in carcinology with high doses but also in psoriasis patients treated with low doses. Hepatic damage related to methotrexate includes elevation of aminotransferases, portal fibrosis and cirrhosis. But data on methotrexate toxicity show small risk of serious liver disease in RA patients. Long duration of therapy and age (> 60 years) have been found to be independent risk factors for the development of hepatic disease. Other identified risk factors are alcohol intake, diabetes, obesity and prior history of hepatitis B or C. The American College of Rheumatology has published guidelines about monitoring patients for liver toxicity. Hepatic tests and Hepatitis B and C serologic studies are recommended before starting treatment with methotrexate. Liver biopsy is only recommended in case of alcoholism, prolonged abnormalities of aminotransferases and chronic hepatitis B or C infection. - Methotrexate and hepatitis B or C infection These infections are endemic in tropical areas. Chronic hepatitis B or C is a contra indication for methotrexate therapy, due to the immuno-suppressive effect of the drug. Positive ELISA tests to C virus must be confirmed with RIBA tests to avoïd false positive tests which have been reported in Africa. The "healthy" HBs Ag carrier state is not in theory a contra indication for methotrexate therapy but the risk of hepatitis B reactivation needs a close monitoring. The biological tests required for are sophisticated and quite impossible in routine practice in tropical areas. So HBs Ag carrier state is usually incompatible with methotrexate treatment. Studies would be useful to prove that in endemic areas of viral hepatitis B and C as in western countries, methotrexate is enough safe to become the main first-line treatment of rheumatoid arthritis.
9822289 In vitro differentiation of peripheral blood T cells towards a type 2 phenotype is impaire 1998 Nov We have examined the capacity of peripheral blood T cells from RA patients to be polarized in vitro towards a type 1 (T1) or a type 2 (T2) phenotype. Peripheral blood T cells from RA patients and from healthy donors were primed by 1 week of culture with soluble OKT3 in the presence of polarizing cytokines. The recovered T cells were restimulated and their cytokine secretion profile determined. Priming of T cells from RA patients in the presence of recombinant (r)IL-2 plus rIL-12 induced a shift towards a TI pattern, characterized by increased production of interferon-gamma, that was more pronounced than in the case of healthy donors. Conversely, priming of T cells from RA patients in the presence of IL-4 failed to induce a shift towards a T2 profile after 1 week, whereas it induced T cells from healthy donors to acquire such a profile characterized by heightened production of IL-4, IL-5 and IL-13. However, a T2 polarization profile emerged in T cells from RA patients that were primed in the presence of rIL-4 and subsequently maintained in culture in rIL-2 alone for 1 or 2 additional weeks. We conclude that in vitro differentiation of peripheral T cells towards a type 2 phenotype is impaired in RA. Nevertheless, conditions required to drive peripheral T cells towards a type 2 phenotype were established. Administration of autologous polyclonal T cells expressing a type 2 cytokine secretion profile is proposed as a therapeutic strategy in RA.
15529574 Lectin-binding profile of serum IgA in women suffering from systemic autoimmune rheumatic 2000 In many pathological states changes in the carbohydrate part of serum glycoproteins occur, the etiopathogenic role or diagnosis significance of these abnormally glycosylated glycoproteins being relevant in many instances. The aim of this study was to determine the glycosylation pattern of the serum immunoglobulin A (IgA) in young women suffering from systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), by comparison with that in healthy ones. We used lectin proteins as bivalent reagents to selectively and specifically recognize and bind the different oligosaccharides at the surface of the IgA molecules and precipitate them. The serum IgA level in the SLE and RA women included in this study was of 4 and respectively 6 times greater than in control women. Our experiments revealed for the IgA isolated from SLE women a very low degree of glycosylation, as follows: in the Fc region, we detected a markedly reduced level of the unbisected, biantennary oligosaccharides (by 72.8%) and of the unbisected, tri- and tetraantennary oligosaccharides (by 40%), accompanied by a slightly increased level of the bisected (by 14.7%) and fucosylated (by 13.3%) oligosaccharides; in the hinge region, a marked degalactosylation (by 74.4%) of the oligosaccharides was revealed; the sialylation degree of the IgA molecules was thus reduced by 71.2%. Related to it, it is reasonable to presume a certain role of the degalactosylated IgA fraction in renal tissue deposition of IgA in SLE patients, as it has been ascribed to this fraction in IgA nephropathy. Referring to the IgA isolated from RA women, we showed that it selectively bound the lectins, but lacked the property to be lectin-precipitated, most probably due to an altered arrangement of the oligosaccharide chains at the surface of the glycoprotein.
11583978 Fractalkine: a novel angiogenic chemokine in rheumatoid arthritis. 2001 Oct Angiogenesis is an important aspect of the vasculoproliferation found in the rheumatoid arthritic (RA) pannus. We have previously implicated members of the CXC chemokine family as potent angiogenic mediators in RA. We investigated the possibility that the sole member of the CX(3)C chemokine family, fractalkine (fkn), induces angiogenesis and that fkn might mediate angiogenesis in RA. Recombinant human fkn significantly induced migration of human dermal microvascular endothelial cells (HMVECs), a facet of the angiogenic response, in the pmol/L range in a concentration-dependent manner (P < 0.05). Fkn also induced the formation of significantly more endothelial tubes on Matrigel than did a negative control (P < 0.05). Fkn significantly induced 2.3-fold more blood vessel growth than control in the in vivo Matrigel plug assays (P < 0.05). We identified HMVEC expression of the fkn receptor, CX(3)CR1. Next, we determined if RA synovial fluid (SF)-induced angiogenesis was fkn-dependent. SFs from six RA patients immunodepleted of soluble fkn induced 56% less migration of HMVECs than did sham-depleted RA SFs (P < 0.05). In vivo, immunodepletion of fkn from six RA SFs significantly inhibited their angiogenic activity in Matrigel plug assays (P < 0.05). Immunodepletion of fkn from five RA synovial tissue homogenates inhibited their ability to induce angiogenesis in in vivo Matrigel plug assays (P < 0.05). These results establish a new function for fkn as an angiogenic mediator and suggest that it may mediate angiogenesis in RA.
10891888 Anti-TNF therapies in rheumatoid arthritis, Crohn's disease, sepsis, and myelodysplastic s 2000 Aug 1 An attempt has been made in this article to summarize the state-of-the-art clinical experience with the use of anti-TNF therapies in four diseased states with special emphasis on myelodysplastic syndromes. Given the central role of TNF-alpha in initiating and perpetuating the chronic damage produced in the diseased organs by controlling a cascade of pro-inflammatory cytokines, as well as its acute role in sepsis, theoretically speaking, neutralization of this peptide was a natural therapeutic choice. Results of the initial clinical trials appear encouraging and sometimes dramatic in their efficacy. The mechanism of response however, is interesting in that even when TNF-alpha is directly targeted by a monoclonal antibody, the resulting benefits can frequently not be attributed to TNF suppression alone. Rather, it appears that a more general effect on the T-lymphocytes is also contributing to the responses being seen. This raises the new possibility of combining anti-cytokine and anti-T-cell strategies to treat at least the more chronic diseases such as Crohn's disease and myelodysplastic syndromes. Continued clinical trials testing these strategies are clearly warranted.
11740751 Low contact stress mobile bearing total knee arthroplasty: results at 5 to 13 years. 2001 Dec A total of 139 mobile bearing knee arthroplasties in 104 patients were evaluated at a mean follow-up of 7.8 years (range, 5-13 years). There were 80 cemented knees, 50 uncemented, and 9 hybrid (cemented tibia, uncemented femur). Ten knees were revised. Four knees were revised for aseptic loosening of an uncemented tibial component, and 1 knee was revised for loosening of an uncemented femoral component. One knee was revised for a recurrent dislocating bearing, and 1 knee was revised for instability. No mechanical loosening occurred in the cemented components. Three knee arthroplasties were revised for infection. A total of 66 patients (92 knees) were evaluated clinically and radiographically. Radiographic evaluation showed a 27% incidence of radiolucent lines for the femur and a 31% incidence of radiolucent lines for the tibia. No components were considered radiographically loose. The survivorship of mobile bearing knee arthroplasties was 93% at an average follow-up of 7.8 years. Aseptic loosening was statistically higher in uncemented components (P=.0051).
10825583 Germ-free mice do not develop ankylosing enthesopathy, a spontaneous joint disease. 2000 Jun Ankylosing enthesopathy (ANKENT) is a naturally occurring joint disease in mice with numerous parallels to human ankylosing spondylitis (AS). Similarities between AS and ANKENT include not only affected tissue (joint entheses) but also association of the disease with genetic background, including MHC genes, gender, and age. Young males with the C57Bl/10 background have been described to suffer from ANKENT and, among H-2 congenic strains, high frequency of afflicted joints has been recorded in B10.BR (H-2(k)) males. Interestingly, the incidence of ANKENT is higher in conventional (CV) males that in their specific-pathogen-free (SPF) counterparts. The latter finding suggests that microbes could play a role as an ANKENT-triggering agent. To further examine this hypothesis we have established a germ-free (GF) colony of B10.BR mice and observed ANKENT incidence in both GF males and their conventionalized (ex-GF) male littermates; 20% of ex-GF males developed ANKENT before 1 year of age. In contrast, no joint disease was observed under GF conditions (p < 0.0001). Our results show that live microflora is required in ANKENT pathogenesis.
9361164 The use of folates concomitantly with low-dose pulse methotrexate. 1997 Nov Toxicities related to low-dose weekly methotrexate are largely due to its antifolate properties. Preexisting folate deficiency is associated with methotrexate toxicity in some patients. At the onset of methotrexate therapy and throughout therapy, the physician should be vigilant regarding one or more nutrient deficiencies. A multivitamin and, where appropriate, specific daily folic acid supplements should be employed. The only regimen known presently (through controlled trials) to treat side effects is the low-dose folinic acid (leucovorin) protocol outlined herein. Folic acid may be helpful to treat mild gastrointestinal symptoms. Folinic acid supplementation should be considered prophylactically in those requiring methotrexate who are at increased risk of hepatic disease. Other possible factors besides methotrexate should always be considered with the onset of new patient complaints or laboratory abnormalities. Claims that folic acid therapy is safer and more convenient than folinic acid seem unwarranted when one reviews the literature carefully. Cost differences between folic acid supplementation and folinic acid supplementation have been exaggerated.
9812572 [HLA-DRB1 alleles genotyping in patients with rheumatoid arthritis in Chinese]. 1997 To explore the role of HLA-DRB1 genes in the development of rheumatoid arthritis (RA) and the correlations between HLA-DR alleles and clinical manifestations of patients with RA we studied 86 patients and 106 race matched controls in whom HLA-DR typing was performed by the method of DNA amplification with sequence-specific primers (PCR-SSP). The subtypes of HLA-DR4 were determined by the method of hybridization of PCR products with sequence-specific oligonucletides (PCR-SSO). The absence or presence of HLA-DR4 and its subtypes was evaluated with the clinical and serological characteristics of the patients. Compared with controls, an increased gene frequency of HLA-DR4 (48.8% vs 17.9%, P < 0.001) and a decreased frequency of HLA-DR5 (16.3% vs 27.4%, P = 0.06) were found. The DRB1 * 0405 accounted for 61.9% of DR4+ RA patients and 21.1% of DR+4 controls (P < 0.01). There was no difference between the DR4+ and DR4- patients with respect to age, sex, duration of disease, extra-articular manifestations including secondary Sjogren's syndrome. But rheumatoid factor (RF) was associated with HLA-DR4 (P < 0.05). According to the X-ray stage, the patients of DR4+ were more severe than those of DR4- (P < 0.05). HLA-DR4 and DR4 subtype of DRB1 * 0405 were related to the development of RA in Chinese. HLA-DR4 can be a useful prognostic marker in the patients with RA.
10065477 [Rheumatic diseases of the ankle joint and tarsus]. 1999 Jan Diseases of the hindfoot are associated with considerable functional impairment and therefore may hamper patients' movements during gait considerably. Because of biomechanical overload, articular structures, tendons and ligaments are prone to early degenerative changes during the course of rheumatic diseases as visible with plain film radiography, sonography (US), or magnetic resonance imaging (MRI). Findings may occur as arthritis of major joints or in the form of fibroostitis and bursitis of the os calcis. Despite the progressive course of rheumatic diseases and characteristic imaging findings, high variability of X-ray signs may occur. Plain film radiograms and high-resolution ultrasonography play a key role in imaging rheumatic diseases of the hindfoot. MRI supports imaging diagnosis in selected cases. The principal goals of diagnostic imaging are precise and reproducible documentation of morphologic abnormalities and differentiated analysis for planning proper conservative or surgical treatment.
11716371 Comparison of fixed-bearing and mobile-bearing total knee arthroplasties. 2001 Nov The purpose of the current study was to directly compare the results of fixed-bearing and mobile-bearing total knee arthroplasties in the same patient who had bilateral simultaneous total knee replacements. A fixed-bearing total knee prosthesis (AMK) was implanted in one knee and a mobile-bearing total knee prosthesis (LCS) was implanted in the other knee in 116 patients. The average age of the patients was 65 years (range, 33-70 years). The average followup was 7.4 years (range, 6-8 years). Clinical and radiographic followup was done using Knee Society and Hospital for Special Surgery knee rating systems at 6 weeks, 3 months, 6 months, 1 year after surgery, and yearly thereafter. Total knee score, pain score, mean functional score, and range of motion were comparable in both groups. Two knee replacements (2%) in one patient with AMK prostheses were revised because of complete wear of tibial bearing polyethylene. One knee replacement (1%) in one patient with an LCS prosthesis was revised because of dislocation of the medial tibial bearing polyethylene and one knee replacement (1%) in one patient with an LCS prosthesis was revised because of complete wear of the medial tibial bearing polyethylene. No knee had aseptic loosening or osteolysis in either group. After a minimum followup of 6 years, the results of fixed- and mobile-bearing total knee prostheses in the current series are favorable. However, there is no evidence to prove the superiority of the mobile-bearing total knee design.
11280103 Healthcare resource utilisation and costs of treating NSAID-associated gastrointestinal to 2001 OBJECTIVE: The aim of the study was to perform an economic analysis of a new therapy in 11 countries (Australia, Belgium, Finland, France, Germany, Italy, The Netherlands, Spain, Sweden, Switzerland and the UK) to assess the cost of treating the gastrointestinal (GI) events associated with the use of nonsteroidal anti-inflammatory drugs in patients with osteoarthritis and rheumatoid arthritis. METHODS: Estimates of GI event-related costs were based on the results of resource utilisation questionnaires. Resources required for the treatment and follow-up of GI events were identified and converted into costs from society and payer perspectives. RESULTS: From the perspective of society, the total per-event cost of managing GI-related events varies from $US51 to $US772 for GI discomfort, from $US108 to $US1100 for anaemia, from $US145 to $US1200 for ulcer and from $US1923 to $US5473 for serious GI events requiring hospitalisation. From the payer perspective, the total per-event cost varies from $US47 to $US680 for GI discomfort, from $US144 to $US762 for anaemia, from $US229 to $US795 for ulcer and from $US1787 to $US6729 for serious GI events requiring hospitalisation. The total cost is driven by hospital expenses for those events requiring hospital admission. For GI discomfort, physician consultations are generally the cost driver, whereas for ulcer and anaemia, cost is primarily driven by the rate of endoscopy. CONCLUSIONS: Costs associated with nonsteroidal anti-inflammatory drug-related GI events differ significantly across countries as a result of variations in resources consumed and price/tariff policies.