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D H Yoo

Publications and source records attributed to D H Yoo.

At least 19 recordsLinked to original sources
PubMed2005

The influence of a polymorphism at position -857 of the tumour necrosis factor alpha gene on clinical response to etanercept therapy in rheumatoid arthritis.

OBJECTIVES: We aimed to test whether polymorphisms in the etanercept target genes TNFA and LTA are associated with clinical responses to etanercept therapy in RA patients. METHODS: Clinical responses of 70 patients treated with etanercept were determined according to the ACR criteria. We genotyped 13 single-nucleotide polymorphisms (SNPs) within TNFA and LTA and tested whether they influenced the responses to 12 weeks of etanercept therapy. Univariate and multivariate analyses were performed to compare allele, genotype and haplotype distributions between responders and non-responders. RESULTS: Association of the -857C/T SNP at the TNFA promoter was marginally significant when patients were divided into responders and non-responders according to improvement criteria ACR20 or ACR70. When ACR70 responders (the best responders) were compared with ACR20 non-responders (the worst responders), however, the association was prominent [odds ratio (OR) = 12, 95% confidence interval (CI) = 1.4-105, P = 0.0077, P(corrected) = 0.054], as the frequency of the T allele was 5% in the ACR20 non-responders but 39% in the ACR70 responders. Moreover, the ratio of ACR70 responder number to ACR20 non-responder number among T-allele carriers was >10-fold higher than in the C-allele homozygotes (OR = 12, 95% CI = 1.2-120, P = 0.033). CONCLUSIONS: RA patients with the T allele of TNFA -857C/T SNP respond better to etanercept therapy than homozygotes for the C allele, indicating that, when the results have been confirmed, this SNP could become a useful genetic marker for predicting responses.

Adult↗
PubMed2005

Macrophagic myofasciitis unrelated to vaccination.

Macrophagic myofasciitis (MMF) is known to be closely associated to vaccination containing aluminium as an adjuvant. Here we describe a case of MMF unrelated to vaccination, and presented as focal tender muscle in a 59-year-old woman. Magnetic resonance imaging showed evidence of unilateral myofasciitis involving muscles and fascias of the vastus lateralis. Open biopsy showed a unique pathological pattern of MMF. Our case suggests that other causes unrelated to vaccination need to be investigated in the pathogenesis of MMF, and MMF could be considered in the differential diagnosis of patients with focal muscle tenderness.

Biopsy↗
PubMed2005

A case report: isolated a heavy chain monoclonal gammopathy in a patient with polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy and skin change syndrome.

A 45-year-old South-Korean man presented with abdominal distension, progressive paresthesia and motor weakness of both lower extremities. Our case was identified as polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy and skin change (POEMS) syndrome based on diagnostic criteria. Circulating M components of POEMS syndrome consist mainly of IgG or IgA-lambda and rarely IgM-lambda, IgG-kappa or isolated light chains. In this case, the M-band on serum protein electrophoresis and isolated IgA heavy chain on serum immunofixation electrophoresis were demonstrated, but there was no abnormal light chain. We suggest that this case may be associated with a pattern of abnormal secretion of monoclonal protein or a coincidence of a heavy chain disease in POEMS syndrome, even though the latter possibility may be very rare.

Bone Marrow↗
PubMed2005

The association between fcgammaRIIIB polymorphisms and systemic lupus erythematosus in Korea.

Polymorphisms of FcgammaR have been proposed as genetic factors that influence susceptibility to SLE. FcgammaRIIIB polymorphism in systemic lupus erythematosus (SLE) have been studied in various populations, but the results were inconsistent. The aim of this study was to determine the association of FcgammaRIIIB polymorphism in Korean lupus patients. One-hundred and eighty-three SLE patients (166 female, 17 male) meeting 1982 ACR criteria and 300 Korean disease-free controls were enrolled. Genotyping for the FcgammaRIIIB NA1/NA2 was performed by PCR of genomic DNA using allele-specific primers. There was no significant skewing in the distribution of the three FcgammaRIIIB genotypes, and alleles between SLE and the controls. The frequency of FcgammaRIIIB genotypes in SLE patients and controls was FcgammaRIIIB NA1/NA1 27.9% versus 26%, NA1/NA2 55.2% versus 51.7%, NA2/NA2 16.9% versus 22.3%, respectively. The gene frequencies of NA1 allele were 0.56 in the SLE and 0.52 in controls, respectively. Among clinical manifestations, thrombocytopenia was more common in FcgammaRIIIB NA2/NA2 genotype (P = 0.04, OR 2.4, 95% CI 1.0-5.4), and NA2 allele (P = 0.03, OR 1.7, 95% CI 1.1-2.8). Although FcgammaRIIIB polymorphism was not associated with the development of SLE in Korean, thrombocytopenia was associated with FcgammaRIIIB NA2/NA2 genotype, and NA2 allele.

Adult↗
PubMed2003

Independent association of HLA-DR and FCgamma receptor polymorphisms in Korean patients with systemic lupus erythematosus.

OBJECTIVES: To determine the distribution of HLA-DR type and FcgammaRIIa/IIIa polymorphisms, and to analyse the combined effects of these genes for susceptibility in Korean systemic lupus erythematosus (SLE) patients. METHODS: A total of 299 SLE patients meeting 1982 ACR criteria and 144 Korean disease-free controls were enrolled. Genotyping for the FcgammaRIIa 131 R/H and FcgammaRIIIa 176 F/V was performed by polymerase chain reaction (PCR) of genomic DNA using allele-specific primers. HLA-DRB1 typing was performed by the PCR-SSOP method. RESULTS: There was significant skewing in the distribution of the three FcgammaRIIa genotypes between the SLE patients and the controls [P = 0.002 for R/R131 vs R/H131 and H/H131, relative risk (RR) 2.6 (95% CI 1.3-5.2)], but not in FcgammaRIIIa genotypes. HLA-DRB1*15 allele was significantly more prevalent among SLE patients than the control population [P < 0.02, RR = 1.7 (1.1-2.6)]. HLA-DRB1 genotypes or allele frequencies of the SLE patients with nephritis did not differ significantly from those of the SLE patients without nephritis. We analysed the combined effects of the two candidate genes on SLE susceptibility. HLA-DRB1*15 allele was a significant predictor of SLE in individuals who were not homozygous for FcgammaRIIa-R/R131 [RR = 2.1 (1.2-3.7), P < 0.008], and the FcgammaRIIa-R/R131 genotype vice versa [RR = 5.3 (1.9-15.4), P < 0.001]. However, an additive or synergistic effect of both susceptible genes on relative risk for SLE was not evident. CONCLUSIONS: Our results suggest that FcgammaRIIa-R/R131 homozygote and HLA-DRB1*15 allele are independent risk factors in Korean SLE patients without additive or synergistic effects.

Adult↗
PubMed2003

Quality of marital life in Korean patients with spondyloarthropathy.

The objectives of this study were to assess the quality of marital life (QML) in patients with spondyloarthropathy (SpA) in Korea and to identify possible gender differences in QML in patients with SpA. This was a case-control study at the outpatient unit of a tertiary care medical centre. Subjects were the patient group, composed of 47 married patients with SpA, and a comparison group composed of 47 healthy married adults with similar demographic characteristics. QML was measured using the Marital Satisfaction Inventory, Revised. As a result, QML was similar for both the male patients and the healthy men. However, the female patients had higher scores on the global distress scale (59.8 +/- 6.3 vs. 53.8 +/- 5.6, P=0.021) and the aggression scale (50.5 +/- 7.9 vs. 44.3 +/- 5.4, P=0.016) than the female comparison group. At the same time, the female patients demonstrated higher scores on the global distress scale (59.8 +/- 6.3 vs. 54.7 +/- 7.2, P=0.035) than the male patients. In conclusion, QML in Korean males with SpA was not greatly different from that of the male comparison group. However, QML in the female patients was characterised by higher global distress and a higher probability of aggression from their partner, but no significant sexual dissatisfaction.

Adaptation, Psychological↗
PubMed2003

Actinomycin D renders cultured synovial fibroblasts susceptible to tumour necrosis factor related apoptosis-inducing ligand (TRAIL)-induced apoptosis.

OBJECTIVE: To investigate the expression of tumour necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) receptors in cultured synovial fibroblasts from rheumatoid arthritis (RA) and osteoarthritis (OA) patients, and to examine their susceptibility to TRAIL-induced apoptosis in the presence or absence of metabolic inhibitors. METHODS: The expression of TRAIL receptors in synovial fibroblasts was examined by Western blot and immunohistochemistry. Expression of TRAIL-receptor 1 (TRAIL-R1), FLICE-inhibitory protein (Fas-associating protein with death domain-like interleukin-1-converting enzyme), and Bcl-2 was assessed by Western blot. Synovial cell viability was measured by 2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide assay (XTT), and apoptosis was determined both by DNA content analysis after propidium iodide staining and Annexin V stain. RESULTS: TRAIL-R1 was constitutively expressed on cultured synovial fibroblasts from RA and OA, however, expression of TRAIL-R2 and TRAIL-R3 was not observed by immunohistochemistry and Western blot. Cultured synovial fibroblasts were resistant to apoptosis by TRAIL alone, but combined treatment of TRAIL with actinomycin D (ActD: 200 ng/mL), cycloheximide (CHX: 10 microg/mL), or proteasome inhibitor (MG132: 20 microM) induced apoptosis in a dose-dependent manner. The apoptosis was completely or partially inhibited by various caspase inhibitors, implicating an involvement of caspase pathway in TRAIL-induced apoptosis in the presence of these metabolic inhibitors. Expression of TRAIL-R1, FLIPL, and Bcl-2 did not account for the apoptosis by the combined treatment of TRAIL with ActD. CONCLUSIONS: Although TRAIL-R1 was constitutively expressed; cultured synovial fibroblasts were resistant to apoptosis by TRAIL. ActD, CHX, and MG132 rendered cultured synovial fibroblasts susceptible to TRAIL-induced apoptosis by a caspase-dependent mechanism. However, the exact mechanism of sensitization by these metabolic inhibitors remains to be determined.

Apoptosis↗
PubMed2002

Increased expression of pro-inflammatory cytokines and metalloproteinase-1 by TGF-beta1 in synovial fibroblasts from rheumatoid arthritis and normal individuals.

Transforming growth factor (TGF)-beta1 is expressed abundantly in the rheumatoid synovium. In this study, the inflammatory effect of TGF-beta1 in rheumatoid arthritis (RA) was investigated using cultured fibroblast-like synoviocytes (FLS) from RA and osteoarthritis (OA) patients, as well as non-arthritic individuals. mRNA expressions of IL-1beta, tumour necrosis factor (TNF)-alpha, IL-8, macrophage inflammatory protein (MIP)-1alpha and metalloproteinase (MMP)-1 were increased in RA and OA FLS by TGF-beta1 treatment, but not in non-arthritic FLS. Enhanced protein expression of IL-1beta, IL-8 and MMP-1 was also observed in RA FLS. Moreover, TGF-beta1 showed a synergistic effect in increasing protein expression of IL-1beta and matrix metalloproteinase (MMP)-1 with TNFalpha and IL-1beta, respectively. Biological activity of IL-1 determined by mouse thymocyte proliferation assay was also enhanced by 50% in response to TGF-beta1 in the culture supernatant of RA FLS. DNA binding activities of nuclear factor (NF)-kappaB and activator protein (AP)-1 were shown to increase by TGF-beta1 as well. These results suggest that TGF-beta1 contributes for the progression of inflammation and joint destruction in RA, and this effect is specific for the arthritic synovial fibroblasts.

Arthritis, Rheumatoid↗
PubMed2002

Angiotensin-converting enzyme gene polymorphism and vascular manifestations in Korean patients with SLE.

Systemic lupus erythematosus (SLE) is an inflammatory multisystem disease of unknown etiology with immunologic aberrations. Many studies have shown that genetic and environmental factors are implicated in the development of SLE. Angiotensin-converting enzyme (ACE) affects various immune phenomena through the renin-angiotensin and kallikrein-kininogen systems by creating angiotensin II and inactivating bradykinin. We investigated the correlation between insertion/ deletion polymorphism of the ACE gene and the clinical manifestations of SLE, especially vascular involvement and lupus nephritis. Two-hundred and eleven Korean patients fulfilling the ACR criteria and 114 healthy subjects were enrolled. The ACE genotype was determined by polymerase chain reaction using genomic DNA from peripheral blood. The nephritis patients were classified by the WHO classification. In addition, the activity and chronicity index were used to assess the severity of renal involvement. We evaluated vascular involvement by the presence or absence of hypertension, Raynaud's phenomenon, livedo reticularis, antineutrophil cytoplasmic antibody and the SLICC/ACR Damage Index. The gene frequency of ACE gene polymorphism was as follows: II 39 vs 34%, ID 41 vs 50%, DD 20 vs 16% in SLE patients and controls, respectively. There was no difference in genotype frequency between both groups. There were no significant differences between the distribution of ACE gene genotypes and lupus nephritis and its related parameters, including WHO classification, activity index, chronicity index, renal dysfunction and amount of 24 h urinary protein. The ACE genotypes and alleles did not affect the presence of vascular manifestations evaluated, but the frequency of DD genotype was significantly low in SLE patients with Raynaud's phenomenon compared to those without Raynaud's phenomenon (P = 0.002 for ACE ID vs DD and II, OR 2.7, 95% CI 1.43-5.09; P=0.023 for ACE DD vs ID and II, OR 0.33, 95% CI 0.12-0.89). Also skewing from DD to II genotype was noted in patients with anti-Sm antibody compared to those without anti-Sm antibody (P = 0.025 for ACE DD vs ID and II, OR 0.21, 95% CI 0.05-0.93). The onset age of serositis was older in patients with the ID genotype than the others (ID= 34.5+/-10.8, II + DD = 25.6+/-10.2, P= 0.002). Also the onset age of malar rash was older in patients with II genotype than the others (II=26.7+/-8.4, ID+DD=21.3+/-9.0; P=0.021). The patients with I allele showed a significantly higher frequency of serositis (P = 0.022). Taken together, the I/D polymorphisms of ACE gene did not affect susceptibility of SLE, lupus nephritis and the vascular manifestations, including Raynaud's phenomenon, in Korean SLE patients, although the DD genotype was negatively associated with Raynaud's phenomenon among SLE patients. However, it would be valuable to evaluate the role of other genes potentially related to vascular events, such as endothelin, nitric oxide or angiotensin II receptor as well as ACE gene.

Adult↗
PubMed2001

Effects of peroxisome proliferator-activated receptor-gamma (PPAR-gamma) on the expression of inflammatory cytokines and apoptosis induction in rheumatoid synovial fibroblasts and monocytes.

This study was performed to investigate whether peroxisome proliterator-activated receptor-gamma (PPAR-gamma) exerted an anti-inflammatory effect on rheumatoid synovial cells and inhibited dysregulated proliferation. The expression of PPAR-gamma mRNA in cultured human synoviocytes and THP-1 cells was analysed by RT-PCR. PPAR-gamma was expressed in normal, osteoarthritis (OA), rheumatoid arthritis (RA) synovial cells as well as a human monocytic cell line, THP-1. In RA and OA synoviocytes, the induction of inflammatory cytokine mRNA expression such as TNF-alpha and IL-1beta was significantly inhibited by the natural PPAR-gamma agonist, 15 deoxy-Delta(12,14)prostaglandin J(2)(15d-PGJ(2)). The effect of PPAR-gamma on the nuclear factor (NF)-kappaB activity was tested by electrophoretic mobility shift assay (EMSA). Both troglitazone and 15d-PGJ(2)markedly inhibited TNF-alpha-induced NF-kappaB activation at 30 microM. However, PPAR-gamma agonist neither reduced proliferation nor induced apoptosis in RA synoviocytes when measured by XTT assay and fluorescence activated cell sorter (FACS) analysis. In contrast, it induced apoptosis in a dose-dependent manner in THP-1 cells and augmented TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis as well. In conclusion, these data demonstrate that PPAR-gamma is expressed in human synoviocytes and THP-1 cells, and the PPAR-gamma activation inhibits expression of inflammatory cytokines in RA synoviocytes. Furthermore, PPAR-gamma activation induces apoptosis by itself and augments TRAIL/Apo2L-induced apoptosis in THP-1 cells. These results suggest that PPAR-gamma agonists may provide a new therapeutic approach for RA.

Apoptosis↗
PubMed2001

Induction of remission with intravenous immunoglobulin and cyclophosphamide in steroid-resistant Evans' syndrome associated with dermatomyositis.

Evans' syndrome is characterised by the simultaneous or sequential occurrence of Coombs'-positive haemolytic anaemia (AIHA) and immune thrombocytopenia without underlying aetiology. It has been found to be associated with collagen vascular diseases, especially systemic lupus erythematosus (SLE) and scleroderma. However, Evans' syndrome with dermatomyositis is very rare. A 59-year-old woman, who had been taking high-dose prednisolone for a month and cyclosporin for 10 days for dermatomyositis, developed purpura on the left popliteal fossa. The platelet and haemoglobin levels decreased to 77,000/mm3 and 9.8 g/dl, respectively. Antiplatelet antibody was positive. Thrombocytopenia responded to intravenous immunoglobulin (IVIG) for a short time, but further decreased in a week. Her blood film showed features of haemolytic anaemia. Laboratory findings showed reticulocytosis and a positive direct Coombs' test. Bone marrow examination showed a mild hyperplasia of erythroid precursors and megakaryocytes. The patient was successfully treated with cyclophosphamide in addition to oral prednisolone. AIHA in connective tissue disease may develop gradually and show a benign clinical course in most patients. Therefore, we suggest that patients with dermatomyositis and anaemia should always be checked for haemolysis if there is no other explanation.

Anemia, Hemolytic, Autoimmune↗
PubMed2001

Cross-cultural adaptation and validation of Korean Western Ontario and McMaster Universities (WOMAC) and Lequesne osteoarthritis indices for clinical research.

OBJECTIVE: Our aims were to translate WOMAC and Lequesne osteoarthritis (OA) indices into Korean (KWOMAC, KLequesne) and confirm their reliability, validity, and responsiveness. DESIGN: The WOMAC and Lequesne indices were translated into Korean by three translators and translated back into English by three different translators. Fifty consecutive patients with OA were asked to rate the comprehensibility of the questions on a 4-point scale. The comprehensibility (responding with 'good' and 'very good') ranged from 78% to 99%. Test-retest was performed in another 47 patients with knee OA. The final 53 patients with knee OA, within the context of a clinical trial of two non-steroidal antiinflammatory drugs for 4 weeks, were studied to assess the internal consistency, construct validity, and responsiveness of the Korean versions. RESULTS: The test-retest reliability of the KWOMAC 3 subscales and the KLequesne yielded intraclass correlation coefficients of 0.79-0.89 and 0.87. The Cronbach standardized alphas were 0.81-0.96 and 0.75, respectively. For the construct validity, the correlation coefficients of both the KWOMAC subscales and the KLequesne with patient pain assessment and patient global assessment were between 0.30 and 0.70 and the KWOMAC subscales correlated with the KLequesne (0.41-0.55). For responsiveness, the KWOMAC and KLequesne scores significantly improved by 4-week post-treatment compared with pre-treatment; effect size values were between 0.41 and 0.69 for the KWOMAC subscales and 0.70 for the KLequesne; and the relative efficiency values of the KWOMAC subscales vs the KLequesne were between 0.87 and 0.90. CONCLUSIONS: The reliability, validity, and responsiveness of the KWOMAC and the KLequesne are confirmed.

Adult↗
PubMed2001

FcgammaRIIa/IIIa polymorphism and its association with clinical manifestations in Korean lupus patients.

The aim of this study was to determine the distribution of the FcgammaRlla and FcgammaRIIIa polymorphisms and their association with clinical manifestations in Korean lupus patients. Three hundred SLE (systemic lupus erythematosus) patients (48 male, 252 female) meeting 1982 ACR criteria and 197 Korean disease-free controls were enrolled. Genotyping for FcgammaRlla 131 R/H and FcgammaRIIIa 176 F/V was performed by PCR of genomic DNA using allele-specific primers and the FcgammaRIIIa genotype was confirmed by direct sequencing of PCR product in some cases. There was significant skewing in the distribution of the three FcgammaRIIa genotypes between the SLE and the controls (P=0.002 for R/R131 vs R/H131 and H/H131, OR 2.5 (95% Cl 1.4-4.5), but not in FcgammaRIIIa genotypes. FcgammaRIIa-R allele was a significant predictor of lupus nephritis, as compared with SLE patients without nephritis (P=0.034 for R131 vs H131, OR 1.4 (95% Cl 1.03-1.9)), but proliferative nephritis (WHO class III and IV) was less common in patients with FcgammaRlla-R/R131 and in FcgammaRIIa-R allele. In 300 SLE patients, high binding allele combination H131/V176 was less common in SLE with nephritis than in SLE without nephritis. Hemolytic anemia was less common in R131/F176 allele combination among four FcgammaRIIa/FcgammaRIIIa allelic combinations. Male SLE patients showed a higher frequency of renal involvement, serositis, thrombocytopenia, malar rash and discoid rash than female SLE, and male SLE had a higher frequency of FcgammaRIIa-R/R131 or R131-allele than male controls, but FcgammaRIIa or FcgammaRIIIa genotypes had no association with renal involvement in male SLE patients. FcgammaRIIa-H/H131 showed a higher frequency of hemolytic anemia and less pulmonary complications in male SLE. Female SLE patients showed higher frequency of any hematologic abnormality, lymphopenia, anticardiolipin antibody (+) and anti-Ro antibody (+) than male SLE, and had earlier onset of first symptoms. There was no skewing in FcgammaRIIa or FcgammaRIIIa genotypes between female SLE and female controls, but FcgammaRIIa-R131 allele showed skewing between female SLE with nephritis and female SLE without nephritis. The age at onset of thrombocytopenia was earlier in FcgammaRIIa R/R131 among three FcgammaRIIa genotypes, and serositis in FcgammaRIIIa-F/F176 among three FcgammaRIIIa genotypes. FcgammaRIIa-R131 homozygote was a major predisposing factor to the development of SLE and FcgammaRIIa-RI31 homozygote and R131 allele were a predisposing factor, and H131/V176 was a protective allele combination in lupus nephritis. In contrast to other ethnic patients, in our study cohort, clinical manifestation was different between male and female, and FcgammaRIIa and FcgammaRIIIa showed somewhat different clinical associations between the genders.

Adolescent↗
PubMed2001

Lupus flare associated with growth hormone.

This case illustrates a young man with an 11 y history of systemic lupus erythematosus who developed lupus flare after a 9-month use of growth hormone (GH) for the treatment of growth retardation. The course of disease was improving after GH cessation and treatment with high dose corticosteroids and intravenous cyclophosphamide pulse therapy.

Adult↗
PubMed2000

Seronegative spondyloarthropathy initiated by physical trauma.

We undertook this study to demonstrate the pattern of onset and the course of arthritis on the traumatised joint in spondyloarthropathy (SpA) initiated by physical trauma. Among 288 patients with SpA, 12 (4.2%) whose arthropathies were associated with trauma were reviewed retrospectively. There were seven patients with ankylosing spondylitis (AS), three with juvenile onset AS and two undifferentiated SpA. The type of trauma was direct injury to the joint and injuries at other sites, except in spinal surgery, for example. In eight cases the initial evidence of disease was peripheral arthritis. The disease first occurred in traumatised joints in five cases. Only three cases showed recurrent inflammatory episodes in the traumatised joints throughout the disease course. SpA initiated by trauma initially manifested as peripheral arthritis at the traumatised joints in about half of the cases. Inflammatory episodes preferentially involved other joints apart from the traumatised joints throughout the whole course of the disease.

Adolescent↗
PubMed2000

Mixed connective tissue disease associated with skin defects of livedoid vasculitis.

A 21-year-old woman who had a 2-year history of mixed connective tissue disease (MCTD) developed rapidly evolving ulcers consistent with livedoid vasculitis (LV) in all distal extremities. She presented clinically with Raynaud's phenomenon, polyarthritis and swollen hands; serologically with high titres of ANA and anti-nRNP; and immunogenetically with HLA-DR4 and HLA-DR53. Although there was initial success in treatment except for the skin defects over the ankles, the patient died from disseminated intravascular coagulation. We suggest that LV may be a poor prognostic manifestation in MCTD.

Adult↗
PubMed2000

Posterior tibial neuropathy by a Baker's cyst: case report.

Baker's cysts are rare cause of peripheral nerve entrapment and only a few cases of tibial nerve entrapment resulting from the popliteal cyst in the calf muscle have been reported in the literature. We present a case of rheumatoid arthritis complicated by a Baker's cyst with a tibial nerve entrapment. It is important to diagnose a Baker's cyst early and to differentiate it from thrombophlebitis, a popliteal aneurysm, tumor or muscle tear to effect optimal therapy and to obviate a potential neuropathy. Prompt recognition of these cases may save the patients unnecessary procedures and delay in treatment.

Arthritis, Rheumatoid↗