bluuebunny/crossref_metadata_2025_split huggingface dataset:
Magnetic resonance imaging of sacroiliac joint inflammation
Authors: Ahlström H. , Feltelius N. , Nyman R. , Hällgren R. 
Published: February 2007

AbstractA consecutive series of 27 patients with symptoms compatible with sacroiliitis underwent magnetic resonance imaging (MRI) of the sacroiliac joints. The diagnostic sensitivity of MRI was similar to that of computed tomography or conventional radiography. However, MRI seems to have the potential of providing unique information about the disease process in sacroiliitis by demonstrating abnormalities in subchondral bone and periarticular bone marrow. The results of this study suggest that early inflammatory changes in sacroiliitis occur in the subchondral structures of the sacroiliac joints.
Hla antigens in juvenile Arthritis
Authors: Fernandez‐Viña Marcelo A. , Fink Chester W. , Stastny Peter 
Published: February 2007

AbstractUsing DNA techniques, we investigated the role of HLA—DR, DQ, and DP alleles in susceptibility to juvenile arthritis (JA). We studied 2 groups of patients with JA having a different disease prognosis and course. The pauciarticular form is usually benign, while the polyarticular disease frequently leads to joint destruction and disability. Persistent pauciarticular disease developed preferentially in patients having HLA—DRw13‐Dw18 and DQw6‐Dw18, but these antigens did not confer susceptibility in patients whose disease converted to the polyarticular form. HLA—DPw2.1 was an additional susceptibility factor for patients with JA of pauciarticular onset. In the polyarticular form of JA, HLA—DPw3 was the major factor for susceptibility, giving a relative risk of 10.3 (P < 0.0001). In addition, we found that DRw8.1 and DQw4 were increased, and HLA—DR4 was markedly decreased, in patients with pauciarticular and polyarticular disease. These results indicate that in addition to some shared factors, distinct HLA class II alleles are important in pauciarticular or polyarticular JA. We conclude that typing with oligonucleotide probes may be useful in predicting the outcome in some children with arthritis.
Modulation of the effects of interleukin‐1 on glycosaminoglycan synthesis by the urine‐derived interleukin‐1 inhibitor, but not by interleukin‐6
Authors: Seckinger Philippe , Yaron Ilana , Meyer Frank A. , Yaron Michael , Dayer Jean‐Michel 
Published: February 2007

AbstractInterleukin‐1 (IL‐1) has been shown to regulate glycosaminoglycan (GAG) synthesis. We therefore investigated whether an IL‐1 inhibitor or IL‐6 modulates IL‐1 biologic activities in human synovial cells and cultured articular cartilage. We found that in the presence of a constant amount of IL‐1β, stimulation of hyaluronic acid (HA) synthesis by the IL‐1 inhibitor was inhibited in a dose‐dependent manner. Similarly, the decrease in sulfated GAG synthesis induced by IL‐1 was reversed by the addition of the IL‐1 inhibitor. In contrast, IL‐6 did not affect the production of HA, prostaglandin E2, or collagenase in synovial cells, nor did it affect GAG in organ cultures when tested in the presence or absence of IL‐1β. Hence, IL‐6 was ineffective in modulating IL‐1 bioactivities on HA or sulfated GAG synthesis. These results emphasize the importance of IL‐1 and IL‐1 inhibitor in connective tissue destruction and raise questions concerning the role of IL‐6 in this pathogenesis.
Organ distribution of the ro (SS‐A) antigen in the guinea pig
Authors: Itoh Yasuhiko , Kriet John D. , Reichlin Morris 
Published: February 2007

AbstractUsing an anti—Ro (SS‐A—specific “sandwich” enzyme‐linked immunosorbent assay (ELISA) and Western immunoblotting, we determined the Ro (SS‐A) content (both quantitative and qualitative) in saline‐perfused organs of the guinea pig. All tissue extracts contained substantial concentrations of Ro (SS‐A) antigen and could be grouped into 3 categories based on quantitative reactivity in the sandwich ELISA. The 60‐kd and 52‐kd molecular forms of Ro (SS‐A) present in tissue extracts were similar to those described in Wi‐L2 extracts, and the 54‐kd molecular form of Ro (SS‐A) in guinea pig erythrocytes was similar to that found in human erythrocytes. The tissue distribution of the isoforms of Ro (SS‐A) was shown by Western immunoblotting to vary in different tissues, and the reactivity to the 60‐kd Ro (SS‐A) was correlated with the activity seen in the ELISA. Both the 60‐kd and 52‐kd Ro (SS‐A) bands in guinea pig liver extracts were very weak on Western immunoblots, in contrast to the high concentration of Ro (SS‐A) antigen in the ELISA. Other data suggest the possible existence of a unique form of Ro (SS‐A) in the liver. Guinea pig tissues have 4 Y RNA that are equivalent to the 4 human RNA—hY1, hY3, hY4, and hY5—present in HeLa cells, while guinea pig red blood cells have only one Y RNA, which is equivalent in size to human hY4. This heterogeneity of the Ro (SS‐A) antigen suggests that there is differential expression of the various Ro (SS‐A) genes in different tissues and expands the possibilities for tissue‐specific pathologic events involving the Ro (SS‐A)/anti—Ro (SS‐A) system.
Cutaneous vasculitis associated with Pheochromocytoma
Authors: Kulp‐Shorten Carol L. , Rhodes Richard H. , Peterson Hugh , Callen Jeffrey P. 
Published: February 2007

AbstractWe describe a patient who presented with constitutional symptoms, severe hypertension, and purpuric lesions over the knees, thighs, and penis. The patient was eventually diagnosed as having multiple endocrine neoplasia type II, with cutaneous leukocytoclastic vasculitis. The cutaneous vasculitis persisted despite treatment with high‐dose systemic corticosteroids, but rapidly resolved after the removal of bilateral pheochromocytomas. This case demonstrates cutaneous leukocytoclastic vasculitis in association with pheochromocytoma.
Progression of osteoarthritis of the hand and metacarpal bone loss. A twenty‐year followup of incident cases
Authors: Sowers Maryfran , Zobel Donna , Hawthorne Victor M. , Carman Wendy , Weissfeld Lisa 
Published: February 2007

AbstractWe examined the prospective relationship between metacarpal bone mass and osteoarthritis (OA) of the hand, using incidence data from the historical cohort in the Tecumseh Community Health Study (Tecumseh, MI). Women were examined for radiographic evidence of OA and for bone mass twice, 20–23 years apart (1962–1965 and 1985; 683 subjects with an age range of 55–74 in 1985). Two measures of OA were evaluated: the highest score assigned to any of the 32 wrist/hand joints, and the sum of scores for all wrist/hand joints. After adjustment for age, women who were classified as having OA (by either measure of OA) in 1985 were more likely to have more cortical area at baseline, which indicates greater bone mass. Women who developed OA in the 23‐year period were more likely to experience a significantly greater widening of the medullary cavity over time, an indicator of increased bone resorption. Women with increasing levels of OA involvement also had an increased likelihood of greater cortical area loss. We conclude that women who later developed OA were more likely to have higher baseline bone mass than women who did not develop OA, but these women also had a greater likelihood of bone loss over time.
Association of HLA–Dw16 with rheumatoid arthritis in Yakima Indians. Further evidence for the “shared epitope” hypothesis
Authors: Willkens Robert F. , Nepom Gerald T. , Marks Cara R. , Nettles James W. , Nepom Arbara S. 
Published: February 2007

AbstractRheumatoid arthritis (RA) is prevalent in Yakima Indians, a Native American tribe. HLA–DR4, the HLA specificity commonly associated with RA in Caucasians, is rare among the Yakima. Using a specific oligonucleotide probe that recognizes DR4 nucleotide sequences associated with RA, a rare HLA–Dw16 gene was identified in 83% of Yakima patients with RA and in 60% of Yakima control subjects. This shared sequence encodes a discrete class II epitope that is highly correlated with RA in both DR4 positive and DR4 negative individuals.
Application of the polymerase chain reaction and immunofluorescence techniques to the detection of bacteria in Yersinia‐triggered reactive arthritis
Authors: Viitanen Anna‐Mari , Arstila T. Petteri , Lahesmaa Riitta , Granfors Kaisa , Skurnik Mikael , Toivanen Paavo 
Published: February 2007

AbstractLeukocytes in synovial fluid and peripheral blood samples from patients with Yersinia‐triggered reactive arthritis were analyzed after DNA amplification using the polymerase chain reaction. The primers applied were specific for the virulence plasmid–coded 1crE genes of Yersinia enterocolitica O:3 and Yersinia pseudotuberculosis III. No Yersinia DNA was observed within the synovial fluid cells or peripheral blood cells by polymerase chain reaction techniques. However, Yersinia antigens were detected in the synovial fluid cells by immunofluorescence techniques. These results suggest that only parts of the causative agents, not the entire microbe, can enter the joint and initiate the inflammation that leads to a reactive arthritis.
Systemic lupus erythematosus in a boy with chronic granulomatous disease: Case report and review of the literature
Authors: Manzi Susan , Urbach Andrew H. , McCune Ann B. , Altman Harold A. , Kaplan Sandra S. , Medsger Thomas A. , Ramsey‐Goldman Rosalind 
Published: February 2007

AbstractWe describe a patient with X‐linked chronic granulomatous disease (CGD) who developed systemic lupus erythematosus, which was characterized by photosensitivity, malar rash, glomerulonephritis, leukopenia, hypocomplementemia, antinuclear antibodies, and anti–double‐stranded DNA antibodies, at age 3. The patient's mother is an asymptomatic carrier of CGD, and her other son (the patient's half‐brother) also has CGD. Neither the mother nor the brother has clinical or serologic evidence of systemic lupus erythematosus. Previous cases of discoid lupus–like skin lesions have been reported both in carriers and in patients with CGD. Our patient represents the first reported case of an individual with convincing clinical, serologic, and pathologic evidence of systemic lupus erythematosus. The association between defective host defense mechanisms and autoimmune phenomena has been described previously in patients with Job's syndrome and in patients with B cell and T cell deficiency disorders, including the acquired immunodeficiency syndrome. The relationship between the known leukocyte defects in CGD and the pathogenesis of a lupus‐like illness is unclear.
Seronegative juvenile rheumatoid arthritis and mast cell–associated gastritis
Authors: Lindsley Carol B. , Miner Philip B. 
Published: February 2007

AbstractWe describe 4 children with seronegative inflammatory arthritis who had persistent, severe nausea and abdominal pain over several months, in spite of vigorous medical therapy, including antacids and histamine H2 receptor antagonists. Endoscopy and biopsy of gastric and duodenal mucosa showed antral gastritis and an increased number of mast cells in 3 of the 4 patients. In the fourth patient, urinary histamine levels were elevated. These findings suggest an association between inflammatory arthritis and localized mast cell disease in some individuals. Further studies are needed to determine whether this association represents an independent syndrome or whether mast cell–related disease is secondary to long‐term treatment with nonsteroidal antiinflammatory drugs in children with mild arthritis.
Synovial membrane histology and immunopathology in rheumatoid arthritis and osteoarthritis. In vivo effects of antirheumatic drugs
Authors: Haraoui Boulos , Pelletier Jean‐Pierre , Cloutier Jean‐Marie , Faure Marie‐Pierre , Martel‐Pelletier Johanne 
Published: February 2007

AbstractWe examined the histologic and immunopathologic features of the synovial membrane of 18 patients with rheumatoid arthritis (RA) and 12 patients with osteoarthritis (OA) who had undergone total knee arthroplasty. Patients were classified into 5 groups according to therapeutic regimen and disease: RA treated with nonsteroidal antiinflammatory drugs (NSAIDs), RA treated with NSAIDs and prednisone, RA treated with NSAIDs and methotrexate (MTX), OA treated with analgesics, and OA treated with NSAIDs. There were no significant between‐group differences in the percentages or the distribution pattern of the infiltrating T cell subsets (CD4, CD8), HLA–DR, or interleukin‐2 receptor‐bearing cells. However, inflammatory indices, which included the thickness of the lining cell layer and the density of the mononuclear cell infiltrate, were significantly higher in the RA patients treated with prednisone and those treated with MTX (P < 0.05). Similarly, fibrosis was markedly reduced in these 2 groups. The RA patients treated with NSAIDs alone and the 2 groups of patients with OA demonstrated similar profiles. These data suggest that prednisone and MTX may inhibit the development of fibrosis without altering the subsets of the inflammatory cell population. This observation raises the possibility that the action of these 2 drugs may be partly mediated by the suppression of inflammatory mediators that are responsible for fibroblast activation.
Temporal arteritis with normal erythrocyte sedimentation rates presenting as occipital neuralgia
Authors: Jundt Jeffrey W. , Mock David 
Published: February 2007

AbstractA retrospective review of 46 patients with biopsy‐proven giant cell (temporal) arteritis revealed 8 (17%) whose initial presentation was occipital pain. The most likely etiology of occipital pain in these patients was occipital artery inflammation. A Westergren erythrocyte sedimentation rate < 40 mm/hour was noted at presentation in 6 of these 8 patients. Giant cell arteritis should be considered in the differential diagnosis of elderly patients who present with occipital pain and demonstrate a normal erythrocyte sedimentation rate.
Association of the complement allele c4aq0 with primary Sjögren's syndrome in japanese patients
Authors: Moriuchi Junko , Ichikawa Yukinobu , Takaya Masatoshi , Shimizu Hiroaki , Arimori Shigeru , Tsuji Kimiyoshi , Wakisaka Akemi , Dawkins Roger 
Published: February 2007

AbstractWe studied allotypes of the fourth component of complement (C4) and factor B in 76 patients with Sjögren's syndrome (SS) and in 63 normal subjects. C4A‐null (C4AQO) was found in 10 of 28 patients who had primary SS, compared with 1 of 63 control subjects (P ⩽ 0.005). In contrast, no significant difference in the frequency of any C4 allotype was observed between patients with secondary SS and control subjects. An association of HLA–DRw53 with primary SS in Japanese patients has been reported. Since there is no linkage disequilibrium between DRw53 and C4AQO, it is possible that at least 2 genes in the major histocompatibility complex may determine susceptibility to the development of primary SS in the Japanese population.
Fatal pulmonary venoocclusive disease secondary to a generalized venulopathy: A new syndrome presenting with facial swelling and pericardial tamponade
Authors: Liang Matthew H. , Stern Steve , Fortin Paul R. , Louie Diane C. , Marsh James D. , Mudge Gilbert H. , Murphy George 
Published: February 2007

AbstractWe describe a patient who developed fatal pulmonary artery hypertension secondary to diffuse venulitis. This otherwise healthy young woman first presented with generalized venulopathy, with chemosis, facial swelling, pleural effusions, and pericardial tamponade. The symptoms partially responded to steroid therapy, but over a 2‐year course, a rapidly progressive and fatal venoocclusive disease developed. No other primary condition was diagnosed, and at autopsy, the patient had striking venulitis throughout, including the pulmonary bed. We believe that this is a unique case of pulmonary hypertension resulting from a generalized venulopathy.
Symptoms of Raynaud's syndrome in patients with fibromyalgia. A study utilizing the Nielsen test, digital photoplethysmography, and measurements of platelet α2‐adrenergic receptors
Authors: Bennett Robert M. , Clark Sharon R. , Campbell Stephen M. , Ingram Shirley B. , Burckhardt Carol S. , Nelson Donna L. , Porter John M. 
Published: February 2007

AbstractTwenty‐nine female patients with fibromyalgia were questioned about symptoms of cold intolerance and Raynaud's syndrome; objective documentation of cold‐induced vasospasm was obtained by a Nielsen test. Twelve patients (41%) had abnormal Nielsen test results, and 11 patients (38%) had elevated levels of platelet α2‐adrenergic receptors. There was a positive correlation between the percentage of change in finger systolic pressure on cooling (Nielsen test) and the number of α2‐adrenergic receptors. There was poor correlation between Raynaud's syndrome symptoms and an abnormal Nielsen test result. Digital photoplethysmography showed a normal waveform in 2 of 3 patients. We hypothesize that a subgroup of patients with fibromyalgia syndrome have an up‐regulation of α2‐adrenergic receptors as a cause of their exaggerated reaction to cold.
In vitro regulation of B cell differentiation by interleukin‐6 and soluble CD23 in systemic lupus erythematosus B cell subpopulations and antigen‐induced normal B cells
Authors: Klashman David J. , Martin Robert A. , Stevens Ronald H. , Martínez‐Maza Otoniel 
Published: February 2007

AbstractPolyreactive systemic lupus erythematosus (SLE) B cells were compared with antigen‐induced SLE and normal B cells for their interleukin‐6 (IL‐6) and soluble CD23 requirements. Unlike normal B cells, secretion of antibody by SLE B cells in serum‐free medium was not enhanced by exogenous IL‐6. Anti–IL‐6 antibodies inhibited immunoglobulin production in cultures of normal and SLE B cells, which suggests that IL‐6 is required for B cell differentiation. SLE culture supernatants had elevated levels of IL‐6, which explains the poor response of the SLE cells to exogenous IL‐6. Soluble CD23 enhanced the responses of cells from normal subjects and SLE patients.
A double‐blind study of deflazacort and prednisone in patients with chronic inflammatory disorders
Authors: Gray Richard E. S. , Doherty Sheelagh M. , Galloway John , Coulton Les , Kanis John A. , de Broe Marc 
Published: February 2007

AbstractDeflazacort and prednisone were given to 26 patients with rheumatoid arthritis, polymyalgia rheumatica, or other chronic inflammatory diseases, in a double‐blind study. Deflazacort rapidly and effectively suppressed disease activity in a manner supporting its assumed therapeutic potency of 83% that of prednisone. Prednisone induced a rapid increase in the level of daily calcium excretion that was not evident with deflazacort. Cortisol secretion was acutely inhibited by prednisone, but not by deflazacort. Neither corticosteroid had a significant effect on glucose metabolism, at the doses studied. Treatment with deflazacort may be an effective alternative to prednisone treatment, with fewer adverse effects on levels of calcium and cortisol, in patients with severe inflammatory conditions warranting the use glucocorticoids.
Induction of neutrophil‐mediated cartilage degradation by interleukin‐8
Authors: Elford Peter R. , Cooper Philip H. 
Published: February 2007

AbstractNeutrophil influx into the inflamed joint is a characteristic feature of disease flares in patients with rheumatoid arthritis. Recently, a protein produced by monocytes and fibroblasts that has chemoattractive/activating properties for neutrophils has been identified and characterized. This protein has been called interleukin‐8 (IL‐8). In this study, we cocultured neutrophils with 35S‐sulfate–labeled cartilage and found that the addition of recombinant human IL‐8 (rHuIL‐8) caused rapid, neutrophil‐mediated cartilage degradation that was the result of induction of neutrophil degranulation by the cytokine. With 10−7M rHuIL‐8, 23% of the radiolabel was released into the culture medium in 4 hours, compared with a 9% release without the factor. At concentrations of up to 10−6M, rHuIL‐8 had no direct effect upon cartilage breakdown. These findings indicate that IL‐8 may participate in the pathogenesis of rheumatoid arthritis through the induction of neutrophil‐mediated cartilage damage.
Epidemiologic and immunogenetic aspects of polymyalgia rheumatica and giant cell arteritis in northern Italy
Authors: Salvarani Carlo , Macchioni Pierluigi , Rossi Fulvia , Castri Concetta , Capozzoli Nicholas , Baricchi Roberto , Boiardi Luigi , Chiaravalloti Franco , Portioli Italo , Zizzi Fabio , Mantovani Wilma 
Published: February 2007

AbstractWe studied the epidemiology of giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) in a Mediterranean population. Ninety‐nine patients with PMR and/or GCA were identified over a 9‐year period (1980–1988) in Reggio Emilia, Italy. The average annual incidence of PMR and GCA was 12.7/100,000 and 6.9/100,000, respectively, in a population aged 50 years or older. Frequencies of HLA antigens were determined in 49 patients with PMR and/or GCA who were followed by staff at our rheumatology unit during the 1980–1988 period. When compared with HLA findings in 242 healthy controls, DR4 was not found to be significantly associated with PMR (24% in PMR patients versus 14% in controls). Patients with GCA also showed an increased frequency of DR4 compared with controls (36% versus 14%), but this difference was also not statistically significant. The immunogenetic features of PMR and GCA and the relationship between the immunogenetic and epidemiologic patterns in different populations are discussed.
Serum keratan sulfate. Quantitative and qualitative comparisons in inflammatory versus noninflammatory arthritides
Authors: Mehraban Fuad , Finegan Candace K. , Moskowitz Roland W. 
Published: February 2007

AbstractThe concentration of keratan sulfate (KS) epitope was measured in the serum of patients with osteoarthritis (OA) or rheumatoid arthritis (RA) by enzyme‐linked immunosorbent assay and compared with that in the serum of patients with primary fibromyalgia syndrome (PFS) and of controls who had no joint disease. By Student's t‐test, the mean serum KS concentrations in OA and RA patients measured with monoclonal antibodies (MAb) 5‐D‐4 and 2‐D‐3 were significantly increased over those in the PFS and normal groups; similar findings were observed using a nonparametric test, except that levels in RA patients showed no difference from those in PFS patients and normal subjects. There was no significant correlation between joint scores or disease duration and KS levels in OA or RA patients. Gel filtration of sera revealed mainly large, polydisperse KS‐bearing fragments which eluted in a broad profile. KS purified from sera by immunoaffinity chromatography consisted mainly of high‐density proteoglycans. Electrophoresis of pooled high‐density KS fractions in polyacrylamide‐agarose gels followed by Western blotting with MAb 5‐D‐4 showed diffuse bands with relative mobilities corresponding to large proteoglycans. These findings are consistent with attachment of KS to protein core fragments of various sizes; KS in patient sera is comparable in size with that in normal sera. Elevations of serum KS levels occur in the presence of cartilage degradation, but do not quantitatively define the extent or duration of articular involvement.