bluuebunny/crossref_metadata_2025_split huggingface dataset:
Polyarthritis resembling juvenile rheumatoid arthritis in a girl with chronic granulomatous disease
Authors: Lee B. W. , Yap H. K. 
Published: February 2007

AbstractChronic granulomatous disease (CGD) is an uncommon disorder affecting neutrophil function, and is characterized by recurrent and severe pyogenic infections. Associated autoimmune disorders, in particular lupus‐like disorders, are found in carriers of X‐linked CGD and in patients with both the X‐linked and the autosomal recessive (AR) forms of the disease. We describe a girl with the AR form of CGD and with rheumatoid factor–positive polyarthritis resembling juvenile rheumatoid arthritis. This association has been reported previously only in a single case report of a patient with probable CGD. The present report further substantiates the association between autoimmune phenomena and CGD.
Increased incidence of a resonance in the phosphodiester region of 31p nuclear magnetic resonance spectra in the skeletal muscle of fibromyalgia patients
Authors: Jubrias Sharon A. , Bennett Robert M. , Klug Gary A. 
Published: February 2007

AbstractObjective. To determine if patients with fibromy algia syndrome (FMS) are more susceptible to activityinduced muscle damage than are healthy subjects.
Methods. Eleven FMS patients and 10 healthy subjects performed concentric and eccentric exercise with their dominant and nondominant forearms, respectively. 31P magnetic resonance spectroscopy (to assess inorganic phosphate [Pi] and phosphocreatine [PCr]) and dolorimetry (to assess pain) were performed before and 20 minutes after exercise and at 4 subsequent 24‐hour intervals.
Results. Neither group exhibited increased Pi/ PCr ratios or reduced dolorimetry scores following the exercise protocols. FMS patients did display a phosphodiester resonance at a higher rate than healthy subjects (37% versus 12%), but this was not related to the exercise.
Conclusion. Unchanged Pi/PCr ratios and dolorimetry scores following acute exercise provide evidence against the hypothesis that FMS patients are more susceptible to activity‐induced muscle damage than are healthy subjects, although Pi/PCr and pain may not adequately document such damage. The frequent occurrence of phosphodiester in the spectra of FMS patients may indicate a sarcolemmal abnormality in these subjects.
Breast‐feeding and the onset of rheumatoid arthritis
Authors: Brennan Paul , Silman Alan 
Published: February 2007

AbstractObjective. In a recent study we demonstrated that the postpartum period, particularly after the first pregnancy, is a time of increased risk for the development of rheumatoid arthritis (RA). The present study was undertaken to investigate whether this risk might be explained by breast‐feeding.
Methods. Through a nationwide media campaign, we identified 187 women who had developed RA within 12 months of a pregnancy, and we compared their breast‐feeding histories with those of 149 similarly aged women chosen from the patient registers of a nationwide group of general practitioners.
Results. In all, 88 of the women with RA developed the disease after their first pregnancy. Eighty‐one percent of these 88 women had breast‐fed. This was higher than the breast‐feeding prevalence of 50% in the 129 controls whose first pregnancy had resulted in a live birth (adjusted odds ratio [OR] 5.4, 95% confidence interval 2.5–11.4). There was a smaller increased risk of breast‐feeding after a second pregnancy in the RA cases (OR 2.0) and no increase after a third pregnancy (OR 0.6). The increase in risk was greatest in those cases whose disease was erosive and who were rheumatoid factor positive.
Conclusion. In a small group of susceptible women, exposure to breast‐feeding after the first pregnancy is associated with a significant increase in risk for RA development. We postulate that this may reflect hormonal influences, specifically the high level of the proinflammatory hormone prolactin.
The lag time between onset of symptoms and diagnosis of rheumatoid arthritis
Authors: Chan KIN‐Wei A. , Felson David T. , Yood Robert A. , Walker Alexander M. 
Published: February 2007

AbstractObjective. Rheumatoid arthritis (RA) may be biologically reversible if treated in the first several months, yet it is unknown whether patients are diagnosed that early. We investigated the lag time between symptom onset and diagnosis of RA in a population with excellent access to rheumatology care.
Methods. Using review of medical records, we evaluated all patients newly diagnosed as having RA from 1987 through 1990, at a health maintenance organization in central Massachusetts. Total lag time from symptom onset to first definite diagnosis was divided into medical encounter lag time (from symptom onset to first medical encounter) and diagnosis lag time (from first medical encounter to diagnosis).
Results. The median total lag time was 36 weeks (range 4 weeks to > 10 years). The median medical encounter lag time was 4 weeks (not all patients included in the analysis). The median diagnosis lag time was 18 weeks. Diagnosis lag time was shorter for patients with progressive disease and positive rheumatoid factor on the initial test. Of 25 patients with symmetric arthritis and positive rheumatoid factor, only 5 (20%) were diagnosed within 2 months, and 10 (40%) were diagnosed more than 6 months after symptom onset.
Conclusion. RA diagnosis is usually delayed for several months after symptoms begin, in large part because of delay in diagnosis by the physician. Thus, the goal of initiating treatment extremely early may be unrealistic for most patients.
The sensitivity and specificity of computerized databases for the diagnosis of rheumatoid arthritis
Authors: Gabriel Sherine E. 
Published: February 2007

AbstractObjective. To examine the accuracy of a computerized medical database for the diagnosis of rheumatoid arthritis (RA).
Methods. The complete medical records of all prevalent cases of RA (according to the 1987 American College of Rheumatology diagnostic criteria) on January 1, 1987 were reviewed to determine the sensitivity, specificity, and predictive value of database diagnoses compared with those obtained by medical record review. Agreement between database and medical record diagnoses was calculated using the kappa statistic.
Results. Computerized database diagnoses of RA had a sensitivity of 89%, a specificity of 74%, a positive predictive value of 57%, and a negative predictive value of 94% compared with diagnoses based on clinical information abstracted from the complete medical record. Agreement between database and medical record diagnoses was poor (K = 0.54).
Conclusion. The sole reliance on such databases for the diagnosis of RA can result in substantial misdiagnosis.
Chloroquine reduces the bioavailability of methotrexate in patients with rheumatoid arthritis
Authors: Seideman Peter , Albertioni Freidoun , Beck Olof , Eksborg Staffan , Peterson Curt 
Published: February 2007

AbstractObjective. To evaluate the effects of a single dose of chloroquine (CQ) on the pharmacokinetics of methotrexate (MTX) in patients with rheumatoid arthritis.
Methods. Eleven patients (ages 41–75 years) who were taking oral doses of MTX (15 mg/week) were studied after a dose of MTX alone and after a dose of MTX plus CQ (250 mg). Plasma and urine samples were collected for 24 hours after dose intake, and the concentrations of MTX and its major metabolite 7‐hydroxymethotrexate were determined by high‐performance liquid chromatography.
Results. Administration of CQ together with MTX caused a reduction in the area under the plasma MTX concentration versus time curve (AUC). The median value of individual AUC ratios (MTX/MTX + CQ) was 1.6 (95% confidence interval 1.2–3.6).
Conclusion. The most likely mechanism for the interaction is that CQ reduces the bioavailability of MTX. This gives a possible explanation for a suggested reduction in MTX‐associated liver toxicity by coadministration of CQ. The significance of the interaction for the therapeutic effect remains to be elucidated.
Treatment of refractory rheumatoid arthritis with a chimeric ANTI‐CD4 monoclonal antibody
Authors: Moreland Larry W. , Pratt Parks W. , Bucy Ralph P. , Jackson Bettie S. , Feldman Janie W. , Koopman William J. 
Published: February 2007

AbstractObjective. To evaluate CD4+ T cell counts of rheumatoid arthritis (RA) patients at 18 and 30 months after treatment with a chimeric anti‐CD4 monoclonal antibody (MAb), cM‐T412, in a phase I trial.
Methods. Of the 25 RA patients who received the MAb, 23 were available for followup at 18 and 30 months. Levels of circulating CD4+ T cells were measured by flow cytometry.
Results. Circulating CD4+ T cell levels in these 23 RA patients remained below normal at 18 and 30 months posttreatment. More profound CD4+ T cell depletion was noted in the higher‐dose groups (300 and 700 mg).
Conclusion. Prolonged suppression of circulating CD4+ T cells was noted both in single‐infusion and multiple‐infusion groups 18 and 30 months after cM‐T412 treatment. The depression was more pronounced in patients who received multiple infusions of cM‐T412. The prolonged decrease in CD4+ T cell numbers suggests that the capacity to reconstitute CD4+ T cells in this patient population (treated with methotrexate) is limited. One patient, who was also receiving methotrexate and prednisone, died 18 months after receiving 100 mg of cM‐T412. No other significant adverse effects, in particular, no opportunistic infections, were reported in these 23 RA patients at 18 and 30 months of followup.
Regression of collagen‐induced arthritis with taxol, a microtubule stabilizer
Authors: Brahn Ernest , Tang Chris , Banquerigo Mona Lisa 
Published: February 2007

AbstractObjective. To investigate the capacity of taxol, a microtubule stabilizer, to inhibit collagen‐induced arthritis (CIA), a model of rheumatoid arthritis.
Methods. Louvain rats were immunized with type II collagen (day 0) to induce arthritis. Taxol was administered beginning on day 2 (prevention protocol) or at arthritis onset on day 9 (in either a high‐dose or low‐dose suppression protocol). Rats were assessed clinically and radiographically for arthritis severity. Cellular and humoral immune responses to type II collagen were also evaluated.
Results. Institution of taxol prior to arthritis onset completely precluded the development of CIA (P < 0.0001 versus controls). It also suppressed established clinical disease (high‐dose protocol P < 0.0000001; low‐dose protocol P < 0.0001) and radiographic erosions (high‐dose protocol P < 0.00001; low‐dose protocol P < 0.001) compared with controls. Levels of IgG antibodies, but not delayed‐type hypersensitivity, to type II collagen were reduced after taxol administration.
Conclusion. Taxol completely prevented the induction of CIA and caused significant regression of existing arthritis.
Expression of ICAM‐R (ICAM‐3), a novel counter‐receptor for LFA‐1, in rheumatoid and nonrheumatoid synovium
Authors: El‐Gabalawy Hani , Gallatin Michael , Vazeux Rosemay , Peterman Gary , Wilkins John 
Published: February 2007

AbstractObjective. To study the distribution of intercellular adhesion molecule receptor (ICAM‐R, or ICAM‐3), a novel ligand for the leukointegrin lymphocyte function‐associated antigen 1 (LFA‐1), in normal and rheumatoid synovial membranes and to compare this with the distribution of ICAM‐1, ICAM‐2, vascular cell adhesion molecule 1 (VCAM‐1), and endothelial leukocyte adhesion molecule 1 (ELAM‐1).
Methods. We performed immunohistochemical analyses of frozen sections of normal and rheumatoid synovial tissue using monoclonal antibodies to the molecules examined.
Results. ICAM‐1 staining was detectable on the vascular endothelium and the synovial lining cells of both normal and rheumatoid synovial membranes. A variable proportion of lymphocytes infiltrating rheumatoid tissues expressed ICAM‐1. ICAM‐2 staining was demonstrable in the vascular endothelium of both normal and inflamed tissues, the latter demonstrating a significantly higher proportion of positive vessels. ELAM‐1 staining was not detectable in normal synovial membranes but was seen on the endothelium of a limited number of rheumatoid synovial vessels, usually close to the synovial lining cell layer. VCAM‐1 staining was intense in both normal and rheumatoid synovial lining cells, but vascular staining was weak in both. In contrast, ICAM‐R staining was not detected in association with any synovial blood vessels, but was widely expressed by lymphocytes and macrophages. Cells of the lining layer did not stain for ICAM‐R.
Conclusion. Although ICAM‐R is a ligand for LFA‐1 and shares considerable sequence homology with ICAM‐1 and ICAM‐2, it does not appear to be expressed by the endothelium of normal or inflamed synovial vessels. Intense expression of ICAM‐R by rheumatoid synovial lymphocytes and macrophages suggests that it may play a role in processes requiring cell‐cell contact, such as antigen presentation and homotypic aggregation.
Preferential utilization of a novel vλ3 gene in monoclonal rheumatoid factors derived from the synovial cells of rheumatoid arthritis patients
Authors: Ermel Richard W. , Kenny Thomas P. , Wong Alice , Solomon Alan , Chen Pojen P. , Robbins Dick L. 
Published: February 2007

AbstractObjective. To further our understanding about the molecular genetics of rheumatoid factor (RF) in rheumatoid arthritis (RA).
Methods. The heavy and light chain variable region (V) genes of 5 new human monoclonal IgM RFs were cloned and sequenced using the polymerase chain reaction and the dideoxynucleotide termination method.
Results. The results reveal the recurrent usage in two RA patients of a novel Vλ3 germline gene, designated Humlv3c93. Specifically, in 2 of 3 RFs (C93 and D53) from one patient, the light chains in the Vλ gene‐encoded region were identical to each other and to the light chain of an RF (H4) from another patient. Serologically, the light chains of these 3 RFs were classified as members of the Vλ3b sub‐subgroup. Each of the RFs was encoded by a different VH gene. Both C93 and D53 bound specifically with human and rabbit IgG, whereas H4 was monospecific for rabbit IgG.
Conclusion. Since the 1v3c93 gene is not homologous to any reported Vλ sequence from natural auto‐antibodies, it is possible that 1v3c93 may represent a disease‐specific RF‐related Vλ gene. Moreover, the amino acid sequence CSGGSCY in the third complementarity‐determining regions of 2 of the RF heavy chains is encoded by the DLR2 gene segment and has been found previously in 2 other RA‐derived RFs, and thus may play a significant role in antigen binding.
Association of patterns of labial salivary gland inflammation with keratoconjunctivitis SICCA
Authors: Daniels Troy E. , Whitcher John P. 
Published: February 2007

AbstractObjective. To determine the association between patterns of inflammation in labial salivary glands (LSG) and the ocular component of Sjögren's syndrome (SS).
Methods. We classified LSG biopsy specimens from 618 patients with suspected SS as showing focal lymphocytic sialadenitis (FLS), other chronic sialadenitis (CS), or other diagnoses. We then determined the association of the other component of primary SS, keratoconjunctivitis sicca (KCS), with FLS, CS, parotid flow rate, and xerostomia.
Results. FLS, rather than CS, was associated with a diagnosis of KCS (X = 191, P < 0.0001). The severity of KCS correlated directly with the severity of FLS (r = 0.52, P < 0.0001), but not of CS, and correlated inversely with parotid flow rate in those patients who had FLS (r = ‐0.29), but not in those who had CS (r = −0.03). Xerostomia was marginally associated with KCS (X2 = 5, P = 0.02).
Conclusion. The stronger KCS association found in patients whose LSG biopsies show FLS makes FLS the best criterion presently available for diagnosing the salivary component of SS. CS is a common feature of labial salivary glands but is neither associated with SS nor an end stage of primary SS. Histopathologic examination of salivary tissue is currently essential for diagnosing primary SS as well as secondary SS in which KCS is lacking, especially cases to be included in studies of SS.
Treatment of lyme arthritis
Authors: Steere Allen C. , Levin Robert E. , Molloy Philip J. , Kalish Robert A. , Abraham Iii James H. , , Liu Nancy Y. , Schmid Christopher H. 
Published: February 2007

AbstractObjective. To test treatment regimens for Lyme arthritis.
Methods. Patients were randomly assigned to treatment with doxycycline or amoxicillin plus probenecid for 30 days. Patients who had persistent arthritis for at least 3 months after treatment with oral antibiotics or parenteral penicillin were given intravenous ceftriaxone for 2 weeks.
Results. Eighteen of the 20 patients treated with doxycycline and 16 of the 18 patients who completed the amoxicillin regimen had resolution of the arthritis within 1–3 months after study entry. However, neuroborreliosis later developed in 5 patients, 4 of whom had received the amoxicillin regimen. Of 16 patients (2 from the oral antibiotic study and 14 additional patients) who had persistent arthritis despite previous oral antibiotics or parenteral penicillin, none had resolution of the arthritis within 3 months after ceftriaxone therapy. The HLA‐DR4 specificity and OspA reactivity were associated with a lack of response.
Conclusion. Lyme arthritis can usually be treated successfully with oral antibiotics, but patients may still develop neuroborreliosis. Patients with certain genetic and immune markers may have persistent arthritis despite treatment with oral or intravenous antibiotics.
Serum levels of soluble interleukin‐2 receptor
Authors: Uziel Yosef , Krafchik Bernice R. , Feldman Brian , Silverman Earl D. , Rubin Laurence A. , Laxer Ronald M. 
Published: February 2007

AbstractObjective. To determine whether circulating serum levels of soluble interleukin‐2 receptor (sIL‐2R) are elevated in patients with localized scleroderma, and if levels of sIL‐2R can differentiate between active and inactive disease.
Methods. Seventeen patients with localized scleroderma were categorized by overall physician assessment into active, inactive, and indeterminate groups, according to disease activity. Serum sIL‐2R levels were analyzed and correlated with disease activity.
Results. The mean sIL‐2R level was significantly higher (P = 0.005) in those with active disease (1,675 ± 823 units/ml) than in those with inactive disease (722 ± 218 units/ml).
Conclusion. Serum sIL‐2R levels are elevated in patients with localized scleroderma. When present, elevated sIL‐2R levels appear to be able to differentiate active from inactive disease. This fact also suggests cell‐mediated immune activation in this condition. Further serial studies are required to assess the value and sensitivity of sIL‐2R levels in measuring changes in disease activity.
Racial differences in the distribution of systemic sclerosis–related serum antinuclear antibodies
Authors: Kuwana Masataka , Okano Yutaka , Kaburaki Junichi , Tojo Takeshi , Medsger Thomas A. 
Published: February 2007

AbstractObjective. To determine racial differences in the frequencies of systemic sclerosis (SSc)–related serum antinuclear antibodies (ANA).
Methods. We tested serum samples from 275 Japanese, 416 North American Caucasian, and 24 North American black SSc patients for 8 SSc‐related serum ANA, using indirect immunofluorescence, double immunodiffusion, and radioimmunoprecipitation assays.
Results. In comparing the 3 racial groups, we found that anti–U1 RNP, anti–RNA polymerase I, II, and III, and anti–U3 RNP antibodies were the most frequently detected antibodies in Japanese, Caucasian, and black patients, respectively. Anti–PM‐Scl antibody was found exclusively in Caucasians.
Conclusion. The production of SSc‐related serum ANA is related to immunogenetic background.
Influence of disease manifestation and antineutrophil cytoplasmic antibody titer on the response to pulse cyclophosphamide therapy in patients with wegener's granulomatosis
Authors: Reinhold‐Keller Eva , Kekow Jörn , Schnabel Armin , Schmitt Wilhelm H. , Heller Martin , Beigel Arwed , Duncker Gernot , Gross Wolfgang L. 
Published: February 2007

AbstractObjective. To assess the effectiveness of pulse cyclophosphamide (CYC) in the treatment of Wegener's granulomatosis (WG) and to identify the patients who are responsive to the treatment.
Methods. The prospective study included 43 patients with biopsy‐proven WG. Clinical, radiographic, laboratory, and immunologic data were evaluated for predicitive values regarding the outcome of pulse CYC therapy.
Results. Only 42% of the patients showed complete or partial remission that lasted at least 6 months after cessation of pulse CYC therapy. These responders had a higher frequency of disease activity limited to the upper and lower respiratory tract (39%, versus 8% in the nonresponder group; P < 0.05) and had lower titers of classic antineutrophil cytoplasmic antibody (cANCA) prior to treatment (<1:64 42%, versus 6% in the nonresponder group; P < 0.05). In the 58% of patients who did not respond to pulse CYC treatment, there was both systemic disease involving more than 4 organ systems (mainly, the heart, nervous system, eye, and skin) and constitutional symptoms. Serious side effects induced by pulse CYC occurred in only 1 patient.
Conclusion. Based on these findings, pulse CYC therapy appears to be effective in WG patients with moderate disease activity and low titers of cANCA, but of little benefit in patients with severe WG. Pulse CYC should therefore not be used as first‐line therapy in patients with severe and rapidly progressing forms of WG associated with high titers of cANCA.
Comparative inhibitory effects of bucillamine and d‐penicillamine on the function of human b cells and t cells
Authors: Hirohata Shunsei , Lipsky Peter E. 
Published: February 2007

AbstractObjective. Clinical trials have suggested that the efficacy of bucillamine (BUC) in rheumatoid arthritis (RA) may be superior to that of D‐penicillamine (DP), although the basis of the differences remains unclear. Previous studies have revealed that BUC has unique immunomodulatory effects that depend upon its capacity to form an intramolecular disulfide (BUG‐ID). We therefore examined the effects of BUC‐ID on the in vitro function of human B cells and T cells compared with those of DP, at their pharmacologically attainable concentrations.
Methods. IgM production was induced in highly purified B cells from healthy donors by stimulation with Staphylococcus aureus Cowan 1 (SAC) plus interleukin‐2 (IL‐2) or with immobilized anti‐CD3–activated CD4+ T cells. Interferon‐γ (IFNγ) production was induced in CD4+ T cells by stimulation with immobilized anti‐CD3.
Results. BUC‐ID suppressed IgM production iduced by SAC + IL‐2 as well as that induced by immobilized anti‐CD3–activated CD4+ T cells, whereas DP suppressed the latter more markedly than the former. DP (3 μg/ml) significantly suppressed IFNγ production by immobilized anti‐CD3–stimulated CD4+ T cells, but not IgM production induced by SAC + IL‐2 stimulation. By contrast, BUC‐ID (0.3 μg/ml) significantly suppressed IgM production induced by SAC + IL‐2, but not T cell IFNγ production. Of note, BUC‐ID did not suppress IL‐6 production by SAC‐activated B cells.
Conclusion. These results indicate that the target cells of BUC and DP in vivo might be different, with the former inhibiting the function of B cells and the latter that of T cells. The data suggest the possibility that BUC may have a different effect in RA patients compared with the effect of DP, and may be effective in patients who do not respond to DP.