Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This clinicopathologic study of patients with chronic graft-versus-host disease (GVHD) after allogeneic marrow transplantation emphasizes the most prominent feature of the syndrome, the cutaneous aspects, and describes the ophthalmic-oral sicca syndrome with sialoadenitis and the neurologic findings. Chronic cutaneous GVHD affected 19 of 92 recipients surviving 150 days or more. In 6 patients chronic GVHD presented as a continuation of acute GVHD; in 8 it occurred after the resolution of acute GVHD; and in 5 it arose without preceding acute GVHD, ie, de novo late onset. Two cutaneous types were distinguished. The generalized type affected 16 patients and ran a progressive course resulting in late complications of poikiloderma, diffuse dermal and subcutaneous fibrosis, and contractures. Microscopically, it resembled generalized morphea and lupus erythermatosus hypertrophicus et profundus. The local type affected 3 patients with a more variable picture of poikiloderma, dermal sclerosis, and contractures. Microscopically, it resembled lupus of erythematosus profundus and scleroderma. Guidelines for defining and subclassifying chronic cutaneous GVHD are proposed.
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PMID:Chronic cutaneous graft-versus-host disease in man. 2 21

ECG changes in 49 patients with rheumatoid arthritis, 18 with ankylosing spondylitis, 47 with systemic lupus erythematosus, 17 with dermatomyositis, 21 with scleroderma and 7 with polyarteritis nodosa were compared with ECG changes in 106 control subjects. The classification of ECG findings was based mainly on the Minnesota Code. Compared with control subjects, pathological Q--QS, ST segment and T wave patterns were more common in all patient groups--including dermatomyositis, in which cardiac involvement has rarely been reported. P terminal force (PTF) was higher in the patient group. Conduction defects were probably more common in connective tissue diseases, whereas differences in ectopic beats, arrhythmias, QRS duration and QRS axis and R wave amplitude were not significant. The only significant difference between the steroid-treated patients and those without such treatment was the higher frequency of ST changes in the steroid-treated group. The results imply that heart affection is common in all connective tissue diseases. The several mechanisms underlying the cardiac involvement are reflected in many ways in the electrocardiograms of these patients, including an increased frequency of ECG changes mimicking those met in coronary heart disease.
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PMID:Electrocardiographic findings in patients with connective tissue disease. 3 14

Antibodies to single-stranded R.N.A. were found by counter immunoelectrophoresis in all of 40 sera from patients with scleroderma. These antibodies were specific to the uracil bases of R.N.A. Antibodies to R.N.A. were also found in 20 of 40 sera from patients with systemic lupus erythematosus (S.L.E.), but in none of forty controls. Antibodies to R.N.A. found in S.L.E. sera could be differentiated immunochemically from those found in scleroderma in that they were more heterogeneous and could react selectively with either uridine or uridine monophosphate. Antibodies ot D.N.A. were more frequent in S.L.E. than in scleroderma. That antibodies to D.N.A. are actually present in scleroderma and precipitin lines are not the result of cross reactivity with anti-R.N.A. antibodies is indicated by the finding that 10 of the 18 scleroderma sera which reacted with D.N.A. also reacted with thymidine, a base present in D.N.A. but not in R.N.A.
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PMID:Uracil-specific anti-R.N.A. antibodies in scleroderma. 4 13

In a previous study, all 40 sera from patients with scleroderma, 20 of 40 sera from SLE patients, but none of 40 sera from normal controls, were found to have antibodies to ssRNA. All scleroderma sera were also found to react with HSA-coupled uridine and UMP and their reaction with HSA-coupled uridine and UMP and their reaction with ssRNA could be inhibited by uracil, uridine, and UMP. To characterize further these uracil-specific anti-RNA antibodies found in scleroderma and compare them with the anti-RNA antibodies found in SLE, we tested their reactivity with Poly (U) and with Poly (A)-Poly (U) and all but one failed to react with Poly (A)-Poly (U). This same serum was the only one in which the reaction with Poly (U) could not be inhibited with uracil. Reactivity of SLE sera was strikingly different from that found in scleroderma sera. Seventeen of 34 SLE sera studied reacted with ssRNA but only four of these reacted with Poly (U). Conversely, two SLE sera that reacted with Poly (U) did not react with ssRNA. Fifteen reacted with Poly (A)-Poly (U) and only two of these failed to react with ssRNA. Five SLE sera which were reactive with ssRNA did not precipitate with Poly (A)-Poly (U). All SLE sera which reacted with Poly (U) could be inhibited with uracil, although less effectively than in scleroderma. Reactivity with Poly (A)-Poly )U) was not inhibited with uracil nor with adenosine. These findings confirm that antibodies to RNA that are found in scleroderma are directed to uracil and thus specific to ssRNA, whereas RNA antibodies found in SLE sera are heterogeneous and directed to either the base, to the site of union of the base and sugar moiety to the ribose backbone, or to the helical structure of double stranded RNA. These differences and the respective antigenic specificities of these anti-RNA antibodies found in scleroderma and SLE may be theoretically important.
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PMID:Immunochemical characterization of the anti-RNA antibodies found in scleroderma and systemic lupus erythematosus. I. Differences in reactivity with Poly (U) and Poly-(A) Poly (U). 5 Mar 53

The rheology of the blood was studied in 20 patients with Raynaud syndrome. Sixteen patients had scleroderma, two had nonspecific angiitis, one had systemic lupus erythematosus, and one had Raynaud disease. Viscosity measurements were performed on whole blood, plasma, and suspensions of 45% red blood cells (RBCs). In autologous plasma, over a wide range of shear rates. The relative viscosity, an index of RBC aggregation, was obtained by dividing the RBC viscosity in autologous plasma (at a hematocrit value of 45%) by the plasma viscosity. Concentrations of the plasma globulins and fibrinogen were also measured. The mean plasma viscosity was significantly (P less than .01) elevated over established normal controls. The mean RBC viscosity and the relative viscosity were significantly (P less than .01) elevated over normal controls, as were fibrinogen and the globulins. These studies demonstrate increased blood viscosity and red blood cell aggregation, which may constitute an important hindrance to flow.
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PMID:Blood viscosity, plasma proteins, and Raynaud syndrome. 5 42

Sixty-eight determinations of leukocyte chemotaxis were performed in 42 patients suffering from systemic lupus erythematodes (17 cases), rheumatoid arthritis (15 cases) and scleroderma (10 cases). In contrast to the results of others, this study showed a deficiency in only 15 of 42 cases (35.7%). Impairment of chemotaxis was always transitory and demonstrable only during acute phases of disease. Intrinsic deficiency of PMN leukocytes as well as deficiency of plasma factors were related to the clinical and biological course of the disease and to the treatment.
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PMID:[Chemotaxis of human polymorphonuclear cells in vitro. Study of inflammatory rheumatic diseases]. 5 33

The methods currently used for the detection of ANA have been analyzed, with emphasis on their practical application to the diagnosis of the CTD. The use of the indirect IF-ANA test was recommended as a screening procedure to detect ANA. The need to standardize the technique using a single substrate and fluorescent conjugates with uniform F/P ratios was stressed. Most importantly, the value of titrating ANA for the diagnosis of the CTD was discussed. ANA titers higher than 1/500 are usually very significant clinically, often found in spontaneous or drug-induced SLE and few other CTD. The immunologic aspects of ANA and their potential value as aids in the diagnosis and management of the CTD were discussed. Anti-nDNA antibodies have been found to have a high degree of specificity for SLE and high titers of these antibodies correlate well with low levels of serum complement and severity of kidney involvement. The spectrum of ANA in the sera from patients with SLE has been expanded with the finding of anti-Sm antibodies which, when detected by gel precipitation with prototype serum, have been found so far only in SLE. Some of these antibodies have been found to have prognostic significance. Patients with MCTD and a group of patients with SLE have high titers of serum ANA with specificity for an RNase-sensitive component of ENA. The group of SLE patients defined by the presence of these antibodies (anti-Mo) have a better prognosis and in general develop only mild nephritis or have no kidney involvement at all. High titers of pure antinucleolar antibodies probably are found almost exclusively in the sera of patients with scleroderma. Some ANA have organ specificity, and GS-ANA have been found in all patients with Felty's syndrome and in a large proportion of patients with RA. One of the great advances in the field has been the recognition that ANA can be induced in the human and in experimental animals by the use of a number of therapeutic agents. Some of these agents can also induce a clinical picture resembling spontaneous SLE, though kidney involvement does not occur or is extremely mild. It is interesting that the whole spectrum of ANA can be found in drug-induced LE except anti-nDNA antibodies which have been associated to the pathogenesis of immune complex nephritis in spontaneous SLE. There is no doubt that research on ANA has contributed a great deal to the understanding of the CTD and will continue to be a valuable tool for the clinician and the investigator.
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PMID:Antinuclear antibodies (ANA): immunologic and clinical significance. 6 98

Studies of antinuclear antibodies (ANA) were carried out in 39 cases of systemic scleroderma and for comparison in 19 cases of systemic lupus erythematosus (SLE) and 4 of mixed connective tissue disease (MCTD) using indirect immunofluorescence (IF) methods under standard conditions. The results on three different substrates--monkey esophagus, guineapig lip and rat liver--are reported. In 48.7% of scleroderma cases ANA showed a substrate specificity. The highest percentage of positive results in scleroderma was obtained on monkey esophagus (97.4%) and the lowest on rat liver (61.5%). In SLE and MCTD, in contrast, only about 13% of the sera displayed such specificity. If only sera with substrate specificity are considered, the positive results on monkey esophagus and rat liver are 94.7% and 21.1%, respectively. Titers of sera reacting positively on 2 or 3 substrates were mostly in agreement, although some sera both in systemic scleroderma and SLE showed higher titers on monkey esophagus. The IF pattern was usually the same regardless of the substrate, Tests for ANA in scleroderma should be performed on at least 2 substrates simultaneously.
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PMID:Substrate specificity of antinuclear antibodies in scleroderma. 6 98

Studies of antinuclear antibodies (ANA) were carried out in 39 cases of systemic scleroderma and for comparison in 19 cases of systemic lupus erythematosus (SLE) using indirect immunofluorescence (IF) methods under standard conditions. The results on three different substrates--monkey esophagus, guinea pig lip and rat liver--are reported. In 48.7% of scleroderma cases ANA showed a substrate specificity. The highest percentage of positive results in scleroderma was obtained on monkey esophagus (97.4%) and the lowest on rat liver (61.5%). In SLE, in contrast, only about 13% of the sera displayed such specificity. If only sera with substrate specificity are considered, the positive results on monkey esophagus and rat liver are 94.7% and 21.1%, respectively. Titers of sera reacting positively on 2 or 3 substrates were mostly in agreement, although some sera both in systemic scleroderma and SLE showed higher titers on monkey esophagus. The IF pattern was usually the same regardless of the substrate. Tests for ANA in scleroderma should be performed on at least 2 substrates simultaneously.
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PMID:Tissue specificity of antinuclear antibodies in scleroderma. 10 22

150 cases of chronic inflammatory lung diseases of unknown aetiology and assumed hyperergic (immuno-reactive) pathogenesis were examined for hypertensive pulmonary arterial lesions and for chronic cor pulmonale. Hypertensive lesions of the small pulmonary arteries were found in more than half of the cases with chronic disorders of long duration, but were inconspicuous in diseases of acute progressive character. Hypertensive lesions were found regularly in chronic interstitial pneumonia, frequently in scleroderma and rheumatoid arthritis and occasionally in dermatomyositis and disseminated lupus erythematosus. Chronic Cor pulmonale occurred in 16% of the cases with hypertensive arterial lesions of grade I (hypertrophy of media) and in 50% of grade II/III (hypertrophy of media and intimal fibrosis). Interstitial lung fibrosis plays an important role in the pathogenesis of cor pulmonale: two thirds of the cases with interstitial lung fibrosis had developed cor pulmonale and all the cases with cor pulmonale also had interstitial lung fibrosis. Hypertensive arterial lesions of grade IV-VI according to Heath and Edwards (angiitis, plexogenic and angiomatoid lesions) have been described in severe cases of pulmonary hypertension (congenital cardiac shunts, primary pulmonary hypertension). In secondary forms of pulmonary hypertension, as represented by our material, these changes are of little importance.
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PMID:[Hypertensive lesions of pulmonary arteries in chronic inflammatory lung diseases (author's transl)]. 15 72


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