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G Sturfelt

Publications and source records attributed to G Sturfelt.

At least 19 recordsLinked to original sources
PubMed1992

Cardiovascular disease in systemic lupus erythematosus. A study of 75 patients form a defined population.

All patients with systemic lupus erythematosus in a prospective, epidemiologically based study within a defined area in southern Sweden were invited to participate in an investigation of cardiac function. From 1981 to 1988, 101 patients were included in the study, and 75 of them were investigated according to a fixed protocol by echocardiography, Doppler cardiography, electrocardiography (ECG) at rest and at exercise, and myocardial scintigraphy (in patients whose ECG became abnormal during exercise). IgG anticardiolipin antibodies (IgG aCL) were determined by ELISA. Twenty of the 75 patients (27%) had valvular disease and 12 of these (60%) had increased concentrations of IgG aCL, compared with 12 of 55 (22%) without valvular disease (p less than 0.01). Pericardial effusion was detected in 14 patients (19%) during the study period. Mild pulmonary hypertension was found in 11 patients (16%), who also had increased frequency of IgG aCL. Myocardial infarction had occurred in 7 patients, 3 of whom were women less than 40 years of age. Echocardiography revealed regional hypokinesis or akinesis in 5 of the patients with myocardial infarction. Exercise testing revealed low work capacity in 13 of 54 patients (24%), the limiting symptoms being mainly exhaustion or musculoskeletal pain. An abnormal resting ECG was found in 9 of the patients participating in the exercise test. During exercise, abnormal ST-depression was observed in 8 patients, 2 of whom developed angina. Myocardial scintigraphy was performed in 6 of these patients, revealing reversible uptake defects in all. Prolonged glucocorticoid treatment was associated with valvular abnormalities as well as myocardial infarction. Valvular abnormalities and IgG aCL appeared to be risk factors for cerebral infarction.

Adult↗
PubMed1992

Detection and characterization of immunoconglutinins in patients with systemic lupus erythematosus (SLE): serial analysis in relation to disease course.

The levels of IgA, IgG and IgM immunoconglutinins (IK) were assessed in sera from 20 patients with SLE which were followed for 8-month periods. At the time of the exacerbation, IgG IKs were significantly increased to 226 +/- 90 arbitrary units (mean +/- s.e.m.) compared with both the minimum value of 75 +/- 28 in the SLE patients and with 31 +/- 2 in healthy controls (P < 0.05). There was no difference between SLE patients and controls in the levels of IgM and IgA IKs. Most of the SLE patients in this material showed maximal IgG IK levels before exacerbation, but there was no correlation between the clinical disease index and the levels of IgG IK. The specificity of IgG IKs showed a broad diversity for microtitre-fixed C3b, iC3b, C3c and C3dg. The antibodies were of IgG1, IgG3 and in two patients, IgG4 subclass. IgG IKs were correlated to the C3d/C3 ratio which suggested that the IK responses were secondary to C3 activation. In summary, unlike other conditions associated with complement activation where elevated IgM IKs are common, an increase in IgG IK levels was observed. It is possible that this diverging IK response contributes to the pathophysiology of the disease.

Antibody Specificity↗
PubMed1992

Two UV-induced episodes of myelitis in a patient with systemic lupus erythematosus.

Two flares of acute myelitis were observed in a 31-year-old woman with previously known mild SLE. The two myelitic episodes both occurred within 1 week after intense sun exposure, and for this reason photobiological induction of the manifestation is considered likely. The diagnostic utility of MRI in the acute situation and the possible influence of sex-steroids on SLE manifestations are also illustrated by this case.

Acute Disease↗
PubMed1992

Western blot analysis of human IgG reactive with the collagenous portion of C1q: evidence of distinct binding specificities.

An enzyme-linked immunosorbent assay (ELISA) with purified collagenous C1q fragments in the solid phase was used for detection of C1q-specific immunoglobulins in the sera of twelve patients with systemic lupus erythematosus (SLE) or the SLE-like disease hypocomplementemic urticarial vasculitis syndrome (HUVS). By clinical criteria, four patients had SLE, and three HUVS. Five patients had overlap syndromes. All patients demonstrated high concentrations of C1q-specific IgG and markedly low concentrations of circulating C1q. Detection of C1q-specific IgG in SLE sera was facilitated by employment of saturating concentrations of collagenous C1q fragments in the solid-phase ELISA. When added to SLE serum, immune complex-fixed C1q inhibited binding of IgG to the C1q fragments, whereas addition of C1q alone had limited inhibitory effects. Under similar conditions, using approximately equimolar amounts of C1q relative to solid-phase C1q fragments, no ELISA inhibition was obtained after addition of C1q or immune complex-fixed C1q to a HUVS serum. Even in large excess, purified C1q did not inhibit binding of HUVS-IgG to solid-phase C1q fragments. Thus, possible interactions between HUVS-IgG and native Clq are probably of low affinity. By Western blot analysis, IgG reactive with the B and C chains of C1q was found in the eight patients with evidence of HUVS, five of whom also showed IgG binding to C'-C' and A'-B' dimers of collagenous C1q fragments. Sera from SLE patients were negative by Western blot analysis. It seems likely that C1q-specific IgG in SLE primarily recognizes assembled C1q molecules or collagenous C1q fragments expressing conformational epitopes of bound C1q. Interestingly, patients with evidence of HUVS fairly consistently had zymogen (C1r-C1s)2 complexes in their serum, while patients with SLE showed high concentrations of complexes containing Cl inhibitor, C1r and C1s. Different binding specificities of C1q-reactive IgG could be of importance with regard to pathogenetic mechanisms in SLE and HUVS. There was no correlation between findings of C1q-specific IgG and a variety of autoantibodies associated with SLE and SLE-like disease.

Adolescent↗
PubMed1992

Effects of ultraviolet irradiation on natural killer cell function in systemic lupus erythematosus.

In vitro irradiation with long wavelength ultraviolet light (UV-A), in clinically relevant dosages, of a natural killer cell line containing cell preparations from 17 control subjects reduced natural killer cell cytotoxicity with the cell line K562 as target. The spontaneous function of natural killer cells from 12 patients with systemic lupus erythematosus (SLE) correlated inversely with the one hour erythrocyte sedimentation rate, but not with glucocorticoid doses. After UV-A exposure, natural killer cells from patients with SLE exert either increased or decreased cytotoxicity, and the direction of change is inversely correlated with the spontaneous natural killer cell function.

Adolescent↗
PubMed1992

Effects of coagulation temperature on measurements of complement function in serum samples from patients with systemic lupus erythematosus.

Blood samples from 15 patients with systemic lupus erythematosus (SLE) and 15 healthy blood donors were allowed to coagulate for one hour at room temperature, followed by one hour at 4 or 37 degrees C. The complement activity of the serum samples was assessed by three different functional assays. Serum samples from patients with SLE obtained by coagulation at 37 degrees C had a lower complement activity than serum samples from blood coagulated at 4 degrees C when the capacity of the serum samples to solubilise precipitable immune complexes and to support the attachment of complement factors to solid phase immune complexes was determined. Haemolytic complement activity was not affected by the coagulation temperature. The content of C1q binding immune complexes in paired serum samples obtained after coagulation at 4 and 37 degrees C was similar and the size distribution of the immune complexes, determined by high performance gel permeation chromatography, was also similar. This study shows that the results of functional complement assays, applied to serum samples from patients with SLE cannot be compared unless the conditions for blood coagulation and serum handling are defined and are the same. The data also indicate that assays measuring complement mediated solubilisation of immune complexes and the fixation of complement factors to solid phase immune complexes are more sensitive indicators of complement activity than the haemolytic assay.

Adult↗
PubMed1992

Serum levels of the soluble interleukin-2 receptor are dependent on the kidney function.

We have investigated the influence of kidney function on soluble interleukin-2 receptor (S-IL-2R) serum levels. S-IL-2R is a glycoprotein with a molecular weight of 45 kDa. The serum concentration of S-IL-2R was positively correlated to serum creatinine (r = 0.35) and complement factor D (r = 0.30), a low molecular weight protein, and the reciprocal value of S-IL-2R was negatively correlated to 51Cr-EDTA clearance (r = -0.35). When measuring S-IL-2R and factor D in a wide range of serum creatinine (140-1,380 mumol/l), a high positive correlation was found between factor D and serum creatinine. S-IL-2R and serum creatinine had r = 0.92 and r = 0.79, p = 0.0001, respectively. The correlation coefficient between factor D and S-IL-2R was 0.86. S-IL-2R is used as a marker for an increased activity of the immune system and in a variety of lymphoproliferative disorders. However, it is important to keep in mind that a reduced kidney function may contribute to the increased S-IL-2R levels seen in different immune diseases. Therefore, renal function should be taken into account in the interpretation of elevated plasma concentrations of S-IL-2R.

Complement Factor D↗
PubMed1991

C1 subcomponent complexes and C2 cleavage in active systemic lupus erythematosus.

We studied the activation and C1 inactivator-dependent dissociation of the first component of complement, the C1q(C1r-C1s)2 complex, in relation to recruitment of the classical activation pathway in the circulation of 24 patients with systemic lupus erythematosus (SLE). The patients were divided into three groups on a clinical basis, and were investigated during flares of disease activity. Group I had mild symptoms, group II major extrarenal manifestations, and group III manifest renal disease. High serum concentrations of trimer complexes containing C1 inactivator, activated C1r and zymogen C1s(C1 IA-C1r-C1s) were found in the majority of the patients. Some patients with high C1 IA-C1r-C1s concentrations showed no evidence of classical pathway activation, indicating that C1 activation was controlled by the action of C1 IA at the C1r level. By contrast, formation in serum of tetramer complexes in which C1 IA was firmly bound to both C1r and C1s (C1 IA-C1r-C1s-C1 IA) was associated with C2 and C3 cleavage in EDTA plasma, and with manifest hypocomplementemia. Low C1 IA-C1r-C1s-C1 IA values were observed in conjunction with substantial C2 cleavage in a few patients. Thus, C1 IA-C1r-C1s-C1 IA may not always be a sensitive indicator of classical pathway activation. Efficient recruitment of the classical pathway was related to disease severity, with some overlap between the clinical groups. In conclusion, C1 dissociation with formation of C1 IA-containing complexes was consistently found in patients with active SLE. The results suggested that C1 IA-dependent control of C1 activation was of biological significance in the disease.

Adolescent↗
PubMed1990

Effects of sulindac and naproxen on prostaglandin excretion in patients with impaired renal function and rheumatoid arthritis.

PURPOSE: The purpose of the current investigation was to study the influence of sulindac and naproxen on renal function and urinary excretion of the stable hydration product of prostacyclin, 6-keto-PGF1 alpha, in patients with arthritis and impaired renal function. PATIENTS AND METHODS: In a placebo-controlled, double-blind, cross-over design, the effects of 7 days of oral sulindac 200 mg twice a day were compared with naproxen 500 mg in the morning and 250 mg in the evening in 10 patients with polyarthritis and stable impaired renal function. Inulin and para-amino-hippurate sodium were used to calculate glomerular filtration rate and renal plasma flow. The excretion rate of 6-keto-PGF1 alpha was measured in urine collected overnight. After patients ingested drugs in the morning, urine was collected in fractions by spontaneous voiding. Venous blood samples were drawn repeatedly for assay of electrolytes, creatinine, proteins, hormones, and drugs. Grip strength and Ritchie articular index were recorded as indicators of symptomatic antiarthritic effectiveness. RESULTS: Naproxen decreased urine levels of 6-keto PGF1 alpha by 59% (p less than 0.01). Sulindac had no effect on renal prostaglandin excretion. Naproxen reduced the glomerular filtration rate and renal plasma flow by 18% (p less than 0.05) and 13% (p less than 0.05), respectively, while no significant change was observed during the sulindac treatment periods. Serum levels of creatinine and complement factor D were unaffected by either drug. Plasma renin activity decreased during naproxen and sulindac treatments by 38% (p less than 0.05) and 22% (p less than 0.05). No significant change in plasma aldosterone was observed during the two drug treatments, but urinary aldosterone declined significantly (p less than 0.05) by 34% with naproxen. Albuminuria decreased (p less than 0.05) during both naproxen (41%) and sulindac treatment (72%), while the albumin/creatinine clearance ratio decreased by 59% (p less than 0.05) only during treatment with sulindac. N-acetyl-beta-D-glucosaminidase in urine was not changed by either drug. Sulindac and naproxen had no discernible effects on base excess, excretion of water, sodium, or potassium, or on osmolal clearance. However, serum potassium increased slightly but significantly (p less than 0.01) during treatment with naproxen. Sulindac sulfide, the active metabolite of sulindac, could not be traced in the urine from any of the patients. Mean arterial blood pressure declined significantly (p less than 0.05) during sulindac treatment but did not change during treatment with naproxen. Both drugs produced equal clinical improvement as measured by grip strength and the Ritchie articular index. CONCLUSION: The results suggest that when sulindac and naproxen are given in clinical equipotent doses to patients with impaired renal function, sulindac does not affect renal prostaglandin synthesis or renal function, whereas naproxen induces suppression of renal prostaglandin synthesis and a further decrease in renal function.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

Estimating the incidence of systemic lupus erythematosus in a defined population using multiple sources of retrieval.

We studied the age-specific incidence of SLE in a defined population in southern Sweden during 1981-86. Female incidence was 5.4/100,000/year and male incidence 1/100,000/year. In comparison with previous studies, incident cases were characterized by a high age at diagnosis with the highest incidence in age groups 55-64 and 65-74, approximately 7.5/100,000/year. The incidence was low in children under 15 years of age, 0.4/100,000/year, and unexpectedly so in the 15-24 decade, 1.2/100,000/year. Patient retrieval was based on four separate sources: a computerized diagnosis register; referrals from both public health care physicians and private practitioners; and records of ANA positive individuals from the single laboratory serving the area. All incident patients were present in at least two of these sources and 11 patients were present in three. We interpret the high amount of overlap between retrieval sources, without patients detected in only one source, as evidence for a high degree of completeness in our retrieval of SLE patients.

Adolescent↗
PubMed1990

Autoantibodies against neutrophil cytoplasm components in systemic lupus erythematosus and in hydralazine-induced lupus.

Anti-neutrophil cytoplasm antibody (ANCA) has been shown to be no marker of systemic lupus erythematosus (SLE) including lupus nephritis or of progressive systemic sclerosis (PSS). Antibodies against myeloperoxidase (anti-MPO) and elastase, two granulocyte lysosomal enzymes, were found in patients with SLE but not in those with PSS, except for one patient who had anti-MPO. Anti-MPO was present in 21% of patients with SLE, and at low concentrations in about 80% of these cases. Anti-elastase was found in four patients with SLE. In another group of six patients with a SLE-like syndrome induced by anti-hypertensive treatment with the anti-hypertensive hydralazine, anti-MPO antibodies occurred in all six, and anti-elastase antibodies in five. Monitored during a 2-year follow-up period, anti-MPO antibodies were found to persist, whereas anti-elastase antibodies were rapidly eliminated, after withdrawal of the drug.

Autoantibodies↗
PubMed1990

Homozygous C4A deficiency in systemic lupus erythematosus: analysis of patients from a defined population.

Homozygous C4A deficiency was found at a prevalence of 16% (13/80 patients) in systemic lupus erythematosus (SLE). The patients represented all diagnosed cases retrieved from a defined population in Southern Sweden, which minimizes the influence of patient selection. Photosensitivity was more common among C4A-deficient patients than among other SLE patients (p less than 0.05). Otherwise, clinical features were similar in the two groups. In addition, no differences were found with regard to presence of various autoantibodies (anti-dsDNA, anti-Sm, anti-RNP, anti-SSA, anti-SSB, rheumatoid factors and anti-cardiolipin). In patients expressing both C4A and C4B isotypes, C4B/C4A quotients were fairly stable in plasma irrespective of disease activity. This argues against preferential break-down of either isotype during complement activation in the disease. The increased photosensitivity of C4A-deficient patients partly resembles the findings in patients with complete deficiencies of classical pathway components.

Antibodies, Antinuclear↗
PubMed1990

A novel assay for neutrophil clustering activity of human sera: relation to disease activity and neutropenia in systemic lupus erythematosus.

A simple and reproducible method for the measurement of serum neutrophil clustering activity was developed. High clustering activity was found in 19/30 patients with active systemic lupus erythematosus (SLE), and 14/20 of those with severe disease flares. In contrast, 0/10 patients with quiescent SLE and 2/20 patients with rheumatoid arthritis had high neutrophil clustering activity. Particularly high clustering activity was found in patients with SLE with lupus glomerulonephritis and in certain patients with central nervous system disease. An inverse correlation was found between neutrophil clustering activity and peripheral blood neutrophil count in patients with SLE not treated with glucocorticoids, and clustering activity was high in all patients with low neutrophil counts in this group. A moderate correlation was found between neutrophil clustering activity and C1q binding circulating immune complexes. Non-steroidal anti-inflammatory drugs and glucocorticoids had little direct effect on neutrophil clustering activity.

Agranulocytosis↗
PubMed1990

Recurrent cerebral infarction and the antiphospholipid syndrome: effect of intravenous gammaglobulin in a patient with systemic lupus erythematosus.

A 23 year old woman with systemic lupus erythematosus and antiphospholipid syndrome developed severe thrombocytopenia (5-10 X 10(9)/l) and cerebral infarction. Treatment with high doses of corticosteroids and cytostatic drugs was not effective. The condition was successfully treated only when three courses of intravenous gammaglobulin at 400 mg/kg daily was added. A clear relation was found between the immunoglobulin infusions and rising platelet counts, whereas an effect on the levels of anticardiolipin antibodies could not be recorded. The findings suggested that the mechanisms responsible may be modification and solubilisation of immune complexes or interference with anticardiolipin binding to platelet membranes, or both.

Adult↗
PubMed1990

The spleen is not a major synthetic site of alternative pathway components.

The serum concentrations of the complement proteins C1q, C1s, C4, C3, factor D, factor B, properdin, C1 inactivator, factor I and factor H were determined in 7 patients before and after splenectomy. The concentrations of C1q, factor D and properdin were moderately decreased 1-2 days after surgery, while the other components were virtually unchanged. During the course of 4 weeks the values either returned to normal, or were slightly increased. In general, the findings could be ascribed to the inflammatory plasma protein response and were similar in cholecystectomized patients. The results provided no evidence of significant complement protein synthesis in the human spleen.

Adult↗
PubMed1990

Absence of circulating antineutrophil cytoplasm antibodies (ANCA) in severe vasculitis associated with rheumatoid arthritis.

Sixteen patients with classical rheumatoid arthritis (RA) complicated by severe vasculitis were studied and compared with a matched control group of 17 RA patients without vasculitis. A control group of 24 patients with unrelated disease was also included. Neither antineutrophil cytoplasmic antibodies (C-ANCA) nor anti-myeloperoxidase (anti-MPO) were found. Granulocyte specific antinuclear antibodies ("GS-ANA") were found in a higher frequency in the vasculitis group (75%) than in the RA control group (41%), but the difference was not statistically significant. No patient in the control group without RA had "GS-ANA".

Aged↗