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Biomedical subjects

U Mårtensson

Publications and source records attributed to U Mårtensson.

27 records · Page 2Linked to original sources
PubMed1977

Studies of C1 subcomponents in chronic urticaria and angioedema.

C1q, C1r, C1s, C3, C4 and C-1 IA were determined by electroimmunoassay in sera from 150 patients with chronic urticaria or angioedema. Abnormal C1q and C1s levels were found in about 30% of the patients. In seven sera C1r was not measurable due to the appearance of diffuse precipitates. The levels of C3 and/or C4 were decreased in five sera with aberrations of C1 subcomponents in the electroimmunoassay. None of the patients showed reduced C-1 IA levels in the electroimmunoassay. The presence in sera of abnormal C1 subcomponent complexes was studied by crossed immunoelectrophoresis. Sera from 11% of the patients contained C1r-C1s complexes. Increased amounts of alpha2 complexes (C-1r-C-1-S-C-1 IA) were found in 33% of the patients. A major part of the C1q in sera yielding abnormal C1r precipitates had the same electrophoretic mobility as isolated C1q and was not associated with the C1qrs complex. C1 activity in hemolytic tests was low in these sera as well as in sera with decreased C1q levels. In the esterolytic assay for C-1 IA low values were found in 14 patients. Repeated sampling and family studies in appropriate cases gave no evidence for genetically determined deficiencies of C1q, C1r or C-1 IA.

Angioedema↗
PubMed1976

C1R levels in normal human sera determined by electroimmunoassay.

C1r levels in normal adults were determined by electroimmunoassay. The 95 per cent range was 71-133 per cent of a normal reference pool. C1r values were well correlated to the levels of C1q (r = 0.708) and of C1s (r = 0.768). The interplate variation of the method on double determinations was 3.4 (SD). C1r values in normal sera not appreciably affected by storage at room temperature or by repeated freezing and thawing. The C1r antigen in EDTA plasma was found to be labile.

Complement C1↗
PubMed1976

C1 subcomponent conplexes in normal and pathological sera studied by crossed immunoelectrophoresis.

Selected pathological sera gave three molecular species of C1s protein on crossed immunoelectrophoresis in the presence of calcium. C1s precipitates were obtained at the origin and in the beta1 and alpha2 regions. 12 normal sera gave C1s protein peaks at the origin and in alpha2 position. One of the normal sera also contained a small amount of the beta1 C1s protein. The C1s protein at the origin represented macromolecular C1. The alpha2 peak was a complex composed of C1 IA, C1s and C1r proteins. This complex was preformed in serum and did not show C4 cleaving activity. The molecular species in the beta1 region was shown to be a calcium-dependent complex of C1r and C1s, probably in proenzyme form. the C1r-C1s complex formed macromolecular C1 on addition of purified C1q to serum. During electrophoresis activation of C1 subcomponents was initiated by a mechanism involving CIr with generation of CIs activity in eluted fractions corresponding to the position of macromolecular C1 as well as in the beta region. The significance of beta1 C1s complexes or of alpha2 C1s complexes in normal and pathological sera was discussed.

Angioedema↗
PubMedDate not supplied

Prospective analysis of C1 dissociation and complement activation in patients with systemic lupus erythematosus.

OBJECTIVE: To evaluate the results of complement analysis for assessment of disease activity and severity, and prediction of flares in systemic lupus erythematosus (SLE). METHODS: Patients with mild extra-renal flares, severe extra-renal flares or flares of lupus glomerulonephritis were followed for eight months, with investigations being performed every second month. Findings in initial samples four months before the flares were compared with findings in a control group with stable disease. C-reactive protein, and circulating C1q, C4 and C3 were determined together with two types of complexes containing C1 inhibitor (C1 INH), C1 INH-C1r-C1s and C1 INH-C1r-C1s-C1 INH, and the C3 breakdown product C3d. RESULTS: Enhanced formation of C1 INH-C1r-C1s appeared to be a marker of low specificity and was mainly seen in patients with extra-renal disease. Concentrations of C1 INH-C1r-C1s-C1 INH, C3d, C1q and C3 clearly varied according to disease activity in patients with severe disease. Interestingly, high C1 INH-C1r-C1s-C1 INH values were found four months before the flares in all but one patient with lupus glomerulonephritis. Assessment of the relative predictivity for a subsequent flare indicated low C1q to be the most reliable marker, the predictivity of the complexes being: low C1q > high C1 INH-C1r-C1s-C1 INH > low C3 > high C3d > low C4. CONCLUSION: The importance of C1q and C1-related events in SLE may be underestimated. In addition, our results demonstrate the relevance of serial complement analysis for the assessment of disease activity and severity.

Adolescent↗