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L Brinch

Publications and source records attributed to L Brinch.

80 records · Page 5Linked to original sources

The in vivo metabolism of C3 in human glomerulonephritis and after renal transplantation.

Metabolic investigations of complement component C3 have been performed to study pathogenetic mechanisms in patients with glomerulonephritis and after renal transplantation. Purified and biologically active 125I-labelled C3 was given intravenously together with 131I-albumin to nine patients with different forms of glomerulonephritis and nine allograft recipients at different stages after renal transplantation. Control studies were performed in 16 normal individuals. The fractional catabolic rate (FCR) of the proteins was calculated with the metabolic clearance method (U/P ratio) and/or by analysis of the plasma radioactivity disappearance curve. An increased FCR of C3 was found in three patients with glomerulonephritis. A modestly elevated FCR of C3 was found in all but one of the transplant patients as calculated by the U/P ratio, while the FCR was high in only two when calculated from plasma radioactivity disappearance. Slight increases of C3 catabolism were found during two suspected rejection episodes, but may have been due to a general increase in protein turnover. The serum level of C3 was reduced in two recipients and in one of these the FCR of the protein was elevated. The remaining patients had normal or increased C3 levels. Judged from these results, activation of complement was only of modest importance in the patients studied.

Adolescent↗

The in-vivo metabolism of C3 in ankylosing spondylitis.

Turnover studies with radioactively labelled C3 were performed in 7 patients with ankylosing spondylitis and in 14 healthy individuals . As a group the patients had a moderately higher fractional catabolic rate of C3 than the controls. A possible explanation is that the complement system is activated by immune complexes. The serum levels of C3 were high. The hypercatabolism was therefore more than compensated for by an increased synthesis rate.

Adult↗

The in vivo metabolism of C3 in hepatobiliary disease associated with ulcerative colitis.

To study possible pathogenetic mechanisms in hepatobiliary disease associated with ulcerative colitis (UC), we performed a metabolic investigation of component C3 of the most important effector of humoral immunity, the complement system. Purified and biologically active C3 was labelled with 125I and injected together with 131I-albumin into seven patients. All had hepatobiliary disease, and total colectomy had previously been performed for severe UC in all patients. The results were compared with those for 16 normal individuals. The fractional catabolic rates (FCR) were calculated by the metabolic clearance method and by analysis of the plasma radioactivity disappearance curve. An increase in the FCR of C3 was found in the patient group, indicating that humoral immune mechanisms may be of pathogenetic importance in hepatobiliary disease associated with UC. The increased FCR was compensated for by and increased synthesis rate of the protein.

Adult↗

The metabolism of C3 in adult coeliac disease.

To study possible pathogenetic mechanisms in adult coeliac disease, we performed a metabolic investigation of a component (C3) of the most important effector of humoral immunity, the complement system. Purified and biologically active C3 was labelled with 125I and injected together with 131I-labelled albumin into six patients with adult coeliac disease exhibiting different degrees of disease activity. The same labelled preparations were given to 12 normal individuals. Plasma and urine radioactivity were studied for a total of 8 days. Fractional catabolic rates (FCR) and synthesis rates were calculated by the metabolic clearance method. Other mathematical methods were not used because a final straight exponential was not always obtained, probably owing to extravascular sequestration of protein. An increased FCR was found in most patients, with the highest values seen in active, untreated disease. This suggests that activation of complement by immune complexes may be a pathogenetic factor in adult coeliac disease.

Celiac Disease↗

Metabolic studies of C3 in man.

The results of metabolic studies with radioactively labelled C3 in 14 healthy individuals are presented. Plasma volume determined by labelled C3 was generally higher than when determined by labelled albumin, and different batches of C3 behaved differently during the early part of the experiments. These phenomena are probably caused by C3 inhomogenities which are difficult to detect by usual biochemical and immunological methods. We have, therefore, excluded the first 24 h of the experiments from the mathematical analysis. In this way, rather narrow limits for the metabolic parameters have been obtained.

Albumins↗