Serum Complement Levels in Systemic Lupus Erythematosus and Other Diseases

Gl, Asherson

doi:10.1111/imj.1960.9.1.57

Cited by 21 publications

(8 citation statements)

References 26 publications

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“…The values for CH60 and C3 concentration did not correlate closely with the degree of cholestasis as measured by the serum levels of alkaline phosphatase and bilirubin. However, raised values for total haemolytic complement activity have been found in patients with cholestasis due to large duct biliary tract obstruction (Jordan, 1953;Mandel and Lange, 1955;Asherson, 1960;Farini et al, 1970;Pagaltsos et al, 1971). The value for CH50 was also raised in a patient with cholestasis due to chlorpromazine (Asherson, 1960).…”

Section: Discussionmentioning

confidence: 99%

“…However, raised values for total haemolytic complement activity have been found in patients with cholestasis due to large duct biliary tract obstruction (Jordan, 1953;Mandel and Lange, 1955;Asherson, 1960;Farini et al, 1970;Pagaltsos et al, 1971). The value for CH50 was also raised in a patient with cholestasis due to chlorpromazine (Asherson, 1960). It would appear, therefore, that cholestasis could be a non-immunological cause of an increase in the total haemolytic complement activity.…”

Section: Discussionmentioning

confidence: 99%

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Serum complement in chronic liver disease

Potter¹,

Trueman²,

Jones³

1973

Gut

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SUMMARY Total serum haemolytic complement activity (CH50) and the serum concentrations of both the third and fourth components ofthe complement system (C3 and C4) have been measured in 29 control subjects, 92 patients with chronic hepatocellular disease, and eight patients with large duct biliary tract obstruction. The mean C4 concentration was reduced in all types of chronic liver disease studied. However, the mean CH50 and C3 values were increased in compensated primary biliary cirrhosis, were relatively normal in non-cirrhotic chronic active hepatitis, and were decreased in cryptogenic cirrhosis, particularly when ascites was present. There was a significant correlation between CH50 and C3 in patients with chronic liver disease but no correlation between CH5o and C4 or between C3 and C4. Raised values for CH50 and C3 in primary biliary cirrhosis may be due at least in part to concomitant cholestasis since these values tend to be raised in patients with large duct biliary tract obstruction. Although primary biliary cirrhosis, chronic active hepatitis, and cryptogenic cirrhosis are considered to be part of a spectrum of chronic liver disease associated with disturbed immunity, the results of this study emphasize that there are clearly definable differences between these diseases in terms of the pattern of changes in serum complement.Although some types of chronic liver disease, such as chronic active hepatitis, primary biliary cirrhosis, and cryptogenic cirrhosis are usually associated with evidence of disturbed immunity, so far no immune mechanism has been demonstrated to be of fundamental importance in the pathogenesis of these diseases. One well established cause of cell lysis and death involves the complement system, classically activated by antigen-antibody interaction on a cell surface (Rapp and Borsos, 1970). If this immune process is responsible for liver cell injury in patients with chronic liver disease, there may be associated changes in serum complement. However, changes in the complement system may also arise as a consequence of the disease process itself.It has previously been shown that patients with chronic liver disease tend to have a reduced total serum complement haemolytic activity (Goldner, 1929;Jordan, 1953;Asherson, 1960;Townes, 1967; Inai, Fujikawa, Naguki, Takahashi, Ozono, and Ishida, 1967;Farini, Gambari, Fagiolo et al, 1970;Pagaltsos, Smith, Eddleston, and Williams, 1971; De Meo and Anderson, 1972;Torisu, Yokoyama, Kohler, Durst, Martineau, Schroter, Amemiya, Groth, and Starzl, 1972) and a reduced serum concentration of the third component of comple-

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Serum complement in chronic liver disease

Potter¹,

Trueman²,

Jones³

1973

Gut

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“…The mechanism for this elevation is at present not understood, but overproduction of complement components is a plausible explanation. Elevations of serum complement levels have been seen during the active phases of obstructive jaundice (50), thyroiditis (51), aCl.lte rheu matic fever (52-54), rheumatoid arthritis (55), periarteritis nodosa (SS), dermatomyositis (55 ), acute myocardial infarction (52), ulcerative colitis (56), sarcoidosis (57), typhoid fever (58), diabetes (59), acute gout, Reiter's syndrome, and acute polyarthritis (60). (61).…”

Section: Acquired Abnormalities Of the Complement System Elevated Commentioning

confidence: 99%

“…Some patients with liver disease also have low complement levels, and it has been thought that these patients are also making some complement com ponents in a defi cient manner (50,60). Studies of individual components are lacking.…”

Section: Decreased Synthesis Of Complement (Components)mentioning

confidence: 99%

Complement in Human Disease

Schur¹,

Austen²

1968

Annu. Rev. Med.

111

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“…Asherson (2) and Deicher, Holman, and Kunkel (3) now have demonstrated other common serum factors in SLE that fix complement with cytoplasmic components, including mitochondria and microsomes from a variety of animal and human sources. The observation of low serum complement levels in active SLE (4)(5)(6)(7)(8)(9)(10) suggests the possibility that complement-fixing antigen-antibody interactions might occur in vivo and play a role in the pathogenesis of the disease.…”

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confidence: 99%

Effects of Antibodies on Mitochondria*

Davis¹,

Bollet²

1962

J. Clin. Invest.

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Since the demonstration of the lupus erythematosus phenomenon by Hargraves, Richmond, and Nforton (1), a great deal of attention has been paid to the numerous antibody-like serum factors in patients with active systemic lupus erythematosus (SLE). Until recently, this attention has been concentrated on those factors that react with whole nuclei or nuclear subunits, such as DNA and histone. Asherson (2) and Deicher, Holman, and Kunkel (3) now have demonstrated other common serum factors in SLE that fix complement with cytoplasmic components, including mitochondria and microsomes from a variety of animal and human sources. The observation of low serum complement levels in active SLE (4-10) suggests the possibility that complement-fixing antigen-antibody interactions might occur in vivo and play a role in the pathogenesis of the disease.Antibodies which react with these mitochondria in. vivo might interfere with important metabolic functions, since mnitochondria contain enzymes involved in the regulation of oxidation and highenergy bond formation. A study of the effect of induced antimitochondrial antibodies in rabbits on mitochondrial enzyme activity was therefore undertaken to define the possible metabolic effects of such antibodies preliminary to study of the effects of the antimitochondrial antibodies found in SLE. This report describes several effects of antimitochondrial serum in various immunologic systems; such serum caused inhibition of mitochondrial enzymes, particularly those in the electron transport chain. A heat-labile serum component, presumably complement, potentiated inhibition of DPNH oxidase by mitochondrial antibody. Preparation of antisera. Five-to 10-pound New Zealand white rabbits, maintained on Purina rabbit chow at will, were given injections of rat liver mitochondria prepared in Freund's adjuvant, made in 25-ml lots that contained 2 g of mitochondrial protein, 10 ml of Bayol F, 5 ml Falba, and 62.5 mg of heat-killed human tubercle bacilli (H30Rv). Controls included unimmunized rabbits and rabbits given adjuvant prepared as above except that sucrose was substituted for the mitochondrial suspension. Subcutaneous injections of 2 ml were given at 1, 2, and 4 weeks. At 6 weeks, and at varying intervals thereafter, subcutaneous booster injections of suspensions of mitochondria in sucrose were given to maintain a high antibody titer. Some rabbits received only one injection of adjuvant suspension followed by boosters of graded doses of antigen in sucrose intravenously twice a week. Blood obtained from marginal ear veins was allowed to clot at room temperature; the serum was inactivated at 560 C for 30 minutes and stored at -200 C. Antiserum to a purified bovine enzyme, L-glutamic dehydrogenase, was prepared in a similar fashion by use of an ammonium sulfate suspension (Sigma) as the antigen (13).Globulin fractions of many sera were prepared by amnmonium sulfate precipitation. Ammonium sulfate was added slowly to the serum to a final concentration of 1.6 M. After overnight refrigeration, the precip...

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Serum Complement Levels in Systemic Lupus Erythematosus and Other Diseases

Cited by 21 publications

References 26 publications

Serum complement in chronic liver disease

Serum complement in chronic liver disease

Complement in Human Disease

Effects of Antibodies on Mitochondria*

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