Murine type II collagen arthritis. Association of an acute-phase response with clinical course.

The acute-phase reactant, C-reactive protein, is a good index of disease activity in patients with rheumatoid arthritis. We examined the murine acute-phase reactant, serum amyloid P, as an index of disease in type II collagen-induced arthritis in 3 mouse strains. The onset of type II collagen-induced arthritis, which is characterized by paw swelling, is associated with a significant, but transient, elevation of serum amyloid P.

Differing acute phase responses in Crohn's disease and ulcerative colitis.

Thirty eight patients with Crohn's disease and 30 patients with ulcerative colitis have been assessed using the technique of faecal excretion of 111Indium granulocytes to quantify precisely acute inflammatory activity. At the time of each faecal granulocyte measurement the serum concentration of the acute phase protein C-reactive protein and the erythrocyte sedimentation rate were estimated. C-reactive protein concentration was significantly higher in Crohn's disease than ulcerative colitis both overall and particularly in relation to given levels of granulocyte excretion.

C-reactive protein in patients undergoing cardiac surgery.

Among 25 patients undergoing cardiac surgery with the aid of cardiopulmonary bypass, 13 who recovered uneventfully all had normal (less than 2 mg/litre) levels of serum C-reactive protein pre-operatively. In contrast, 10 of the 12 patients who suffered from various postoperative complications, including two who died, had abnormally raised levels of C-reactive protein pre-operatively. All patients showed a major acute phase response to surgery with peak C-reactive protein levels at about 46 hours but, whereas the uncomplicated cases showed a characteristic smooth biphasic pattern of declining levels thereafter, the complicated cases all exhibited significant alterations of this pattern.

Continuous subcutaneous insulin infusion does not provoke significant acute-phase response.

C-reactive protein (CRP), the classical acute-phase reactant, and serum amyloid A protein (SAA), the putative precursor of AA-type amyloid fibrils, were measured in 62 diabetic patients. They were all attending their regular clinic appointments and had been asymptomatic during the 2 wk preceding sampling. CRP and SAA levels were similar in 18 patients on continuous subcutaneous insulin infusion (CSII), 27 patients treated by conventional insulin therapy (CIT), nine treated by diet only, and eight treated by diet and oral hypoglycemic agents, and were almost entirely within the normal range.

Circulating human leucocyte elastase in patients with inflammatory bowel disease.

The plasma concentration of human leucocyte elastase (HLE), measured by enzyme immunoassay as the complex with alpha 1-proteinase inhibitor, was determined in 94 patients with active and inactive inflammatory bowel disease. In Crohn's disease and in ulcerative colitis human leucocyte elastase levels were raised significantly above normal when the disease was active, and fell on remission. The mean human leucocyte elastase level in 31 cases of active Crohn's disease was significantly greater than the mean human leucocyte elastase level in 23 patients with active ulcerative colitis (p = 0.

Serum C-reactive protein concentration in the management of infection in patients treated by continuous ambulatory peritoneal dialysis.

In a prospective study over 21 months, serum C-reactive protein (CRP) concentration was measured serially in 39 consecutive patients undergoing continuous ambulatory peritoneal dialysis. All patients with peritonitis mounted a CRP response, and the height of the response correlated well with the severity and extent of the peritoneal damage. Patients who recovered uneventfully after antimicrobial treatment showed a prompt fall in CRP from its peak value towards normal.

Serum C-reactive protein measurement in the detection of intercurrent infection in Oriental patients with systemic lupus erythematosus.

In a prospective study serum C-reactive protein (CRP) concentrations were measured during 28 febrile episodes in 27 Oriental patients with systemic lupus erythematosus (SLE). Although active SLE was associated with only a modest rise in serum CRP level, intercurrent infection provoked substantially higher levels. Serum CRP thus provides a sensitive objective test for this complication in SLE patients of all ethnic groups.

Correlation of disease activity in systemic vasculitis with serum C-reactive protein measurement. A prospective study of thirty-eight patients.

In a prospective study over 2 years, serum C-reactive protein (CRP) concentration and erythrocyte sedimentation rate were measured serially in thirty-eight patients with various types of necrotizing systemic vasculitis. The CRP concentration was always elevated in patients with active vasculitis and fell rapidly in association with clinical remission induced by immunosuppression. During periods of complete remission, in the absence of any intercurrent condition, the value remained within the normal range.

Serum C-reactive protein in polymyalgia rheumatica. A prospective serial study.

A prospective serial study of 13 well-documented, previously untreated cases of polymyalgia rheumatica was undertaken in order to assess the behavior of the nonspecific indices of disease activity, erythrocyte sedimentation rate and serum C-reactive protein (CRP) concentration, during induction of disease remission by prednisolone therapy. The clinical manifestations of all patients responded rapidly and completely to steroids, and the serum CRP value, which was raised in all patients at presentation, fell to normal at a rate which precisely reflected the clinical improvement. The erythrocyte sedimentation rate also fell, but did so much more slowly than the CRP concentration and, in half the patients, was still not normal after 14 days.

Serum C-reactive protein response to therapeutic embolisation: possible role in management.

In a prospective study over 12 months, serum C-reactive protein concentration was measured serially in 20 consecutive patients who underwent therapeutic embolisation for various forms of malignancy and in 13 patients who had diagnostic coeliac or hepatic angiography without embolisation. All the patients who underwent successful embolisation showed a C-reactive protein response and in all cases the height of the response correlated well with the estimated size of the embolised tumour. Patients who recovered uneventfully showed a prompt fall in C-reactive protein from its peak values towards normal.

Immunohistochemical studies of C-reactive protein and apolipoprotein B in inflammatory and arterial lesions.

Interactions in vivo between C-reactive protein (CRP) and apolipoprotein B (apo-B)-containing lipoproteins were sought in inflammatory lesions and atherosclerosis. CRP was demonstrated immunohistochemically on the surface of some muscle fibres in locally induced inflammatory lesions in the rabbit, but apoB was not detected in the same distribution. CRP was not detected in catheter-induced aortic endothelial injuries in the rabbit, in arterial lesions containing apoB from cholesterol-fed rabbits, in apoB-containing human fatty streaks or in advanced human atherosclerotic lesions.

Continuous subcutaneous insulin infusion does not induce a significant acute phase response of serum amyloid A protein.

In a study of 23 matched pairs of Type 1 (insulin-dependent) diabetic patients receiving continuous subcutaneous insulin infusion or conventional insulin injection therapy respectively, there were no significant differences in serum levels of the acute phase proteins, serum amyloid A and C-reactive protein. These results do not support the suggestion that continuous subcutaneous insulin infusion stimulates serum amyloid A production or that it carries a risk of inducing reactive systemic amyloidosis.

In vivo turnover studies of C-reactive protein.

The in vivo plasma clearance rate of the acute phase reactant C-reactive protein (CRP) was studied in mice and rats. The clearance rate of 125I-human CRP in mice and 125I-rat CRP in rats showed a T1/2 of approximately 4 h. The T1/2 was independent of circulating levels of CRP and was not affected by the presence of C-polysaccharide (CPS), a ligand to which CRP binds.

A comparison of the erythrocyte sedimentation rate and serum C-reactive protein concentration in elderly patients.

Fifty-five consecutive admissions to an acute geriatric unit were studied prospectively. Individuals were classified according to the obvious presence or absence of an active disease process on admission and their serum C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were measured then and five days later. There was no significant difference between the ESR values in the two groups either on admission or at day 5, nor was there any significant change between admission and day 5.

Human serum amyloid P component, a circulating lectin with specificity for the cyclic 4,6-pyruvate acetal of galactose. Interactions with various bacteria.

Serum amyloid P component (SAP), a normal plasma glycoprotein, has recently been shown to have Ca2+-dependent binding specificity for methyl 4,6-O-(1-carboxyethylidene)-beta-D-galactopyranoside (MO beta DG) [Hind, Collins, Renn, Cook, Caspi, Baltz & Pepys (1984) J. Exp. Med.

Studies of the in vivo synthesis and catabolism of serum amyloid P component (SAP) in the mouse.

The production of mouse serum amyloid P component (SAP), a major acute phase protein of liver origin, was studied immunocytochemically using the peroxidase staining technique. SAP was not detectable in the cytoplasm of hepatocytes from normal, unstimulated mice, nor was it observed before 24 h after an acute phase stimulus. 125I-labelled mouse SAP was cleared from the plasma in vivo with a half-life of 7.

Calcium-dependent aggregation of human serum amyloid P component. Inhibition by the cyclic 4,6-pyruvate acetal of galactose.

Serum amyloid P component is a normal plasma glycoprotein which is the precursor of amyloid P component, a minor but universal constituent of amyloid deposits. When isolated human P component is exposed to free ionised Ca2+ it aggregates and precipitates. This phenomenon is completely inhibited by the presence of 10(-4)-10(-2) M methyl 4,6-O-(1-carboxyethylidene)-beta-D-galactopyranoside, a recently synthesised specific ligand for amyloid P component.

Isolation and characterization of C-reactive protein from the dog.

Using calcium-dependent affinity chromatography on Sepharose-bearing, covalently-coupled pneumococcal C-polysaccharide, a protein was isolated from the serum of dogs that had undergone general anaesthesia and major surgery. This protein was confirmed as the canine analogue of C-reactive protein (CRP) in other species by virtue of its electron microscopic appearance, subunit composition and behaviour as an acute phase reactant. Dog CRP had an apparent molecular weight of approximately 100,000 and was composed of five subunits of approximately 20,000 MW each.

In vivo turnover studies of C-reactive protein and lipoproteins in the rabbit.

Clearance from the plasma of 125I-labelled rabbit C-reactive protein (CRP) was significantly slower in animals undergoing an acute phase response (T1/2, mean +/- s.d., 6.

Circulating human C-reactive protein binds very low density lipoproteins.

Native human CRP in solution formed complexes with the abnormal lipoprotein beta-VLDL in serum of patients with type III hyperlipoproteinaemia. CRP also formed complexes in sera from individuals with type IV and type V hyperlipoproteinaemia. The binding was calcium-dependent and inhibitable by free phosphoryl choline.

The failure of ascorbic acid therapy to alter the induction or remission of murine amyloidosis.

It has been claimed that ascorbic acid enhances the in vitro degradation of AA amyloid fibrils. This raises the possibility that ascorbic acid may be of benefit in systemic AA amyloidosis, a condition with serious morbidity and mortality for which there is as yet no specific treatment. The effect was therefore tested of oral or injected supplements of ascorbic acid on the induction of AA amyloidosis in mice.