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Biomedical subjects

I Brandslund

Publications and source records attributed to I Brandslund.

14 recordsLinked to original sources

[Costs and prices of laboratory services].

Cost accounting is performed in private and public laboratories. Guidelines for these activities are required and with this objective in mind, the Board of the Danish Society of Clinical Chemistry commissioned a working group to produce a position paper which is presented now in this report. The report discusses the objectives, the principles and the general requirements for cost accounting. The significance of information on costs for the clinicians' rational use of the laboratory is also illustrated. The working group points out that prerequisites for lucid and appropriate costing guidelines are clarification of which purposes information on costs are meant to serve, identification of the relevant cost centers and quality assurance of laboratory services to a defined extent. It is common practice to express laboratory costs as costs per test. The report advocates calculation of the cost per patient contact, i.e. the overall costs for laboratory service in a given investigative situation.

Accounting

Specificities of monoclonal antibodies against the complement C3d split product.

The only specific method at present for the quantification of the complement split product C3d, the double-decker rocket immunoelectrophoretic assay, is work intensive and expensive. We investigated the possibilities for developing an ELISA for the direct quantification of C3d in plasma. Available antibodies were examined for their specificity for C3 and its degradation products by the PAGE immunoblotting method. None of the antibodies were specific for C3d, as cross-reactivities against C3 and/or C3b and C3bi were demonstrable.

Animals

Metabolism of C3 and factor B in patients with congenital factor I deficiency.

The metabolism of complement factor B and C3 was analyzed in three previously described patients with congenital deficiency of factor I (C3b/C4b inactivator). Samples taken at steady state contained elevated levels of Ba and Bb, whereas native factor B was not detectable. Following plasma infusion in two of the patients Ba was rapidly cleared (within 8-12 hr) from the circulation and native factor B increased transiently, reaching normal levels within 22-24 hr. In parallel with the increase in Ba, factor B decreased during the following days, reaching preinfusion level after seven days. This was in contrast to a continued increase in C3 concentration, which was still within the normal range 15 days after infusion, despite the presence of only trace amounts of native B. In vitro complement activation experiments, employing purified C3Nef IgG as alternative pathway activator and aggregated IgG as classical pathway activator, were performed on selected serum samples (base-line, 12 hr and 15 days postinfusion samples) from the plasma infusion series. It was demonstrated that (a) C3Nef could not induce alternative pathway C3-conversion in factor B depleted samples and (b) C3-degradation by CP-activation could still occur in B-depleted samples, although at a much slower rate compared to normal human serum. These results may partly explain the difference in kinetics of factor B and C3 metabolism seen after plasma infusion in patients with factor I deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

Autoantibodies

Lumbar disc surgery and variations in C-reactive protein, erythrocyte sedimentation rate and the complement split product C 3 d.

Lumbar disc surgery was performed in fifty consecutive patients and variation in erythrocyte sedimentation rate (ESR), complement C 3 d, and C-reactive protein (CRP) levels before and after surgery were recorded. Preoperative values were within normal limits in all patients. Postoperatively, CRP increased immediately, with a maximum of 28.5 mg/l on the 2nd day and were normalized within 6 days. The maximum ESR elevation occurred after the 6th day and was followed by a slow decrease. After 12 weeks some patients still had an elevated ESR. Plasma C 3 varied pari passu with the ESR. Uncomplicated recovery after lumbar disc surgery seems to be indicated by a normalization of CRP, regardless of ESR values. Therefore, ESR may not be so useful as an indicator of disc space inflammation as previously accepted.

Adult

Neutrophil lysosomal enzyme release and complement activation during cardiopulmonary bypass.

Complement activation and neutrophil degranulation were concomitantly studied during uncomplicated cardiopulmonary bypass (CPB). Plasma concentrations of complement factor C4, complement split product C3d, the neutrophil lysosomal enzyme elastase complexed with alpha 1-proteinase inhibitor (PI) and fibronectin were measured in 12 patients, C3d and elastase/PI increased significantly during CPB (volume-corrected results). The C3d rise was almost linear, whereas elastase/PI showed exponential increase. Mean elastase/PI and mean C3d concentrations at different times during CPB covaried closely. The study showed that during CPB neutrophil lysosomal enzyme release is intimately related to complement activation, although activation of the two systems may be caused by a common third activator within the extracorporeal circuit.

Adult

Screening for complement deficiencies in unselected patients with meningitis.

Two hundred and nine patients consecutively admitted to hospital with a tentative diagnosis of meningitis were screened for complement deficiency by measuring classical and alternative pathway serum haemolytic complement activity and the plasma concentration of C3d. Abnormal test results were followed up by quantitative immunochemical measurements of individual complement components. No patients with homozygous complement deficiency were found in our material. One patient with pneumococcal meningitis with probable heterozygous C2-deficiency was identified. Patients with purulent meningitis of various etiologies or meningococcal disease had significantly increased plasma C3d concentration at admission compared to patients with serous meningitis or without meningitis. Furthermore, increased plasma level of C3d at admission in patients with purulent meningitis or meningococcal disease was associated with an increased lethality. Our findings do not support the hypothesis that complement deficiency is commonly associated with sporadically occurring meningococcal disease or purulent meningitis.

Adolescent

Plasma concentrations of complement split product C3d and immune complexes after procainamide induced production of antinuclear antibodies.

Seventeen patients treated with procainamide for cardiac ventricular arrhythmias were followed for up to 40 weeks. Immunological data as a clue to developing the systemic lupus erythematosus (SLE)-like syndrome was emphasized. Ten patients developed antinuclear antibodies (IgG or IgM), but no increase in the plasma concentration of the complement split product C3d or immune complexes, measured by two different methods, was demonstrated. This finding is in contrast to the high levels of both C3d and immune complexes in SLE. The discrepancy may be caused by a lack of immune complex mediated complement activation by the procainamide induced antibodies, or may be due to a difference in severity of disease. The acetylator phenotype of the patients was determined but due to the low frequency of fast acetylators no comparison of the immunological response of the two phenotypes could be done.

Aged

A family with complement factor I deficiency.

A family with inherited factor I deficiency is described. The proband was a 19-year-old Caucasian female with one episode of meningococcal meningitis and one episode of suspected septicaemia of unknown cause. Two obligate and two probable heterozygotes with factor I levels below the lower limit of the reference range were identified. None of these exhibited increased susceptibility to infectious diseases. The inheritance was autosomal codominant. In addition, molecular heterogeneity of factor H in plasma from the proband but not from any other family members was demonstrated by crossed immunoelectrophoresis. The migration of factor H component of fast electrophoretic mobility was retarded by antibodies to C3c and C3d, suggesting the presence of a fluid-phase complex between factor H and excess C3b generated by the uncontrolled activity of the amplification loop.

Adult

Circadian and diurnal variation of circulating immune complexes, complement-mediated solubilization, and the complement split product C3d in rheumatoid arthritis.

Nine patients with active classical rheumatoid arthritis (ARA criteria) were studied with reference to circadian variation of immunological and clinical parameters. Complement-mediated solubilization (CMS) of immune complexes (IC) and the level of circulating IC were found to be inversely related with low CMS and increased IC levels in the morning, and vice versa in the afternoon. Bed rest and exercise did not influence these fluctuations. The C3d concentration in plasma was increased but showed no diurnal or circadian periodic fluctuations when the levels were corrected for fluctuations in plasma albumin concentration. Clinical assessment by means of pain score exhibited marked variations, with high scores in the morning, and lower in the daytime, whereas measurements of Ritchie's joint index showed no consistent pattern. The circadian variations in CMS, serum IC and clinical parameters indicate the need to collect blood specimens and perform clinical examinations of patients at a fixed time of day.

Adult

Gastrointestinal blood loss caused by controlled-release and conventional acetylsalicylic acid tablets.

Gastrointestinal blood loss has been studied following oral administration of the novel controlled-release acetylsalicylic acid tablet preparation Acetard and the instant-release acetylsalicylic acid tablet Magnecyl (Ph. Nord. 63). Acetard contains micro-encapsulated acetylsalicylic acid crystals having an in vitro release time of approximately 4 hours. The investigation was carried out as a two-part, randomized cross-over trial, and with a test dosage of either 1 g X 4 or 2 g X 2 per day, given to 10 and 14 male students, respectively, during two 5-day periods separated by a one week interval. The dosage of the plain formulation was maintained at 1 g X 4 daily in both parts of the investigation. Faeces were collected every 24 hours throughout the trial, covering a total of 4 weeks. Blood loss was measured using the 51Cr labelling technique. Acetard was found to cause statistically significantly less gastrointestinal blood loss as compared with the plain formulation, irrespective of whether Acetard was given twice or four times a day.

Adult