PubMed · 7515838
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M W Turner. 1994. Mannose binding protein.. https://doi.org/10.1042/bst0220088
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Current clinical practice relies heavily on serologic testing for the prompt and accurate diagnosis of rheumatic diseases. Serologic testing should be used to support the findings of the history and physical examination, and, in some cases, to monitor disease activity. The inflammation of the rheumatoid arthritis (RA), polymyalgia rheumatica, and temporal arteritis can be assessed by the erythrocyte sedimentation rate (ESR). The C-reactive protein (CRP, an acute-phase protein) test, which is newer, correlates more closely than ESR with clinical and radiographic parameters of RA inflammation. The rheumatoid factor test is nonspecific as a screen for RA, and some argue that it is also insensitive (accounting for the existence of "seronegative" RA). High titers of rheumatoid factor are associated with progressive joint inflammation, erosions, and disability. Antinuclear antibody (ANA) tests are likewise nonspecific, but ANA subtypes have proved to be very specific for subtypes of connective tissue diseases. Examples are the presence of anti-DNA antibody in systemic lupus erythematosus; anti-centromere antibody in the CREST syndrome of scleroderma; anti-histone antibody in drug-induced lupus; and anti-Ro antibody in neonatal lupus. Anti-neutrophil cytoplasmic antibodies (ANCA) are a new group of auto-antibodies seen in Wegener's granulomatosis. Brief case descriptions are presented to illustrate appropriate selection of these antibody tests as well as tests for antiphospholipid antibodies and cryoglobulins.
The propensity of therapeutic doses of HI-6 (50 mg/kg) in combination with atropine sulphate (17 mg/kg), antidotes used to treat organophosphate poisoning, to induce the acute phase response (APR) in the laboratory rat was examined. A single intraperitoneal injection of HI-6, either alone or with atropine, caused a rapid doubling of the plasma corticosterone concentration. However, this increase was short-lived in comparison with corticosterone kinetics during the typical, turpentine-induced APR. The elevated glucocorticosteroid concentration did not affect acute phase protein (APP) gene transcription or mRNA and protein synthesis in the livers of oxime/atropine-treated rats. On the basis of these findings, we concluded that the administered doses of HI-6 and atropine did not induce the generalised, non-specific APR.
In vitro experiments have suggested that interleukin (IL)-6 may contribute to human immunodeficiency virus (HIV) burden and to immunological abnormalities in HIV-infected patients. We had the opportunity to directly address this question in vivo through the virological and immunological monitoring of HIV-infected patients treated with an anti-IL-6 monoclonal antibody (mAb) for a lymphoma (ANRS 018 trial). Sixteen courses of anti-IL-6 mAb administration, performed in 11 patients, were studied. All patients were at a late stage of HIV infection. The HIV load and the immunological status were determined at the initiation of each course and at its end, 21 days later. The mAb induced no significant change of HIV load, as evaluated by p24 antigenemia, plasma viremia, and quantification of circulating HIV RNA by reverse transcriptase-polymerase chain reaction and branched DNA techniques. The anti-IL-6 mAb also did not affect CD4+, CD8+, and CD19+ circulating cell counts, nor the serum concentrations of sIL-2R and of sCD8. In contrast, the mAb completely abrogated acute-phase reaction, as demonstrated by the normalization of C-reactive protein and fibrinogen circulating levels (p = 0.013 and p = 0.008, respectively). It increased serum albumin concentration. The latter effect was restricted to patients with a spontaneously low albuminemia (p = 0.01). It decreased B-lymphocyte hyperactivity, as reflected by decreased IgG and IgA serum levels (p = 0.008 and p < 0.001, respectively), and by a decreased production of IgG in vitro (p = 0.017). In contrast, the IgM hyperproduction was not affected by the mAb. Therefore, increased IL-6 production in HIV-infected patients at a late stage of the infection may not stimulate HIV replication in vivo, but it may represent a key mechanism contributing to the metabolic and immunological dysbalance of the disease.