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Biomedical subjects

K DeCeulaer

Publications and source records attributed to K DeCeulaer.

6 recordsLinked to original sources

CD4 TCRBV CDR3 analysis in prevalent SLE cases from two ethnic groups.

We examined CD4+ T cell TCRBV-CDR3 transcripts from 19 lupus patients and 16 controls to test the hypothesis that CD4+ TCRBV-CDR3 expression in SLE differs from normals. Within the disease group we also performed exploratory analyses to determine the association between risk of oligoclonality and HLA-DRB specificities and the duration of the CDR3 patterns. Oligoclonal patterns consistent with CDR3 restriction were three times more likely in SLE than in controls (OR = 3.7). TCRBV1, BV4, BV5.1, BV7, BV9, BV18 and BV22 gene segment CDR3 patterns of oligoclonality were seen exclusively among lupus patients. HLA-DRB3 increased the risk of oligoclonal expression in SLE. In four patients studied over time, the pattern of TCRBV-CDR3 expression was stable in a second sample obtained 6-14 months later. The increased frequency of CD4+ T cell TCRBV-CDR3 oligoclonal expression in SLE when compared to controls and the persistence of these patterns are consistent with an expanded pool of autoreactive CD4 T cells in SLE which recognize peptides derived from autoantigens. The association of HLA-DRB3 genes with increased risk of CDR3 oligoclonality among the SLE subjects is compatible with the hypothesis that molecules encoded by HLA-DRB3 may facilitate autoantigen recognition by CD4 T cells.

Adult↗

Systemic lupus erythematosus, rheumatoid arthritis and HLA phenotypes in Jamaicans.

The HLA phenotypes were investigated in 30 Jamaican patients with Systemic Lupus Erythematosus (SLE), 30 with Rheumatoid Arthritis (RA) and 40 healthy controls. HLA phenotypes were determined by the microcytoxicity technique, using commercially prepared typing trays. In this study, the HLA phenotypic associations with SLE (HLA-B14, RR 4.3: HLA-A28, RR 4.3) were not statistically significant. However, a statistically significant lack of HLA-A9 (p < 0.01; CP < 0.1) was observed in SLE patients compared to healthy controls. In RA patients, a statistically significant association was noted with HLA-A2 (RR 5.1; CP < 0.01). No HLA class II associations were noted with SLE. Class II associations with RA did not achieve statistical significance but included those previously established in other populations. The preliminary data obtained from this study indicate differences in the patterns of HLA phenotypes in Jamaican patients with SLE and RA compared to those observed in such patients elsewhere. Further studies involving larger groups of patients and typing at the serological, cellular and molecular levels are clearly warranted.

Arthritis, Rheumatoid↗

Asymptomatic cardiac involvement in systemic lupus erythematosus.

Cardiologic and laboratory parameters were studied in 21 patients with systemic lupus erythematosus (SLE) with cardiopulmonary symptoms (CPS), 20 SLE patients without CPS and 45 age- and sex-matched healthy controls. The most frequent cardiac abnormalities in patients with CPS included pericardial effusion (24%), ventricular enlargement (20%), mitral regurgitation (19%) and tricuspid regurgitation (14%). No structural abnormalities were observed in SLE patients without CPS. Mean calculated and derived echocardiographic values in both groups of SLE patients differed significantly from those observed in normal controls (p < 0.004). Patients with CPS had significantly lower mean values of ejection fraction (p < 0.05) and fractional shortening (p < 0.03). However, the frequencies of functional abnormalities in patients with CPS did not differ significantly from those observed in patients without CPS. There were no remarkable laboratory findings in SLE patients with CPS compared to those without. The finding that some SLE patients may have functional cardiac abnormalities in the absence of CPS is an important one. It raises the question as to whether asymptomatic cardiac involvement in SLE is a separate entity or whether it heralds symptomatic cardiopulmonary involvement.

Adolescent↗

Infective arthritis due to Blastocystis hominis.

A patient with rheumatoid arthritis taking prednisone developed Blastocystis hominis acute diarrhoea, which was associated with increased inflammation and effusion of the left knee. B hominis organisms were found in synovial fluid from the left knee. The patient responded dramatically to metronidazole treatment. B hominis may become disseminated in immunosuppressed patients with diarrhoea and may cause infective arthritis.

Adult↗

Plasma haemoglobin and complement activation in sickle cell disease.

The role of haemolysis in producing deficient complement function in homozygous sickle cell disease was studied by measuring indices of complement activation and of haemolysis in 30 asymptomatic patients. Plasma concentration of C3d (an index of increased C3 turnover) was elevated in 40% of patients, and modest decreases in serum concentration of C3 and functionally (haemolytically) active factor B were found. There was a positive correlation between C3d and plasma haemoglobin concentration (r = 0.56, p less than 0.005). Reticulocyte count and foetal haemoglobin concentration also contributed to variation in C3d, though to a lesser extent than plasma haemoglobin. Intravascular haemolysis in sickle cell disease may produce activation of complement and thus cause partial depletion of functional factor B and C3. This may reduce the immune function of the alternative pathway.

Adolescent↗