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Biomedical subjects

L S Teh

Publications and source records attributed to L S Teh.

At least 19 recordsLinked to original sources
PubMed2001

Mannose binding lectin and FcgammaRIIa (CD32) polymorphism in Spanish systemic lupus erythematosus patients.

OBJECTIVE: Mannose binding lectin (MBL) and FcgammaRII (CD32) polymorphisms have both been implicated as candidate susceptibility genes in systemic lupus erythematosus (SLE). The aim of this study was to evaluate the relationship of these polymorphisms with SLE. METHODS: We studied a cohort of 125 SLE patients from Barcelona, Spain and 138 geographically matched controls. Sequence-specific primer-polymerase chain reaction (SSP-PCR) amplification was used to determine CD32 and MBL structural polymorphisms. MBL haplotypes were established using sequence-specific oligonucleotide probing techniques. RESULTS: Patients carried the MBL codon 54 mutant allele more frequently than controls [odds ratio (OR) 2.2; 95% confidence interval (CI) 1.2-4.0; P=0.007] and the haplotype HY W52 W54 W57 was found to be significantly lower in cases compared with controls (OR 0.6; 95% CI 0.4-0.9; P=0.016). CONCLUSION: The MBL gene codon 54 mutant allele appears to be a risk factor for SLE, whilst haplotypes encoding for high levels of MBL are protective against the disease. Differences between controls and patients were not significant when considering the FcgammaRIIa polymorphisms; similar results were observed for renal affectation.

Acute-Phase Proteins↗
PubMed2000

Tumor necrosis factor receptor II (TNFRII) exon 6 polymorphism in systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a complex autoimmune disease that exhibits extensive clinical heterogeneity. Several studies have suggested a role for tumor necrosis factor alpha (TNFalpha) in SLE and recently, the locus encompassing the TNF receptor II (TNFRII), which is a mediator of TNF effect, was amongst the candidate loci suggested by genetic linkage studies of multi-case SLE families. Komata et al. reported an association between a polymorphism at position 196 (R allele) of TNFR II and SLE in Japanese patients. We have typed SLE patients from two different ethnic populations, Spanish and UK Caucasoids, for this polymorphism using a polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP)-based technique. No significant differences in allele or genotype frequencies were found between cases and matched controls in either population. The TNFRII 196R allele does not appear to be associated with SLE susceptibility in either Spanish or UK populations.

Alleles↗
PubMed1998

Complement C4B null allele status confers risk for systemic lupus erythematosus in a Spanish population.

Genetic susceptibility to systemic lupus erythematosus (SLE) may vary amongst different populations. In UK patients, genes encoded in the HLA class II (DQA*0501/DRB1*0301) and class III [C4A*Q0 and tumour necrosis factor (TNF) polymorphisms] subregions appear to contribute to disease susceptibility. We have examined HLA-DRB1, C4 and TNF microsatellites in 50 Spanish SLE patients and 48 matched controls. HLA-DRB1*0301 was increased in patients but did not achieve statistical significance (41% vs. 25.5%). C4A*Q0 was not increased in patients, but C4B*Q0 allele frequency was significantly increased compared with the controls (29% vs. 6%; OR: 6.0). TNF c2 microsatellite allele frequency was also increased in SLE patients. The C4B null allele (C4B*Q0) appears to play an important role in SLE susceptibility in the Spanish population.

Alleles↗
PubMed1997

A dysfunctional allele of the mannose binding protein gene associates with systemic lupus erythematosus in a Spanish population.

OBJECTIVE: To determine dysfunctional mannose binding protein (MBP) status of Spanish patients with systemic lupus erythematosus (SLE) and to determine whether MBP and complement C4 null alleles contribute in an additive way to SLE susceptibility. METHODS: The frequencies of MBP alleles (characterized by polymorphisms at codon 54 and codon 57 of exon 1) were determined by the amplification refractory mutation system-polymerase chain reaction in 50 Spanish patients with SLE and 49 matched controls. Mutant genotypes for the codon 54 mutation were confirmed using a Ban I restriction enzyme digest method. Complement C4 allotyping was achieved by agarose gel electrophoresis of neuraminidase/carboxypeptidase B digested plasma samples followed by immunofixation and staining. RESULTS: At least one dysfunctional MBP allele, unable to activate complement, was present in 52% of patients with SLE and in 31% of controls (OR = 2.4, 95% CI 1.1-5.6). Complement C4 null alleles (either C4A or C4B) were present in 61% of patients and 43% of controls (OR = 2.1, 95% CI 0.9-4.9). A dysfunctional MBP allele and C4 null allele were present in 41% of patients and 16% of controls (OR = 3.2, 95% CI 1.2-8.1). CONCLUSION: The presence of a dysfunctional MBP allele is a risk factor for developing SLE in this Spanish population and may affect susceptibility in an additive way with C4 null alleles.

Acute-Phase Proteins↗
PubMed1997

Ascorbic acid absorption in patients with systemic sclerosis.

OBJECTIVE: To investigate whether reduced circulating levels of ascorbic acid in patients with systemic sclerosis (SSc) are a result of malabsorption. METHODS: Eight patients with SSc, but with no evidence of bacterial overgrowth, and 8 healthy controls were recruited. On the first day of study, each subject was given orally an aliquot of [14C] ascorbic acid, which was then "flushed out" by oral intake of unlabeled ascorbic acid for the following 7 days. Plasma samples were collected at specified intervals and urine was collected continuously over the 8 day study period. [14C] content of plasma and urine were measured by scintillation counting. For each subject, a plasma [14C] decay curve was drawn. Each subject's ascorbic acid absorption was assessed using the area under the curve (AUC) and the apparent renal clearance (CLr[app]). Ascorbic acid intake was assessed using dietary history and food composition tables. RESULTS: There were no differences in the dietary intake of vitamin C (p = 0.16) and body mass indices (p = 0.91) between patients and controls. The plasma [14C] AUC and CLr(app) were similar between patients and controls [AUC patient mean (standard deviation, SD) = 37.1 (6.8), AUC control mean (SD) = 38.6 (9.9), p = 0.74; CLr(app) patient mean (SD) = 0.57 (0.24), CLr(app) control mean (SD) = 0.47 (0.27), p = 0.45]. CONCLUSION: There was no evidence of impaired absorption of ascorbic acid in patients with SSc without bacterial overgrowth compared to healthy controls.

Absorption↗
PubMed1996

Antibody deficiency associated with gold treatment: natural history and management in 22 patients.

OBJECTIVE: To perform a clinical and immunological study of patients with rheumatoid arthritis who develop subnormal serum immunoglobulins on gold treatment; to clarify the nature of the defect in antibody production and determine the natural history of this adverse reaction; to use this information to suggest guidelines for the detection, investigation, and management of this complication. METHODS: 22 patients who developed subnormal levels of one or more immunoglobulin isotypes while receiving gold treatment were recruited over a 10 year period from the practice of a single rheumatologist. Antibody production was assessed by measurement of total immunoglobulins and of specific antibody production against polysaccharide and protein antigens, with test immunisation if necessary. RESULTS: Two broad patterns of antibody deficiency were identified: (1) (n = 11) mild, affecting only one immunoglobulin isotype and with normal specific antibody production. These patients were in general able to continue gold without further deterioration in antibody production. (2) (n = 11) severe, affecting two or three immunoglobulin isotypes, with defective specific antibody production. Six patients developed significant infections and were treated with immunoglobulin. Gold was discontinued in all. Normal antibody production recovered in nine patients, and in all but one followed for more than one year. No relation was seen between duration/dose of gold and antibody deficiency. CONCLUSIONS: Gold-induced antibody deficiency may be more common than usually recognised. A spectrum of deficiency exists, with some patients developing infective complications. Antibody production should be monitored in patients on gold treatment.

Adult↗
PubMed1995

Sustained-release transdermal glyceryl trinitrate patches as a treatment for primary and secondary Raynaud's phenomenon.

A randomized, double-blind, placebo controlled, cross-over study was conducted to determine the clinical efficacy of and patient tolerance to sustained-release glyceryl trinitrate (GTN) patches in the treatment of Raynaud's phenomenon. The patients studied were those with primary Raynaud's disease (n = 21) and patients with Raynaud's phenomenon secondary to systemic sclerosis (n = 21). GTN patches (0.2 mg/h) were found to be effective in reducing the number (P < 0.05) and severity of Raynaud's attacks (P < 0.05) in both groups of patients. Objective assessments by infrared thermography did not show any significant improvement when the patients were on GTN patches (P > 0.05). Headaches, refractory to treatment, led to the withdrawal of eight patients from the study and occurred in approximately 80% of the remaining patients. Thus, in spite of the subjective efficacy, the frequent headaches will limit the use of GTN patches in Raynaud's phenomenon. Elucidating the mechanism of action of the beneficial and adverse effects of GTN at the molecular level may shed light on the pathogenesis of Raynaud's phenomenon and its treatment.

Administration, Cutaneous↗
PubMed1994

HLA-DRB genes and antiribosomal P antibodies in systemic lupus erythematosus.

Antibodies to the ribosomal P protein are specific for SLE but their prevalence varies in different ethnic groups. In a group of Chinese SLE patients from Malaysia who have a high prevalence of this antibody, we have found an increased frequency of an uncharacterized HLA-DRB gene allele, DR16X, in patients who are positive for anti-P antibodies compared to antibody negative patients (31.3% vs 3.2%, P < 0.01, Pcorr not significant, relative risk = 13.6). DR16X has only been found in south east Asian populations and may be a genetic factor which influences the high prevalence of anti-P antibodies in Chinese.

Alleles↗
PubMed1993

Anti-P antibodies are associated with psychiatric and focal cerebral disorders in patients with systemic lupus erythematosus.

In a cross-sectional study, 62 patients with systemic lupus erythematosus were assessed using standardized psychiatric and psychological methods; systemic disease activity was scored using the British Isles Lupus Assessment Group and the Lupus Activity Criteria Count indices. IgG and IgM anti-P antibodies were measured by ELISA using a synthetic 22 amino acid peptide as the relevant antigen. IgG and IgM anti-P antibodies were significantly associated with neuropsychiatric disorders (psychiatric and neurological) but failed to distinguish patients with psychiatric disorders from those with neurological disorders. These antibodies were not associated with cognitive impairment or systemic disease activity.

Antibodies↗
PubMed1993

Antiribosomal P protein antibodies in different populations of patients with systemic lupus erythematosus.

We report a significantly increased prevalence of antiribosomal P protein antibodies in Malaysian Chinese patients (38%) with SLE compared to white Caucasian (13%) and Afro-Caribbean (20%) patients. The increased prevalence was not due to a generalized increase in autoantibody production because anti-dsDNA and anti-SSA antibodies were present in comparable frequencies in the three ethnic groups while anti-Sm and anti-SSB antibodies were rarely found in the Malaysian Chinese patients.

Antibodies, Anti-Idiotypic↗
PubMed1992

Antibodies to protein P in systemic lupus erythematosus.

A synthetic peptide was used to develop an enzyme linked immunosorbent assay (ELISA) to detect antibodies to the ribosomal proteins P0, P1, and P2. Significantly increased levels of IgG antibodies to protein P were found in 16% (18/116) of patients with systemic lupus erythematosus but slightly increased levels were detected in 2% (2/98) of patients with rheumatoid arthritis and one normal control subject. No association was observed between the presence of IgG antibodies to protein P and either lupus psychosis or depression. Sequential studies in individual patients failed to show an association between antibody levels and the development of psychosis.

Antibodies↗