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1.
Rev. méd. Chile ; 131(1): 11-18, 2003. tab
Article in Spanish | LILACS | ID: lil-342217

ABSTRACT

Background: Polymorphisms of Fc receptors for IgG (FcgR) have been proposed as a genetic factor that influences susceptibility for systemic lupus erythematosus (SLE). Human FcgRIIa has 2 codominantly expressed alleles, H131 and R131, which differ at amino acid position 131 in the second extracelular domain (histidine or arginine respectively) and differ substantially in their ability to bind human IgG2. The H131 allele binds IgG2 efficiently, whereas R131 binds it poorly. Because IgG2 is a poor activator of the classical complement pathway, the H131 is essential for the disposal of IgG2 immune complexes. Aim: To determine the distribution of FcgRIIA genes in a cohort of Chilean SLE patients, with or without a history of lupus nephritis. Patients and methods: We studied 52 Chilean SLE patients fulfilling the 1982 American College of Rheumatology (ACR) criteria, 20 of whom had a history of nephritis, and 44 ethnically matched disease-free controls. FcgRIIa allotypes were genotyped by PCR. Results: No significant association was observed between the low affinity FcgRII receptor (FcgRIIa-R131) and the presence of SLE or lupus nephritis. However, genotype frequencies in SLE patients but not in controls, departed from the proportions predicted by the Hardy-Weinberg equilibrium, suggesting this locus might be related to the disease. Conclusions: Our results suggest that in Chilean patients with SLE, as well as in many other populations, the R131 allotype is not a major factor predisposing to the development of SLE or lupus nephritis


Subject(s)
Humans , Lupus Erythematosus, Systemic/genetics , Polymorphism, Genetic/genetics , Immunoglobulin G , Receptors, IgE , Alleles , Genotype , Kidney Diseases
2.
Rev. méd. Chile ; 127(4): 411-20, abr. 1999. tab
Article in Spanish | LILACS | ID: lil-243911

ABSTRACT

Background: Patients with inactive systemic lupus erythematosus (SLE) and elevated high affinity double-stranded anti-DNA antibodies (anti-dsDNA), measured using Farr technique, would have a risk of relapse that fluctuates between 40 to 80 percent according to different series. Aim: To study the association between anti-dsDNA levels measured using Farr technique and disease activity and their predictive capacity for relapses. Material and methods: Anti-dsDNA antibodies were measured according to Farr method in 60 healthy subjects, 69 patients with other connective tissue diseases and in 120 patients with SLE. Farr positive were considered those individuals with anti-dsDNA levels over 10.4 IU/ml. Disease activity, assessed using MEX-SLEDAI score was related with anti-dsDNA levels in 101 patients. Forty seven patients with inactive disease were followed for 17ñ14 months. Results: Anti-dsDNA levels were 3ñ2.5 IU/ml (range 1-26) in subjects without LED, and 127ñ500 IU/ml (range 1-5280) in patients with LED. Sixty subjects had an active SLE and 43 (72 percent) were Farr positive; in 41 the disease was inactive and 13 (32 percent) were Farr positive (p <0.001), OR 5.45. Twelve of the 47 followed patients had a relapse and 10 (83 percent) were Farr positive. Of those that did not have a relapse, 13 (37 percent) were Farr positive (p< 0.02, RR 5.22). Six of 15 patients that were followed for more than on year (40 percent), were Farr positive. Conclusions: Elevated anti-dsDNA antibodies measured using Farr technique in patients with inactive generalised lupus erythematosus, predicted the risk of relapse. However less than half of patients with inactive disease and elevated Farr relapsed in a period of one year. The need to treat patients with inactive SLE and positive Farr should therefore be considered debatable


Subject(s)
Humans , Male , Female , Adolescent , Adult , Middle Aged , Antibodies, Antinuclear , Radioimmunoprecipitation Assay/methods , Lupus Erythematosus, Systemic/diagnosis , Prednisone/therapeutic use , Return of Old Symptoms , Predictive Value of Tests , Mixed Connective Tissue Disease/complications , Lupus Erythematosus, Systemic/complications , Lupus Erythematosus, Systemic/immunology , Lupus Erythematosus, Systemic/drug therapy
3.
Rev. méd. Chile ; 126(1): 33-41, ene. 1998. ilus, tab
Article in Spanish | LILACS | ID: lil-210407

ABSTRACT

Background: Neuroendocrine factors play an important role in the expression of autoimmune disease. Proclatin (PRL) can induce T-cell proliferation and macrophage activation. Elevated PRL levels have been described in patients with rheumatoid arthritis and (RA). Aim and Methods: We studiend immunological and clinical effects of PRL suppression in 9 RA patients with active disease, treated for 3 months with bromocriptiner (BRC), an inihibitor of PRL secretion. Results: BRC induced a significant depression of the peripheral blood mononuclear cells response to antigen (p=0.008) and mitogen (p=0.008) which was significantly correlated with improvements in the HAQ disability index (r=0.68; p=0.04) and grip strength (r=0.7; p=0.02). Also, the in-vitro production of IL-2, nitric oxide and poliamines -that are critical for the proliferative response of lymphoid cells- decreased significantly. The group experienced significant improvement of grip strength (p=0.028) and the HAQ disability index (p=0.025), whereas 4 individuals archieved clinical improvement according to the American College of Rheumatology preliminary definition. We conclude that BRC treatment induces a significant depression of in-vitro immune function in RA patients and these changes are related to parameters of disease activity. The effects of BRC on immune function and disease activity in RA patients warrant further investigation


Subject(s)
Humans , Female , Middle Aged , Arthritis, Rheumatoid/drug therapy , Bromocriptine/pharmacokinetics , Polyamines/blood , Arthritis, Rheumatoid/immunology , Prolactin/blood , Rheumatoid Factor/isolation & purification , Range of Motion, Articular/drug effects , Interleukin-2 , Postmenopause/drug effects
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