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1.
Rev. méd. Chile ; 137(10): 1367-1374, oct. 2009.
Article in Spanish | LILACS | ID: lil-534046

ABSTRACT

Despite the availability of newer therapeutic interventions to improve clinical outcome in patients with Systemic Lupus Erythematosus (SLE), the incidence of infections as a cause of morbidity and mortality has not changed over the past 30 years. SLE itself increases the risk of infection, due to genetic (complement deficiencies) and acquired factors such as functional asplenia (humoral immunodepression) and the use of immunosuppressive drugs. These medications increase the risk of opportunistic infections that are associated with an altered cellular immune response. The main etiologic infectious agents in SLE patients are common bacterial pathogens, especially capsulated ones. The most common sites are lung, skin, bladder, brain and systemic infections. The main risk factor for infection is the history of a previous one. The clinical approach to SLE patients with suspected infectious diseases must consider the possibility of a flare up of the underlying disease, posing an additional problem to the clinician.


Subject(s)
Humans , Lupus Erythematosus, Systemic/microbiology , Lupus Erythematosus, Systemic/prevention & control , Lupus Erythematosus, Systemic/therapy , Risk Factors
2.
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
3.
Rev. méd. Chile ; 130(2): 209-214, feb. 2002. ilus, tab
Article in Spanish | LILACS | ID: lil-313184

ABSTRACT

Eosinophilic fasciitis (EF) is a scleroderma-like disease of unknown etiology characterized by cutaneous swelling and induration that affects predominantly the extremities, elevated immune globulins, and peripheral eosinophilia. We report three patients with clinical, laboratory and pathologic characteristics of EF. The main symptoms were cutaneous and included "peau d' orange", groove signs and induration of the affected extremities. Two patients had skin changes after exercising and one had a hypothyroidism. None had extra-cutaneous manifestations. All patients had peripheral eosinophilia. Pathologic findings were thickening and inflammation of the fascia and normal epidermis. Only one patient was treated with prednisone 30 mg daily and showed only moderate improvement. There is no follow up information about the other two cases. EF is a rare disorder classified at times as scleroderma variants. However, its clinical picture, capillary microscopy findings, pathology and prognosis differentiate it from systemic sclerosis


Subject(s)
Humans , Male , Female , Adult , Middle Aged , Eosinophilia , Fasciitis
4.
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
6.
Rev. méd. Chile ; 123(2): 215-24, feb. 1995. tab, ilus
Article in Spanish | LILACS | ID: lil-151175

ABSTRACT

Cyclosporine may be useful in the treatment of rheumatoid arthritis refractory to other immunosupressive agents, in doses of less than 10 mg/kg/day to minimize its nephrotoxic potential, that is enhanced with prolonged use of concomitant administration of antiinflammatory drugs. We report 15 patients aged 50 ñ 12 years with erosive rheumatoid arthritis lasting 5 ñ 4 yeras and refractory to other immunosupressive agents. They were studied during one year and received cyclosporine in initial doses of 2.5 mg/kg/day that were increased to 5 mg/kg/day, assessing clinical response, blood pressure and serum creatinine. Nine patients, that received a maximal dose of 3.4 ñ 0.7 mg/kg/day during 7 ñ 4 months, improved; a 30 percent increase in creatinine was observed in 3, blood pressure raised in six and 2 bad hepatic toxicity. in the 6 patients that did not improve, the mean treatment lapse was 4 ñ 3 months and the maximal dose achieved was 2.7 mg/kg/day; creatinine increased in one and blood pressure increased in 4. It is concluded that although the clinical response to cyclosporine was good, only 4 patients completed one year of treatment, due to the frequent secondary effects of the drug


Subject(s)
Humans , Male , Female , Adult , Middle Aged , Arthritis, Rheumatoid/drug therapy , Cyclosporine/administration & dosage , Arthritis, Rheumatoid/complications , Follow-Up Studies , Cyclosporine/adverse effects , Creatinine/blood , Blood Pressure , Clinical Protocols
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