The prevalence of celiac disease autoantibodies in patients with systemic lupus erythematosus

OBIECTIVE: Systemic lupus erythematosus has been associated with false positive autoantibodies for primary biliary cirrhosis, chronic active hepatitis, Sjogren's syndrome, rheumatoid arthritis, thyroid disorders, syphilis, and scleroderma. An increased prevalence of autoantibodies are found in celiac disease and systemic lupus erythematosus, which share the human lymphocyte HLA-B8 and HLA-DR3 histocompatibility antigens. This study examines the prevalence of celiac disease autoantibodies in systemic lupus erythematosus patients. METHODS: Patients observed in the Department of Rheumatology at our institutions in San Antonio, Texas with known systemic lupus erythematosus were offered participation in the study. One hundred three of the 130 patients contacted agreed to participate. Patients were excluded if they were pregnant or medically unable to undergo endoscopy. All volunteers were tested for the serological presence of IgA and IgM antigliadin and IgA antiendomysial antibodies. Those with positive serology underwent esophagogastroduodenoscopy with duodenal mucosal biopsy. RESULTS: Twenty-four of 103 (23.3%) systemic lupus erythematosus patients tested positive for either antigliadin antibody, whereas none of the 103 patients tested positive for antiendomysial antibody. None of the 24 antigliadin positive patients were found to have endoscopic or histological evidence of celiac disease, making the false positive rate of antigliadin antibody 23%. CONCLUSION: The presence of false positive antigliadin antibodies in patients with systemic lupus erythematosus is common. Despite shared human lymphocyte antigen loci there does not seem to be an association between celiac disease and systemic lupus erythematosus.     

Barriers to treatment adherence among African American and white women with systemic lupus erythematosus

OBJECTIVE: To determine whether African Americans with systemic lupus erythematosus (SLE) have poorer treatment adherence than whites, and to determine ethnic group differences in barriers to adherence, and how barriers affect adherence. METHODS: We compared 68 African American and 54 white women with SLE on 19 potential barriers, on 2 adherence behaviors during the past year, and on how the potential barriers relate to each nonadherence behavior. RESULTS: African Americans and whites were similar on most barriers, although African Americans were more likely to rely on religion and were more concerned about long-term medication effects. The 2 ethnic groups were comparable on medication nonadherence, but whites tended to have poorer clinic appointment adherence than African Americans. Finally, we found that barriers related to negative affect (depression, medication concerns, physical symptoms) as well as short-term memory problems and the need for child or elder care were associated with nonadherence among African Americans, whereas perceived treatment inefficacy and lacking trust in physicians were associated with nonadherence among whites. CONCLUSION: Relationships between adherence barriers and nonadherence may be ethnicity specific, suggesting that interventions to address barriers should be targeted to specific groups.     

Human leukocyte antigen and autoantibodies association with juvenile systemic lupus erythematosus

In this study we investigated the association between autoantibodies production and MHC class II alleles in fifty three Egyptian children patients with systemic lupus erythematosus (SLE). A significant association was found between expression of HLA-DR4 and HLA-DR13 genes and the generation of anti-ribonucleoprotein and IgG cardiolipin antibodies respectively, in contrast to the negative association of antinuclear antibodies (ANA) with HLA-DR8 and HLA-DR14. Analysis of HLA-DR alleles and autoantibodies frequencies in relation to different clinical manifestations revealed significant association between HLA-DR13 and vasculitis, while, HLA-DR1 and HLA-DR3 were significantly associated with seizures. In contrast, HLA-DR8, HLA-DR4 and HLA-DR52 alleles were associated with significant protection from arthritis, abnormal kidney function and neuropsychiatric disorders, respectively. SLE autoantibodies, namely anti-DNA antibodies were significantly associated with disturbed kidney function tests and the occurrence of seizures. In contrast, nucleosome antibodies showed no association with renal involvement in childhood onset systemic lupus erythematosus.     

Increased plasma fibronectin in patients with systemic lupus erythematosus

Summary To add to our knowledge of collagen diseases, plasma fibronectin (FN) in patients with systemic lupus erythematosus (SLE) has been measured, and it was determined that the plasma FN value in those with SLE was 454±36 g/ml, is significantly higher than the FN value in normal subjects (234±21 g/ml. Further, the plasma FN value of patients with active SLE was significantly higher (591±46 g/ml than that of patients with non-active SLE (287±31 g/ml. The plasma FN value of SLE patients was also seen to be associated with the peripheral blood platelet count and with the dose level of the corticosteroid hormone administered to patients. In active SLE patients, it was similarly found that the plasma FN value had a significant correlation with the peripheral blood lymphocyte count and with the dose level of the corticosteroid hormone given to patients. Since the plasma FN value is known to be high in untreated SLE patients, it was felt that the increase of the FN value in SLE patients is not due to the effect of the corticosteroid but to the disease itself.     

Increased serum RANTES in patients with systemic lupus erythematosus

The aim of this study was to investigate the serum RANTES (regulated on activation, normal T-cell expressed and secreted) level in patients with systemic lupus erythematosus (SLE), and the associations with disease activity and clinical laboratory indexes. Twenty-seven SLE patients and 27 normal controls were enrolled in this study. Serum RANTES was measured by enzyme-linked immunosorbent assay (ELISA). The clinical and laboratory parameters of the patients were also recorded. Results showed that serum RANTES level was significantly elevated in SLE patients when compared with normal controls. Serum RANTES level was correlated with C3, ANA, anti-dsDNA antibodies, anti-Sm antibodies, and anti-SSB antibodies. Nevertheless, no association of serum RANTES level with SLEDAI was found. Taken together, serum RANTES level was significantly higher in SLE patients, suggesting that RANTES might be involved in the pathogenesis of SLE.     

Anti-ige autoantibodies in systemic lupus erythematosus

IgG and IgM autoantibodies directed against IgE were determined in 95 serum samples from 67 patients with systemic lupus erythematosus, by an enzyme-linked immunosorbent assay. IgM anti-IgE autoantibodies were found in 18 patients (27%) and IgG anti-IgE autoantibodies were detected in 23 patients (34%). The specificity of the immunoassay was confirmed by the ability to inhibit binding with IgE myeloma, but not other immunoglobulin isotypes and the demonstration that the reactivity was directed to the Fc ε fragment of IgE. The IgG fraction of certain sera with anti-IgE activity was capable of inducing histamine release from control basophils and cutaneous mast cells. Clinical associations with the presence of anti-IgE activity were sought by retrospective chart analysis of 61 patients. Significant correlation was found with articular involvement, lymphadenopathy, and anti-DNA antibodies (P < 0.05). Anti-IgE autoantibodies are observed in a significant number of patients with systemic lupus erythematosus and may contribute to the pathogenesis of the vascular and articular lesions characteristic of this disease.     

Antinuclear autoantibodies in systemic lupus erythematosus

PURPOSE OF REVIEW: The production of autoantibodies against nuclear antigens is the hallmark of systemic lupus erythematosus. Among the large number of autoantibodies known, only a limited number appear to be clinically important. The various autoantibodies have different clinical significance in lupus patients. In this review, we will discuss the various antinuclear autoantibodies detected in lupus patients, their potential pathogenic role, and their usefulness in clinical practice. RECENT FINDINGS: Recent advances include the clear demonstration of autoantibody transport into living cells, a process that clearly includes interactions with a number of cellular components that may play a role in cellular dysfunction and disease. Also, the anti-Sm B/B' response originates from a single antigenic epitope that appears to be the same structure in different patients, before spreading to other epitopes and becoming the typically mature, complex humoral autoimmune anti-Sm autoantibody response. SUMMARY: The existing data strongly support a central role of autoantibodies in the pathogenesis of lupus. Better characterization of autoantibodies, their mechanisms of production, and their interactions with various cellular constituents will clarify the pathogenesis of this disease.     

Anti-prolactin autoantibodies in paediatric systemic lupus erythematosus patients.

The aim of this study was to determine the frequency of anti-prolactin autoantibodies and the relationship among anti-prolactin autoantibodies, serum prolactin (PRL) levels and lupus activity in paediatric patients with systemic lupus erythematosus (SLE) using a transversal study. One-hundred and three consecutive paediatric SLE patients were tested for serum anti-PRL autoantibodies and PRL levels. Clinical disease activity was scored using the SLEDAI index. Anti-PRL autoantibodies were measured by means of gel filtration. The frequency of anti-PRL autoantibodies was 6.7% (7/103), on the basis of the amount of immunoreactive PRL eluted in molecular weight fraction corresponding to IgG (150 kDa). No anti-PRL autoantibodies were found in normoprolactinaemic patients. By contrast, 21.8% (7/32) hyperprolactinaemic patients (hPRL) had anti-PRL autoantibodies. There was a correlation between anti-PRL autoantibody and serum levels of PRL (r(s) = 0.98, P = 0.0001). Lupus activity was present in 64/103 (62.1%) patients, without a significant difference in the frequency of anti-PRL autoantibodies when compared to inactive lupus (7.8 vs 5.1%, P > 0.05). Higher levels of serum PRL were associated with lupus activity regardless of other variables (39.6% vs 17.9%, P = 0.05). Patients with anti-PRL autoantibodies had higher levels of serum PRL than those without anti-PRL autoantibody (41.85 vs 17.77 ng/ml, P = 0.01) and significantly different frequency of hPRL (100 vs 26%, r = 0.4531, P < 0.001). We have identified a subset of paediatric SLE patients with hPRL and anti-PRL autoantibodies. Anti-PRL autoantibodies were associated with hPRL state and antibody titres correlated positively with serum PRL levels. These data suggest that anti-PRL autoantibodies could be responsible for hPRL in a subset of SLE patients. An increase in serum PRL levels proved to be related to lupus activity, but there was no statistical relationship between anti-PRL autoantibodies and lupus activity.     

Human leukocyte antigen haplotype and autoantibodies of a family with systemic lupus erythematosus

A search for HLA haplotypes of a family of five indicated that four members had the same haplotype. Systemic lupus erythematosus (SLE) had already developed in three of these four people. SLE has now developed in the remaining person, and the result is that all the members of the family having the same haplotype will develop SLE. Regarding these four SLE patients, the types of autoantibodies and the symptoms were different in each person, so the idea that this haplotype is strongly related to the onset of SLE but minimally related to the symptoms was suggested.     

Human leukocyte antigen haplotype and autoantibodies of a family with systemic lupus erythematosus

Abstract

A search for HLA haplotypes of a family of five indicated that four members had the same haplotype. Systemic lupus erythematosus (SLE) had already developed in three of these four people. SLE has now developed in the remaining person, and the result is that all the members of the family having the same haplotype will develop SLE. Regarding these four SLE patients, the types of autoantibodies and the symptoms were different in each person, so the idea that this haplotype is strongly related to the onset of SLE but minimally related to the symptoms was suggested.     

TREX1 polymorphisms associated with autoantibodies in patients with systemic lupus erythematosus

Three-prime repair exonucleases 1 and 2 (TREX1 and TREX2) play a role in the metabolism and clearance of DNA. The objective of this study was to confirm whether polymorphisms of TREX1 and TREX2 are associated with genetic susceptibility to systemic lupus erythematosus (SLE), and examine associations with autoantibodies (auto-Abs) in SLE. We investigated the genetic variants in 24 Korean individuals by direct sequencing. The genotype distributions of single-nucleotide polymorphisms (SNPs) and haplotypes were analyzed with multiple logistic regression models while controlling for covariates. We identified 12 and 5 SNPs of TREX1 and TREX2, of which −20260G>C, −389T>C, −381C>T, and +531C>T SNPs of TREX1; −23386G>C, −14703G>A, −7279C>T, and +1747C>T SNPs of TREX2; and each of three haplotypes were selected for larger scale genotyping (n = 1,053). No statistically significant association with the risk of SLE was observed in TREX1 and TREX2. TREX1 polymorphism −20260G>C showed protective effect on the production of anti-Ro Ab, and +531C>T in exon 16 and ht2 [G–T–C–T] showed also protective effect on the production of anti-dsDNA Ab, although the effect of +531C>T disappeared after multiple correction. An erratum to this article can be found at     

The prevalence of dyslipoproteinemia in Thai patients with systemic lupus erythematosus

Fasting blood samples taken from 93 pairs of outpatient systemic lupus erythematosus (SLE) women and matched controls were assessed for total cholesterol (TC), triglyceride (TG), high-density lipoprotein (HDL)- and low-density lipoprotein (LDL)-cholesterol. The demographic data, clinical manifestations, Mexican-SLE Disease Activity Index (MEX-SLEDAI), Systemic Lupus International Collaborating Clinics/American College of Rheumatology (SLICC/ACR) damage index and medication prescribed in the SLE patients were reviewed. A significant elevation of TG levels was observed in the SLE patients compared to controls (mean+/-SD 113.3+/-59.5 versus 77.7+/-45.7 mg/dL, P < 0.001). The HDL-c level was also significantly lower in SLE patients than controls (mean+/-SD 49.7+/-12.7 versus 65.0+/-14.8 mg/dL, P < 0.001). The percentage of samples with low HDL-c (<35 mg/dL) was higher in the SLE group (9.7%) than controls (0%; P = 0.002). The LDL-c and TC levels were comparable in both groups. The use of antimalarial drugs was negatively associated with TC (OR 0.22, 95%CI 0.08-0.61) and LDL-c levels (OR 0.27, 95%CI 0.09-0.80). The increased prevalence of dyslipoproteinemia in SLE patients in this report has confirmed the results of previous studies and emphasized the importance of controlling this modifiable cardiovascular risk factor by the combination of lifestyle modification and medical treatments.     

High frequency of Smith autoantibodies in Omani patients with systemic lupus erythematosus

This study was conducted to investigate the frequency and significance of some antinuclear autoantibodies in Omani patients with systemic lupus erythematosus (SLE). Anti-nuclear antibodies (ANA), anti-double stranded-DNA (anti-dsDNA), and anti-Smith (anti-Sm) autoantibodies were investigated in 60 Omani patients clinically diagnosed with SLE according to the American College of Rheumatology Criteria. The SLE group included 57 females and 3 males with an average age of 26 years. In addition, a group of 60 healthy Omanis (26 females and 34 males; average age 25 years) was used as a control. ANA patterns and autoantibody profile were assayed by indirect immunofluorescence assay using Hep-2 cells and liver/kidney/stomach tissue, respectively. Anti-dsDNA were examined by enzyme-linked immunosorbent assays; anti-Sm antibodies were measured by immunoblotting technique. Out of the 60 SLE patients, 59/60 (98.3%) were seropositive for ANA. Anti-dsDNA and anti-Sm each was detected in 50/60 (83.3%) of the Omani patients. The homogenous pattern of ANA was detected in 30/60 (50%) of patients, whereas the frequency of fine-speckled and coarse-speckled was 16/60 (26.7%) and 6/60 (10%), respectively. High titers (≥1:320) of ANA was detected in 56/60 (93.3%) of SLE patients. High titers of anti-Sm were detected in 22/60 (33.3%) of patients. High titers (>100 IU/ml) of anti-dsDNA were detected in 40/60 (66.7%) of patients. In the control group, ANA were detected in 8/60 (13.3%) but at low titers, whereas anti-dsDNA and anti-Sm were not detected in the healthy control group. This study shows that anti-Sm is as important as the anti-dsDNA for confirming the diagnosis of SLE and that anti-Sm occurs at a much higher frequency (83.3%) than that reported in other populations indicating the importance of this specific autoantibody for the diagnosis and possibly prognosis of Omani SLE patients.     

Antineutrophil cytoplasmic autoantibodies in systemic lupus erythematosus

Although antineutrophil cytoplasmic antibodies (ANCA) were first associated with the primary vasculitides, it is now clear that 15-20% of patients with lupus have detectable ANCA. In this short review we confirm that the major link is with perinuclear ANCA (pANCA) but not cytoplasmic ANCA (cANCA). ANCA to myeloperoxidase are associated with drug-induced lupus. There may be a link between pANCA levels and disease activity in some patients although the links to specific organ involvement are not proven. ANCA in lupus must be interpreted cautiously with particular attention paid to laboratory technique, the size, age and genetic background of the populations studied.     

Increased risk of cancer in patients with systemic lupus erythematosus.

To evaluate the risk of cancer in patients with systemic lupus erythematosus (SLE) a series of 205 consecutive patients (182 women and 23 men) were followed up for cancer through the files of the Finnish Cancer Registry. The follow up consisted of a total of 2340 person years. Fifteen cancers were diagnosed against 5.7 expected (relative risk (RR) 2.6, 95% confidence interval (CI) 1.5 to 4.4). Among the women there were four non-Hodgkin's lymphomas against 0.09 expected (RR 44, CI 11.9 to 111) and two soft tissue sarcomas against 0.04 expected (RR 49, CI 6.0 to 177). When evaluated by a case control study previous treatment with cytostatic drugs showed no influence on the occurrence of cancer in this series of patients with SLE.     

Increased prevalence of renal disease in systemic lupus erythematosus families with affected male relatives

OBJECTIVE: To distinguish familial differences from sex-related differences in the clinical manifestations of systemic lupus erythematosus (SLE). METHODS: A total of 372 affected individuals from 160 multiplex SLE pedigrees were analyzed. Twenty-five of these pedigrees contained at least 1 affected male relative. Comparisons of the presence of each of the 11 1982 American College of Rheumatology criteria for SLE were made between female family members with affected male relatives and those without affected male relatives, using Fisher's exact tests. RESULTS: The presence of renal disease was significantly increased in female family members with an affected male relative when compared with those with no affected male relative (68% and 43%, respectively; P = 0.002). This trend remained after stratifying by race and was most pronounced in European Americans. A familial basis for differences in hematologic and immunologic manifestations was also suggested, while arthritis and dermatologic features appeared to be most influenced by sex. CONCLUSION: Our results demonstrate that the increased prevalence of renal disease previously reported in men with SLE is, in large part, a familial rather than sex-based difference, at least in multiplex SLE families. Distinguishing familial from sex-related differences may facilitate efforts to understand the genetic and hormonal factors that underlie this complex autoimmune disease.