J Clin Gastroenterol. 2008 Mar;42(3):252-5.
Adult celiac disease followed by onset of systemic lupus erythematosus.
Freeman HJ
.
Department of Medicine (Gastroenterology), University of British Columbia, Vancouver, BC.
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BACKGROUND: Celiac disease has been associated with autoimmune disease (eg, autoimmune thyroiditis) and the appearance of different autoantibodies (eg, antidouble-stranded DNA). Conversely, tissue transglutaminase antibodies have been detected in autoimmune disorders, including systemic lupus erythematosus (SLE), but cases of celiac disease with SLE have been only rarely recorded.
METHODS: In this study, 246 patients with biopsy-defined celiac disease were evaluated for a prior diagnosis of SLE on the basis of American Rheumatological Association-defined clinical and serologic parameters. RESULTS: There were 6 patients with celiac disease and SLE, or 2.4%, including 4 females and 2 males. Their mean age at diagnosis of celiac disease was 44.7 years and SLE 50 years. In all patients, the diagnosis of SLE was established from 2 years to more than 10 years after the diagnosis of celiac disease, with a mean of 5.3 years. The celiac disease in all 6 patients responded to a gluten-free diet with histologic normalization of the small intestinal biopsies. Despite this small bowel biopsy response, SLE appeared later in the clinical course of the celiac disease.
CONCLUSIONS: This study suggests that SLE occurs far more frequently in biopsy-defined celiac disease than is currently appreciated, and detection may be more likely if the period of clinical follow-up of the celiac disease is prolonged.
PMID: 18223501 [PubMed - indexed for MEDLINE]
Scand J Gastroenterol. 2009;44(2):168-71.
Gliadin IgG antibodies and circulating immune complexes.
Eisenmann A
,
Murr C
,
Fuchs D
,
Ledochowski M
.
Department of Clinical Nutrition, Medical University of Innsbruck, Austria.
OBJECTIVE: Circulating immune complexes (CICs) in blood are associated with autoimmune-diseases such as
systemic lupus erythematosus, immune complex
glomerulonephritis,
rheumatoid arthritis and
vasculitis. However, slightly increased serum concentrations of such CICs are sometimes also found in healthy individuals. The objective of the current study was to assess whether food antigens could play a role in the formation of CICs. MATERIAL AND METHODS: A total of 352 (265 F, 87 M), so far, healthy individuals were tested for CICs containing C1q and immunoglobulin G (IgG) as well as for gliadin IgG antibodies using the ELISA technique. Additionally, fructose and lactose malabsorption was assessed using hydrogen breath tests.
RESULTS: In our study, 15.3% (54/352) of the patients presented with elevated CIC concentrations (above 50 microg/ml) and 6.5% (23/352) of the study population were positive for gliadin IgG antibodies (above 20 U/ml). CIC concentration levels were significantly higher in the group with elevated gliadin IgG antibodies (CIC median: 49.0 microg/ml) compared with the group with normal levels of gliadin IgG antibodies (CIC median: 30.0 microg/ml; Mann-Whitney U-test, U=1992; p <0.001). As expected, there was no difference in CIC concentrations (Mann-Whitney U-test, U=6106; p=0.783) and gliadin IgG (Mann-Whitney U-test, U=3761; p=0.411) between patients in the fructose or lactose malabsorber groups and the subjects without malabsorption.
CONCLUSIONS: The results of this study indicate that certain food antigens (e.g.
gluten) could play a role in the formation of CICs. An association between CICs and fructose or lactose malabsorption seems to be improbable.
PMID: 18819035 [PubMed - indexed for MEDLINE]