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PubMed2004

Novel concepts and treatments for autoimmune disease: ten focal points.

Understanding the development of autoimmunity is a crucial step toward improving the management, not only of autoimmune diseases, but also of tumors and primary immunodeficiency syndromes. The rapid expansion of knowledge on autoimmunity is fueling the development of a novel approach known as targeted immunotherapy. The present review will concentrate on ten areas where major advances have been achieved: 1) early regulation of B-cell mediated autoimmunity; 2) thymic regulation of tolerance to tissue-restricted antigens via the transcription factor AIRE; 3) role for a population of regulatory T cells (CD4+ CD25+ Tregs) with unique effects; 4) major role for dendritic cells in the development of autoimmunity in conditions such as lupus; 5) role for T cells in autoimmune diseases; 6) role for T cells in rheumatoid arthritis, with new data from a murine model of spontaneous arthritis related to a ZAP-70 mutation; 7) role for the environment via innate immunity, in particular mediated by the toll-like receptors (TLR); identification of new autoantigens with the description of sense-antisense peptides (e.g., proteinase 3-complementary proteinase 3); the immunosenescence concept, which suggests that some autoimmune diseases may be related to premature aging of the immune system; 10) identification of new immunotherapy targets, including costimulation pathway molecules (CD28, CTLA4), original activation systems (BAFF/BLyS), and receptors such as TLRs. These exciting insights into the pathogenic mechanisms underlying immune dysfunction will play a key role in advancing the field of immunorheumatology.

Autoimmune Diseases↗

PubMed2004

T-cell vaccination against anti-CD4 autoimmunity in HIV-1 infected patients.

BACKGROUND: Highly active antiretroviral therapy (HAART) is frequently associated with only partial restoration of CD4 T-cell levels. Autoimmunity to CD4 T-cells may account for the persistence of the CD4 T-cell lymphopenia in such cases. OBJECTIVE: To document T-cell autoimmunity to CD4 in HIV-infected patients and to determine if T-cell vaccination against CD4 autoimmunity is feasible and safe. STUDY DESIGN: Seven out of 20 HIV-infected patients undergoing HAART who manifested T- cell reactivity to rCD4, gp120 and to recall antigens (Tetanus toxoid and Candida) were treated with T-cell vaccines composed of glutaraldehyde treated autologous, activated T-cells, and enriched in anti CD4-reactive T-cells. The response of the seven vaccinated patients was compared to seven non-vaccinated HIV-1 infected subjects. RESULTS: Five out of seven responded with a decrease in anti-CD4 autoimmunity, associated with a persistent increase in their CD4 T-cell levels; just one of the control patients showed increased CD4 levels. No change in HIV plasma viral loads and no adverse effects were detected in any of the T-cell vaccinated patients. CONCLUSIONS: The persistence of CD4 T-cell lymphopenia despite effective anti-retroviral treatment may be associated with anti-CD4 autoimmunity. T-cell vaccination with autologous autoimmune CD8 T-cells may decrease such autoimmunity and increase CD4 T-cell numbers.

AIDS Vaccines↗

PubMed2006

Herbal medicine Gamgungtang down-regulates autoimmunity through induction of TH2 cytokine production by lymphocytes in experimental thyroiditis model.

The crude herbal formulation, Gamgungtang (GGT), has been shown to protect animals against a wide range of spontaneously developing or induced autoimmune diseases. We have previously reported that GGT shows marked down-regulation of several experimental autoimmune diseases. Although very effective at preventing thyroid infiltrates in mice immunized with mouse deglycosylated thyroglobulin and complete Freund's adjuvant and in spontaneous models of thyroiditis, it completely failed to modify experimental autoimmune thyroiditis (EAT) induced in mice immunized with mouse thyroglobulin and lipopolysaccharide. In this study, in an effort to elucidate the mechanisms by which GGT suppresses EAT, and autoimmunity in general, we investigated the in vivo effects of this drug on the Th1/Th2 lymphocyte balance, which is important for the induction or inhibition of autoreactivity. Naive SJL/J mice were treated orally for 5 days with GGT (80 mg/(kg day)). Spleen cells were obtained at various time points during the treatment period and were stimulated in vitro with concanavalin A. Interleukins IL-4, IL-10 and IL-12, transforming growth factor-beta (TGF-beta) and interferon-gamma (IFN-gamma) cytokine production was evaluated at the protein levels of the cytokines in the medium and mRNA expressions. A significant upregulation of IL-4, IL-10 and TGF-beta was observed following treatment with GGT, which peaked at day 5 (IL-10) or day 10 (IL-4). On the other hand, IL-12 and IFN-gamma production were either unchanged or decreased. It seems therefore that GGT induces in vivo a shift towards Th2 lymphocytes which may be one of the mechanisms of down-regulation of the autoimmune reactivity in EAT. Our observations indicate that down-regulation of TH1 cytokines (especially IL-12) and enhancement of Th2 cytokine production may play an important role in the control of T-cell-mediated autoimmunity. These data may contribute to the design of new immunomodulating treatments for a group of autoimmune diseases.

Animals↗

PubMed2005

Bone marrow transplantation as a strategy for the treatment of autoimmune hearing loss in MRL/Mp-lpr/lpr mice.

Sensorineural hearing loss (SNHL) has been reported to develop as a main part of or in combination with systemic and organ-specific autoimmune diseases. The aim of the current study is to treat autoimmune SNHL in MRL/Mp-lpr/lpr (MRL/lpr) mice, a murine model of systemic autoimmune disease, using allogeneic bone marrow transplantation (BMT), which replaces recipient bone marrow cells with bone marrow cells from a non-autoimmune-prone donor. The results indicate that BMT can be used to treat SNHL; cochlear pathology, serum autoantibodies and lupus nephritis are ameliorated. Therefore, it is conceivable that the autoimmune SNHL in the MRL/lpr mice results not from defects in the cochlea, including the stria vascularis, but from defects in the bone marrow, and BMT would therefore provide a curative effect on inner ear autoimmune dysfunction associated with systemic autoimmune diseases.

Acoustic Stimulation↗

PubMed2006

Could diabetic retinopathy be an autoimmune disease?

Diabetic retinopathy is a common and progressive complication of diabetes mellitus. It is characterized by the loss of pericytes, hypertrophy of basement membrane, microaneurysms formation, increased vascular permeability, capillary occlusions, neovascularisation and fibrovascular proliferation. The pathogenesis of diabetic retinopathy is still insufficiently understood, although some reports have implicated the role of the immune system. We hypothesize that, according to some current data diabetic retinopathy could also be considered as an autoimmune disease. The finding of antipericyte and antiendothelial cell autoantibodies in the circulation of diabetic patients strongly suggests that some autoimmune activity has been involved in the early pathophysiology of diabetic retinopathy. There is even more evidence that implicates the presence of autoimmune mechanisms in the proliferative stage of this disease: elevated levels of tumor necrosis factor-alpha, interleukin-8 and soluble interleukin-2 receptor in the serum of diabetic patients, increased vitreous concentration of the interleukin-6 and interleukin-8 in patients with proliferative retinopathy. Furthermore, preretinal membranes in diabetic patients contain deposits of immunoglobulins, activated complement components, monocytes, T and B lymphocytes, fibroblastes and lymphokynes. In diabetic patients human leukocyte antigen DR and DQ expression on the retinal vascular endothelial cells as well as on pigment and nonpigment epithelial cells was found. These antigens are normally restricted to immunocompetent cells and play an important regulatory role in the immune response. Their aberrant expression has been found on nonlymphoid cells in various autoimmune diseases whilst abnormal expression of DR and DQ antigens at sites where they do not normally exist would result in autoimmunity by converting the target cell into a functional antigen-presenting cell. In conclusion, although the pathogenesis of diabetic retinopathy is not completely understood it is known that the immune system is certainly involved in its development. However, there is increasing evidence of the presence of some autoimmune processes in the early stages of diabetic retinopathy and particularly in its proliferative phases. Consequently, diabetic retinopathy could also be considered as an autoimmune disease.

Autoimmune Diseases↗

PubMed2006

Loss of autoimmune T cells correlates with brain diseases: possible implications for schizophrenia?

T-cell-mediated autoimmunity participates in physiological defense, maintenance and repair of the adult brain. However, unless such autoimmune responses to insults are rigorously controlled, they might lead to an autoimmune disease or other immune-related defects, where destructive activity outweighs the beneficial effect. Here, we discuss these apparently contradictory effects of autoimmunity in schizophrenic patients, whose typical immune aberrations have prompted recent speculation about an autoimmune-related etiology. We found that, although schizophrenic patients have active immune systems, they often lack autoimmune clones specifically reactive to a major myelin protein, myelin basic protein (MBP). This, in conjunction with our discovery in rodents that T cells that recognize brain-resident proteins are needed for normal cognitive functioning, led us to propose an immune-based neurodevelopmental hypothesis, in which autoimmune-T-cell deficiency is suggested to cause onset or progression of schizophrenia.

Adolescent↗

PubMed2005

Consequence or coincidence? The occurrence, pathogenesis and significance of autoimmune manifestations after viral vaccines.

BACKGROUND: Viruses and virus-induced lymphokines may have an important role in the pathogenesis of autoimmunity (Schattner A. Clin Immunol Immunopathol; 1994). The occurrence and significance of autoimmune manifestations after the administration of viral vaccines remain controversial. METHODS: Medline search of all relevant publications from 1966 through June 2004 with special emphasis on search of each individual autoimmune manifestation and vaccination, as well as specifically searching each viral vaccine for all potential autoimmune syndromes reported. All relevant publications were retrieved and critically analyzed. RESULTS: The most frequently reported autoimmune manifestations for the various vaccinations, were: hepatitis A virus (HAV)--none; hepatitis B virus (HBV)--rheumatoid arthritis, reactive arthritis, vasculitis, encephalitis, neuropathy, thrombocytopenia; measles, mumps and rubella vaccine (MMR)--acute arthritis or arthralgia, chronic arthritis, thrombocytopenia; influenza--Guillain-Barre syndrome (GBS), vasculitis; polio--GBS; varicella--mainly neurological syndromes. Even these 'frequent' associations relate to a relatively small number of patients. Whenever controlled studies of autoimmunity following viral vaccines were undertaken, no evidence of an association was found. CONCLUSIONS: Very few patients may develop some autoimmune diseases following viral vaccination (in particular - arthropathy, vasculitis, neurological dysfunction and thrombocytopenia). For the overwhelming majority of people, vaccines are safe and no evidence linking viral vaccines with type 1 diabetes, multiple sclerosis (MS) or inflammatory bowel disease can be found.

Adult↗

PubMed2000

Autoimmune hemolytic anemia in patients with systemic lupus erythematosus.

PURPOSE: We sought to evaluate the clinical and serologic associations with, and outcomes of, autoimmune hemolytic anemia, as compared with other types of anemia, in patients with systemic lupus erythematosus (SLE). SUBJECTS AND METHODS: We studied 41 consecutive patients with SLE with clinically manifest autoimmune hemolytic anemia, including 27 (66%) in whom hemolysis was the initial disease manifestation. We matched each patient for age and disease duration with a patient with SLE with anemia resulting from a different cause. RESULTS: The 41 patients had a total of 50 episodes of autoimmune hemolytic anemia. The recurrence rate was 4 per 100 person-years. Cases and controls had similar mean (+/- SD) lupus activity indexes (2.1 +/- 1.5 vs 2.4 +/- 1.3, P = 0.5). Patients with autoimmune hemolytic anemia at any time could be distinguished from patients with other causes of anemia, because they were more likely to have elevated titers of IgG anticardiolipin antibodies [odds ratio (OR) = 5.8; 95% confidence interval (CI), 1.4 to 24] and thrombosis (OR = 4.6; 95% CI, 1.0 to 21). Autoimmune hemolytic anemia at the onset of SLE was independently associated with renal involvement (OR = 5.4; 95% CI, 1.0 to 28), thrombocytopenia (OR = 7.3; 95% CI, 1.1 to 48), and possibly thrombotic episodes during follow-up (OR = 11; 95% CI, 0.8 to 160) when compared with controls with other types of anemia at the onset of SLE. CONCLUSIONS: Autoimmune hemolytic anemia usually occurs at the onset of SLE, and its recurrence rate is low among treated patients. The association with IgG anticardiolipin antibodies and thrombosis suggests that the occurrence of autoimmune hemolytic anemia may define a subgroup of patients with SLE who have characteristic serologic and clinical manifestations.

Adult↗

PubMed1986

Clinical characteristics and prognosis of myasthenia gravis with other autoimmune diseases.

Of 277 patients with myasthenia gravis (MG) who underwent thymectomy, including 78 with thymomatous MG, 33 patients had other autoimmune diseases. The clinical characteristics of MG with other autoimmune disease were investigated. Graves's disease and rheumatoid arthritis were the most common autoimmune diseases seen. The association rate of autoimmune disease in patients with thymomatous MG (3.8%) was significantly lower than that in patients with nonthymomatous MG (15.1%). The positive rate for a germinal center in the thymus was significantly higher in patients with other autoimmune disease than in those without such disease. Thymectomy was effective for MG in patients with an associated disease as well as in those without such a complication. The clinical course of the associated autoimmune disease did not seem to be adversely affected by thymectomy. Therefore, thymectomy should be performed in MG patients with other autoimmune disease.

Arthritis, Rheumatoid↗

PubMed2001

Treating endometriosis as an autoimmune disease.

OBJECTIVE: To review the literature on the role of autoimmunity in the etiology of endometriosis, compare the similarities in the pathophysiologies between endometriosis and autoimmune diseases, and discuss the use of immunomodulators currently used to treat autoimmune diseases as potential therapies for endometriosis. DESIGN: The literature on endometriosis and other autoimmune diseases was reviewed, and summary data are presented. RESULTS: Endometriosis shares many similarities with autoimmune diseases such as rheumatoid arthritis, Crohn's disease, and psoriasis. These similarities include elevated levels of cytokines, decreased cell apoptosis, and T- and B-cell abnormalities. Because the use of immunomodulators and inflammatory modulators has proven to be an effective means of medical management for these autoimmune diseases, similar therapies may prove useful in treating endometriosis. CONCLUSION(S): Although substantial evidence indicates that endometriosis at least shares many similarities with autoimmune diseases, endometriosis is primarily treated by using compounds that induce a hypoestrogenic environment. A review of the literature combined with the shortcomings of current means of medical management for endometriosis support the postulate that treatment of endometriosis with immunomodulators and inflammatory modulators is warranted.

Adjuvants, Immunologic↗

PubMed1988

Lymphocytes infiltration induces dysfunction in autoimmune myocarditis: role of SRS-A.

In this paper it was examined whether it could reproduce "in vitro", some of the myocardial dysfunction see "in vivo" in autoimmune myocarditis. The isolated atria from mice hyperimmunized with heart exhibited a lymphomononuclear cell infiltration and alteration in contractility: dysrhythmia and decrease in tension. These alterations highly resembled that triggered by spleen lymphocytes from autoimmune myocarditis mice, when they reacted with normal atria. This effect appears to be specific since cells sensitized to an irrelevant antigen were inactive, and was not secondary to allogenic interaction. The free-cell supernatant of autoimmune cells was inactive, point out the requirement of lymphocyte-heart contact. The most likely effectors of lymphocytes-induced alteration of atria contractility were T-lymphocytes. Beta-lymphocyte subset had no effect. Inhibitors of lipoxygenase(s) pathway of arachidonic acid metabolism, inhibited induced alterations of contractility and the SRS-A receptor blocker, FPL-55712 improved cardiac function. In addition LTC4 release was increased either in autoimmune myocarditis hearts and in normal hearts challenged with autoimmune cells; the hearts proving to be responsible of leukotriene synthesis. Normal or immune cells alone failed to release LTC4. Lipoxygenase(s) inhibitors diminished LTC4 release while indomethacin could not reverse the effect. It is concluded that mononuclear cells infiltrates occurring in hearts with autoimmune myocarditis mice are related to cardiac impairment, being critical in the myocardial dysfunction etiology. The way suggested for these phenomena to take place is, at least in part, the harmful effect of SRS-A released by hearts when specific antigens of myocardial tissue are recognized by autoimmune cells.

Animals↗

PubMed1998

Cell biology of autoimmune diseases.

Autoimmune diseases such as insulin-dependent diabetes mellitus, rheumatoid arthritis, and multiple sclerosis are common in the western world and are often devastating diseases which pose serious health problems. The key feature of such diseases is the development and persistence of inflammatory processes in the apparent absence of pathogens, leading to chronic breakdown of selected tissues. To date, no comprehensive explanation can be given for the onset or persistence of autoimmunity. As a rule, the chronic activation of helper T lymphocytes reactive against self proteins appears to be crucial for fueling the destructive autoimmune process, but why this occurs remains to be established. In this review, we present an overview on the rules that govern activation of T lymphocytes and on the factors that control it. The contribution of both genetic and environmental factors are discussed, clarifying that most autoimmune disease are of multifactorial origin. Special emphasis is given to the contribution of infectious events and the role of stress proteins in the process. In attempts to dissect the mechanisms involved in autoimmunity and to develop ways of blocking disease, experimental animal models are widely employed. We describe the various experimental models that exist for the study of multiple sclerosis, diabetes, and other autoimmune diseases and on the experience that has been gained in such models with experimental therapies to block the activation of self-reactive T lymphocytes. The lessons that can be drawn from these studies provide hope that continued efforts will lead to the successful development of antigen-specific strategies which block the development of autoimmunity also in humans.

Animals↗

PubMed1997

Neurobehavioral alterations in autoimmune mice.

Inbred MRL, NZB and BXSB strains of mice spontaneously develop a systemic, lupus-like autoimmune disease. The progress of autoimmunity is accompanied with a cascade of behavioral changes, most consistently observed in tasks reflective of emotional reactivity and the two-way avoidance learning task. Given the possibility that behavioral alterations may reflect a detrimental consequence of autoimmune-inflammatory processes and/or an adaptive response to chronic malaise, they are tentatively labeled as autoimmunity-associated behavioral syndrome (AABS). It is hypothesized that neuroactive immune factors (pro-inflammatory cytokines, brain-reactive antibodies) together with endocrine mediators (corticotropin-releasing factor, glucocorticoids) participate in the etiology of AABS. Since AABS develops natively, and has a considerable face and predictive validity, and since the principal pathway to autoimmunity is known, AABS may be a useful model for the study of CNS involvement in human autoimmune diseases and by extension, for testing autoimmune hypotheses of several mental disorders (major depression, schizophrenia, Alzheimer's disease, autism and AIDS-related dementia).

Animals↗

PubMed2000

Clinical significance of anti-neutrophil cytoplasmic antibodies (ANCA) in autoimmune liver diseases.

BACKGROUND/AIMS: The clinical relevance of anti-neutrophil cytoplasmic antibodies (ANCA) in autoimmune liver disease is unclear. Defining the antigenic specificities of ANCA in these diseases may improve their clinical significance. METHODS: We studied the target antigens of ANCA in 88 patients with autoimmune hepatitis, 53 patients with primary biliary cirrhosis, and 55 patients with primary sclerosing cholangitis by indirect immunofluorescence, antigen-specific enzyme-linked immunosorbent assays, and immunodetection on Western blot, using an extract of whole neutrophils as a substrate. We related the data to clinical symptoms of autoimmune liver disease. RESULTS: By indirect immunofluorescence, ANCA were present in 74% of patients with autoimmune hepatitis, 26% of patients with primary biliary cirrhosis, and 60% of patients with primary sclerosing cholangitis. Major antigens were catalase, alpha-enolase, and lactoferrin. The presence of ANCA as detected by indirect immunofluorescence was associated with the occurrence of relapses in autoimmune hepatitis, with decreased liver synthesis function in primary biliary cirrhosis and in primary sclerosing cholangitis, and with increased cholestasis in primary sclerosing cholangitis. ANCA of defined specificities had only limited clinical relevance. CONCLUSIONS: ANCA as detected by indirect immunofluorescence seem associated with a more severe course of autoimmune liver disease. The target antigens for ANCA in these diseases include catalase, alpha-enolase, and lactoferrin. Assessment of the antigenic specificities of ANCA in autoimmune liver disease does not significantly contribute to their clinical significance.

Adolescent↗

PubMed1998

Is severe cryptogenic chronic hepatitis similar to autoimmune hepatitis?

BACKGROUND/AIMS: It has been reported that severe cryptogenic chronic hepatitis may be a subgroup of autoimmune hepatitis. The aims of this study were to investigate the clinical features, liver function tests, human leukocyte antigens and response to immunosuppressive therapy in severe cryptogenic chronic hepatitis, and to compare the findings in such patients with those in patients with autoimmune hepatitis. METHODS: History of alcohol and hepatotoxic drug intake, markers of metabolic liver disease, autoantibodies (antinuclear antibody, smooth muscle antibody, antibody to liver/kidney microsome type 1), and viral markers (HBsAg, HBV DNA, anti-HCV, HCV RNA) were negative in all severe cryptogenic chronic hepatitis patients (histological activity index > 9 and alanine aminotransferase level > 2 x normal). Fifteen cryptogenic patients (13 women; mean age, 33 +/- 16 years) and seven autoimmune patients (seven women; mean age, 28 +/- 3.9 years; five type 1; two type 2a) received prednisolone and azathioprine for at least 2 years. RESULTS: Cryptogenic chronic hepatitis patients were similar to patients with autoimmune hepatitis with respect to age, sex, clinical presentation, liver function tests and Knodell scores at admission. HLA phenotype frequencies were comparable between cryptogenic and autoimmune groups: BW6 (77% vs. 100%), DR4 (62% vs. 57%), and HLA B8 (15% vs. 43%). The rates of complete and partial remissions achieved during therapy were 87% vs. 57% and 13% vs. 29%, respectively (p > 0.05). CONCLUSIONS: The clinical, biochemical and HLA phenotypic features, and the responsiveness to immunosuppressive therapy in severe cryptogenic chronic hepatitis support the idea that it may be an autoimmune liver disease similar to autoimmune hepatitis.

Adult↗

PubMed2000

Assessment of autoimmunity-inducing potential using the brown Norway rat challenge model.

The development of autoimmune disease in humans is thought to occur as a result of the interactions of a genetic predisposition of the host and environmental factors. There is evidence that treatment with certain drugs and exposure to environmental toxicants increase the risk associated with the development and severity of autoimmune disease. When exposed to certain chemicals, Brown Norway (BN) rats develop autoimmune disease similar to human systemic lupus erythematosus (SLE) characterized by elevation of antibody levels to self and non-self antigens which can result in the formation of immune complexes and lead to a fatal glomerulonephritis. A unique characteristic of the BN rat model is that the increase in IgE is self-limiting with levels eventually returning to normal. The objective of these studies was to determine if the BN rat and the self-limiting nature of the IgE response could be used in identifying compounds capable of initiating autoimmune responses. Two compounds known to produce autoimmunity, mercuric chloride and D-penicillamine, were studied as were, trichloroethylene and silicone gel, two agents suspected of inducing autoimmune disease. The results indicated that the BN rat model may prove useful for detecting compounds with the potential to produce autoimmunity, particularly if a HgCl(2) challenge is incorporated into the evaluation.

Animals↗

PubMed2001

Aldosterone and prednisolone control of cochlear function in MRL/MpJ-Fas(lpr) autoimmune mice.

Recently this laboratory showed aldosterone, a mineralocorticoid that only enhances sodium transport, was as effective as the glucocorticoid prednisolone in restoring cochlear function in autoimmune mice. To further test this relationship between sodium transport and autoimmune hearing loss, dosage comparisons were made of prednisolone and aldosterone control of the auditory dysfunction in autoimmune MRL/MpJ-Fas(lpr) mice. Mice were tested at 2 months of age to establish baseline auditory brainstem response (ABR) thresholds, hematocrit, serum immune complexes, and anti-nuclear antibodies. Mice were then given different doses of prednisolone or aldosterone in their drinking water for 2 months. After the treatment period, most untreated water controls showed elevation of ABR thresholds due to the ongoing autoimmune disease. However, the steroid groups had significantly more mice with improved or unchanged thresholds. Both steroids improved stria vascularis morphology, although aldosterone appeared to be more effective. The immune suppressive prednisolone caused a dose-related improvement in levels of serum immune complexes and hematocrit, hallmarks of systemic autoimmune disease. Aldosterone, which has no immune suppressive function, did not alter systemic disease. The comparable efficacy of prednisolone and aldosterone in restoring auditory function suggests steroid reversal of autoimmune hearing loss in mice is due to increasing stria vascularis sodium transport and not suppression of systemic autoimmune reactions.

Aldosterone↗

PubMed2000

Usefulness of screening program for celiac disease in autoimmune thyroiditis.

We determined the prevalence of celiac disease in subjects with autoimmune thyroiditis compared with sick and healthy subjects. The screening was performed with IgA-class endomysium antibody, by indirect immunofluorescence using human umbilical cord as the antigenic substrate. Six of the 172 patients with autoimmune thyroiditis were found to be anti-endomysium positive (3.4%) and five of these underwent intestinal biopsy, which showed total villous atrophy. By contrast, 3 (0.75%) of 396 patients with nongastroenterologic malignancies and 10 (0.25%) of 4000 blood donors were found to have celiac disease. The prevalence of autoimmune diseases was significantly higher in patients with both celiac disease and autoimmune thyroiditis than in patients with autoimmune thyroiditis alone (P = 0.01). This study confirms that celiac disease is increased among patients with autoimmune thyroiditis. We suggest that these patients may benefit from screening for celiac disease so as to eliminate symptoms and limit the risk of developing other autoimmune disorders.

Adolescent↗