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PubMed1990

Polyglandular autoimmune syndrome type II in patients with idiopathic Addison's disease.

The frequency of polyglandular autoimmune syndrome Type II, (idiopathic or autoimmune Addison's disease associated with autoimmune thyroid disease, and/or insulin-dependent diabetes mellitus), was retrospectively investigated in 44 patients (26 females and 18 males) with idiopathic Addison's disease (median age at onset 32.5 years, range 8-62; median observation time 17 years, range 0.5-41) evaluated between 1966 and 1988 in the Department of Endocrinology, General Hospital, Malmö. Twenty-two patients (16 females and 6 males) fulfilled the criteria for polyglandular autoimmune syndrome Type II and of these 16 had autoimmune thyroid disease and 9 insulin-dependent diabetes mellitus. In 7 of 9 patients insulin-dependent diabetes mellitus developed prior to Addison's disease, whereas autoimmune thyroid disease was diagnosed before as well as after Addison's disease and with a similar age distribution as Addison's disease. In conclusion, the present study indicates that polyglandular autoimmune syndrome Type II occurs in about 50% of patients with idiopathic Addison's disease and that autoimmune thyroid disease is more common than insulin-dependent diabetes mellitus in these patients. The present study also indicates that insulin-dependent diabetes mellitus precedes Addison's disease in a majority of these patients and usually develops at a young age, whereas autoimmune thyroid disease precedes as well as succeeds Addison's disease and occurs at all ages in these patients.

Addison Disease↗

PubMed2003

Autoimmunity in Wiskott-Aldrich syndrome: risk factors, clinical features, and outcome in a single-center cohort of 55 patients.

OBJECTIVES: To evaluate the occurrence of autoimmune and inflammatory complications in Wiskott-Aldrich syndrome (WAS) and to determine risk factors and the prognosis of such complications with the aim of improving the definition of treatment options. METHODS: We reviewed the records of 55 patients with WAS evaluated at Necker-Enfants Malades Hospital (Paris) from 1980 to 2000. RESULTS: Forty patients (72%) had at least 1 autoimmune or inflammatory complication. Autoimmune hemolytic anemia was detected in 20 cases (36%); in all cases, onset occurred before the age of 5 years. Other complications included neutropenia (25%), arthritis (29%), skin vasculitis (22%), cerebral vasculitis (7%), inflammatory bowel disease (9%), and renal disease (3%). The median survival of the entire population was 14.5 years. Two autoimmune complications and 1 biological factor were predictive of a poor prognosis in this population: autoimmune hemolytic anemia, severe thrombocytopenia recurring after splenectomy, and high serum immunoglobulin M (IgM) levels before splenectomy. Autoimmune hemolytic anemia was significantly more observed in patients with high serum IgM level. CONCLUSIONS: High serum IgM concentration before splenectomy was identified as a risk factor for autoimmune hemolytic anemia; however, it must be confirmed. Autoimmune hemolytic anemia and severe thrombocytopenia recurring after splenectomy were 2 indicators of a poor prognosis. Those results suggest that patients with WAS and IgM levels more than mean + 2 standard deviations before splenectomy should be placed under strict surveillance. Furthermore, severe autoimmune complications should lead, as early as possible, to hematopoietic stem cell transplantation using the best available donor.

Adolescent↗

PubMed2005

The role of infections in the pathogenesis of autoimmune diseases.

The autoimmune diseases result from inappropriate responses of the immune system to self antigens. The etiology of autoimmune diseases remains largely unknown but candidate etiologic factors include genetic abnormalities and infections. Although there are considerable data supporting the role of infections in a variety of autoimmune diseases, this role has been unequivocally established in only a few autoimmune diseases. The difficulty in establishing the infectious etiology of autoimmune diseases stems from several factors such as the heterogeneity of clinical manifestations in individual autoimmune diseases and the time interval between infection and autoimmune disease. The data on this association derive from clinical observations, epidemiological studies and research using laboratory techniques, protein sequence database screening and animal models. Infectious agents can cause autoimmune diseases by different mechanisms, which fall into two categories: antigen specific in which pathogen products or elements have a central role e.g. superantigens or epitope (molecular) mimicry, and antigen non-specific in which the pathogen provides the appropriate inflammatory setting for "bystander activation". The most important mechanisms are molecular mimicry and superantigens. As far as molecular mimicry is concerned the recent data on the degeneracy of T cell recognition shifted the focus from searching for linear sequence homology to looking for similarity of antigenic surfaces. Special mention has to be made to retroviruses as they have some unique means of inducing autoimmunity.

Animals↗

PubMed1998

Peptide-based molecular analyses of HLA class II-associated susceptibility to autoimmune diseases.

Recent advances in knowledge of crystal structures of MHC class II molecules has advanced understanding of the molecular basis for interactions between peptides and HLA class II molecules. Polymorphism of HLA class II molecules influences structures of peptides bound to HLA class II molecules. To better understand mechanisms related to particular HLA class II alleles and autoimmune diseases, it is important to identify self-peptides presented by disease-susceptible HLA class II molecules and triggering disease-causative autoreactive T cells. Autoimmune diseases occur in Caucasians, Blacks and Asians, albeit with a different incidence. In some autoimmune diseases, disease-susceptible HLA class II alleles are closely related but different, and clinical manifestations of diseases differ among ethnic groups. These phenomena strongly suggest that difference in autoimmune self-peptide(s) in the context of disease-susceptible HLA class II molecules may explain the different clinical manifestations of diseases. Therefore, a comparison among disease-susceptible HLA class II alleles, autoimmune self-peptides and clinical manifestations of autoimmune diseases in different ethnic groups would be instructive. We directed efforts to determining: (1) HLA-class II alleles specific to Asian populations and which are associated with susceptibility to autoimmune diseases, (2) binding-peptide motifs for these HLA class II molecules, and (3) self-peptides presented by susceptible HLA class II molecules to stimulate autoreactive T cells related to the development of autoimmune diseases in Asians. In this review, our related recent investigations are described and the uniqueness of HLA class II-associated autoimmune diseases in Asians is given emphasis.

Amino Acid Sequence↗

PubMed1997

Immunogenetics and the cause of autoimmune disease.

Autoimmune disease results from the action of environmental factors on a predisposed genotype. In this review, the role of genetic susceptibility in the aetiology of autoimmune disease is examined. As the genetics of autoimmune diabetes has been studied more intensively than that of other autoimmune diseases, supporting evidence is drawn principally from that example. Autoimmune diseases are not inherited as entities but as constitutions which confer an increased probability of developing disease. It is proposed that there are two components to autoimmune disease susceptibility. One confers susceptibility to autoimmunity per se, while the other determines tissue specificity. In this review, the concept of liability is introduced as a tool used in quantitative genetics and is applied to the analysis of autoimmune diabetes by considering a threshold model. In this example, empirically derived incidence figures are used to calculate heritability which is a relative measure of the influence of genetics and environmental factors. The validity of applying the concept of liability to diabetes is confirmed by examining the values of heritability calculated from empirical data obtained from different kindred relationships, and by confirming that the assumptions on which liability is based are supported by recent gene mapping data. Finally, the physiological significance of liability is considered and its significance to the cause of autoimmunity discussed.

Animals↗

PubMed2001

Local transgenic expression of granulocyte macrophage-colony stimulating factor initiates autoimmunity.

Mechanisms leading to breakdown of immunological tolerance and initiation of autoimmunity are poorly understood. Experimental autoimmune gastritis is a paradigm of organ-specific autoimmunity arising from a pathogenic autoimmune response to gastric H/K ATPase. The gastritis is accompanied by autoantibodies to the gastric H/K ATPase. The best characterized model of experimental autoimmune gastritis requires neonatal thymectomy. This procedure disrupts the immune repertoire, limiting its usefulness in understanding how autoimmunity arises in animals with intact immune systems. Here we tested whether local production of GM-CSF, a pro-inflammatory cytokine, is sufficient to break tolerance and initiate autoimmunity. We generated transgenic mice expressing GM-CSF in the stomach. These transgenic mice spontaneously developed gastritis with an incidence of about 80% after six backcrosses to gastritis-susceptible BALBc/CrSlc mice. The gastritis is accompanied by mucosal hypertrophy, enlargement of draining lymph nodes and autoantibodies to gastric H/K ATPase. An infiltrate of dendritic cells and macrophages preceded CD4 T cells into the gastric mucosa. T cells from draining lymph nodes specifically proliferated to the gastric H/K ATPase. CD4 but not CD8 T cells transferred gastritis to nude mouse recipients. CD4(+) CD25(+) T cells from the spleen retained anergic suppressive properties that were reversed by IL-2. We conclude that local expression of GM-CSF is sufficient to break tolerance and initiate autoimmunity mediated by CD4 T cells. This new mouse model should be useful for studies of organ-specific autoimmunity.

Adoptive Transfer↗

PubMed2006

Autoimmune diseases in asthma.

BACKGROUND: Previous research has suggested an inverse relationship between T-helper 2-related atopic disorders, such as asthma, and T-helper 1-related autoimmune diseases. One controversial hypothesis postulates that asthma provides a protective effect for the development of autoimmune-related disorders. OBJECTIVE: To assess the rate of newly diagnosed autoimmune disorders in a large cohort of young adults. DESIGN: Using cross-sectional data from the Israeli Defense Force database, the authors analyzed the prevalence of autoimmune disorders in asthmatic and nonasthmatic military personnel between 1980 and 2003. A follow-up study traced newly diagnosed autoimmune disorders among asthmatic and nonasthmatic individuals from the time of enrollment in military service until discharge (22 and 36 months for women and men, respectively). SETTING: General community. PATIENTS: 307,367 male and 181,474 female soldiers in compulsory military service who were between 18 and 21 years of age. MEASUREMENTS: Cases of type 1 diabetes mellitus, vasculitis, immune thrombocytopenic purpura, inflammatory bowel disease, rheumatoid arthritis, and the antiphospholipid syndrome. RESULTS: Of 488,841 participants at enrollment, significantly more women than men had autoimmune disorders. Compared with asthmatic women, nonasthmatic women had a significantly higher prevalence of all autoimmune disorders except for the antiphospholipid syndrome. Type 1 diabetes mellitus, vasculitis, and rheumatoid arthritis were less prevalent in men with asthma than in those without. During the follow-up period, vasculitis and rheumatoid arthritis were more frequently diagnosed in nonasthmatic persons of both sexes. There was a significantly higher incidence of immune thrombocytopenic purpura, inflammatory bowel disease, and the antiphospholipid syndrome in nonasthmatic women and a statistically significantly higher incidence of type 1 diabetes mellitus in nonasthmatic men. LIMITATIONS: The study was limited to a population of young military recruits; therefore, its findings are not necessarily applicable to the general population. Because of the noninterventional nature of the study, it describes associations but cannot prove causality. CONCLUSIONS: Asthma status may affect the prevalence of major autoimmune disorders. Preexisting asthma seems to protect against the development of autoimmune disorders to varying degrees in men and women.

Asthma↗

PubMed2001

[The environment and autoimmunity--from external causes to inner conflicts].

Autoimmune disorders result from a breakdown of immunologic tolerance leading to an immune response against self-molecules. In most instances the events that initiate the immune response to self-molecules are unknown, but a number of studies suggest associations with environmental and genetic factors and certain types of infections. The concordance of autoimmune diseases among identical twins is virtually always less than 50%, often in the 25-40% range. This observation, as well as epidemic clustering of some autoimmune diseases following xenobiotic exposure, reinforces the thesis that autoimmune disease is secondary to both genetic and environmental factors. In addition, because of individual genetic susceptibilities based not only on major histocompatibility complex differences but also on differences in toxin metabolism, lifestyles, and exposure rates, individuals will react differently to the same chemicals. With these comments in mind it is important to note that there have been associations of a number of xenobiotics with human autoimmune disease, including mercury, iodine, vinyl chloride, canavanine, organic solvents, silica, L-tryptophan, particulates, ultraviolet radiation, and ozone. In addition, there is discussion in the literature that raises the possibility that xenobiotics may also exacerbate an existing autoimmune disorder. In this article these issues are discussed, in particular, the evidence for the role of environmental agents in the initiation or progression of autoimmune conditions. With the worldwide deterioration of the environment, this is a particular important subject for human health. This is best illustrated by the epidemics of eosinophilic myalgia syndrome with shared characteristics that occurred about 20 years ago. Another example is the toxic oil syndrome of Spain in 1981 involving cooking oil led to both acute and chronic disease as well as formation of auto-antibodies to collagen, DNA, and skeletal muscle. Currently the question is risen whether there is a link between environmental estrogens and autoimmune disorders, especially since these illnesses are reported possibly more frequent. Yet for the time being, an answer is not available, since the current state of science with respect to autoimmunity and environmental agents is still in the early stages of hazard identification.

Autoantibodies↗

PubMedDate not supplied

[Immunoablation or otherwise followed by hematopoietic cell stem as intensive treatment of severe autoimmune diseases].

The treatment of severe autoimmune diseases has been recently revitalized by the increasing utilization of clinical interventions aimed at ablating/abrogating autoimmune lymphoid clones followed (but not in certain procedures) by transplantation of allogeneic, but also autologous, hematopoietic stem cells. Two different investigative avenues have paved the way to specific clinical studies. The first originates from the epochal murine experiments of the '70s, and has been greatly expanded in the last decade. A graft-versus-autoimmunity effect could also be demonstrated. In addition, it could also be shown that induced experimental autoimmune diseases such as adjuvant arthritis and autoimmune encephalomyelitis could, surprisingly, be cured following autologous transplantation. The first results in humans were observational and derived from studies including patients with coincidental diseases (severe autoimmune diseases plus leukemia/aplasia) treated with allogeneic hematopoietic stem cell transplants. Although the concept of an allogeneic transplant is indisputably more appealing, very few patients with an isolated severe autoimmune disease have been treated using such a therapeutic approach. Reduced intensity conditioned transplants relying on subsequent graft-versus-autoimmunity effects strengthened by donor lymphocyte infusions are being explored cautiously. On the other hand, autologous transplants are being performed quite extensively. To date, transplanted severe autoimmune diseases include multiple sclerosis, connective tissue diseases (systemic sclerosis, systemic lupus erythematosus, rheumatoid arthritis) and many others. It is uncertain if the main mechanism is solely immunoablative, or whether tolerized lymphocytes may also develop during a postulated "window of opportunity" following the transplant.

Animals↗

PubMed2003

[Autoimmune hepatitis].

Autoimmune hepatitis is an unresolving, hepatocellular inflammation of unknown cause that is characterized by the presence of periportal hepatitis on histologic examination, tissue autoantibodies in serum, and hypergammaglobulinemia. By international consensus, the designation autoimmune hepatitis has replaced alternative terms for the condition. Three types of autoimmune hepatitis have been proposed based on immunoserologic findings. Type 1 autoimmune hepatitis is characterized by the presence of antinuclear antibodies (ANA) or smooth muscle antibodies (SMA) (or both) in serum. Seventy percent of patients with type 1 of autoimmune hepatitis are women. This type is the most common form and accounts for at least 80% of cases. Type 2 is characterized by the presence of antibodies to liver-kidney microsome type 1 (anti-LKM1) in serum. Patients with this type of autoimmune hepatitis are predominantly children. Type 3 autoimmune hepatitis is characterized by the presence of antibodies to soluble liver antigen (anti-SLA) in serum. There are no individual features that are pathognomonic of autoimmune hepatitis, and its diagnosis requires the confident exclusion of other conditions. The large majority of patients show satisfactory response to corticosteroid (usually prednisone or prednisolone) therapy. For the past 30 years it has been customary to add azathioprine as a "steroid sparing" agent to allow lower doses of steroids to be used and remission, once achieved, can be sustained in many patients with azathioprine alone after steroid withdrawal. Patients with autoimmune hepatitis who have decompensated during or after corticosteroid therapy are candidates for liver transplantation.

Autoantibodies↗

PubMed2004

Autoimmune hepatitides--update 2004.

This update reports is primarily made to update papers published in 2002 and 2003. A selection had to be realized since a search of the literature yielded more than 1600 journal articles. The prevailing opinion of an international group is especially emphasized. Autoimmune hepatitides (AIH)--as the name already suggests it--are no disease entity. We prefer to classify them under the terms of typical and atypical autoimmune hepatitides. Typical autoimmune hepatitis can be subdivided into a type 1 (with antibodies against nuclear material and/or smooth muscle) and a type 2 (with antibodies against endoplasmic reticulum). In the case of atypical autoimmune hepatitides, the detected autoantibodies would have to be stated. The essential feature of an autoimmune hepatitis is the presence of various high-titer autoantibodies circulating in serum, especially such of the IgG class. Special mention is made of the very rare liver ribosomal antibodies (LRA), which are mainly directed against 80S liver ribosomes and point to a so-called virus-associated autoimmune hepatitis. Also discussed are a genetic disposition, which is still speculative in some points, and the existence of so-called autogenes (physiological, pathological/pathogenic and so-called regulator genes). Various noxae, e.g. viruses, might also be "autogenous". Further research in the field of the autoimmune hepatitides (and also autoimmunity and autoimmune diseases as such) is therefore likely to concentrate on viruses and genes and their interrelations.

Animals↗

PubMed1992

Sjögren's syndrome in relation to other autoimmune diseases.

Autoimmune diseases can be divided into primary autoimmune diseases, in which the immune system is over-reactive, leading to an oligoclonal B cell stimulation, and secondary autoimmune diseases, in which the immune system is completely normal but some autoantigens are slightly altered, and are thus considered to be foreign. Sjögren's syndrome probably has characteristics of both types of autoimmune disease. The primary autoimmune diseases can be divided into organ-specific autoimmune diseases like thyroiditis, gastritis and adrenalitis, and generalised autoimmune diseases, such as systemic lupus erythematosus (SLE) and rheumatoid arthritis. Sjögren's syndrome has characteristics of both types of primary autoimmune disease, and therefore occupies a central position among the other autoimmune diseases. The focal position of the disease in the present issue of The Netherlands Journal of Medicine is because of the symposium organized for the occasion of the fifth anniversary of the "Dutch Association of Patients with Sjögren's Syndrome", of which this issue is the report.

Autoimmune Diseases↗

PubMed2005

Autoimmune disease is a risk factor for the development of non-Hodgkin's lymphoma.

OBJECTIVE: To investigate the relationship of prior autoimmune disease to the development of non-Hodgkin's lymphoma (NHL). METHODS: Patients with NHL (n = 278) seen from 1993 to 2002 were compared with a group of patients with other hematological disorders (controls, n = 317) seen at the same time. All patients were questioned about prior autoimmune disease. Comparisons between NHL patients and controls were based on analysis of a 2 2 table of counts using Fisher's exact test. Analysis of the effect of autoimmune disease on NHL status, controlling for other risk factors, was performed using logistic regression. RESULTS: Thirty-six (13%) NHL patients had a prior autoimmune disease compared to 5% of controls (p = 0.001). Sixty-nine percent of NHL patients with a prior autoimmune disease were female compared to 43% without a prior autoimmune disease, and this was similar in control patients, 69% and 48%, respectively. Twenty percent of all women with NHL had a history of autoimmune disease compared to 7% of women in the control group (p = 0.001). Nineteen of the NHL patients with autoimmune disease (56%) received immunosuppressive treatment compared to 5 (38%) in the controls. CONCLUSION: Autoimmune disease may account in part for the increase in NHL, especially in women.

Autoimmune Diseases↗

PubMed2006

Prevalence of onychomycosis in patients with autoimmune diseases.

BACKGROUND: Onychomycosis is the most common nail disorder in adults. Many studies reported a higher prevalence of onychomycosis among particular patients, such as those with diabetes, poor peripheral circulation or immunosuppression. However, studies of the prevalence of onychomycosis in autoimmune patients who carry many of these predisposing factors have been limited OBJECTIVE: Study the prevalence of onychomycosis in autoimmune compared to non-autoimmune female patients. MATERIAL AND METHOD: A cross-sectional study of the prevalence of onychomycosis in autoimmune patients and non-autoimmune female patients visiting a dermatology clinic over a period of 18 months. One hundred and sixty-five female autoimmune patients were enrolled. RESULTS: The prevalence of onychomycosis in autoimmune patients was 10.2% (95%CI 6.5%, 15.9%) compared to 6.7% (95%CI 3.8%, 11.6%), in non-autoimmune patients (p > 0.05, 2-sided). Of vesiculobullous patients, mainly presenting with pemphigus and who were mostly on immunosuppressive medication, 24% had onychomycosis [p = 0.013; OR 4.39 (95%CI 1.27, 14.89)]. CONCLUSION: Exposure to humid microenvironments was an important factor in the occurrence of onychomycosis (p < 0.05, 2-sided). However, the number of patients with each individual disease was too small to conclude a prevalence of onychomycosis in conjunction with these individual cutaneous autoimmune diseases.

Adult↗

PubMedDate not supplied

Oncogenes, growth factors, and autoimmune diseases (review).

Autoimmune diseases are benign proliferative diseases characterized by the expansion and activation of the autoreactive immune cells and the proliferation of connective tissue elements. Because both cytokines and oncogenes products are necessary for expansion of immune cells, it is possible that inappropriate activation of oncogenes might influence cytokine and lymphokine secretion as well as the expression of immune response genes necessary for the development of autoimmunity in a susceptible individual. At least four gene families of the immune system are involved in the induction and perpetuation of autoimmunity: 1) genes associated with the major histocompatibility complex, 2) germline immunoglobulin genes, 3) T cell receptor genes, and 4) complement genes. The hypothetical genetic locus responsible for the induction of autoimmunity is the "rheumogene". Oncogenes are obvious candidates for rheumogenes and activation of such genes may be necessary for the development of autoimmunity. Certain protooncogenes are activated in systemic lupus erythematosus, rheumatoid arthritis, Sjögren's syndrome, progressive systemic sclerosis, and dermatomyositis, supporting this hypothesis. However, the activation of oncogenes in autoimmunity is not associated with gene translocation, deletions, point mutations, loss of regulatory sequences, or amplification, indicating that autoimmunity involves different mechanisms of oncogene activation than do many malignancies. Oncogene expression in autoimmune diseases tends to mimic the expression of oncogenes in normal activated lymphocytes, macrophages, and fibroblasts. Rheumogenes, if they exist, may be disordered regulatory genes which suppress or enhance the expression of cellular oncogenes in a non-malignant fashion. The existence of regulator gene demethylation and the presence of DNA-binding proteins specific for oncogene regulator sequences provide support for the concept of that regulator gene dysfunction, rather than oncogene activation per se is the more primary event in autoimmune diseases.

Animals↗

PubMed1988

[Multiple autoimmune syndromes].

The possibility of three or more autoimmune diseases occurring in the same patient cannot be fortuitous and suggests a pathogenic relationship between each of them. In the light of 4 personal cases, the authors have recorded 87 reports of such associations in the literature, an analysis of which leads them to propose a classification of three types of multiple autoimmune syndrome. The grouping of these syndromes under a single heading should make the research and analysis of these morbid associations easier. Moreover, the classification adopted by the authors allows a more precise definition of patients with at least two autoimmune diseases and so helps to recognize the onset of a third autoimmune disease at a later date. Multiple autoimmune syndromes can be classified in 3 groups according to the prevalence of their associations one with another. Type I comprises myasthenia, thymoma, polymyositis and giant cell myocarditis, this association having a single pathogenic mechanism. Type II includes the Sjögren's syndrome, rhumatoid arthritis, primary biliary cirrhosis, scleroderma and autoimmune thyroid disorders. Type III groups together 10 autoimmune diseases (autoimmune thyroid disease, myasthenia and/or thymoma, Sjögren's syndrome, pernicious anaemia, idiopathic thrombocytopaenic purpura, Addison's disease, insulin-dependent diabetes, vitiligo, autoimmune haemolytic anaemia, systemic lupus erythematosus) for which a genetic predisposition (phenotype HLA B8 and/or DR3 or DR5) seems to be an important factor.

Adult↗

PubMed1995

The outcome of children referred to a pediatric rheumatology clinic with a positive antinuclear antibody test but without an autoimmune disease.

OBJECTIVE: To assess the diagnostic value of positive antinuclear antibody (ANA) test results in children with musculoskeletal or dermatologic problems but without autoimmune disease at presentation. DESIGN: Retrospective chart review. SETTING: Pediatric rheumatology clinic in a tertiary care center. PATIENTS: Five hundred charts reviewed, comprising all new patients seen, 1978 to 1993. RESULTS: Of 500 children seen, 113 had positive ANA test results available at referral. Of those 113 patients, 72 (64%) had an autoimmune condition diagnosed at initial clinic visit; another 10 (9%) were lost to follow-up. Thirty-one children (27%) had no autoimmune condition diagnosed at initial clinic visit and had clinical follow-up over a mean of 37 months. Nonspecific musculoskeletal complaints and hypermobility accounted for the majority of presentations. Routine hematology data were usually normal. Median ANA titer was 1:160; ANA patterns varied. On follow-up, 25 patients (81%) cleared their symptoms; five (16%) had significant improvement. One patient developed an autoimmune disease (autoimmune hepatitis). CONCLUSIONS: Based on our findings, the vast majority of children who have positive ANA test results but do not have autoimmune conditions at initial diagnosis will not develop an autoimmune condition. ANA testing of children who have musculoskeletal or dermatologic problems in the absence of autoimmune conditions does not reveal new diagnoses, and represents unnecessary laboratory time and expense. The prognosis of children who have positive ANA test results in the absence of autoimmune conditions is usually excellent.

Adolescent↗

PubMed2001

Islet cell autoimmunity in youth onset diabetes mellitus in Northern India.

We characterised a consecutive cohort of 132 youth onset diabetic individuals (age at onset<30 years, mean duration of disease 5.5+/-6.0 years) from North India, by serological determination of the determination of the islet cell autoantibodies, GAD(65) and IA2, and clinically for coexisting autoimmune thyroid disease, malnutrition and pancreatic calcification. Five types of diabetes were delineated: Type 1 (37%), ketosis resistant (32%), Type 2 (13%), fibrocalculous pancreatopathy (11%) and autoimmune polyglandular syndrome (7%). C-peptide response to glucagon was assessed in a representative subset of 50 patients with Type 1, ketosis resistant, and autoimmune polyglandular syndrome. A total of 22.4% of Type 1 and 30% of autoimmune polyglandular syndrome subjects showed both GAD(65) plus IA-2 autoantibody positivity, significantly more than the 4.7% positivity shown by the ketosis resistant type. However, GAD(65) antibody positivity alone was seen in 38% of ketosis resistant subjects which was significantly more than the 14.2 and 10% positivity seen in Type 1 and autoimmune polyglandular groups, respectively. The fibrocalculous pancreatopathy group showed GAD(65) plus IA-2 autoantibody positivity in 14.2% and GAD(65) autoantibody alone positivity in 7.1%. 26 and 60%, respectively, of the Type 1 and autoimmune polyglandular syndrome groups had thyroid microsomal autoantibody positivity. Type 1 showed significantly less C-peptide response to glucagon when compared to the ketosis resistant and autoimmune polyglandular syndrome groups. The controls and Type 2 diabetic individuals tested negative for islet cell autoimmunity markers. These findings demonstrate a role of islet cell autoimmunity in the pathogenesis of four out of the five clinical types of youth onset diabetes seen in North India.

Adolescent↗