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PubMed2000

Stimulation of the developing immune system can prevent autoimmunity.

Both genetic and environmental factors contribute to the development of autoimmunity. Animals and humans exposed to natural infections have a reduced rate of autoimmune diseases. There is increasing evidence that immune stimulation prevents autoimmune diseases. Our hypothesis is that the process of the development of pathogenic cells involved in autoimmunity can be modulated by early stimulation of the immune system in autoimmunity prone individuals This allows for the upregulation of cytokines and growth factors that influence the generation of regulatory cells involved in autoimmunity. As we live in a 'cleaner environment' the decreasing chances of natural infection in the general population may contribute to the induction of autoimmunity because the developing immune system is not exposed to stimulation that may be necessary to generate regulatory cells involved in the modulation and prevention of autoimmunity. Immunization with certain vaccines may provide an alternative approach to stimulate the immune system to modulate or prevent the generation of pathogenic cells involved in autoimmunity by induction of regulatory cells.

Animals↗

PubMed2005

Protective autoimmunity and neuroprotection in inflammatory and noninflammatory neurodegenerative diseases.

Autoimmune diseases are traditionally viewed as an outcome of a malfunctioning of the immune system, in which an individual's immune system reacts against the body's own proteins. In multiple sclerosis (MS), a disease of the white matter of the central nervous system (CNS), the attack is directed against myelin proteins. In this article we summarize a paradigm shift proposed by us in the perception of autoimmune disease. Observations by our group indicating that an autoimmune response is the body's mechanism for coping with CNS damage led us to suggest that all individuals are apparently endowed with a purposeful autoimmune response to CNS injuries, but have only limited inherent ability to control this response so that its effect will be beneficial. In animals susceptible to autoimmune diseases, the same autoimmune T cells are responsible both for neuroprotection and for disease development; the timing and strength of their activity will determine which of these effects is expressed. Individuals with non-inflammatory neurodegenerative diseases need a heightened autoimmunity. We discovered that autoimmunity could be boosted without risk of disease induction, even in susceptible strains, by the use of Copolymer-1 (Copaxone(R)), a weak agonist of a wide range of self-reactive T cells. Here we summarize the basic findings that led us to formulate the concept of protective autoimmunity, the mechanisms underlying its constitutive presence and its on/off regulation, and its therapeutic implications. We also offer an explanation for the commonly observed presence of cells and antibodies directed against self-components in healthy individuals.

Animals↗

PubMed2003

Autoimmunity and hepatitis C.

Hepatitis C is a widespread chronic liver disease leading to cirrhosis and to the complications of portal hypertension. Based on biochemical and clinical features, it is almost indistinguishable from autoimmune hepatitis, which is characterized by the absence of viral infection, and other causes of chronic liver diseases, and represents a classical autoimmune disease with loss of immunological tolerance of liver tissue. Although the differentiation between both diseases is not difficult due the availability of diagnostic viral markers, it is well recognized that not only are autoantibodies present in autoimmune hepatitis frequently detected in hepatitis C, but also that an array of immune-mediated symptoms and diseases occur in patients with chronic hepatitis C. This has prompted research aimed at identifying a link between hepatitis C and autoimmunity, and autoimmune hepatitis in particular. This review focuses on the general immunological mechanisms linking viral infections with autoimmunity and includes the specific features of hepatitis C- and D-associated autoimmunity. Virus infection remains at the center of molecular and cellular research aimed at identifying the forces driving human autoimmunity and autoimmune diseases.

Animals↗

PubMed2026

FPR2/ALX stimulation modulates microglia and natural killer cells to restrict autoimmune astrocytopathy.

Autoantibody- and complement-mediated cytotoxicity can cause autoimmune astrocytopathy that leads to CNS inflammatory demyelination. Formyl peptide receptor 2 (FPR2/ALX) governs the activation and propagation of immune response. However, the precise role of FPR2/ALX in neuroinflammation and the effect of FPR2/ALX stimulation on autoimmune astrocytopathy are poorly understood. Using a mouse model of autoimmune astrocytopathy induced by AQP4-IgG- and complement-mediated cytotoxicity, we found that the stimulation of FPR2/ALX with the small-molecule agonist Quin-C1 led to reduced brain lesion volume, astrocyte loss and demyelination. This was accompanied by enhanced anti-inflammatory activity of microglia and reduced infiltration of lymphocytes in the brain. FPR2/ALX stimulation also led to increased phosphorylation of SYK and AKT in mice with autoimmune astrocytopathy. Notably, the benefits of FPR2/ALX stimulation were attenuated in mice with autoimmune astrocytopathy after microglial depletion using the CSF1R inhibitor PLX5622 or natural killer (NK) cell depletion using an anti-NK1.1 monoclonal antibody. Additionally, the protective effects of FPR2/ALX stimulation were diminished in mice with autoimmune astrocytopathy that received the SYK inhibitor R406. Collectively, our findings demonstrate that FPR2/ALX stimulation may represent a promising therapeutic strategy to attenuate detrimental neuroinflammation in autoimmune astrocytopathy by modulating microglia and NK cells. FPR2/ALX stimulation suppresses autoimmune astrocytopathy: Using a mouse model of autoimmune astrocytopathy, we demonstrated that FPR2/ALX stimulation with the small molecule Quin-C1 reduces the CNS infiltration of lymphocytes and augments the anti-inflammatory activity of microglia, leading to attenuated astrocyte pathology induced by AQP4-IgG and complement-mediated attacks. Mechanistically, the benefits of FPR2/ALX stimulation using Quin-C1 involve microglia, natural killer (NK) cells, and SYK-AKT signaling.

Animals↗

PubMed2001

The effect of treatment with Campath-1H in patients with autoimmune cytopenias.

We describe 21 patients with severe and life-threatening autoimmune cytopenias resistant to standard immunosuppression who were treated with the monoclonal antibody Campath-1H. Four patients had autoimmune neutropenia, four had autoimmune haemolytic anaemia, four had pure red cell aplasia, one had immune thrombocytopenia purpura (ITP), three had autoimmune haemolytic anaemia and ITP (Evan's syndrome), three had autoimmune pancytopenia (ITP, autoimmune neutropenia and autoimmune haemolytic anaemia), one had ITP (associated with acquired Glanzmann's disease) and autoimmune neutropenia, and one had ITP and red cell aplasia. Campath-1H was administered at a dose of 10 mg/d as an intravenous infusion for 10 d. Responses were seen in 15 patients, which were sustained in six. Relapse occurred in eight patients after Campath-1H treatment. Patients entering the study later, received cyclosporine after Campath-1H in an attempt to reduce the incidence of relapse. Three patients received a second course of Campath-1H; all responded but later relapsed. Fourteen patients are alive at a median of 12 months (range 4-61) after Campath-1H. Campath-1H represents an alternative therapeutic option for severe, refractory autoimmune cytopenias.

Adolescent↗

PubMedDate not supplied

Recent progress in the understanding of B-cell functions in autoimmunity.

Our early concepts of the normal role of B cells in immunity focused on their ability to produce antibodies (Ab) and in the case of autoimmune diseases autoAbs, some of which were pathogenic. Over the past 10 years, it has became apparent that B cells display a variety of characteristics, other than Ab production, which could contribute to autoimmunity. They normally play a role in the development of lymphoid architecture, regulating T-cell subsets and dendritic cell (DC) function through cytokine production, and in activation of T cells. Receptors editing is also important in B cells which aids in immunity to infection and, possibly, prevention of autoimmunity. Transgenic animal models have now shown that B cells are necessary for many autoimmune diseases although their Ab products are not required in some cases. Negative signalling by CD5 and other molecules, such as CD22, in maintaining tolerance through recruitment of src-homology two domain-containing protein tyrosine phosphatase-1 has also been documented. In fact, we have now reached a new era whereby the B cell has returned as an important contributor to autoimmune disorders, so that the race is on to characterize signalling regulation via the B-cell receptor and coreceptors. Identification of such molecules and their potential defects should lead to effective ways of controlling the immune response and in particular preventing the development of autoimmune states. The classical view of B cells in the biology of immune responses to infectious and self-antigens (Ag) that they promote immunity primarily by producing Ab turns out to be rather naïve. Indeed, studies over the last few years indicate that this view is far from complete, and suggest that B lymphocytes have extraordinarily diverse functions within the immune system. Furthermore, it is becoming increasingly clear that the pathogenesis of autoimmune diseases cannot solely be accounted for by T cells, and intrinsic abnormalities of B cells have been described in such conditions. In this brief review we highlight some recent observations in the context of B lymphocyte in pathophysiology, and focus on their revival as pivotal players the pathophysiology in autoimmune diseases. Yet, it remains difficult to provide a model of how important B cells are in immunity and autoimmunity.

Animals↗

PubMed2004

Patterns of autoimmunity in primary biliary cirrhosis patients and their families: a population-based cohort study.

BACKGROUND: Primary biliary cirrhosis (PBC) is a chronic liver disease with autoimmune features but uncertain aetiology. Increased risk of PBC among relatives of patients may reflect common environmental factors, or inherited immunogenetic susceptibility. Associations between PBC and other autoimmune diseases have been reported, but their true extent and pattern is unknown. AIM: To examine the prevalence and association patterns of autoimmune disease in a representative group of PBC patients. DESIGN: Clinical cohort study. METHODS: We clinically assessed members of a geographically-based PBC patient cohort (n = 160) for the presence of additional autoimmune disease, using established specific diagnostic criteria. RESULTS: Some 53% of patients had at least one additional autoimmune condition, and 63% had serum autoantibodies other than AMA or ANA. AMA+ patients had a significantly lower prevalence of additional autoimmunity than AMA- patients (49% vs. 79%; p < 0.01). The greatest relative increase in disease prevalence was for scleroderma (8% of patients). Autoimmune disease was present in 14% of first-degree relatives. DISCUSSION: PBC patients and their families have a wide susceptibility to autoimmunity. This observation supports an autoimmune aetiology and suggests that the genetic basis of PBC is likely to be expressed, at least in part, through factors controlling immune tolerance in general.

Adult↗

PubMed1992

Causes and mechanism of autoimmune disease: cyclosporin A as a probe for the investigation.

Organ-specific autoimmune disease can be elicited in rodents by manipulating the thymus/T cells. For example, elimination of a particular T-cell subset causes organ-specific autoimmune diseases, such as thyroiditis and gastritis, in otherwise normal mice. Environmental agents can cause similar autoimmune diseases by affecting the thymus/T cells. Cyclosporin A (CsA), a potent immunosuppressive drug, is an example. When a particular strain of newborn mice are daily administered with CsA for a limited period, they spontaneously develop organ-specific autoimmune disease, such as gastritis with anti-parietal cell autoantibodies, later in life. CsA abrogates the production of CD4+T cells and CD8+T cells in the thymus. Consequently, these T cells are substantially depleted from the peripheral lymphoid organs, especially when the drug is administered from the day of birth. The autoimmune disease is prevented when CsA-treated newborn mice are inoculated with splenic T cells from normal syngeneic adult mice. On the other hand, removal of the thymus immediately after neonatal CsA treatment produces autoimmune disease with a higher incidence and in a wider spectrum of organs, i.e., thyroiditis, sialoadenitis of the salivary gland, gastritis, insulitis of the endocrine pancreas, adrenalitis, oophoritis, or orchitis. Each autoimmune disease is accompanied by the development of circulating autoantibodies specific for the corresponding organ-specific antigens. These findings taken together indicate that CsA causes autoimmune disease not by affecting the target self-antigens, but by interfering with a thymus/T cell-dependent control mechanism on the production/expansion of pathogenic self-reactive T cells. Various other environmental insults (such as ionizing radiation or virus) can also cause similar autoimmune diseases, presumably by a similar mechanism.

Animals↗

PubMed2005

Clinical features of type 1 autoimmune hepatitis in elderly Italian patients.

BACKGROUND: The usual onset of type 1 autoimmune hepatitis occurs at puberty or around menopause, whereas disease presentation in the advanced age is less often reported. AIM: To assess the clinical, immunological and histological features of Type 1 autoimmune hepatitis in elderly Italian patients. METHODS: We assessed, at diagnosis, the clinical and immunological features of 76 consecutive Italian patients with type 1 autoimmune hepatitis, focusing particularly on a subgroup of 20 patients presenting at > or = 65 years (females 95%, median age 72 years, range 65-82). RESULTS: In comparison with the younger group, at the time of autoimmune hepatitis diagnosis, elderly Italian patients are more often asymptomatic (25% vs. 7%; P = 0.04), are more frequently positive for antinuclear autoantibodies (95% vs. 52%; P = 0.0004) and HLA-DR4 (45% vs. 18%; P = 0.03); among the extra-hepatic manifestations, autoimmune thyroid disorders are prevalent in the elderly group (25% vs. 5%; P = 0.02). However, no difference was observed in the histological/biochemical expression of the liver disease and response to immunosuppression. CONCLUSIONS: In elderly Italian patients, autoimmune hepatitis has typical serological and genetic characteristics, is more frequently asymptomatic, although prognosis and response to therapy is similar to that of younger patients. As a concomitant autoimmune thyroid disorder is common, autoimmune hepatitis should be suspected and investigated in elderly patients with autoimmune thyroid disorder and abnormal liver function tests.

Adult↗

PubMed2005

Early disease onset and increased risk of other autoimmune diseases in familial generalized vitiligo.

Generalized vitiligo is an autoimmune disorder in which acquired white patches of skin and overlying hair result from autoimmune loss of melanocytes from involved areas. Although usually sporadic, family clustering of vitiligo may occur, in a non-Mendelian pattern typical of multifactorial, polygenic inheritance. Sporadic vitiligo is associated with autoimmune thyroid disease, pernicious anemia, Addison's disease, and lupus; these same disorders occur at increased frequency in patients' first-degree relatives. Here, we studied 133 'multiplex' generalized vitiligo families, with multiple affected family members. The age of onset of vitiligo is earlier in these 'multiplex' families than in patients with sporadic vitiligo. Affected members of the multiplex vitiligo families have elevated frequencies of autoimmune thyroid disease, rheumatoid arthritis, psoriasis, adult-onset insulin-dependent diabetes mellitus, pernicious anemia, and Addison's disease. Probands' unaffected siblings have elevated frequencies of most of these same autoimmune diseases, particularly if the proband had non-vitiligo autoimmune disease. Familial generalized vitiligo is thus characterized by earlier disease onset and a broader repertoire of associated autoimmune diseases than sporadic vitiligo. This mostly likely reflects a greater inherited genetic component of autoimmune susceptibility in these families. These findings have important implications for autoimmune disease surveillance in families in which multiple members are affected with vitiligo.

Addison Disease↗

PubMed1994

Autoimmunity and heavy metals.

This brief review is focused on those heavy metals (cadmium, gold and mercury) that have strong associations with autoimmunity. Cadmium treatment of rats and mice results in autoimmune responses that vary with species and inbred strain of animals. However, there is no solid evidence demonstrating that the renal pathology observed in humans exposed to cadmium has an autoimmune pathogenesis. More clear-cut are the autoimmune effects of preparations containing gold salts, that have been widely used in the treatment of rheumatoid arthritis. Gold may cause autoimmune thrombocytopenia, immune complex-mediated glomerulonephritis and other autoimmune disorders. Similarly, there is solid evidence that mercury can induce autoimmune disease both in humans and experimental animals. The lessons to be derived from metal-induced autoimmunity relate to structure-activity relationship, pathogenesis, etiology and genetics. They probably apply to xenobiotic-induced autoimmune disease in general.

Animals↗

PubMed2003

Central diabetes insipidus and autoimmunity: relationship between the occurrence of antibodies to arginine vasopressin-secreting cells and clinical, immunological, and radiological features in a large cohort of patients with central diabetes insipidus of known and unknown etiology.

Central diabetes insipidus (CDI) is a rare hypothalamus-pituitary disease due to the deficiency of arginine vasopressin (AVP) synthesis from the hypothalamus and/or secretion from the neurohypophysis. The etiology of CDI is unknown in over one third of cases, classified as idiopathic CDI. The aim of this study was 2-fold: 1) to evaluate the occurrence of circulating autoantibodies to AVP-secreting cells (AVPcAb), and 2) to correlate it to clinical (sex, age of disease onset, disease duration, and degree), immunological (clinical history of autoimmune diseases and presence of related organ-specific autoantibodies), and radiological features (neurohypophyseal bright spot, pituitary stalk thickening, and empty sella) in a large cohort of patients with apparently idiopathic CDI or CDI of known etiology. To this purpose, 150 patients with CDI were studied: 64 idiopathic, 6 familial, 12 associated to granulomatous diseases, and 68 secondary to cranial trauma, tumor, or surgery. AVPcAb were measured by an indirect immunofluorescence method. AVPcAb were found in 23.3% of CDI patients: 21 idiopathic (32.8%) and 14 nonidiopathic (16.3%; chi(2) = 13.1; P < 0.001). AVPcAb were independently associated with age less than 30 yr at disease onset (P = 0.001) in patients with idiopathic CDI and with history of autoimmune diseases (P = 0.006 and P = 0.02, respectively) and radiological evidence of pituitary stalk thickening (P = 0.02 and P = 0.003, respectively) in both idiopathic and nonidiopathic CDI. The likelihood of autoimmunity in one patient with apparently idiopathic CDI with age of disease onset less than 30 yr was 53%, it increased to 91% when history of autoimmune diseases was associated and to 99% when pituitary stalk thickening was further associated. In conclusion, autoimmunity is associated with one third of patients with apparently idiopathic CDI, which should therefore be classified as autoimmune CDI. Autoimmune CDI is highly likely in young patients with a clinical history of autoimmune diseases and radiological evidence of pituitary stalk thickening. Conversely, autoimmunity probably represents an epiphenomenon in patients with nonidiopathic CDI.

Adult↗

PubMed2006

Beneficial autoimmunity participates in the regulation of rheumatoid arthritis.

Antigen specific T cells and B cells recognize their target determinants by antigen specific receptors that are being rearranged in a random manner. These cells then undergo negative and positive selection processes that limit, albeit not eliminate, the escape of self-reactive T and B cells capable of eliciting autoimmune responses. The above processes are referred to as "central selection", and their outcome is the "central tolerance". Auto-reactive T and B cells escaping central tolerance are then subjected to peripheral mechanisms that restrain their auto-aggressive behavior. Different types of regulatory T cells are key players in maintaining actively induced peripheral tolerance. In patients suffering from various autoimmune disorders autoreactive T and/or B cells that escaped central tolerance also circumvented regulatory T cells that could, potentially, eradicate their pathogenicity in the periphery. We have found an additional regulatory mechanism that restrains the harmful activity of these cells at that time. It includes autoimmune B cells that produce neutralizing autoantibodies against numerous inflammatory mediators, mostly cytokines and chemokines, which participate in destructive autoimmunity. These autoantibodies restrain the harmful consequences of inflammatory autoimmune conditions such as in rheumatoid arthritis. Interestingly, this antibody production is elicited during autoimmune diseases, and to a much lesser extent during local inflammation. The specificity of this response is highly restricted to determinants with minimal cross reactivity to other known gene products. Thus, the immune system allows selective breakdown of tolerance in autoimmune conditions. The findings that this beneficial response is turned on by the autoimmune condition, and then regulated by its progression further imply for the existence of a programmed regulatory response of "beneficial autoimmunity". In the current review we describe how this mechanism was discovered in experimental models of rheumatoid arthritis and multiple sclerosis, demonstrate its importance in the natural regulation of these diseases, and finally explore its relevance to human diseases.

Animals↗

PubMedDate not supplied

Serological and clinical markers of autoimmune disease in HCV-infected subjects with different disease conditions.

OBJECTIVE: To investigate whether the serological markers of autoimmunity and the clinical features of autoimmune disease which occur in hepatitis C virus (HCV)-infected subjects are correlated to each other and/or to the clinical pattern of the disease. METHODS: Seventeen symptom-free, anti-HCV antibody positive subjects, 17 patients with chronic hepatitis C, 21 patients with mixed cryoglobulinemia (MC), and as controls 17 anti-HCV negative patients with dyspepsia were enrolled in a prospective study. A patient history, clinical examination, self-administered questionnaire and laboratory investigations (hepatic enzyme levels, serum HCV-RNA and anti-HCV antibody testing, and serum autoantibody profile) were performed to detect liver and/or autoimmune disease. RESULTS: Serological markers of autoimmunity and clinical findings of autoimmune disease were found to be more frequent in the HCV-infected patients considered as a whole than in controls. However, rheumatoid factor and clinical findings of autoimmune disease were more frequent in MC patients, while anti-smooth muscle antibodies not linked to symptoms or signs of autoimmune disease were detected in all groups of HCV-infected individuals, including healthy carriers and subjects who had recovered from a previous HCV infection. CONCLUSION: Anti-smooth muscle antibodies, a serological marker of autoimmunity, are detectable in HCV-infected subjects whatever their clinical status. Clinical findings of autoimmune disease prevalently occur in patients with mixed cryoglobulinemia.

Adult↗

PubMedDate not supplied

Autoimmune polyglandular syndrome type III in monozygotic twins: a case report.

Autoimmune polyglandular syndrome is characterized by the coexistence of several autoimmune diseases, affecting predominantly the endocrine glands. Autoimmune polyglandular syndrome type III, as a subdivision of autoimmune polyglandular syndrome type II, is the co-occurrence of autoimmune thyroid disease with other autoimmune disorders without Addison disease. We present a rare case of autoimmune polyglandular syndrome type III in monozygotic twins. One of the twins also had autoimmune leukopenia. To our knowledge, leukopenia is the first mentioned coexistence in the literature of autoimmune polyglandular syndrome.

Adult↗

PubMed1991

[Autoimmunization: new facts, controversial questions and study prospects].

At present autoimmunization is viewed as a complex of immune responses to unchanged autoantigens, bearing in mind that autoimmune processes can be "physiologic" ("sanitary" and "regulatory") and pathologic, underlying autoimmune diseases and illnesses associated with secondary autoimmune disorders. The "physiologic" autoimmune processes may be an element of the regulatory mechanisms of homeostasis. The pathologic autoimmune processes develop on the basis of the physiologic ones in the presence of immune disorders in the form of varying defects of the suppressor mechanisms of the immune system. Among the mechanisms of autoimmunization, predisposing, initiating and contributory factors may be distinguished. Of paramount importance is thymic dysfunction whose character has not been completely disclosed. The alterations in the lymphoid organs and tissues (target organs) hypersensitivity reactions (with the exception of reagin ones) form the morphological substrate of autoimmune diseases. Distribution of autoimmune diseases into organ-specific and non-organ-specific can be accepted as the working classification.

Antigen-Antibody Reactions↗

PubMed1994

Is multiple sclerosis an autoimmune disease?

It is a commonly held view that multiple sclerosis (MS) may be an autoimmune disease. Most neurology texts list MS as an autoimmune disease and most texts on autoimmunity point to MS as a prime example of an autoimmune disease of the CNS. This view has influenced research into the pathogenesis of MS to the extent that most published work on MS is based on the assumption that it is correct, ignoring other possibilities, unless they can be put into an autoimmune context. Furthermore, most attempts at treating MS have been with agents that influence the immune system. Some of these agents, such as cytoxan and cyclosporin, are drugs with serious side-effects. Hence, it can be argued that over the years some MS patients have suffered because of the autoimmune hypothesis, although in the end and even today, other MS patients may benefit from it. This article examines some of the evidence in support of autoimmune hypotheses of the pathogenesis of MS. We believe that this examination shows that it has not been proven that MS is an autoimmune disease although it underscores the possibility that it may be so. Although it is still a reasonable hypothesis that MS is an autoimmune disease, it has yet to be proven and it would constitute a serious error of omission not to examine other possibilities.

Animals↗

PubMed1994

[Combined endocrine autoimmune syndrome--incidence, forms of manifestation and clinical significance].

UNLABELLED: In a retrospective case finding study we collected data from patients with polyglandular autoimmune syndrome type II (PGAS Type II) who had been treated in our endocrine outpatient clinic between 1975 and 1989. 31 adult patients (25 females and 6 males) fulfilled the criteria for PGAS Type II (association of autoimmune endocrine disease with at least one other--usually endocrine--autoimmune disease or autoantibodies against another organ). Among these patients, 18 had hypothyroidism due to autoimmune thyroiditis, 8 were hyperthyroid (Graves' disease), and 4 had silent autoimmune thyroiditis (without thyroid dysfunction). Insulin dependent (type I) diabetes mellitus (IDDM) was seen in 11, Addison's disease in 7, primary hypogonadism in 5, vitiligo in 6 and pernicious anemia in 5 cases. The presence of antiparietal cell antibodies was demonstrated in 21 of 30 investigated patients. These patients also showed other evidence of autoimmune gastritis, such as increased gastrin (in 10 out of 13), diminished vitamin B12 levels (6 out of 13), atrophic gastritis (9 out of 9), pernicious anemia (6 out of 30) and funicular myelosis (2 out of 30). CONCLUSION: The most common endocrine diseases in our patient group were autoimmune thyroid diseases (97%) followed by IDDM (35%) and Addison's disease (23%). A high percentage (70%) of our subjects had elevated titers of antiparietal cell antibodies. Polyglandular autoimmune syndrome must be suspected in all patients with autoimmune endocrine disease, especially in the presence of relatives suffering from PGAS. Patients at risk should be screened regularly by measuring thyrotropin (ultrasensitive assay), fasting blood glucose levels, and by checking red blood count and antiparietal cell antibodies.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗