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PubMed2003

Genetic underpinnings of autoimmunity--lessons from studies in arthritis, diabetes, lupus and multiple sclerosis.

Autoimmunity has been studied for more than four decades, but its genetic origins have remained a mystery. The recent past has witnessed an exponential growth in our understanding of autoimmunity resulting from both forward and reverse genetic approaches. More than 40 genes have been shown to precipitate systemic autoimmunity when genetically manipulated. In addition, reverse genetic studies in various autoimmune diseases have successfully guided researchers to specific locations on the genome that are associated with disease susceptibility. Buried within these genomic intervals lies a further treasure chest of autoimmunity genes. Efforts to unmask these culprit genes have yielded the very first clues about how an elaborate cast of players may be at work to orchestrate autoimmunity.

Arthritis↗

PubMed2004

A fourfold difference in the incidence of type 1 diabetes between Sweden and Lithuania but similar prevalence of autoimmunity.

We investigated whether other autoimmune disorders in addition to type 1 diabetes are more common in Sweden than Lithuania, and if there are any differences in inheritance patterns of both type 1 diabetes and other autoimmune disorders. Data from 517 children in southeast Sweden and 286 children in Lithuania aged 0-15 years were included in the study. Age- and sex-matched control children were randomly selected. Information was collected by questionnaire. Of the children with diabetes in Sweden, 13.2% had a family member with type 1 diabetes compared to 7% of children with diabetes in Lithuania (P < 0.01) (OR = 2.01). No such difference was seen for other autoimmune diseases in family members of children with diabetes (Sweden 12%, Lithuania 14%, n.s.). Control children in Lithuania had family members with autoimmunity more frequently (15.3%) than control children in Sweden (7.4%, P < 0.001) (OR = 2.26). This difference was most pronounced in mothers. The Lithuanian control children had an autoimmune disease more frequently than the controls in Sweden (4.7% versus 1.5%, respectively, P < 0.001) (OR = 3.21). There seem to be environmental factors that specifically contribute to the development of type 1 diabetes, factors which are less related to the development of autoimmunity in general.

Adolescent↗

PubMed2004

Overlap syndrome of primary biliary cirrhosis and autoimmune hepatitis with unusual initial presentation as fulminant hepatic failure.

Autoimmune hepatitis and primary biliary cirrhosis are generally easy to discriminate on the basis of clinical, laboratory, and histological findings. The presence of anti-mitocondrial antibodies seropositivity and cholestatic clinical, laboratory, and/or histological features in patients with autoimmune hepatitis indicates the overlap syndrome of autoimmune hepatitis and primary biliary cirrhosis. Fulminant hepatic failure is an unusual initial form of presentation of autoimmune hepatitis and primary biliary cirrhosis overlap syndrome. We report the case of a 50-year-old woman with autoimmune hepatitis and primary biliary cirrhosis overlap syndrome who presented with fulminant hepatic failure. Fulminant hepatic failure has a high mortality rate and may require liver transplant. Our patient revealed a good response to corticosteroid and ursodeoxycholic acid therapy. It is important to identify and distinguish autoimmune hepatitis and variant syndromes from other forms of liver disease because of response to corticosteroid therapy.

Cholagogues and Choleretics↗

PubMed2004

Frontal cortical perfusion abnormalities related to gluten intake and associated autoimmune disease in adult coeliac disease: 99mTc-ECD brain SPECT study.

OBJECTIVE: Since brain perfusion abnormalities have been described by single-photon emission computed tomography in some autoimmune diseases, the aim of the present study was to evaluate the incidence of perfusion abnormalities by brain single-photon emission computed tomography in a group of coeliac disease patients, and to investigate whether gluten intake and associated autoimmune diseases may be considered risk factors in causing cerebral impairment. METHODS: Thirty-four adult coeliac patients (16 on a gluten-free diet and 18 on a gluten-containing diet, 18 (53%) with autoimmune diseases) underwent 99mTc-ethyl cysteinate dimer brain single-photon emission computed tomography and qualitative evaluation of brain perfusion was performed together with a semiquantitative estimation using the asymmetry index. Ten subjects on our database, matched for sex, age and ethnic group, who were proved normal by histology ofjejunal mucosa (four males and six females; median age 39 years, range 27-55 years), were included as control group. RESULTS: Twenty-four out of 34 patients (71%) showed brain single-photon emission computed tomography abnormalities confirmed by abnormal regional asymmetry index (>5%; range 5.8-18.5%). Topographic comparison of the brain areas showed that the more significant abnormalities were localised in frontal regions, and were significantly different from controls only in coeliac disease patients on unrestricted diet. The prevalence of single-photon emission computed tomography abnormalities was similar in coeliac disease patients with (74%) and without (69%) associated autoimmune disease. CONCLUSIONS: Abnormalities of brain perfusion seem common in coeliac disease. This phenomenon is similar to that previously described in other autoimmune diseases, but does not appear to be related to associated autoimmunity and, at least in the frontal region, may be improved by a gluten-free diet.

Adult↗

PubMed2004

Autoimmune pancreatitis.

Autoimmune pancreatitis is a type of idiopathic pancreatitis. It is also referred to as sclerosing pancreatitis, lymphoplasmatocytic sclerosing pancreatitis, chronic pancreatitis with irregular stenosis of the main pancreatic duct and as sclerosing pancreatocholangitis. Clinical characteristics of autoimmune pancreatitis are jaundice, abdominal pain, weight loss and diabetes mellitus. Radiologically, there is diffuse enlargement of pancreas with stenosis of pancreatic duct without calcifications in the pancreatic parenchyma. In autoimmune pancreatitis, antibodies against lactoferrin and carbonic anhydrase have been detected, but they are not specific because they are present in some other autoimmune diseases too. Also in autoimmune pancreatitis, there are increased levels of gammaglobulins and characteristically high titres of IgG4, which are a subtype of IgG. Autoimmune pancreatitis is usually treated successfully by prednisolone.

Antibody Formation↗

PubMed2005

Spontaneous scratching behavior in MRL/lpr mice, a possible model for pruritus in autoimmune diseases, and antipruritic activity of a novel kappa-opioid receptor agonist nalfurafine hydrochloride.

Pruritus is a common, distressing and difficult to manage complication of many autoimmune diseases. A suitable animal model of autoimmune disease associated pruritus would contribute to a better understanding of the pathophysiology of this symptom and lead to the development of safe and effective antipruritic agents. We noticed spontaneous scratching behavior in aged MRL/lpr mice, a model of autoimmune disease. This scratching behavior was observed in a specific pathogen-free environment and was more frequent in female mice. In contrast to animal models of dermatitis; NC/Nga mice, the serum IgE and IgG1 levels in MRL/lpr mice were not elevated. These features indicate that this scratching behavior is similar to human autoimmune disease associated pruritus. The antipruritic effects of an antihistamine (chlorpheniramine), an opioid receptor antagonist (naltrexone), and a novel kappa-opioid receptor agonist (nalfurafine hydrochloride [TRK-820]) were evaluated. The frequency of scratching was not reduced by oral administration of chlorpheniramine, suggesting that the behavior is antihistamine-resistant. The oral administration of nalfurafine and subcutaneously administered naltrexone inhibited the scratching behavior without causing gross behavioral changes. In conclusion, MRL/lpr mice scratching behavior is a suitable model of pruritus that occurs in autoimmune diseases, and nalfurafine was shown to be efficacious against this behavior suggesting that it may be beneficial in patients with autoimmune disease associated pruritus.

Age Factors↗

PubMed2004

Increased incidence of autoimmune disorders as a late complication in children with early onset dermatitis and/or milk allergy.

Subjects with atopic dermatitis and autoimmune disorders share some similar immune response disorders. The aim of this study was to see whether subjects with early onset atopic dermatitis run a risk of eventually developing autoimmune diseases. The results of a questionnaire of 145 adolescents (70 f, 75 m, mean age 18.2 years, range 16-23 years) was compared with those of a group of 262 controls (112 f, 150 m, mean age 17.5 years, range 16-21 years), 164 of whom reported no atopic symptoms and were treated as a separate group for statistical analysis. As compared with the non-atopic controls, the study group subjects showed a significantly increased incidence of autoimmune disorders (9% vs. 1%), the relative risk ratio of a subject with infantile onset atopic eczema getting a gastrointestinal (GI) immune-mediated disease being 2.4 (CI(95)2.1-2.8) and of getting some other autoimmune disorder 3.1 (CI(95)2.8-9.7). The positive skin prick tests showed a negative association with the manifestation of a GI or other autoimmune disorder. The subjects with infantile dermatitis also reported recurrent abdominal pains (23% vs. 15%), and milk-induced gastrointestinal symptoms (19% vs. 10%) significantly more even as young adults than the controls. Our study showed that infantile atopy increases a predisposition to autoimmune disorders, suggesting that these two entities might have a common immunological determinant. While a high incidence of chronic GI complaints among the study subjects suggests the ongoing activity of local immune responses. However, more detailed prospective studies are needed to confirm these observations.

Adolescent↗

PubMed2006

Genetic variations in ZFP36 and their possible relationship to autoimmune diseases.

The ZFP36 gene codes for TTP, a regulator of TNF alpha. In mice, TTP deficiency results in a systemic autoimmune inflammatory syndrome with severe arthritis. We hypothesized that genetic variations in ZFP36 are associated with autoimmune disease in humans. The primary objective of this study was to identify human ZFP36 genetic variants in autoimmune disease cases and controls, determine their frequencies in a general clinic population, and construct haplotypes. We resequenced ZFP36 in 316 individuals with autoimmune diseases and identified 28 polymorphisms and determined the frequency of all the known ZFP36 polymorphisms in 484 participants of the Environmental Polymorphism Registry, a regional registry being conducted by the NIEHS. Based on the sequence-verified ZFP36 genotypes, 34 haplotypes were constructed. As a secondary objective, we examined autoimmune disease cases and controls for potential ZFP36 genetic associations. One novel polymorphism, ZFP36*8, a C to T transition in the protein coding domain, was significantly associated with rheumatoid arthritis (RA) in African-Americans (RR=1.23, 95% CI: 1.11-1.36). The data presented here suggest a tentative association between ZFP36 and RA. This finding, as well as the ZFP36 polymorphisms and haplotypes identified here, should form the basis for future association studies in autoimmune diseases.

Adult↗

PubMed2005

Regulatory T-cells and autoimmunity.

Approximately 20% of the population is affected by autoimmune or inflammatory diseases mediated by an abnormal immune response. A characteristic feature of autoimmune disease is the selective targeting of a single cell type, organ or tissue by certain populations of autoreactive T-cells. Examples of such diseases include rheumatoid arthritis, insulin-dependent diabetes mellitus, and systemic lupus erythematosus (SLE), all of which are characterized by chronic inflammation, tissue destruction and target organ malfunction. Although strong evidence links most autoimmune diseases to specific genes, considerable controversy prevails regarding the role of regulatory T-cell populations in the disease process. These cells are now also believed to play a key role in mediating transplantation tolerance and inhibiting the induction of tumor immunity. Though the concept of therapeutic immune regulation aimed at treating autoimmune pathology has been validated in many animal models, the development of strategies for the treatment of human autoimmune disorders remains in its infancy. The main obstacles to this include the conflicting findings of different model systems, as well as the contrasting functions of regulatory T-cells and cytokines involved in the development of such disorders. This review examines the role of regulatory T-cells in the pathogenesis of autoimmunity and describes the therapeutic potential of these cells for the prevention of immune-mediated pathologies in the future. Although much remains to be learned about such pathologies, a clearer understanding of the mechanisms by which regulatory T-cells function will undoubtedly lead to exciting new possibilities for immunotherapeutics.

Animals↗

PubMed2006

Endometriosis associated with defective handling of apoptotic cells in the female genital tract is a major cause of autoimmune disease in women.

Several autoimmune diseases are far more common in women than men. The reasons are unknown. Recent studies have shown that many autoimmune diseases which predominantly affect females are characterized by the production of autoantibodies against components of apoptotic cells. Furthermore, in experimental animals, defective clearance of apoptotic cells in a pro-oxidant inflammatory environment can trigger the production of these autoantibodies and related autoimmune disease. Endometriosis is characterized by defective clearance of apoptotic endometrial cells in a pro-oxidant inflammatory environment. It is proposed that this combination of abnormalities triggers autoantibody production in women affected by endometriosis. A proportion of these women will be genetically predisposed to develop overt autoimmune disease. As endometriosis affects at least 4% of the female population of reproductive age, this phenomenon will have a major effect on the gender prevalence of several related autoimmune syndromes. The hypothesis is supported by epidemiological studies which show a strong association between endometriosis and female-predominant autoimmune disorders.

Apoptosis↗

PubMed2004

Innate and adaptive immune requirements for induction of autoimmune demyelinating disease by molecular mimicry.

Molecular mimicry is the main postulated mechanism by which infectious agents induce autoimmune disease. A number of animal models have been utilized to establish a link between molecular mimicry and autoimmunity. However, a model of infectious disease whereby a natural pathogen expressing a known mimic epitope can induce autoimmunity to a known self-antigen leading to clinical autoimmune disease is still lacking. We have engineered a recombinant Theiler's murine encephalomyelitis virus (TMEV) to express an encephalitogenic myelin proteolipid protein PLP139-151 epitope (PLP-TMEV) and a PLP139-151 mimic peptide naturally expressed by Haemophilus influenzae (HI-TMEV). Infection of mice with either PLP-TMEV or HI-TMEV induces early-onset disease that is associated with the activation of cross-reactive PLP139-151-specific immunopathologic CD4+ Th1 cells. Based on results from this model, we hypothesize, due to the considerable degeneracy in the T cell repertoire, that induction of full-blown autoimmune disease via molecular mimicry is a tightly regulated process requiring multiple factors related to the pathogen expressing the potential mimic epitope. In this review, we will discuss how various factors related to the infectious environment control whether or not autoimmune disease is initiated. Contributing factors include the nature of the innate immune response to the pathogen which determines the immunopathologic potential of the induced cross-reactive T cells, the capacity of the mimic epitope to be processed and presented from its natural flanking sequences in the pathogen-encoded protein, the site(s) of the primary infection in the host and the ability of the pathogen to persist, and the potential requirement for multiple infections with the same or different pathogens.

Animals↗

PubMed2006

[Hepatitis C-autoimmune hepatitis overlap syndrome: five new cases].

PURPOSE: The hepatitis C-Autoimmune hepatitis overlap syndrome is an uncommon condition whose management can be difficult in both diagnosis and treatment. PATIENTS AND METHODS: Five cases of hepatitis C and autoimmune hepatitis overlap syndrome, brought by a retrospective study, are reported. Hepatitis C was proven by a positive HCV viral load and the autoimmune hepatitis was proven by characteristic immunological and/or histological features. RESULTS: All patients were female, the mean age at diagnosis was 54.2 years (+/-6.6), only one patient had a history of autoimmune disease (autoimmune thyroiditis). Four patients had significant autoantibodies levels (over 1/320) and 4 had a high serum gammaglobulin level (over 1.5 times the upper normal limit). Liver biopsy showed characteristic features of autoimmune hepatitis in all cases and characteristic features of chronic HCV infection in 3 cases. Corticosteroid and/or immunosuppressive treatment was given as a first line therapy in 4 cases while an antiviral treatment has been tried in 4 cases with a good viral response in 2 of them. Corticosteroid and/or immunosuppressive treatment enhanced HCV viral load in all cases, however a histological improvement was observed in every case in which a control biopsy has been performed (3 cases). CONCLUSION: This study highlights the deciding contribution of the initial histological findings in the diagnosis of such a HCV/autoimmune hepatitis overlap syndrome; it also demonstrates that histological outcome is not necessarily compromised by corticosteroid and/or immunosuppressive treatment.

Adrenal Cortex Hormones↗

PubMed2004

Idiopathic chronic cough and organ-specific autoimmune diseases: a case-control study.

The marked female predominance in cases of idiopathic chronic cough and its association with mild chronic lymphocytic airway inflammation suggests an underlying autoimmune process. We set out to test the hypothesis that idiopathic chronic cough is associated with other organ-specific autoimmune diseases in a case control study. Twenty-two patients with idiopathic chronic cough and 65 community-matched controls for age and sex who responded to a self-administered questionnaire were asked about the presence of autoimmune disease, other medical problems and drug history. All subjects were invited to have a blood test for an autoimmune screen. Thirteen out of 22 (59%) patients with idiopathic chronic cough and eight out of 65 (12%) age- and sex-matched controls reported organ-specific autoimmune disease (odds ratio 8.8; 95% confidence interval 2.4-31.8, P<0.001). Organ-specific autoantibodies were present in a significantly higher proportion of cases than controls (40% vs. 13%; P = 0.047). These findings suggest a relationship between idiopathic chronic cough and organ-specific autoimmunity.

Adult↗

PubMed2005

Mercury and autoimmunity: implications for occupational and environmental health.

Mercury (Hg) has long been recognized as a neurotoxicant; however, recent work in animal models has implicated Hg as an immunotoxicant. In particular, Hg has been shown to induce autoimmune disease in susceptible animals with effects including overproduction of specific autoantibodies and pathophysiologic signs of lupus-like disease. However, these effects are only observed at high doses of Hg that are above the levels to which humans would be exposed through contaminated fish consumption. While there is presently no evidence to suggest that Hg induces frank autoimmune disease in humans, a recent epidemiological study has demonstrated a link between occupational Hg exposure and lupus. In our studies, we have tested the hypothesis that Hg does not cause autoimmune disease directly, but rather that it may interact with triggering events, such as genetic predisposition, exposure to antigens, or infection, to exacerbate disease. Treatment of mice that are not susceptible to Hg-induced autoimmune disease with very low doses and short term exposures of inorganic Hg (20-200 microg/kg) exacerbates disease and accelerates mortality in the graft versus host disease model of chronic lupus in C57Bl/6 x DBA/2 mice. Furthermore, low dose Hg exposure increases the severity and prevalence of experimental autoimmune myocarditis (induced by immunization with cardiac myosin peptide in adjuvant) in A/J mice. To test our hypothesis further, we examined sera from Amazonian populations exposed to Hg through small-scale gold mining, with and without current or past malaria infection. We found significantly increased prevalence of antinuclear and antinucleolar antibodies and a positive interaction between Hg and malaria. These results suggest a new model for Hg immunotoxicity, as a co-factor in autoimmune disease, increasing the risks and severity of clinical disease in the presence of other triggering events, either genetic or acquired.

Animals↗

PubMed2004

Short- and long-term effects of T-cell modulating agents in experimental autoimmunity.

Due to the easy and reliable induction of a disease condition with many of the features present in human autoimmunity, mercury-induced autoimmunity (mHgAI) in rodents is a favourable autoimmune model. Genetically susceptible (H-2(s)) mice develop in response to mercury (Hg) a systemic autoimmune condition with antinucleolar antibodies (ANoA) targeting the protein fibrillarin, transient polyclonal B-cell activation, hyperimmunoglobulinemia, and systemic immune-complex (IC) deposits. In order to study the short- and long-term effects of treatment with immunomodulating agents on the disease parameters in HgAI, groups of B10.S (H-2(s)) mice were given 6 mg HgCl(2)/l drinking water for 22 weeks. Three weeks initial treatment with cyclosporin A (CyA), a high dose of tacrolimus (HD tacrolimus), or anti-CD4 monoclonal antibody (a-CD4) inhibited induction of ANoA and IC deposit by Hg. This effect persisted for the subsequent 19 weeks when the mice were only treated with Hg. Initial treatment with anti-IL-4 monoclonal antibody (a-IL-4) for 3 weeks inhibited induction of IgE and IC deposits by Hg, but not ANoA. However, subsequent treatment with Hg without a-IL-4 for 19 weeks induced IC deposits. The T-cell modulating agents aggravated some of the HgAI disease parameters: a-CD4 stimulated the polyclonal B-cell activation, a-IL-4 increased the IgG antichromatin antibody response, and a low dose of tacrolimus (LD tacrolimus) enhanced the ANoA, the polyclonal B-cell activation, and the IC deposits. We conclude that a short initial treatment with a-CD4 or CyA efficiently protects against induction of systemic autoimmunity for an extended period of time. However, some of the T-cell modulating agents, especially a low dose of tacrolimus, aggravate autoimmune manifestations not only during ongoing treatment, but also after treatment with these agents has ceased.

Adjuvants, Immunologic↗

PubMed1999

Opposite beta2-glycoprotein I requirement for the binding of infectious and autoimmune antiphospholipid antibodies to cardiolipin liposomes is associated with antibody avidity.

The aim of this study was to investigate the interaction of antiphospholipid antibodies (aPL) from two different populations (patients with autoimmune or infectious disorders) with cardiolipin (CL) arranged in a defined bilayer. beta2-Glycoprotein I (beta2GPI), an apolipoprotein that plays a critical role in the aPL binding to phospholipids, was quantified by dot blot in purified IgG-aPL samples, further classified according to apparent avidity to CL. In solid-phase assays, beta2GPI increased, preferentially, the binding of low-avidity autoimmune aPL to CL but inhibited the binding of low-avidity syphilitic aPL. In the absence of beta2GPI, both autoimmune and infectious aPL induced the leakage of the entrapped fluorescent probe, carboxyfluorescein (CF), from small unilamellar vesicles containing CL. aPL-induced probe leakage was protein concentration-dependent and characterized by a lag-phase onset of 100-120 min. beta2GPI increased the leakage rate induced by low-avidity autoimmune aPL only and inhibited the leakage induced by all syphilitic aPL. The following conclusions were provided: (1) in the absence of beta2GPI, autoimmune and infectious aPL bind to CL in a bilayer, inducing liposome leakage; (2) the leakage mechanism induced by aPL is suggested to be intravesicular; (3) beta2GPI requirement for phospholipid binding in both solid and fluid phase is associated to aPL avidity; (4) CL alone or the CL-beta2GPI complex are the most likely epitopes for autoimmune aPL; (5) aPL from syphilis patients can only form the CL-aPL complex, supporting that beta2GPI is not (part of) the target epitope.

Antibodies, Anticardiolipin↗

PubMed1993

Premature ovarian failure--the prognostic application of autoimmunity on conception after ovulation induction.

OBJECTIVE: To assess whether the presence of autoimmune activity in patients with premature ovarian failure (POF) can predict the response to ovulation induction and conception. DESIGN: Assessment of autoimmune activity in patients with POF, correlating the response to ovulation induction with this autoreactivity. SETTING: Tertiary care academic center. PATIENTS: Forty women with POF, 15 of them treated by ovulation induction because of infertility. INTERVENTIONS: All patients were tested for the presence of autoimmune activity, antibodies against various tissues, and 15 of them were treated with combinations of hMG/hCG, glucocorticosteroids as immunosuppressant, and some of them also with a long-acting GnRH agonist. Those patients not interested in infertility were put on hormone replacement therapy (HRT). MAIN OUTCOME MEASURES: Serum E2 and P were measured during ovulation induction as well as follicular diameter monitoring by transvaginal sonography. Achievement of gestations and their outcome were monitored in the group in which ovulation induction was accomplished. RESULTS: Antibodies against thyroglobulin, nuclear antigens, heart, tissue gluten, or increased levels of immunoglobulin (Ig)M, or decreased levels of complement C3 and C4 were significantly different in the patients with POF than in the control population. Autoreactivity of at least one class of the tested antibodies was found in 31 of 40 patients (77%). In 15 patients with autoimmune activity who have undergone ovulation induction using hMG/hCG, 14 pregnancies were achieved in 8 patients. Two of the pregnancies were spontaneous, and 12 were generated by hMG/hCG and fluocortolone, with or without pretreatment with GnRH-a. Twelve healthy babies were generated by 10 gestations, 3 ended in spontaneous abortions (23%), and 1 is ongoing. All the nonspontaneous pregnancies were achieved in the first three cycles of ovulation induction. CONCLUSIONS: Patients with POF and autoimmune activity, suggesting an autoimmune etiology to the ovarian failure, may respond to ovulation induction and have a conception rate of approximately 40% in three cycles. Those who do not conceive in three treatment cycles have a very low probability to conceive; therefore, further attempts of ovulation induction should be discouraged. However, some patients may spontaneously conceive in association with HRT.

Adult↗

PubMed2004

EUS findings in patients with autoimmune pancreatitis.

BACKGROUND: Autoimmune pancreatitis is an increasingly recognized benign condition with a presentation similar to pancreatic neoplasia but responds to corticosteroid therapy. Clinical features, ERCP, and CT findings have been described. This study assessed the EUS and EUS-guided FNA features of proven autoimmune pancreatitis. METHODS: The diagnosis of autoimmune pancreatitis was based on examination of surgical resection specimens or typical clinical findings (elevated immunoglobulin G level, no evidence of malignancy, characteristic non-EUS imaging studies, and clinical improvement, especially in response to treatment with a corticosteroid). RESULTS: Presenting manifestations in 14 patients included obstructive jaundice, abdominal pain, and weight loss. Ten patients underwent surgery (including exploratory surgery). Six were successfully treated with corticosteroid. EUS revealed diffuse hypoechoic pancreatic enlargement (8/14) or a focal irregular hypoechoic mass (6/14). Features of chronic pancreatitis were not noted. EUS-guided FNA of the pancreas was suggestive of chronic inflammatory pancreatitis in 9 of 12 patients. Celiac and peripancreatic lymphadenopathy (up to 3 cm in diameter) was present in 6 patients. EUS-guided FNA of lymph nodes (3/4) did not reveal evidence of malignancy. Vascular involvement was noted in 3 patients. CONCLUSIONS: The EUS features of autoimmune pancreatitis are easily mistaken for malignancy. However, a diffusely hypoechoic, enlarged pancreas, together with chronic inflammatory cells in aspirated cytologic specimens, is supportive of the diagnosis of autoimmune pancreatitis. When combined with clinical data, EUS and EUS-guided FNA may support a diagnosis of autoimmune pancreatitis, may warrant a trial of corticosteroid, and thereby may prevent unnecessary surgery.

Adolescent↗