Non-endocrine Autoimmune Diseases Research Articles

Interleukin (IL)-23, IL-31, and IL-33 Play a Role in the Course of Autoimmune Endocrine Diseases.

Interleukins (IL)-23, 31, and 33 are involved in the regulation of T helper 17 (Th17)/regulatory T (Treg) cells balance. The role of IL-23, 31 and 33 in non-endocrine autoimmune diseases has been confirmed. Data on the involvement of these cytokines in endocrine autoimmune diseases are limited. This study aimed to determine the involvement of cytokines regulating the T helper 17 (Th17)/regulatory T (Treg) cells axis in the course of autoimmune endocrine diseases. A total number of 80 participants were divided into 4 groups: the autoimmune polyendocrine syndrome (APS) group consisting of APS type 2 (APS-2) and type 3 (APS-3) subgroups, the Hashimoto's thyroiditis (HT) group, the Graves' disease (GD) group and the control (C) group. Fifteen cytokines related to Th17 and Treg lymphocytes were determined in the serum of all participants. Higher levels of IL-23 and IL-31 were found in the APS, GD, and HT groups compared to the C group. Higher levels of IL-23 and IL-31 were also observed in the APS-2 group, in contrast to the APS-3 group. Correlation analysis of variables in the groups showed a statistically significant correlation between the cytokines IL-23, IL-31, and IL-33 in the APS and APS-2 groups, but no correlation in the APS-3 and C groups. IL-23 and IL-31 are independent factors in the course of HT, GD, and APS-2, in contrast to APS-3. The positive correlation between IL-23 and IL-31, IL-23 and IL-33, and between IL-31 and IL-33 in the APS, APS-2 groups, but the lack of correlation in the APS-3 and C groups may further suggest the involvement of these cytokines in the course of Addison's disease.

Evans Syndrome in a Patient with Auto Immune Thyroiditis – A Rare Association

A 46-year-old woman, diagnosed with hypothyroidism, was on treatment with synthetic thyroxine 100 micrograms per day for one year. She complained of recent-onset exertional dyspnoea, and had malaise, lethargy, and pica. Investigations revealed significant anaemia and severe thrombocytopenia, necessitating blood transfusion. She had Coombs-positive autoimmune haemolytic anaemia and immune thrombocytopenic purpura, confirming a diagnosis of Evans syndrome. She also had a positive antinuclear antibody test but had no other notable findings of autoimmune disease, suggesting a diagnosis of primary Evans syndrome. The patient was treated with intravenous dexamethasone for four days, followed by oral prednisolone at 1mg/kg/ day, with supplemental calcium and vitamin D. Thyroperoxidase antibody was positive and there was reduced uptake in thyroid scintigraphy, confirming a diagnosis of autoimmune thyroiditis. Hashimoto’s thyroiditis frequently coexists with non-endocrine autoimmune disorders. Presence of antithyroid antibodies is sometimes observed in Evans syndrome, a condition where there is simultaneous occurrence of autoimmune Haemolytic Anaemia, Cytopoenia and immune thrombocytopenic purpura. However, the development of Evans syndrome in patients with overt hypothyroidism and Hashimoto’s thyroiditis is rare. This case implies the potential existence of a shared immunogenetic pathway among three distinct autoimmune diseases, namely autoimmune haemolytic anemia, immune thrombocytopenic purpura, and Hashimoto’s thyroiditis, in the pathogenesis.

ODP273 Schmidt Syndrome Causing Multiorgan Failure

Abstract Introduction To our knowledge there has not been a case report published on the acute presentation of Schmidt syndrome (Polyglandular Autoimmune Syndrome Type 2) in which all three manifestations of type 1 diabetes mellitus (T1DM), primary adrenal insufficiency, and hypothyroidism were found and diagnosed at the same time. Case Description A 32-year-old male with suspected alcohol abuse presented to the hospital with nausea, vomiting, and weakness of two weeks duration after sustaining a fall. He was admitted for Diabetic Ketoacidosis (DKA) and shock requiring three pressors with unclear etiology. Labs were significant for severe hyponatremia of 113 mmol/L (136-145), elevated anion gap of 22, glucose 206 mg/dL (70-100), bicarbonate 11mmol/L (21-31), beta hydroxybutyrate 5.90 mmol/L (0. 0-0.42), and pH 7.22 (7.35-7.45) with Hemoglobin A1c 14.5% (<5.7). An insulin drip was instituted for DKA and the hyponatremia persisted. Cortisol was found to be suppressed at 3. 0 ug/dL (3.1-22.4) with significantly elevated ACTH 220.4 pg/mL (7.2-63.3) suggesting a new diagnosis of primary adrenal insufficiency. IV hydrocortisone 100 mg q8H was started on day 2 of hospitalization. Thyroid labs showed elevated TSH 10.10 uIU/mL (0.36-3.74) confirming hypothyroidism, prompting initiation of IV levothyroxine. His hospital course was complicated by cardiac arrest and acute respiratory failure requiring intubation. Cardiac work up was negative except for severe non-ischemic cardiomyopathy with significantly reduced ejection fraction of 20-25%. Bronchoscopy was performed and showed no evidence of obstructing pulmonary etiologies. SARS Coronavirus PCR was negative. He also had shock liver along with Disseminated intravascular coagulation (DIC). His kidney function worsened requiring continuous kidney replacement therapy (CRRT). Urine microscopy showed granular casts consistent with acute tubular necrosis. TPO antibodies, adrenal antibodies, GAD antibodies, and Zinc Transporter 8 antibodies all came back positive along with an undetectable C- peptide confirming the diagnosis of Hashimotos hypothyroidism, primary adrenal insufficiency, and T1DM respectively. He was eventually discharged on basal bolus insulin regimen, levothyroxine 75 mcg po daily, fludrocortisone 0. 05 mg po daily, and prednisone 5 mg po daily. The patient had multifactorial shock from an acute presentation of DKA, primary adrenal insufficiency, and hypothyroidism all presenting simultaneously. Conclusion This case illustrates the severe impact of having three endocrine organs affected all at once. The prevalence of Schmidt syndrome is very low at 1: 20,000 in the general population and can be associated with other non-endocrine autoimmune disorders. Prevalence of autoimmune thyroid disease is 70%, T1DM 50%, and Addison's disease is almost 100%. Due to the low prevalence, one needs a high clinical suspicion with the correct lab findings to diagnose this disease. Incorrect diagnoses or a late diagnosis can lead to life threatening consequences to the patient. The mainstay of treatment is hormone replacement, with corticosteroids given before thyroid replacement. Presentation: No date and time listed

Intestinal barrier permeability in patients with hashimoto's thyroiditis associated to non-endocrine autoimmune disorders

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Generation and Characterization of iPS Cells Derived from APECED Patients for Gene Correction.

APECED (Autoimmune-Polyendocrinopathy-Candidiasis-Ectodermal-Dystrophy) is a severe and incurable multiorgan autoimmune disease caused by mutations in the AIRE (autoimmune regulator) gene. Without functional AIRE, the development of central and peripheral immune tolerance is severely impaired allowing the accumulation of autoreactive immune cells in the periphery. This leads to multiple endocrine and non-endocrine autoimmune disorders and mucocutaneous candidiasis in APECED patients. Recent studies have suggested that AIRE also has novel functions in stem cells and contributes to the regulatory network of pluripotency. In preparation of therapeutic gene correction, we generated and assessed patient blood cell-derived iPSCs, potentially suitable for cell therapy in APECED. Here, we describe APECED-patient derived iPSCs’s properties, expression of AIRE as well as classical stem cell markers by qPCR and immunocytochemistry. We further generated self-aggregated EBs of the iPSCs. We show that APECED patient-derived iPSCs and EBs do not have any major proliferative or apoptotic defects and that they express all the classical pluripotency markers similarly to healthy person iPSCs. The results suggest that the common AIRE R257X truncation mutation does not affect stem cell properties and that APECED iPSCs can be propagated in vitro and used for subsequent gene-correction. This first study on APECED patient-derived iPSCs validates their pluripotency and confirms their ability for differentiation and potential therapeutic use.

Screening of Organ-Specific Autoantibodies in a Large Cohort of Patients with Autoimmune Thyroid Diseases

Background: Autoimmune diseases tend to cluster in the same individual or in families. Four types of autoimmune polyglandular syndromes (APS) have been described based on the combination of endocrine and/or non-endocrine autoimmune diseases. In particular, type-3 APS is defined by the association of an autoimmune thyroid disease (ATD) and other autoimmune diseases and has a multifactorial etiology. The natural history of autoimmune diseases is characterized by three stages: potential, subclinical, and clinical. Methods: To determine the prevalence of organ-specific autoantibodies (anti-adrenal, anti-ovary [StCA], anti-pituitary [APA], anti-parietal cells [PCA], anti-tissue transglutaminase [tTGAb], anti-mitochondrial [AMA], anti-glutamic acid decarboxylase [GADA], anti-nicotinic acetylcholine receptor) in patients with ATD and to define the stage of the disease in patients with positive autoantibodies. From January 2016 to November 2018, 1502 patients (1302 female; age 52.7 ± 14.7 [mean ± standard deviation] years, range 18-86 years) with ATD (1285/1502 [85.6%] with chronic autoimmune thyroiditis and 217/1502 [14.4%] with Graves' disease) were prospectively enrolled. Results: The most common organ-specific autoantibodies were PCA (6.99%) and GADA (2.83%), while the prevalence of the remaining autoantibodies was ≤1%. All autoimmune diseases, but celiac disease, were predominant at the potential stage. Sex, ATD type, smoking habit, and coexistence of other autoimmune diseases correlated with the susceptibility to develop chronic atrophic gastritis (CAG) or autoimmune diabetes mellitus. Conclusions: The association between ATD and CAG was the most common manifestation of type-3 APS, mainly at the potential stage, that could lead to appropriate follow-up for early detection and timely treatment of the disease.

Schmidt’s Syndrome Presenting as Diabetic Ketoacidosis and Adrenal Crisis: A Case Report and Review of Literature

Introduction: Schmidt’s Syndrome, is a rare endocrine disorder defined by the combined occurrence of Addison disease, autoimmune thyroid disease, and type 1 diabetes mellitus. The rarity of the condition and the presentation of adrenal insufficiency and hypothyroidism often lead to misdiagnosis with life-threatening consequences for the patients. We report a case presenting with adrenal insufficiency and diabetic ketoacidosis who was diagnosed with Schmidt’s Syndrome. Case Description: We describe the case of a 38-year-old male with a past medical history of hypothyroidism, who was admitted for worsening abdominal pain, nausea, vomiting, fevers, and chills. Physical exam revealed underweight male with marked dehydration, diaphoresis, in moderate abdominal pain. Initial vital signs and laboratory panel raised suspicion for adrenal insufficiency and diabetic ketoacidosis. Blood pressure 82/42mmHg, HR of 121, sodium 128mmol/L, potassium 6.8mmol/L, chloride 104mmol/L, bicarbonate 5mmol/L, BUN 20mg/dl, Creatinine 1.5mg/dl, Glucose 402mg/dl, TSH 60, and serum osmolality 319mosm/kg. The electrolyte derangements and vital signs improved after the initiation of the high-dose steroids and insulin. The patient was transitioned to a regimen of hydrocortisone/ fludrocortisone, levothyroxine, and insulin basal/bolus and was discharged in clinically stable conditions to follow up with an endocrinologist. Discussion: The prevalence of Schmidt’s syndrome is 1:20,000 in the general population and a 3:1 ratio of females to males. Autoimmune thyroid disease is present in 70–75%, T1DM in 40–60%, and Addison’s disease in 40–50%. This syndrome can be associated with other non-endocrine autoimmune disorders, such as vitiligo, myasthenia gravis, Sjogren’s syndrome, rheumatoid arthritis, and primary antiphospholipid syndrome. The initial step in diagnosis should be checking serum morning cortisol levels to identify adrenal insufficiency. Autoimmune antibodies play an important role to confirm the diagnosis including 21-hydroxylase, 17-hydroxylase, thyroid peroxidase, glutamic acid decarboxylase, islet cells, anti-tissue transglutaminase antibodies, parietal cell, and anti-intrinsic factor antibodies. Currently, treatment is limited to hormone replacement in patients with organ failure. But it is crucial to replace corticosteroids before starting thyroid replacement in patients with adrenal insufficiency. Conclusion: A high level of diagnostic suspicion is required for the diagnosis of Schmidt’s syndrome when encountering a patient with autoimmune disease. The diagnosis of this syndrome is often delayed, causing adverse events. With this case presentation, we add to the data pool of Schmidt’s syndrome with the ability to significantly improve patients outcomes with early diagnosis and hormone replacement.

A rare simultaneous manifestation of polyglandular autoimmune syndrome type II.

SummaryPolyglandular autoimmune syndrome type II is a rare condition defined by the presence of autoimmune primary adrenal insufficiency along with autoimmune thyroid disease and/or type-I diabetes. Onset of these conditions will usually be separated by several years, though in rare instances it can occur simultaneously. This syndrome can also be associated with various non-endocrine autoimmune diseases, such as vitiligo and alopecia. Coeliac disease is less commonly associated with polyglandular autoimmune syndrome type II and is more commonly associated with polyglandular autoimmune syndrome type III. Here we describe an interesting case of a young male presenting with simultaneous manifestation of Addison’s disease and Graves, with coincident asymptomatic coeliac disease, as a rare manifestation of polyglandular autoimmune syndrome type II.Learning points:Polyglandular autoimmune syndrome type II is rare, has female predominance, and peak onset in the third and fourth decades of life.Onset of Addison’s disease will usually precede or follow onset of type-I diabetes or autoimmune thyroid disease by several years in this syndrome.Simultaneous onset can occur, as in this case.Coeliac disease is uncommonly associated with this syndrome.Coeliac disease is more commonly associated with polyglandular autoimmune syndrome type III.Coeliac disease should be screened for in patients with associated autoimmune conditions, such as type-I diabetes or autoimmune thyroid disease.

Recurrent Pregnancy Loss in Women with Hashimoto's Thyroiditis with Concurrent Non-Endocrine Autoimmune Disorders.

Background: An increased rate of recurrent miscarriage has been described in patients with autoimmune thyroid disease. However, there is a lack of studies that assess the rate of recurrent pregnancy loss (RPL) in patients with Hashimoto's thyroiditis (HT) isolated or with concurrent non-endocrine autoimmune disorders (NEAD). The objective of the study was to assess the rate of RPL in patients with HT isolated or accompanied with non-endocrine autoimmune diseases. Methods: This is a retrospective observational cohort study with a systematic review of the NEAD with concurrent HT in an outpatient Endocrinology Unit at a University Hospital. Among the 3480 consecutively examined women with HT, 87 patients met the criteria of RPL and represented the study group. Sixty-five of them had isolated HT and 22 women had HT+NEAD. Results: The rate of RPL in women with HT was 2.1% versus 5.64% observed in women with HT+NEAD (odds ratio = 2.78 [95% confidence interval 1.70-4.57]; p < 0.0001). On subdivision, this difference was still evident in euthyroid patients (p < 0.0001), while it disappeared in hypothyroid women (p = 0.21). The RPL did not correlate with the autoantibody concentrations nor in women with isolated HT nor in those with HT+NEAD. The presence of antiphospholipid syndrome (APS) explained RPL in 3 out of 22 (14%) patients with HT+NEAD, the remaining being related to different autoimmune disorders. Interestingly, even subtracting the patients with APS, RPL was more frequent in patients with poly-autoimmunity than in patients with isolated HT (p = 0.0013). Conclusions: The co-presence of NEAD is correlated with a higher risk of RPL in women with HT. The association with APS may explain only a fraction of RPL rate in patients with poly-autoimmunity.

Аутоиммунные полигландулярные синдромы

Autoimmune polyglandular syndromes (APS) are the primary defeat of the autoimmune process of 2 peripheral endocrine glands and more, leading, as a rule, to their insufficiency, often combined with various organ-specific non-endocrine autoimmune diseases.

Autoimmune polyglandular syndromes

Autoimmune polyglandular syndromes (APS) are the primary defeat of the autoimmune process of 2 peripheral endocrine glands and more, leading, as a rule, to their insufficiency, often combined with various organ-specific non-endocrine autoimmune diseases.

Down syndrome with Graves' disease: A lesser thyroid association

Down syndrome is a common cause of mental retardation in pediatric population. These individuals also have increased prevalence of both endocrine and nonendocrine autoimmune disorders with thyroid disorder being the most common endocrine disorder reported. Autoimmune disorders in these patients are associated with early presentation. Hypothyroidism is the most common autoimmune thyroid disease while Graves' disease is rare in patients of Down syndrome. We hereby present a case of Graves' disease in a patient with Down syndrome that clinically presented with symptoms of hyperthyroidism. Early definitive treatment is recommended in view of challenges of compliance to treatment in these mentally challenged individuals.

High prevalence of comorbid autoimmune diseases in adults with type 1 diabetes from the HealthFacts database.

Patients with type 1 diabetes (T1D) are at risk for other autoimmune diseases (ie, polyautoimmunity). The prevalence and risk factors of this phenomenon have been underreported in adults and ethnic minorities, and data are lacking regarding non-endocrine autoimmune diseases. Study population data were gathered from HealthFacts, a deidentified patient database compiled from electronic medical records systems in the US. Patients with an International Classification of Diseases diagnosis code specifying T1D were included in the study, whereas those with a diagnosis of type 2 diabetes were excluded. The cross-sectional study cohort comprised 158 865 adults with T1D (mean [±SD] age 51.4 ± 18.9 years, 52.5% female). The most common autoimmune diseases were thyroid disease (20.1%), systemic rheumatic diseases (3.4%), rheumatoid arthritis specifically (2.0%), and gastrointestinal autoimmune diseases (1.4%). Most of the autoimmune diseases were more common in women (eg hypothyroidism, hyperthyroidism, celiac disease, rheumatoid arthritis, lupus, and Sjögren syndrome). Caucasians were more likely than other ethnicities to have an additional autoimmune disease. The prevalence of autoimmune diseases increased with increasing age, significantly in women, such that 38.5% of women over 80 years of age had an additional autoimmune disease, compared with 17.9% of women aged ≤29 years. Additional autoimmunity represents a significant comorbidity in patients with T1D. Autoimmune diseases are more common in Caucasians and in women, and increase with age. Clinicians treating patients with T1D should be aware of the risk factors for additional autoimmune diseases.

Autoimmune endocrine diseases.

The endocrine system is interested by several autoimmune diseases, characterized by different impact and severity, according to the organs involved. Autoimmune thyroid disorders (i.e. Hashimoto's thyroiditis and Graves' disease) and type 1 diabetes mellitus are the most common autoimmune endocrine disorders, while hypophysitis, adrenalitis (90% of cases of primary hypocortisolism or Addison's disease), POF and hypoparathyroidism represent quite rare conditions. Autoimmune endocrine diseases can also coexist in the same individuals and cluster in families. Some of these associations are nosologically codified in the so-called autoimmune polyglandular syndromes, but autoimmune endocrinopathies can also be accompanied by other non-endocrine autoimmune disorders (i.e. connective tissue, skin or gastrointestinal diseases). Pathophysiology generally results from a complex interplay among genetic predisposition and environmental/endogenous factors. In the diagnostic process, measurement of organ-specific autoantibodies, both with a causative role or as an epiphenomenon, is often fundamental and integrates the assessment of hormone axes and the targeted imaging studies.

Polyglandular autoimmune syndromes.

In recent years, scientific knowledge pertaining to the rare ORPHAN polyglandular autoimmune syndrome (registered code ORPHA 282196) has accumulated. To offer current demographic, clinical, serological and immunogenic data on PAS. Review of the pertinent and current literature. Polyglandular autoimmune syndromes (PAS) are multifactorial diseases with at least two coexisting autoimmune-mediated endocrinopathies. PAS show a great heterogeneity of syndromes and manifest sequentially with a large time interval between the occurrence of the first and second glandular autoimmune disease. PAS cluster with several non-endocrine autoimmune diseases. In most endocrinopathies of PAS, the autoimmune process causes an irreversible loss of function, while chronic autoimmune aggressions can simultaneously modify physiological processes in the affected tissue and lead to altered organ function. The rare juvenile PAS type I is inherited in a monogenetic manner, whereas several susceptibility gene polymorphisms have been reported for the more prevalent adult types. Relevant for a timely diagnosis at an early stage is the screening for polyglandular autoimmunity in patients with monoglandular autoimmune disease and/or first degree relatives of patients with PAS. The most prevalent adult PAS type is the combination of type 1 diabetes with autoimmune thyroid disease. Early detection of specific autoantibodies and latent organ-specific dysfunction is advocated to alert physicians to take appropriate action in order to prevent full-blown PAS disease.

BREG cells in Hashimoto's thyroiditis isolated or associated to further organ-specific autoimmune diseases

Hashimoto thyroiditis (HT) may occur isolated or associated with other non-endocrine autoimmune disorders (NEAD). No data are available about Breg cells in these disorders and this represented the aim of the study. Th17 and Breg cells subset were characterized on peripheral blood mononuclear cells isolated from 18 healthy donors (HD), 19 patients with isolated HT and 26 patients with HT+NEAD. Th17 were higher in patients with isolated HT than in HD but no further changes were seen in patients with HT+NEAD. CD24hiCD38hi unstimulated Breg cells were similar in HT patients and in HD, but significantly higher in patients with HT+NEAD than in both HT and in HD. CD19+CD24hiCD27+ Breg memory phenotype was similar in HD and in HT patients, but decreased in patients with HT+NEAD (23.4%vs38.5%). Upon CpG-stimulation, CD24hiCD38hi IL-10+ Breg cells were higher in HT patients than in HD (3.9%vs1.8%) but similar in patients with HT+NEAD (2.4%).

Endocrinology and interdisciplinary consultation in internal medicine : Illustrated using the example of polyglandular autoimmune syndrome

Polyglandular autoimmune syndromes encompass several endocrine and nonendocrine autoimmune disorders with variable onset and phenotype. Rheumatoid and gastroenterological symptoms in patients with autoimmune polyglandular syndromes are suggestive of additional rheumatoid gastrointestinal and hepatological autoimmune diseases. Autoimmune gastritis, celiac disease, autoimmune hepatitis, rheumatoid arthritis, Sjögren syndrome, and systemic Lupus erythematodus are of particular clinical relevance. In addition, unspecific rheumatoid and gastrointestinal attendant symptoms of the existing autoimmune endocrinopathy must be considered. Furthermore, certain disorders of polyglandular autoimmune syndromes, e. g., type1 diabetes are frequently associated with particular gastrointestinal diseases such as small bowel bacterial overgrowth. An optimal patient-centered care of subjects with autoimmune diseases requires acomprehensive differential diagnostic work up and emphasizes the importance of an interdisciplinary cooperation.

POLYGLANDULAR AUTOIMMUNE SYNDROME ASSOCIATED WITH MULTIPLE AUTOIMMUNE CONDITIONS AND ATOPIC DERMATITIS - AN UNUSUAL MANIFESTATION OF A POLYAUTOIMMUNITY PHENOTYPE.

The polyglandular autoimmune syndrome (PAS) type III is a rare condition defined as the coexistence of autoimmune thyroid disorder with other endocrine autoimmune diseases, including type 1 diabetes, without adrenal dysfunction. PAS may associate with other non-endocrine autoimmune diseases, overlapping with the multiple autoimmune syndromes (MAS). We present a case of PAS III/ MAS type 3, including autoimmune thyroiditis, autoimmune diabetes, vitiligo, lupus erythematosus, associated with adult-onset atopic dermatitis, a combination not reported previously. A 40 years old woman, registered as nurse working in dialysis unit, previously diagnosed with vitiligo, euthyroid autoimmune thyroiditis and disseminated granuloma annulare, with personal and familial history of atopic disorders, presented in our clinic for disseminated eczematous and lichenoid cutaneous rashes. She was tested positive for antinuclear, anti-double stranded DNA and anti-histone antibodies, with inflammatory syndrome and marginal lymphopenia and she was diagnosed with systemic lupus erythematosus (SLE). Subsequently, moderate hyperglycemia, positive anti-glutamic acid decarboxylase antibodies and low C-peptide level prompted the diagnosis of autoimmune diabetes. Recurrent flexural eczematous rashes, with negative epicutaneous tests but positive specific IgE tests for common allergens fulfilled the clinical criteria for the diagnosis of atopic dermatitis. The clinical, immunological and glycemic status were controlled with low doses of oral prednisone (<0.5 mg/kg), methotrexate (10mg/week), antimalarials, metformin, emollients and photoprotection. After changing her workplace, the immunosuppressive treatment could be discontinued, and the patient maintained normal immunological and biochemical profile at 6 months follow-up.This case brings a unique perspective on the evolution, associations spectrum and the management challenges of endocrine polyautoimmunity associated with atopic diathesis.

A Case of Type III Autoimmune Polyglandular Syndrome

&lt;p&gt;The autoimmune polyglandular syndromes (APS) are groups of syndromes comprising a combination of endocrine and nonendocrine autoimmune diseases. Among of those four types of APS, the main characteristics of the 3 APS are autoimmune thyroid diseases associated to other autoimmune diseases, excluding Addison’s disease. Type 3 APS are also subdivided into 3A, 3B, 3C, and 3D. Recently, we experience a case of APS manifesting 3A, 3C, and 3D subtype. A 28-year-old woman developed type I diabetes. According to her medical history, she had Graves’ disease, vitiligo, auimmune hemolytic anemia and systemic lupus erythematosus (SLE). The antoantibodies associated with Graves’ disease, SLE, and type I diabetes showed positive findings. We report this case with literatures review.&lt;/p&gt;

Schmidt's Syndrome – Case report and review of literature

Autoimmune polyglandular syndrome (APS) is a broad spectrum of various autoimmune endocrinopathies and may show similarities with other endocrine or non-endocrine autoimmune diseases. APS-2, also known as Schmidt's syndrome, is characterized by diabetes mellitus type 1, hypothyroidism and Addison's Disease. Here we present a case of Schmidt's syndrome presenting with a left cerebellar mass.