Autoimmune Thyroid Disease and Keratoconus: Is There an Association?

Presence of Other Autoimmune Diseases in Subjects with Autoimmune Thyroid Disease

AB0553 Prevalence of Autoimmune Thyroid Disease in Malaysian SLE Patients

Autoimmune thyroid disease in Egyptian patients with rheumatoid arthritis

A case of polymyositis associated with Hashimoto's thyroiditis

Autoimmune diseases are chronic conditions initiated by the loss of immunological tolerance to self-antigens. They constitute heterogeneous group of disorders, in which multiple alterations in the immune system result in a spectrum of syndromes that either target specific organs or affect the body systematically. Recent epidemiological studies have shown a possible shift of one autoimmune disease to another or the fact that more than one autoimmune disease may coexist in a single patient or in the same family. Numerous autoimmune diseases have been shown to coexist frequently with thyroid autoimmune diseases. AUTOIMMNUNE THYROID DISEASE AND OTHER ORGAN SPECIFIC NON-ENDOCRINE AUTOIMMUNE DISEASES: This part of the study reviews the prevalence of autoimmune thyroid disease coexisting with: pernicious anaemia, vitiligo, celiac disease, autoimmune liver disease, miastenia gravis, alopecia areata and sclerosis multiplex, and several recommendations for screening have been given. AUTOIMMUNE THYROID DISEASE AND OTHER ORGAN NON-SPECIFIC NON-ENDOCRINE AUTOIMMUNE DISEASES: Special attention is given to the correlation between autoimmune thyroid disease and rheumatoid arthritis, systemic lupus erythematosus, syndrome Sjögren, systemic sclerosis and mixed connective tissue disease. Screening for autoimmune thyroid diseases should be recommended in everyday clinical practice, in patients with primary organ-specific or organ non-specific autoimmune disease. Otherwise, in patients with primary thyroid autoimmune disease, there is no good reason of seeking for all other autoimmune diseases, although these patients have a greater risk of developing other autoimmune disease. Economic aspects of medicine require further analyzing of these data, from cost/benefit point of view to justified either mandatory screening or medical practitioner judgment.

Objectives. (1) To determine the prevalence of autoimmune thyroid disease among patients with autoimmune rheumatic disorders seen at the Philippine General Hospital. (2) To determine clinical features that are associated with the occurrence of autoimmune thyroid disease in these patients. Methodology. This is a cross sectional analytical study that included 155 adult Filipinos diagnosed with an autoimmune rheumatic disorder. Clinical characteristics were recorded. Serum thyrotropin, thyroxine, triiodothyronine, anti-thyroid peroxidase antibody, anti-thyroglobulin antibody and urinary iodide excretion were determined. The prevalence of autoimmune thyroid disease was computed. Associations between clinical factors and autoimmune thyroid disease were determined. Results. Overall 21.94% of the population had autoimmune thyroid disease. There was significant association between duration of the autoimmune rheumatic disorder and autoimmune thyroid disease (p-= 0.018). No significant association was noted with the other clinical factors although there was an almost significant association observed for the presence of goiter (p=0.054). Conclusion. Autoimmune thyroid disease commonly occurs in patients with autoimmune rheumatic disorders. As such, it is important to consider screening these patients for the coexistence of thyroid disease to help prevent the complications associated with thyroid dysfunction and avoid adding up to the morbidity of the existing autoimmune rheumatic disorder.

The pathogenesis of Graves-Basedow's disease is similar to that of Hashimoto’s disease (chronic autoimmune thyroiditis) and it is assumed that these two forms are the opposite poles of the same autoimmune disease. The name of the first disease derives from the surnames of two scientists who described it in the literature: Robert James Graves (1835) and Karl Adolf von Basedow (1840). The first description of the second disease was presented in 1912 by Hakaru Hashimoto. Genetic, environmental and endogenic factors are involved in the pathogenesis of autoimmune diseases. Genetic predisposition to an autoimmune disease depends on many genetic loci, of which three seem to be most important: alleles of the major histocompatibility system genes (human leukocyte antigen – HLA), mainly of class II HLA-DR3 and DR5; alleles of the gene encoding antigen-4 associated with the cytotoxic T lymphocyte (cytotoxic T lymphocyte associated antigen-4 – CTLA-4) and alleles of the gene encoding the lymphocytic tyrosine phosphatase (Protein Tyrosine Phosphatase Non Receptor – Type 22 - PTPN22). Epidemiological studies also confirm that genetic factors are responsible for autoimmune thyroid diseases with a high prevalence in patients’ relatives, especially among monozygotic twins. The environmental factors responsible for the presence of thyroid autoantigens on thyrocyte surface include viral infection, extreme stress, an excessive iodine content in diet, the action of some drugs (interferon α, amiodarone) and a huge number of chemical compounds in polluted surroundings. The most important endogenic factors include female sex and the phenomenon of foetal microchimerism in pregnant women. An organ-specific suppressor T lymphocyte defect develops in genetically predisposed people, which leads to an excessive stimulation of the T-helper lymphocytes. As a consequence, B lymphocytes experience excessive stimulation with subsequent production of plasma cells, which are responsible for the disproportionate production of antibodies against thyroid antigens – mainly the TSH receptor, thyroglobulin and thyroid peroxidase. In Graves-Basedow's disease, TSH receptor is the main autoantigen against which the antithyroid antibodies are directed. High titres of ATG and anti-TPO may suggest the coexistence of Hashimoto’s disease. In 80% cases of Graves-Basedow's disease, TSHR antibodies are stimulatory (thyroid stimulating immunoglobulins – TSI). In some cases, antibodies that inhibit thyrotropin binding to thyroid cells are produced (thyrotropin binding inhibiting immunoglobulins – TBII), which may lead to the development of hypothyroidism. In Hashimoto’s disease, cytotoxic lymphocytes, able to destroy thyroid follicular cells, receive considerable stimulation. Apart from cytotoxic lymphocytes, macrophages and the phenomenon of programmed cell death (apoptosis) also take part in the process of thyrocyte destruction. Clinical diagnosis of Graves-Basedow's disease is based on the detection of evenly enlarged thyroid gland with tactile fremitus and/or audible vascular murmur and the occurrence of the typical ophthalmic changes. Some patients also suffer from pretibial myxoedema and thyroid acropathy. Ultrasonography is a very useful imaging tool in the diagnosis of Graves-Basedow's disease – the thyroid gland is usually enlarged and has a homogenous, hypoechoic structure. Scintigraphy is not obligatory in each case of Graves-Basedow's disease, but it is very helpful in patients with the features of nodular structure and in the form without the goitre in which diagnostic difficulties occur. In the classical form of Hashimoto’s disease, a painless goitre of intensified cohesion presents with a butterfly-like shape because of the palpable pyramidal lobe. Patients complain of pressure and feeling of obstruction within the neck, and can report swallowing disorders and hoarseness. Chronic autoimmune thyroiditis can also occur in the atrophic, focal and juvenile form. Additionally, there are two variants of Hashimoto’s disease: postpartum thyroiditis and silent, painless thyroiditis. High anti-TPO antibody concentrations confirm the diagnosis of Hashimoto’s disease or any of its variants. The absence of antibodies in serum does not exclude lymphocytic thyroiditis as they are provided by intrathyroid lymphocyte infiltrations. Some authors attribute a special diagnostic significance to fine-needle aspiration biopsy in seronegative forms. Ultrasound thyroid examination is helpful in establishing correct diagnosis. Heterogeneous and distinctly hypoechoic structures of the thyroid gland are typical sonographic manifestations.

Comorbidity profiles among patients with alopecia areata: The importance of onset age, a nationwide population-based study

IntroductionThe pathogenesis of autoimmune thyroid diseases is complicated and not completely known. Among the causes of thyroid autoimmunity, we distinguish genetic predisposition and environmental factors. Graves’ disease and Hashimoto’s thyroiditis are associated with a disturbance of immune tolerance of thyroid antigen molecules. The IL2RA gene is located on chromosome 10 and encodes the interleukin 2 receptor (IL2RA), which is expressed by the regulatory T-cells (Tregs) responsible for suppression. It has been shown that this gene and its polymorphism occur in people with various autoimmune diseases (e.g. type 1 diabetes mellitus, rheumatoid arthritis, Graves’ disease, or multiple sclerosis). The FAIM2 gene is located on chromosome 12 and encodes the molecule involved in the apoptosis inhibition process. The PADI4 gene is located on chromosome 1, and its expression is associated with activation of T-cells, differentiation of macrophages, which leads to increased inflammation.AimThe aim of the study was to analyze the polymorphisms of the IL-2RA (rs7093069), FAIM2 (rs7138803) and PADI4 (rs1748033) genes and their correlation to thyroid hormones and anti-thyroid antibodies in pediatric patients with Graves’ disease and Hashimoto’s thyroiditis compared to the control group.Material and MethodsThe study was performed in 180 patients with GD (mean age 16.5 ± 2), 80 with HT (mean age, 15.2 ± 2.2), and 114 children without any autoimmune diseases (mean age 16.3 ± 3) recruited from the endocrinology outpatient clinic. Three single nucleotide polymorphisms (SNPs): rs7138803-FAIM2, rs7093069-IL-2RA, and rs1748033 PADI4 were determined by TaqMan SNP QuanStudio 12K Flex-OpenArray genotyping with PCR and correlated to thyroid hormones and anti-thyroid antibodies.ResultsRs7090369-IL-2RA allele T was more frequent in patients with AITDs (33.7% in GD vs 28.7% in HT, p = 0.077, OR = 1.52) compared with healthy children (25%). Allele T of that gene predisposes to the occurrence of autoimmune thyroid diseases, especially GD and TT genotype gives a statistically significant 5.2 times higher risk of GD (p = 0.03, OR = 5.26) and increased risk of HT (p = 0.109, OR = 4.46). Allele A rs7138803-FAIM2 is more frequent in patients with GD (p = 0.071, OR = 1.45) and HT (p = 0.028, OR = 1.8). In our data the presence of GG genotype of that gene significantly reduces the risk of autoimmune thyroid diseases (p = 0.05, OR = 0.42). Allele C rs1748033PADI4 and its CC genotype were more frequent in patients with autoimmune thyroid diseases, but it was not statistically significant. The occurrence of CT genotype significantly reduces the risk of HT (p = 0.03, OR = 0.4).Conclusions1). Polymorphisms rs7138803-FAIM2 and rs1748033-PADI4 are more frequent in patients with autoimmune thyroid diseases, more frequent in patients with Hashimoto’ thyroiditis, but the occurrence of GG rs7138803-FAIM2 genotype could reduce the risk of thyrocyte apoptosis inhibition. 2). The TT rs7093069-IL2RA genotype may increase the risk of autoimmune thyroid diseases. 3). Analysis of polymorphisms of given genes in clinical practice will allow to determine predisposition to autoimmune thyroid disease development, to find symptoms of thyroid gland dysfunction earlier and to use appropriate treatment.

Vulvar lichen sclerosus (VLS) is defined as a chronic inflammatory skin disease that most often involves lesions on the mucous membranes of the vulva with a tendency to progress to the anal skin. The etiopathogenesis of VLS remains unknown and is likely multifactorial. Data emphasize the role of immunological factors - more than 25% of VLS cases coexist with autoimmune diseases. The purpose of the present study was to determine the correlation of the prevalence of anti-thyroid antibodies - IgG class antibodies against thyroid peroxidase and IgG class antibodies against thyroglobulin in women with vulvar lichen sclerosus, and the appropriateness of screening tests for autoimmune thyroid diseases in women with vulvar lichen sclerosus. Fifty women with vulvar lichen sclerosus were enrolled in the study. The control group consisted of 41 healthy women. A detailed medical history was taken with all patients, followed by laboratory determinations - anti-thyroid antibodies - IgG class antibodies against thyroid peroxidase and IgG class antibodies against thyroglobulin. Antibodies to thyroid peroxidase were present in 12% of the study group with vulvar lichen sclerosus and 4.88% of the control group, and this difference was not statistically significant (p = 0.41). Anti-thyroglobulin antibodies were detected in 4% of the patients with vulvar lichen sclerosus and 4.88% of the control group, and this difference was not statistically significant either (p = 0.76). The study did not confirm the association of VLS with autoimmune thyroid diseases. Undoubtedly, based on the data available in the literature, further studies are needed to determine the mechanisms behind the association between vulvar lichen sclerosus and autoimmune thyroid diseases.

To the Editor: We refer to the article by Ansaldi et al. (1), which presents autoimmune thyroid disease associated with celiac disease (CD) in children. According to their results, autoimmune thyroid disease was found in 90 of 343 (26.2%) patients with CD and in 20 (10%) of the control subjects (P = 0.001). We recently performed a study to evaluate the prevalence of autoimmune thyroid disease in children with CD in Eastern Turkey. Our study group consisted of 77 children with CD in whom the diagnosis was performed according to the accepted criteria of the European Society for Pediatric Gastroenterology and Nutrition (2). Of subjects included in the study, 34 (44.2%) were boys and 43 (55.8%) were girls. Mean age was 9.36 ± 4.05 years (range, 1 to 18 years). Forty healthy subjects matched for sex and age were included as a control group. CD was ruled out in these children on the basis of serological screening tests (antiendomysial antibody immunoglobulin A and antigliadin antibody immunoglobulin G). Thyroid function was assayed by measuring the levels of thyroid-stimulating hormone, free T3, free T4, thyroid microsome antibodies and antithyroglobulin antibodies. There was no serologic or clinical sign of another autoimmune disease in patients with CD except for one patient with autoimmune hepatitis. Both thyroid microsome antibodies and antithyroglobulin antibodies were positive in this patient but she was euthyroid. Hypothyroidism was observed in four (5.2%) children with CD; it was not observed in any of the controls. Medical treatment was started for all the patients with hypothyroidism. Hyperthyroidism was not observed in our patients, but it was observed in one of the control subjects (2.5%). We found that seven of 77 (9.1%) patients were positive for thyroid microsome antibodies and six of 77 (7.8%) were positive for antithyroglobulin antibodies; two of 77 showed both positive thyroid microsome antibodies and antithyroglobulin antibodies. Therefore, in 11 of 77 (14.3%), at least one antibody directed against thyroid tissue was positive. In the control group, only one patient had antithyroglobulin antibodies positivity; he was euthyroid. CD is an autoimmune disorder characterized by inflammation, villous atrophy and crypt hyperplasia of the small bowel mucosa. An association between CD and other autoimmune disorders-such as insulin-dependent diabetes, Addison's disease, systemic lupus erythematous, rheumatoid arthritis, alopecia areata and autoimmune endocrine diseases-has been described (1,3-6). Of these, autoimmune thyroid disease is commonly seen in CD (3). Collin et al. (3) reported that thyroid involvement would be evident in as many as 10% to 15% of all CD subjects and clearly more frequently than in control subjects. The growth of knowledge of the pathogenesis of CD that has taken place in recent years indicates that CD is a disease of autoimmune etiology (4). The greater frequency of thyroid disease among children with CD compared with healthy individuals justifies a routine assessment of thyroid functions. Forchielli et al. (6) and Kowalska et al. (4) reported that incidences of autoimmune thyroid disease associated with CD were 37.6%, and 41.1%, respectively. Ansaldi et al. (1) reported the frequency of CD in the largest pediatric series of CD as 26.2%. Interestingly, in the mentioned study, the reported frequency of autoimmune thyroid disease in control subjects was higher than in other studies (10%). It was not clear in the text whether the controls were tested for CD serology. This investigation is particularly important in countries where the prevalence of CD is relatively high. Hakanen et al. (5) detected autoimmune thyroid disease in patients with CD and controls as 13.9% and 2.1%, respectively. Toscano et al (7) described similar results for autoimmune thyroid disease associated with CD. In conclusion, we found the frequency of autoimmune thyroid disease associated with CD to be 14.3% in Turkish children. This result was similar to other published data. We emphasize the importance of screening selected controls for celiac serology, especially in countries where celiac prevalence is relatively high, to avoid overestimation the prevalence of thyroid disease in healthy children. Mukadder Ayşe Selimoğlu Vildan Ertekin Atatürk University, Medical Faculty Department of Pediatric Gastroenterology, Hepatology and Nutrition, Erzurum, Turkey

Thyroid function abnormalities and thyroid autoantibodies have been frequently described in patients with rheumatologic autoimmune diseases, such as Sjögren's syndrome, rheumatoid arthritis, systemic lupus erythematosus and scleroderma. Limited data are available regarding the prevalence and clinical characteristics of autoimmune thyroiditis in other rheumatologic disorders, such as rheumatic fever and juvenile systemic lupus erythematosus. The authors review the association of endocrine autoimmune and rheumatic autoimmune diseases, assessing various age groups and clinical conditions. The bibliographic survey was conducted through the search for scientific articles indexed in the general health sciences databases, such as Latin American and Caribbean Health Sciences Literature (LILACS), Medline/PubMed, and Scientific Electronic Library Online (SciELO). The following descriptors were used: "rheumatic autoimmune diseases and autoimmune thyroid diseases"; "thyroid disorders and rheumatic diseases"; "thyroiditis and rheumatic diseases"; "autoimmune diseases and thyroid"; and "pediatric rheumatic diseases and autoimmune thyroid diseases". This study showed that, despite contradictory results in the literature, there is a greater prevalence of the association between autoimmune thyroid diseases and rheumatic diseases, highlighting the possibility of common pathogenic mechanisms among them.

Disclosure: B. Cardakli: None. S. Clare: None. A. Mathew: None. M. Kutahyalioglu: None. Background: Polyglandular Autoimmune Syndrome Type II (PAS-II), also known as Schmidt Syndrome, is a rare genetic condition characterized by multiple endocrine dysfunctions most commonly including type 1 diabetes (T1D), adrenal insufficiency, and autoimmune thyroid disease. Uncontrolled hyperthyroidism and adrenal insufficiency can lead to recurrent diabetic ketoacidosis (DKA) in patients with T1D. Clinical Case: A 24-year-old female with a history of T1D was admitted for DKA. Diagnosed at age four, she managed her condition well, with rare DKA admissions previously. She has a strong family history of autoimmune disorders, including T1D, polymyositis, celiac disease, systemic lupus erythematosus, and rheumatoid arthritis. She has been using an insulin pump for the past four years without malfunctions and has consistently adhered to her diabetes therapy. Over the past 12 months, she experienced persistent fatigue, nausea, frequent hypoglycemia, and low appetite, resulting in six DKA admissions, with two occurring just one week apart—unusual given her prior history. During the first admission of the year, she was diagnosed with autoimmune hyperthyroidism. Her thyroid peroxidase antibodies were elevated, and although initially negative, her thyroid-stimulating immunoglobulin became positive three months later. Methimazole was prescribed, with dosage adjusted based on thyroid function tests. Adrenal insufficiency was also suspected at the same admission and confirmed with a positive cosyntropin stimulation test (CST), though her 21-hydroxylase antibody was negative. She began hydrocortisone treatment, discontinued six months later after a negative CST. In her two most recent admissions, uncontrolled hyperthyroidism was suspected to trigger DKA, alongside recurring adrenal insufficiency after common DKA causes were ruled out. Screening for other autoimmune diseases showed normal vitamin B12 levels and a pituitary function panel, including prolactin, IGF-1, LH, FSH, and estradiol, with a negative ANA test. However, she tested positive for celiac disease amidst iron deficiency anemia and vitamin D deficiency. The diagnosis of PAS-II was based on the presence of T1D, autoimmune thyroid disease, and Addison's disease. Her recurrent DKA episodes over the year are attributed to the complex interplay of developing autoimmune disorders, exacerbated by uncontrolled thyroid disease and intermittent adrenal insufficiency. Conclusion: This case highlights the critical importance of considering PAS-II in patients with T1D who present with unexplained DKA, especially those with a strong family history of autoimmune diseases. Early identification through comprehensive screening can aid in prompt management and potentially prevent recurrent episodes. Presentation: Saturday, July 12, 2025

The association of nephropathy with autoimmune thyroid disease (AITD) has been reported previously. However, there is limited information on the relationship between thyroid autoantibodies and nephropathy. A retrospective study was conducted using the medical records of 246 patients with nephropathy, 82 of whom had concurrent AITD. General characteristics, thyroid function, autoantibodies, and the pathological types of nephropathy were analyzed. Immunohistochemistry was used to detect the thyroglobulin antibody (TG-Ab) and thyroid peroxidase antibody (TPO-Ab) in the kidneys. We found nephropathy patients with AITD exhibited higher serum levels of TPO-Ab, TG-Ab, thyroid-stimulating hormone receptor antibody (TR-Ab), and immunoglobulin G (IgG) (P < .05). Compared with the nephropathy without AITD group, the nephropathy with AITD group exhibited higher proportions of membranous nephropathy (MN) and focal segmental glomerulosclerosis (FSGS), and relatively lower proportions of mesangial proliferative glomerulonephritis (MsPGN) and minimal change nephropathy (MCN) (P = .005). TPO-Ab and TG-Ab levels in the kidney were more prevalent in nephropathy patients with AITD than those without AITD (P = .015 and P = .026, respectively). Subgroup analysis demonstrated that serum levels of thyroid stimulating hormone (TSH), TG-Ab, TPO-Ab, immunoglobulin M (IgM), and IgG in the MN group were significantly higher, whereas the levels of free thyroxine (FT4) and estimated glomerular filtration rate (eGFR) were lower, as compared with MN with Hashimoto thyroiditis (HT) group (P < .05). TPO-Ab and TG-Ab expression levels in the kidneys were more prevalent in the MN group than in the MN with HT group (P = .034). The expression levels of FT4, TG-Ab, TPO-Ab, and thyroid-stimulating hormone receptor antibody (TSHR-Ab) in the serum were significantly higher in the MN group than in the MN with Graves disease (GD) group (P < .05). The expression of TPO-Ab in the kidneys was more prevalent in the MN group than in the MN with GD group (P = .011). In sum, the expressions of TPO-Ab and TG-Ab were more prevalent in the kidneys of patients with nephropathy and AITD. Our findings indicate that TPO-Ab and TG-Ab may play a role in the development of AITD-related nephropathy.

Introduction: Psoriasis is a common immunologically mediated inflammatory disease characterized by skin inflammation, epidermal hyperplasia, an increased risk of painful and destructive arthritis, cardiovascular morbidity, and psychosocial challenges. Some autoimmune diseases are mediated by stimulating or blocking auto-antibodies. Auto-antibodies may act as antagonists and bind to hormone receptors, blocking receptor function. It may result in impaired secretion of mediators and gradual dysfunction of the affected organ, e.g., Graves disease and myasthenia gravis.Objective: This study was planned to evaluate the association between anti-thyroid peroxidase antibody (anti-TPO Ab) and anti-thyroglobulin antibody (anti-TG Ab) as biochemical markers in 30 clinically diagnosed psoriasis patients.Materials and methods: This hospital-based, epidemiological case-control study was conducted in the Department of Biochemistry in collaboration with the Department of Dermatology, Venereology, and Leprology at Bhagat Phool Singh Government Medical College for Women, Khanpur Kalan, Sonepat, Haryana, India. Thirty subjects diagnosed clinically with psoriasis and an equal number of age-matched controls with no known autoimmune disease from the outpatient department were also enrolled. The following hormonal tests, i.e., thyroid-stimulating hormone (TSH), free triiodothyronine (FT3), free thyroxine (FT4), and antibodies, anti-TPO Ab and anti-TG Ab, were performed. The study period was one year. The data thus obtained was analyzed using SPSS Statistics version 26.0 (IBM Corp. Released 2019. IBM SPSS Statistics for Windows, Version 26.0. Armonk, NY: IBM Corp). The significance level (p-value) was taken as <0.05.Results: The mean age of psoriasis subjects was 37.83±12.89 years compared to 36.91±12.32 years in the control group and was found to be non-significant (p=0.432), reflecting a similar age distribution. A male preponderance was observed in the present study, where the psoriasis group consisted of 80% males and 20% females, while the control group had 60% males and 40% females. All six psoriasis patients diagnosed with autoimmune thyroid disease (AITD) were euthyroid at the time of enrollment, compared to only one control subject in a subclinical hypothyroid state. The mean values of anti-TPO Ab were 30.93±41.26 IU/mL in psoriasis patients and 11.39±28.42 IU/mL in the control group (p=0.001), while the mean values of anti-TG Ab were 11.21±27.69 IU/mL in psoriatic subjects and 2.49±9.05 IU/mL in the control group (p=0.004). No significant correlation between AITD and psoriasis was found when both parameters were analyzed statistically for correlation; even when one marker was considered, no significant correlation was found. The odds ratio was calculated to find an association between the disease and thyroid autoimmunity. The odds ratio was estimated to be 2.25 for psoriasis and the control group, with a confidence interval of 95% (0.77-6.59) and a p-value of 0.139, which was not statistically significant.Conclusion: Psoriasis, a dermatological disorder, has been seen as related to AITD. The role of early detection of anti-thyroid antibodies, i.e., anti-TPO Ab and anti-TG Ab, can be of prognostic value in AITD and psoriasis.