Antithyroid Microsomal Antibodies Research Articles

Role of Immunotherapy in Down Syndrome Disintegrative Disorder (DSDD)

Objective To describe case series of patients with DSDD, successfully treated with immunotherapy including Intravenous Immunoglobulin (IVIG) at a single academic center. Background Down syndrome is the most common chromosomal disorder, and in most cases, is due to trisomy of chromosome 21. DSDD is underrecognized, rapidly progressive neuropsychiatric syndrome with various postulated etiology including psychological stress, primary psychiatric disorder and autoimmunity. Design/Methods Case-1: A 20-year-old fun loving female with trisomy-21 and infantile spasms started having complex partial seizures, hallucinations, speech regression, tics, abnormal head movement and obsessive-compulsive behavior. Case-2: A 20-year-old female cheerleader with trisomy-21, started having rapid regression in language, cognition, social skills and agitation over one year. Case-3: A 22-year-old female dancer with trisomy-21, started having subacute onset depression, hallucinations, sleep changes, anorexia and speech regression over one year. Results Case-1: MRI brain and cerebrospinal fluid (CSF) studies were normal including negative autoimmune encephalitis panel. Serum thyroglobulin and thyroid peroxidase antibody were high. Prolonged oral steroid therapy helped but caused adverse effects. She was able to return to her premorbid baseline with chronic IVIG therapy every 10 weeks. Case-2: MRI brain and CSF were normal. Serum autoimmune encephalitis panel, thyroglobulin antibody and thyroid peroxidase antibody were negative. Pulse IV steroids improved symptoms, however she regressed after stopping steroids. IVIG every 6 weeks along with electroconvulsive therapy improved neurological symptoms. Case-3: MRI brain and EEG were normal. CSF showed elevated white blood cell count. Serum Thyroid antimicrosomal and thyroglobulin antibody were high. One dose of IVIG caused significant improvement in neurological symptoms for 6 weeks. Conclusions DSDD should be considered in patients with down syndrome with rapid regression. It is often associated with positive thyroid peroxidase antibody suggesting immune mediated etiology. Various immunotherapy treatments have been reported in literature including steroid, IVIG, mycophenolate and rituximab with significant improvement in selected patient with autoimmunity.

Hyperthyroid Phase of Hashimoto's Thyroiditis

Hashimoto thyroiditis (chronic autoimmune thyroiditis) is the most common cause of hypothyroidism in iodine-sufficient areas of the world. This condition, however, can sometimes show hyperthyroidism. A 39-year-old femalewas admitted to hospital due to shortness of breath and tremor four hours before hospitalization. There were nausea, chestpain, cold chills, and palpitation. She was diagnosed with Hashimoto's thyroiditis and routinely received tyrosol,propranolol, and dexamethasone. Physical examination showed cervical mass, afebrile, blood pressure of 130/70 mmHg,pulse rate of 110 beats/minute and respiratory rate of 20 breaths/minute. Laboratory examinations showed WBC 7.53 x 109/L, Hb 11.0 g/dL and platelet count of 168 x 109/L. Chest X-Ray: negative for infiltrates. Several laboratory testswere performed, abnormal results were as follows: FT4 level of 2.96 ng/dL (increased), TSH level of 0.003 µIU/mL(decreased), anti-TPO (antithyroid microsomal antibody) level of 306 IU/ml (increased), and IgE level of 213.6 IU/mL(increased). Peripheral blood smear, coagulation test, serum electrolytes, liver function tests, renal function tests, urinalysis,CEA and Ca 125 were within normal limits. Thyroid ultrasound was performed and showed a benign lesion. Fine needleaspiration biopsy showed lymphocytic Hashimoto's thyroiditis. Echocardiography showed hyperthyroid heart disease. Dueto an increase of anti-TPO and FT4 levels, a decrease of TSH levels and lymphocytic thyroiditis from FNAB, this patient wasdiagnosed with a hyperthyroid phase of Hashimoto's thyroiditis. Thyroid function tests and thyroid antibody tests must bemonitored to distinguish between the hyperthyroid and hypothyroid phase of Hashimoto thyroiditis.

HASHIMOTO’S THYROIDITIS HYPERTHYROID STAGE

Preliminary: Hashimoto thyroiditis (chronic autoimmune thyroiditis) is the most common cause of hypothyroidism in iodine- sufficient areas of the world, but can sometimes show hyperthyroidism. Case: A 39-year-old female was referred due to shortness of breath and tremor, four hours before hospitalization. There was nausea, chest pain, cold chills and palpitation. She was diagnosed with Hashimoto’s thyroiditis and routinely received tyrosol, propanolol and dexamethasone. Physical examination: cervical mass, afebrile, blood pressure 130/70 mmHg, pulse rate 110 x/minute and respiratory rate 20 x /minute. Laboratory examinations showed WBC 7.53 x 109/L, Hb 11.0 g/dL and platelet count 168 x 109/L. Chest X-Ray: negative for infiltrates. Several laboratory tests were performed, abnormal results were as follows: FT4 2.96 ng/dL (increased), TSH 0.003 uIU/mL (decreased), anti-TPO (antithyroid microsomal antibody) 306 IU/ml (increased), Ig E 213.6 IU/mL (increased). Peripheral blood smear, coagulation test, serum electrolytes, liver function tests, renal function tests, urinalysis, CEA and Ca 125 were within normal limits. A thyroid ultrasound resulted in a benign lesion. Fine Needle Aspiration Biopsy concluded in lymphocytic Hashimoto’s thyroiditis. Echocardiography showed hyperthyroid heart disease. Discussion: Due to an increase in anti-TPO and FT4, a decrease in TSH and lymphocytic thyroiditis from FNAB, this patient was diagnosed with Hashimoto’s Thyroiditis Hyperthyroid Stage. Conclusion: Thyroid function tests and thyroid antibody tests must be monitored to decide whether it is hyperthyroid or hypothyroid stage of Hashimoto thyroiditis.

Painless thyroiditis induced by the cessation of a dipeptidyl peptidase-4 inhibitor

We describe the first reported case of painless thyroiditis induced by an abrupt cessation of a dipeptidyl peptidase-4 (DPP-4) inhibitor. A 38-year-old man who had type 2 diabetes mellitus, hypertension, hyperuricemia, and pruritus, was treated with metformin, glimepiride, dapagliflozin, sitagliptin, azelnidipine, trichlormethiazide, febuxostat, and fexofenadine. One year previously, his thyroid-stimulating hormone (TSH) was 1.59 (reference range, 0.34–4.94 U/mL). As his HbA1c value reached to 13%, sitagliptin was switched to dulaglutide. One month later, the HbA1c was 12.3%, TSH was <0.05, FT4 was 3.16 (0.7–1.48 ng/dL), FT3 was 7.79 (1.71–3.71 pg/mL), anti-TSH receptor antibody was 0.7 (0–1.99 IU/L), and thyroglobulin was 159.5 (0–32.6 ng/mL). Additionally, his anti-thyroglobulin and anti-thyroid microsomal antibodies were negative. Thyroid ultrasonography revealed a heterogeneous, hypoechogenic, normal-sized thyroid gland with decreased doppler flow. He was diagnosed with painless thyroiditis and was kept under observation without any change in current medication. One month later, the HbA1c was 12.4%, TSH was 9.06, FT4 was 0.81, FT3 was 2.26, and thyroglobulin was 86.7. Additionally, 2 months later, the HbA1c was 9.8%, TSH was 4.2, FT4 was 1, FT3 was 2.55, and thyroglobulin was 21.92. He continued taking dulaglutide once a week. His thyrotoxicosis disappeared within 3 months without specific drug therapy. Anti-TSH receptor antibody was negative throughout his clinical course. We speculate that the cessation of a DPP-4 inhibitor maybe one of the triggers of painless thyroiditis. However, glucagon-like peptide-1 is not likely a cause for painless thyroiditis because he continues taking dulaglutide once a week to date. Our findings indicate that it is important to examine thyroid function after termination of a DPP-4 inhibitor.

Autoantibody profile in children with Kawasaki disease on long-term follow-up: A prospective study from North India.

To study the profile of autoantibodies on long-term follow-up of children with Kawasaki disease (KD). In this single-center observational cohort study, 50 children who had been diagnosed and treated for KD with a minimum follow-up period of 3years were enrolled. The organ-specific autoantibodies that were assessed in the study included anti-thyroid microsomal antibody (TMA), anti-parietal cell antibody (PCA) and anti-liver kidney microsomal (LKM) antibody. The organ-nonspecific autoantibodies that were studied included anti-endothelial cell antibody (AECA), anti-nuclear antibody (ANA), anti-neutrophil cytoplasmic antibody (ANCA), anti-mitochondrial antibody (AMA) and anti-smooth muscle antibody (SMA). The sample for assessment of serology was taken at a mean follow-up period of 6.41years (±1.95 SD) after diagnosis. Autoantibodies were detected in 11/50 (22%) patients. ANA was detected in three patients, TMA was positive in seven and ANCA was positive in one. These autoantibodies likely develop in children with KD during the acute stage and may persist for many years. There is no concrete evidence to suggest that these children are at increased risk of developing an autoimmune disease in the future. However, there is some justification for prolonged surveillance for development of autoimmune manifestations.

Repairing effects of ICAM-1-expressing mesenchymal stem cells in mice with autoimmune thyroiditis.

The aim of the present study was to determine the repairing effects of intercellular adhesion molecule (ICAM)-1-expressing mesenchymal stem cells (MSCs) in mice with autoimmune thyroiditis. Following induction of an experimental autoimmune thyroiditis (EAT) model, mice were randomly divided into the following groups (n=10 each): i) Normal control; and experimental groups that were subject to EAT induction, including ii) EAT model; and iii) primary MSC; iv) C3H10T1/2/MSC; v) C3H10T1/2-MIGR1/MSC; and vi) C3H10T1/2-MIGR1-ICAM-1/MSC, which were all administered the relevant cells. MSCs were administered via the caudal vein. A blood sample was harvested from the angular vein of each animal 28 days post-treatment and ELISA was used to determine the serum total triiodothyronine, total thyroxine (T4), thyroid-stimulating hormone (TSH), anti-thyroid peroxidase (TPOAb), anti-thyroid microsomal (TMAb) and anti-thyroglobulin (TGAb) antibodies. Hematoxylin and eosin staining was performed to evaluate injury of the thyroid gland by determining the size of the follicle, inflammatory infiltration, colloidal substance retention and epithelial injury. Reverse transcription-quantitative polymerase chain reaction was performed to determine the mRNA expression of interleukin (IL)-4, IL-10, IL-17 and interferon (INF)-γ. Western blot analysis was performed to determine the expression of p38 mitogen-activated protein kinase (p38) and extracellular signal-regulated kinase (ERK). To observe cellular migration in vivo, mice were divided into the following groups, (n=10 each), which were subject to EAT induction: i) CM-DiI-labeled primary MSC; ii) CM-DiI-labeled C3H10T1/2/MSC; iii) CM-DiI-labeled C3H10T1/2-MIGR1/MSC; and iv) CM-DiI-labeled C3H10T1/2-ICAM-1/MSC, which were all administered the relevant cells via the caudal vein. C3H10T1/2-ICAM-1/MSCs were able to ameliorate the expression of T4, TSH, TPOAb, TMAb and TGAb in vivo, attenuate thyroid follicle injury and decrease the splenic index in mice. They were also able to ameliorate the mRNA expression of IL-4, IL-10, IL-17 and INF-γ, and the modulation of the P38 and ERK-signaling pathways in the mouse spleen. Furthermore, ICAM-1 overexpression was able to modulate the nesting of MSCs in the thyroid gland and lung. These findings suggest that C3H10T1/2-ICAM-1/MSC may affect the differentiation, proliferation and migration of immunocytes through modulating the p38 and ERK signaling pathways, and that ICAM-1 may modulate the immunoregulatory effects of MSCs by affecting the migration of MSCs in vivo.

Anemia and hematinic deficiencies in anti-gastric parietal cell antibody-positive and -negative recurrent aphthous stomatitis patients with anti-thyroid antibody positivity.

Serum anti-gastric parietal cell (GPCA), anti-thyroglobulin (TGA), and anti-thyroid microsomal antibodies (TMA) can be found in some recurrent aphthous stomatitis (RAS) patients. This study mainly assessed whether serum GPCA, TGA, TMA and RAS itself played significant roles in causing anemia and hematinic deficiencies in TGA/TMA-positive RAS patients with GPCA positivity (GPCA+/TGA/TMA/RAS patients) or negativity (GPCA-/TGA/TMA/RAS patients). The mean corpuscular volume (MCV) and mean blood hemoglobin (Hb), iron, vitamin B12, and folic acid levels were measured and compared between any two of the four groups of 15 GPCA+/TGA/TMA/RAS patients, 69 GPCA-/TGA/TMA/RAS patients, 240 all autoantibodies-negative RAS patients (Abs-/RAS patients), and 342 healthy control subjects. GPCA+/TGA/TMA/RAS patients had significantly lower mean Hb (for men only) and vitamin B12 levels as well as significantly greater frequencies of Hb, iron, and vitamin B12 deficiencies than healthy control subjects. GPCA+/TGA/TMA/RAS patients had lower serum vitamin B12 level and higher MCV as well as a significantly greater frequency of vitamin B12 deficiency than GPCA-/TGA/TMA/RAS patients. Furthermore, both GPCA-/TGA/TMA/RAS and Abs-/RAS patients did have significantly lower mean Hb, MCV, and iron levels as well as significantly greater frequencies of Hb, iron and vitamin B12 deficiencies than healthy control subjects. There were no significant differences in blood data between GPCA-/TGA/TMA/RAS and Abs-/RAS patients CONCLUSION: Both serum GPCA positivity and RAS itself are the contributing factors causing anemia and hematinic deficiencies in GPCA+/TGA/TMA/RAS patients. RAS itself but not TGA/TMA positivity plays a significant role in causing anemia and hematinic deficiencies in GPCA-/TGA/TMA/RAS patients.

Antigastric parietal cell and antithyroid autoantibodies in patients with recurrent aphthous stomatitis.

Anti-gastric parietal cell antibody (GPCA), anti-thyroglobulin antibody (TGA), and anti-thyroid microsomal antibody (TMA) have not yet been reported in patients with recurrent aphthous stomatitis (RAS). This study mainly assessed the frequencies of the presence of serum GPCA, TGA, and TMA in different types of RAS patients. Serum GPCA, TGA, and TMA levels were measured in 355 RAS patients of different subtypes and in 355 age- and sex-matched healthy control individuals. We found that 13.0%, 19.4%, and 19.7% of 355 RAS patients, 16.7%, 23.3%, and 21.7% of 60 major-typed RAS patients, 12.2%, 18.6%, and 19.3% of 295 minor-typed RAS patients, 18.1%, 20.0%, and 21.9% of 160 atrophic glossitis-positive RAS (AG+/RAS) patients, and 8.7%, 19.0%, and 17.9% of 195 AG-negative RAS (AG-/RAS) patients had the presence of GPCA, TGA, and TMA in their sera, respectively. RAS, major-typed RAS, minor-typed RAS, AG+/RAS, and AG-/RAS patients all had a significantly higher frequency of GPCA, TGA, or TMA positivity than healthy control individuals (all p<0.001). Of 65 TGA/TMA-positive RAS patients whose serum thyroid-stimulating hormone (TSH) levels were measured, 76.9%, 12.3%, and 10.8% of these TGA/TMA-positive RAS patients had normal, lower, and higher serum TSH levels, respectively. We conclude that approximately one-third RAS patients may have GPCA/TGA/TMA positivity in their sera. Because some GPCA-positive patients may develop pernicious anemia, autoimmune atrophic gastritis, and gastric carcinoma, and some TGA/TMA-positive patients may have thyroid dysfunction such as hyperthyroidism and hypothyroidism, these patients should be referred to doctors for further management.

Antigastric parietal cell and antithyroid autoantibodies in patients with desquamative gingivitis.

Desquamative gingivitis (DG) is principally associated with erosive oral lichen planus (EOLP), mucous membrane pemphigoid (MMP), and pemphigus vulgaris (PV). Serum autoantibodies including antigastric parietal cell antibody (GPCA), antithyroglobulin antibody (TGA), and antithyroid microsomal antibody (TMA) were measured in 500 patients with DG, 287 EOLP without DG (EOLP/DG- ) patients, and 100 healthy control subjects. The 500 patients with DG were diagnosed as having EOLP in 455 (91%), PV in 40 (8%), and MMP in five (1%) patients. We found that 37.0%, 43.6%, and 42.6% of 500 patients with DG, 39.6%, 46.4%, and 45.1% of 455 EOLP with DG (EOLP/DG) patients, and 18.5%, 27.5%, and 30.3% of 287 EOLP/DG- patients had the presence of GPCA, TGA, and TMA in their sera, respectively. DG, EOLP/DG, and EOLP/DG- patients all had a significantly higher frequency of GPCA, TGA, or TMA positivity than healthy control subjects (all P-values < 0.001). Moreover, 455 EOLP/DG patients had a significantly higher frequency of GPCA, TGA, or TMA positivity than 287 EOLP/DG- patients (all P-values < 0.001). Of 210 TGA/TMA-positive patients with DG whose serum thyroid-stimulating hormone (TSH) levels were measured, 84.3%, 6.7%, and 9.0% patients had normal, lower, and higher serum TSH levels, respectively. We conclude that 73.4% DG, 77.1% EOLP/DG, and 47.4% EOLP/DG- patients may have GPCA/TGA/TMA positivity in their sera. Because part of GPCA-positive patients may develop pernicious anemia, autoimmune atrophic gastritis, and gastric carcinoma, and part of TGA/TMA-positive patients may have thyroid dysfunction, these patients should be referred to medical department for further management.

Thyroid Disturbance in Patients with Chronic Hepatitis C Infection: A Systematic Review and Meta-analysis.

The involvement of thyroid autoimmunity and dysfunction in patients with chronic hepatitis C virus (HCV) infection before interferon-α (IFN-α) therapy remains controversial. We performed this meta-analysis to evaluate the association of HCV infection with the presence of anti-thyroid antibodies and dysthyroidism. A literature search was carried out to collect articles dated up to August 2015 to identify observational studies which compared the prevalence of anti-thyroid antibodies and thyroid dysfunction in IFN-α naïve chronic HCV-infected subjects with non-HCV infected controls. Random-effect or fixed-effect meta-analyses were applied and results reported as odds ratios (ORs) with 95% confidence intervals (CIs). Twelve studies were included, involving 1,735 HCV-infected and 1,868 non-HCV infected subjects. Pooled anti-thyroid antibody prevalence tended to be higher in HCV-infected subjects. The prevalence of anti-thyroglobulin antibody (TGAb), anti-thyroid peroxidase antibody (TPOAb), anti-thyroid microsomal antibody (ATMA) were 2.40-fold, 1.96-fold and 1.86-fold higher in HCV-infected subjects than in controls, respectively. The prevalence of hypothyroidism also differed by HCV infection status, with a pooled risk of 3.10 (95%CI: 2.19-4.40) in HCV-infected subjects. However, the results did not show a significant difference in the prevalence of hyperthyroidism between the two groups. Chronic HCV infection may be an independent risk factor for thyroid disturbance. It is advisable for the clinicians to monitor both thyroid antibodies and function in the course of chronic HCV infection, independent of IFN-α treatment.

Hashimoto's thyroiditis and papillary carcinoma in an adolescent girl: A case report.

Hashimoto's thyroiditis with thyroid cancer in childhood is not as common in the adult population. Hashimoto's thyroiditis is an autoimmune disease associated with autoantibodies, and the association between Hashimoto's thyroiditis and papillary carcinoma of the thyroid remains controversial. The present study reported a 15-year-old adolescent girl with the diagnosis of Hashimoto's thyroiditis with thyroid cancer. With the complexity of the clinical manifestations of Hashimoto's thyroiditis, it can be expressed as not only hyperthyroidism or hypothyroidism, but also normal thyroid function. The long-term treatment, and for children with thyroid cancer, early diagnosis is particularly difficult. In the present case, the diagnosis of Hashimoto's thyroiditis is primarily based on clinical manifestations, anti-thyroglobulin antibody and anti-thyroid microsomal antibody. The only diagnostic imaging ultrasound was negative. The present study discussed the possible reason and the identification of this unique case of Hashimoto's thyroiditis with thyroid cancer.

Correlation of serum antithyroid microsomal antibody and autologous serum skin test in patients with chronic idiopathic urticaria.

Background:About 25–45% of patients of chronic urticaria (CU) have been stated to have histamine releasing autoantibodies in their blood. The term autoimmune urticaria is increasingly being accepted for this subgroup of patients. Review of the literature suggests high autologous serum skin test (ASST) positivity and presence of antithyroid microsomal antibodies in patients with autoimmune urticaria.Aims:To study prevalence of ASST positivity and antithyroid microsomal antibodies in chronic “idiopathic” urticaria and to study the correlation between the two parameters.Methods:All patients of chronic idiopathic urticaria satisfying inclusion/exclusion criteria were enrolled in the study after written informed consent. Patients of CU secondary to infections and infestations, physical urticaria including dermatographism, mastocytosis, urticarial vasculitis and those on treatment with immunosuppressive drugs for urticaria were excluded from the study. In all of these patients, complete blood count; ASST, serum T3/T4/thyroid stimulating hormone levels, antithyroid microsomal antibody (AMA) levels were done. Statistical analysis was done by Chi-square test, Fisher exact test and Kappa statistics.Results:Study included 24 males and 26 females with mean age of 39.54 years. Majority of patients belonged to 20–40 years of age. Females showed more ASST positivity. A total of 12 out of 50 (24%) patients showed positive ASST. A total of four out of 12 (33.33%) had positive ASST and raised AMA levels.Conclusion:Only 25% of patients of chronic idiopathic urticaria had positive ASST. ASST and AMA levels were positively correlated in our study. Further studies are required to authenticate this association.

Autoantibody profile in a cohort of South Indian children with Kawasaki disease

Objective: There is no clear data on autoantibody levels in Kawasaki Disease (KD) especially from the Indian Subcontinent. Aim: To look for the presence of organ nonspecific and organ specific antibodies to strengthen the search for an autoimmune cause of KD. We tested the presence of antinuclear antibody (ANA) and antithyroid microsomal antibody (TMA) in children with KD, 6 months after the acute phase. Anti Neutrophil Cytoplasmic Antibody (pANCA, cANCA), Anti Endothelial Cytoplasm Antibody (AECA) and Anti Smooth Muscle Antibody (SMA) was additionally tested in those with elevated titers of ANA and/or TMA. Materials and Methods: Prospective case-control study of 24 children with KD on follow up and an equal number of age and sex matched controls. Historical data about acute phase of illness was obtained from the medical records. After obtaining institutional ethics committee clearance and informed consent from the parents, blood was tested for ANA and TMA by the indirect immunofluorescence method (IIF), using a kit developed by Euroimmun. Positive samples were additionally tested for pANCA, cANCA, AECA and SMA. Relationship of autoantibody elevation and clinical course in the cases was determined. Results: The age of the study group was 4 ΁ 3.2 years. Incomplete KD was seen in 12.5% of the cases. Five cases (21%) had cardiac involvement. All but one with mitral and tricuspid regurgitation resolved after the acute phase of the disease. Only her ANA was elevated. Two children (8%) positive for TMA did not show any cardiac abnormalities. Further antibody testing was negative. All three children with elevated autoantibodies were females. ( P value = 0.02: statistically significant). Conclusion: Elevated autoantibodies in three (12.5%) children after the acute phase may suggest the role of autoimmunity in the etiopathogenesis of KD, even though our observations were not statistically significant.

Hemoglobin, iron, and vitamin B12 deficiencies and high blood homocysteine levels in patients with anti-thyroid autoantibodies

Autoimmune thyroiditis can be diagnosed by measuring patients' serum levels of thyroid stimulating hormone (TSH), anti-thyroglobulin antibody (TGA), and anti-thyroid microsomal antibody (TMA). This study evaluated whether there were hematinic deficiencies, high blood homocysteine levels, and serum gastric parietal cell antibody (GPCA) positivity in patients with TGA or TMA. The blood hemoglobin (Hb), iron, vitamin B12, folic acid, homocysteine and TSH concentrations and the serum GPCA level in 190 TGA- or TMA-positive patients were measured and compared with the corresponding levels in 190 age- and sex-matched healthy control subjects. We found that 31 (16.3%), 27 (14.2%), 12 (6.3%), and 2 (1.1%) TGA- or TMA-positive patients had deficiencies of Hb (Men<13g/dL, Women<12g/dL), iron (< 60μg/dL), vitamin B12 (< 200pg/mL), and folic acid (< 4ng/mL), respectively. Moreover, 25 (13.2%) and 48 (25.3%) TGA- or TMA-positive patients had abnormally high blood homocysteine level and serum GPCA positivity, respectively. TGA- or TMA-positive patients had a significantly higher frequency of Hb (p<0.001), iron (p<0.001), or vitamin B12 deficiency (p=0.001), of abnormally elevated blood homocysteine level (p=0.001), or of serum GPCA positivity (p<0.001) than healthy control subjects. Of 190 TGA- or TMA-positive patients, 8 (4.2%) had lower serum TSH level (< 0.1μIU/mL, suggestive of hyperthyroidism), 163 (85.8%) had serum TSH level within normal range (0.1-4.5μIU/mL), and 19 (10%) had higher serum TSH level (>4.5μIU/mL, suggestive of hypothyroidis). There are significant deficiencies of hemoglobin, iron, and vitamin B12, abnormally high blood homocysteine levels, and serum GPCA positivity in TGA- or TMA-positive patients. In addition, the majority (85.8%) of TGA- or TMA-positive patients had euthyroid and only a small portion (14.2%) of TGA- or TMA-positive patients had either hypothyroidism or hyperthyroidism.

Tubulointerstitial nephritis and uveitis syndrome with transient hyperthyroidism in an elderly patient

A 69-year-old Japanese woman without any specific medical or family history was admitted to our hospital for renal insufficiency with proteinuria. On laboratory examinations, deteriorated renal function (blood urea nitrogen level was 34.9 mg/dL and creatinine level was 1.78 mg/dL) and elevated urinary levels of N-acetyl-β-D-glucosaminidase (23.4 U/L) and β2-microgloblin (20200 μg/L) were observed. We performed a renal biopsy. The biopsied specimen showed severe diffuse infiltration of mononuclear cells into the interstitium, with normal glomeruli, and these findings were compatible with acute tubulointerstitial nephritis (ATIN). At that time, ATIN seemed to be idiopathic. We performed gallium scintigraphy, and the results revealed uptake by the bilateral kidneys, thyroid gland, and right parotid gland. Serum thyroid stimulating hormone (TSH) was undetectable, free triiodothyronine was normal (3.11 pg/mL), and free thyroxine was elevated to 2.4 ng/dL. The titers of antithyroglobulin and antithyroid microsomal and TSH-receptor antibodies were not elevated. Two months later, burning pain and conjunctival congestion developed in both eyes. She had uveitis, as diagnosed by slit-lamp examination. Topical corticosteroid was used for the uveitis with success. We could not detect any cause of the uveitis, so a diagnosis of tubulointerstitial nephritis and uveitis syndrome (TINU syndrome) with associated hyperthyroidism was made. Treatment was started with 15 mg/day of prednisolone. Now her renal function is slowly recovering. There are few reports of TINU syndrome with transient hyperthyroidism. This case suggests the possibility of thyroid dysfunction in patients with TINU syndrome. A laboratory evaluation of thyroid function should be considered in the diagnostic evaluation of TINU syndrome.

A Case of a False-Positive Anti-Myeloperoxidase Antibody ELISA in a Patient with Hypothyroidism

We present a case of a false-positive anti-myeloperoxidase (MPO) antibody result on an ELISA in a patient with anti-thyroid microsomal antibody (TMA)-positive hypothyroidism. A 41-year-old woman presented with dyspnea on exertion. The initial evaluation revealed pericardial effusion associated with hypothyroidism. In addition, microscopic hematuria with normal renal function and positive cytoplasmic anti-neutrophil cytoplasmic antibodies (c-ANCA) on immunofluorescent assay were found. In further evaluation, elevated anti-TMA and MPO antibodies by ELISA. While no definite signs of vasculitis were present, the clinical state improved with thyroid hormone replacement and diuretics. Anti-MPO antibody was still positive in the follow-up tests, and microscopic hematuria persisted. On the basis of previous reports that thyroid peroxidase and MPO molecules contain cross-reactive epitopes that are exposed in denaturated molecules, we suggest that in a patient with anti-TMA-positive hypothyroidism, anti-MPO antibody might also be positive on ELISA without clinical signs of vasculitis.

Steroid-responsive encephalopathy in autoimmune thyroiditis: Clinical spectrum and MRI observations in three cases

Hashimoto's encephalopathy (H.E.) is probably of autoimmune etiology, and manifests with seizures, stroke-like episodes, cognitive decline, neuropsychiatric symptoms, myoclonus. It is presumed to be autoimmune in origin with high serum titers of antithyroid peroxidase antibodies (anti-TPA). Thyroid function might often be normal. The diagnosis is arrived at by excluding other toxic, metabolic and infectious causes of encephalopathies, supportive clinical profile, elevated thyroid antibodies and optimum steroid response. We present the characteristic phenotypic manifestations, magnetic resonance imaging and electroechography observations and response to immunomodulation with follow-up in three cases of H.E. All the three cases manifested with subacute to chronic progressive encephalopathy, cerebellar dysfunction, seizures, behavioral abnormalities and oculomotor disturbances and had evidence of hypothyroidism, elevated titers of anti-TPA and positive thyroid anti-microsomal antibodies. Atypical and uncommon presentations are known. This report emphasizes that a high index of suspicion is often required in cases with “investigation negative encephalopathy” for early diagnosis of H.E.

Prevalence of autoantibodies in patients of psoriasis

Psoriasis is a common chronic inflammatory disease of the skin and joints. Autoantibodies have been reported in psoriasis patients. Objective of the study was to see the prevalence of various autoantibodies in patients of psoriasis and its correlation with gender, age, and type. Anti-nuclear antibody and antibody to double-stranded deoxyribonucleic acid were studied by indirect enzyme linked immunosorbent assay, rheumatoid factor was done by latex agglutination, whereas anti-thyroid microsomal antibody (anti-TMA) was by gelatin agglutination method. About 28.8% of psoriasis cases were positive for atl east one autoantibody. Age of onset (P=0.033) and types of psoriasis (P=0.037) had significant association with gender. Anti-double-stranded deoxyribonucleic acid (P=0.029) and anti-thyroid microsomal antibody (P=0.002) had significant association with types of psoriasis. Gender wise distribution of psoriasis in age group had significant (P=0.03) association with anti-TMA. This study concludes that the autoantibodies are found to be present in psoriasis patients or latent autoimmune diseases develop in psoriasis patients without any clinical symptoms.

HISTOPATHOLOGY OF VGKC ANTIBODY–ASSOCIATED LIMBIC ENCEPHALITIS

We describe histopathology from whole brain in a patient with autoimmune limbic encephalitis with high titers of voltage-gated potassium channels (VGKC) antibodies. ### Case report. A 56-year-old man had a 4-month history of intermittent confusion and two seizures. He appeared well but had periods of confabulation and fear. His history included borderline hypertension. He had stopped smoking. Blood pressure was 147/102 mm Hg. Mini-Mental State Examination score1 was 18/30, indicating disorientation with poor working memory. The patient's VGKC-Ab level was 3,327 pM (normal, 0–100).2 His Na level was 130 mmol/L (normal, 135–145 mmol/L). Antineuronal (anti-Hu and Yo) and thyroid antimicrosomal antibodies, erythrocyte sedimentation rate, C-reactive protein, dsDNA, extractable nuclear antigen, antineutrophil cytoplasmic antibodies, B12, folate, angiotensin-converting enzyme, chest x-ray, and treponemal serology were normal. The patient refused a lumbar puncture. The EEG showed sharp waves over both frontoparietal regions. Brain MRI (T2 and fluid-attenuated inversion recovery) showed left hippocampal atrophy. The patient died in his sleep 7 days after the laboratory studies began. The patient's brain weighed 1,367 g and was macroscopically normal. Paraffin-embedded specimens (4–7 μm thickness) were stained with hematoxylin & eosin (Nissl methods). Immunohistochemistry was performed using antibodies against CD3, CD4, CD8, CD20, CD45, CD68, glial fibrillary acid protein, herpes simplex virus types 1 and 2, measles, cytomegalovirus, SV40, and toxoplasma. Staining for infectious agents was negative. There were no organisms, …

Prevalence of Anti-Thyroid Antibodies in Patients with Primary Thyroid Disorders

To determine prevalence of thyroid antimicrosomal and antithyroglobulin antibodies among patients with primary thyroid disorders. Descriptive cross-sectional study. Kenyatta National Hospital, July 2003 to August 2004. Antimicrosomal antibodies (anti-TPOAbs) were detected in 51.4% of all the patients while 36.1% tested positive for the antithyroglobulin antibodies (anti- TgAbs). Among the hyperthyroid patients, anti-TPOAbs and anti-TgAbs were in 50.8% and 33% respectively while 53.3% and 46.7% of the hypothyroid patients tested positive for anti-TPOAbs and anti-TgAbs respectively. Most of the patients who showed positivity for anti-TgAbs (88.5%) also tested positive for anti-TPOAbs. More than half of the patients with primary thyroid disorders show presence of autoimmune thyroid markers, with anti TPO antibodies being more prevalent.