Hashimoto\'s encephalopathy (HE) has been a poorly understood disease. It has been described in all age group, yet, there is no specific HE marker. Additionally, the treatment data in the available studies are frequently divergent and contradictory. Therefore, the aim of our systematic and critical review is to evaluate the diagnosis and treatment of HE in view of the latest findings. The databases browsed comprised PubMed, Scopus, and Google Scholar as well as Cochrane Library, and the search strategy included controlled vocabulary and keywords. A total of 2443 manuscripts were found, published since the beginning of HE research until February 2024. In order to determine validity of the data collected from studies, bias assessment was performed using RoB 2 tool. Ultimately, six studies were included in our study. HE should be considered in the differential diagnosis in patients with psychiatric and neurological symptoms. According to our findings, negative thyroid peroxidase antibodies (anti-TPOs) may represent a valuable parameter in ruling out HE. Nonetheless, this result cannot be used to confirm HE. Furthermore, the proposed anti NH2-terminal-α-enolase (anti-NAE) is non-specific for HE. The effectiveness of glucocorticoid therapy is 60.94%, although relapse occurs in 31.67% of patients following the treatment. Our review emphasizes the significance of conducting further large-scale research and the need to take into account the potential genetic factor.

Our article examines a rare case where hypothyroidism due to Hashimoto\'s thyroiditis progressed, after a long period (three years) of L-thyroxine substitution, into confirmed hyperthyroidism due to Graves\' disease in a 69-year-old man. The article explores possible mechanisms of this unusual transition based on our case and others reported in the literature. Findings suggest that the coexistence of Hashimoto\'s thyroiditis and Graves\' disease can lead to transitions between hypothyroidism and hyperthyroidism, influenced by the predominance of involved antibodies and residual capacity of thyroid tissue. The authors emphasize the importance of further studies to better understand these transitions and identify at-risk patients. In conclusion, the article highlights the necessity of considering the rare possibility of transition to Graves\' disease in patients presenting with persistent hyperthyroidism despite cessation of L-thyroxine.

Chronic spontaneous urticaria and chronic inducible urticaria (CSU/CindU) are caused by mast cell and basophil activation leading to degranulation and the release of histamine and several other mediators. Three kinds of factors can trigger mast cells in CSU: (1) activation of stimulating receptor(s) on the mast cell membrane, (2) upregulation of certain receptor(s), and (3) intracellular dysregulation in signaling with overexpression of the spleen tyrosine kinase (SYK) or reduced activation of the inhibitory Src homology 2 (SH2)-containing inositol phosphatases (SHIP)-related pathways. In CSU, two major endotypes exist based on the primary receptor activating mechanism: type I hypersensitivity (IgE-mediated, directed against auto-allergens) and type IIb (autoimmune, via IgG autoantibodies directed against IgE or the IgE-receptor). Their treatment responses vary. We discuss in vitro and in vivo biomarkers.
Patients with auto-allergic CSU have clinical characteristics that can distinguish them partly from those with autoimmune CSU. Most importantly, their disease generally presents a less aggressive course, a better response to second generation (up-dosed) antihistamines and a good response to omalizumab, if necessary. Meanwhile, autoimmune CSU/CindU patients fare less well and often need immunosuppressive drugs. Biomarkers that might help endotype CSU/CindU patients and select the most appropriate treatment, dose, and duration, e.g., for autoallergic CSU, high total IgE and IgE against auto-allergens; for autoimmune CSU, low IgE, basopenia, and IgG against autoantigens like thyroid peroxidase and a positive autologous serum skin test (but sometimes also positive in autoallergy). Some biomarkers are easily accessible but of low specificity; others are highly specific but more futuristic.

Background and aims The prevalence of vitamin B12 deficiency is found to coexist in hypothyroid patients, causing the persistence of symptoms concomitant to both diseases even on adequate thyroxine supplementation. Primary objective To study vitamin B12 levels in patients with hypothyroidism. Secondary objective To study the clinical profile of patients with hypothyroidism with special reference to anemia, and to study the association between vitamin B12 deficiency with anti-thyroid peroxidase (anti-TPO) antibodies and anti-thyroglobulin (anti-Tg) antibodies in patients with hypothyroidism. Methods and results A single-centric cross-sectional study was carried out over a period of one year. Among 100 hypothyroid patients, 68% were found to be vitamin B12 deficient, among whom 73.5% were females. Of patients with raised anti-TPO antibodies, 78.6% had vitamin B12 deficiency (p = 0.01), while 78% of patients with raised anti-Tg antibodies were vitamin B12 deficient (p = 0.07). The Pearson correlation coefficient (r) of vitamin B12 with anti-TPO and anti-Tg antibodies was -0.302 (p = 0.002) and -0.253 (p = 0.011), respectively. Conclusion There is a predilection of hypothyroid patients toward developing anemia, with vitamin B12 deficiency as a major etiology. This finding can be correlated with the hematopoietic action of thyroid-stimulating hormones as well as autoimmune thyroid disease predisposing to pernicious anemia.

(1) Background: Previous studies have reported a correlation between serum anti-Thyroglobulin-antibodies (TgAb) and papillary thyroid carcinoma. The aim of our study was to evaluate whether serum TgAb and anti-thyroid-peroxidase antibody (TPO) positivity was also related to pre-neoplastic histological changes such as papillary-like nuclear features (PLNF) and with the presence of lymphocytic infiltrate (LI) in thyroid surgical specimens. (2) Methods: The study was retrospectively carried out on 70 consecutively recruited patients who underwent thyroidectomy for benign process and whose TgAb and TPOAb values were retrieved from clinical records. Histological sections of thyroid surgical samples were revised, looking for PLNF and lymphocytic infiltrate. HBME1 expression was assessed by immunohistochemistry. (3) Results: Our results showed a significant association between TgAb, PLNF, and lymphocytic infiltrate. The presence of TgAb was highly specific, but less sensitive, in predicting the presence of PLNF (sensitivity = 0.6, specificity = 0.9; positive predictive value (PPV) = 0.88; negative predictive value (NPV) = 0.63). TgAb positivity showed a good association with the presence of lymphocytic infiltrate (sensitivity = 0.62, specificity = 0.9; PPV = 0.88 and NPV = 0.68). HBME1 immunoreactivity was observed in the colloid of follicles showing PLNF and/or closely associated with LI. (4) Conclusions: The presence of PLNF and LI is associated with serum TgAb positivity. The presence of TgAb and of LI could be triggered by an altered thyroglobulin contained in the HBME1-positive colloid, and could be a first defense mechanism against PLNF that probably represent early dysplastic changes in thyrocytes.

UNASSIGNED: This study was aimed at determining the frequency of thyroid autoimmunity and subclinical hypothyroidism in patients with hyperprolactinemia due to prolactinoma compared to well-matched healthy controls.
UNASSIGNED: This was a cross-sectional study wherein 78 treatment naïve prolactinoma patients and ninety-two healthy control subjects were recruited. Serum prolactin (PRL), thyroid-stimulating hormone (TSH), total thyroxine (T4), circulating anti-thyroid peroxidase (anti-TPO), and anti-thyroglobulin (anti-Tg) antibody levels were measured in all study subjects. Progression of the antibody-positive population to subclinical hypothyroidism was determined.
UNASSIGNED: The median PRL level among patients was 166 ng/ml (IQR 85-467) compared to 11.4 ng/ml (IQR 8.5-15.9) in controls (P < 0.001). There was no significant difference in levels of T4 (P = 0.83) and TSH (P = 0.82) between the cases and controls. Overall, 25% of patients had the presence of anti-thyroid antibodies as compared to 20% of controls (P = 0.56). SCH was more common in antibody-positive hyperprolactinemia subjects compared with antibody-positive controls.
UNASSIGNED: We did not find an increased prevalence of thyroid autoimmunity among untreated prolactinoma patients compared to healthy controls. At the same time, subclinical hypothyroidism was more common in thyroid antibody-positive patients with hyperprolactinemia than positive controls.

BACKGROUND: Serum anti-thyroid peroxidase antibody (anti-TPO) and anti-thyroglobulin antibody (anti-Tg) levels are key indicators for the diagnosis of autoimmune diseases, especially autoimmune thyroiditis. Before the thyroid autoantibodies turn from negative to positive, it is unknown whether any clinical indicators in the body play a warning role.
OBJECTIVE: To establish an early prediction model of seroconversion to positive thyroid autoantibodies.
METHODS: This retrospective cohort study collected information based on clinical laboratory data. A logistic regression model was used to analyse the risk factors associated with a change in thyroid autoantibodies to an abnormal status. A machine-learning approach was employed to establish an early warning model, and a nomogram was used for model performance assessment and visualisation. Receiver operating characteristic (ROC) curves, calibration curves, and decision curve analyses were used for internal and external validation.
RESULTS: Logistic regression analysis revealed that albumin to globulin ratio, triglyceride levels, and Glutamic acid levels among liver function and some metabolism-related indicators, high density lipoprotein C among metabolism-related indicators, and cystatin C among renal function indicators were all risk factors for thyroid antibody conversion (P < 0.05). In addition, several indicators in the blood count correlated with thyroid conversion (P < 0.05). Changes in the ratio of free thyroxine to free triiodothyronine were a risk factor for positive thyroid antibody conversion (ORfT4/fT3 = 1.763; 95% confidence interval 1.554-2.000). The area under the curve (AUC) of the early warning model based on the positive impact of clinical laboratory indicators, age, and sex was 0.85, which was validated by both internal (AUC 0.8515) and external (AUC 0.8378) validation.
CONCLUSIONS: The early warning model of anti-TPO and anti-Tg conversion combined with some clinical laboratory indicators in routine physical examination has a stable warning efficiency.

Introduction There is scanty evidence regarding the role of autoimmunity in vitiligo, especially in the Asian population. Moreover, the existing studies reported conflicting results. This prompted the investigators to identify the association of thyroid autoimmunity with vitiligo by employing a case-control design in this setting. Methodology The present study was a hospital-based case-control study conducted in one of the tertiary care hospitals of North India. We recruited 30 subjects aged 16-60 years with vitiligo attending the skin and venereal diseases outpatient department. The subjects attending the general medicine outpatient department without having a diagnosis of vitiligo were considered for the control group. Thyroid hormones (FT3 and FT4), thyroid-stimulating hormones, anti-thyroid peroxidase (anti-TPO) antibodies, and anti-thyroglobulin (anti-TG) antibodies were the primary investigations performed among the study subjects. Results The mean age of the study subjects was 31.3 (SD: 13.3) years. Both the case and control groups were comparable based on selected socio-demographic variables (p > 0.05). There was a statistically significant difference in terms of mean anti-TPO and anti-TG values between the case and control groups in which subjects with vitiligo reported significantly higher values (p < 0.05). Conclusion Our study reported a significant elevation in the mean values of the thyroid antibodies (anti-TG and anti-TPO antibodies) in vitiligo subjects compared to control subjects in this setting. Hence, screening for autoimmune thyroid diseases among patients with vitiligo is suggested for the early detection and the initiation of appropriate intervention.

BACKGROUND: Rheumatoid arthritis (RA) is one of the most common chronic non-organ-specific autoimmune diseases; meanwhile, autoimmune thyroid disease (AITD) is the most common organ-specific autoimmune disease that can lead to hypo or hyperthyroidism. Although the etiology of both diseases is complex with a combination of genetic and environmental factors, there are overlaps in genes contributing to the pathogenesis of both diseases. Numerous studies found a correlation between thyroid abnormality and RA in different populations, yet some didn\'t. This study is aimed to evaluate the prevalence of thyroid dysfunction, AITD, and anti-thyroid peroxidase (anti-TPO) positively in Iranian patients with RA.
METHODS: A total of 250 RA patients and 248 patients with non-inflammatory rheumatologic disease were included in this case-control study. All participants underwent complete clinical and laboratory assessments. Participants were also assessed for thyroid function testing, including anti-TPO antibodies.
RESULTS: Thyroid dysfunction was twice as common in RA patients as in controls (OR = 2.16; P-value > 0.001). Overt hypothyroidism was the most common thyroid dysfunction among RA patients (58 out of 84). Anti-TPO positivity was also significantly more common in RA compared with controls (OR = 2.65; P-value > 0.001). The proportion of controls and RA patients with AITD were 9 and 21.5%, respectively. AITD was found 2.8 times more common in RA group than controls (OR = 2.77; P-value > 0.001).
CONCLUSIONS: It was demonstrated that RA was an independent factor associated with thyroid dysfunction and AITD.

UNASSIGNED: The current study aimed to determine association of anti-TPO with LH/FSH in PCOS women.
UNASSIGNED: Current case control study included 33 diagnosed PCOS women and 32 age matched healthy women and were analysed for body mass index (BMI) and waist to hip ratio (WHR), fasting blood glucose (FBG), free T3 (FT3), free T4 (FT4), Thyroid stimulating hormone (TSH), dehydroepiandrostenedione (DHEA-S), total testosterone, follicular stimulating hormone (FSH), luteinizing hormone (LH) and anti thyroperoxidase antibodies (anti-TPO). Data was statistically analysed by Student\'s t - test and Pearson\'s correlation analysis.
UNASSIGNED: Of the total PCOS women, 45% were obese and 34.37% had raised anti-TPO. The biochemical profile of obese PCOS women showed significantly raised FBG (p<0.0001), LH (p<0.0001), Testosterone (p<0.0001) and DHEA-S (p=0.0021) as compared to non-obese PCOS women. The LH/FSH ratio was significantly raised in PCOS women as compared to control (p<0.0001). Pearson\'s correlation analysis showed a significant association of anti-TPO with FBS, testosterone, LH and LH/FSH in obese PCOS and with Testosterone and LH in non-obese PCOS women using SPSS 21.
UNASSIGNED: The current study shows a high prevalence of AITD in euthyroid PCOS women and suggests a strong link of euthyroid obese PCOS women to autoimmunity due to the hyper-anderogenism and a higher LH/FSH ratio.