Ramadan fasting may influence thyroid hormone homeostasis through changes in meal timing, circadian rhythm, and medication adherence. Its clinical impact appears to vary according to baseline thyroid status. This narrative review summarized the available evidence on the effect of Ramadan fasting on thyroid function among healthy, hypothyroid, and hyperthyroid individuals. A structured narrative review of the literature was conducted using PubMed/MEDLINE and Google Scholar from database inception to 2 July 2026. Original research, prospective and retrospective cohort studies, randomized clinical trials, systematic reviews, and relevant clinical guidance documents assessing thyroid function before, during, or after Ramadan were included. Evidence was organized according to thyroid status to facilitate clinical interpretation. Pooled evidence indicates that Ramadan fasting preserves hypothalamic-pituitary-thyroid (HPT) axis function within normal physiological reference ranges in healthy adults. In hypothyroid patients receiving levothyroxine, an increase in post-Ramadan TSH has been observed in several studies, although the contribution of fasting itself versus changes in medication timing, sleep, and circadian patterns remains uncertain; FT4 usually remained stable, and the biochemical change was more evident in patients with higher baseline TSH or poorer control. No single levothyroxine timing regimen consistently outperformed others, although adherence and patient preference were important determinants. In hyperthyroid patients, direct evidence is limited and recommendations are primarily based on expert opinion; fasting may be considered on an individualized basis in clinically stable patients with well-controlled disease, whereas active thyrotoxicosis warrants caution and individualized assessment. Ramadan fasting is usually safe from a thyroid perspective in healthy individuals and most stable hypothyroid patients, but biochemical monitoring and individualized counseling are recommended. Controlled studies in hyperthyroidism and trials evaluating alternative levothyroxine regimens are needed.

This study investigated the thyroid effects of azole fungicide mixtures in male rats, addressing the gap in regulatory assessments that typically focus on single chemicals rather than combined exposures. Using a 28-day rat model, binary and ternary mixtures of azole fungicides were tested at high doses, with thyroid hormone levels, liver enzyme activity, and thyroid tissue changes as the key endpoints. The mixtures caused elevated TSH, reduced T4, increased UGT enzyme activity, and thyroid tissue alterations, including follicular cell hypertrophy and hyperplasia. Interestingly, the mechanism observed with single-compound exposures (hepatic metabolism driving secondary TSH elevation) appeared less prominent in the mixture groups. Whether these responses reflect additive, less-than-additive, or more-than-additive interactions could not be determined without formal dose-response modeling. As the tested dose (NOAELx10) is substantially higher than the human realistic exposure levels permitted under the current regulation, direct extrapolation of the present findings to realistic human exposure conditions is limited. However, the current regulatory evaluation with respect to the effect dose was confirmed. While existing approaches appear adequate, a deeper understanding of thyroid-specific endpoints is needed to ensure that mixture risk assessments remain robust and appropriately protective.

Thyroid disease is a common endocrine disorder in pregnant women and important to recognize. The clinical management relies on biochemical assessment of thyroid function and thyroid autoantibodies from a panel of routinely available tests. A challenge regarding biochemical assessment in pregnancy relates to the physiological adaptations that influence the analyses used for diagnosis and monitoring of maternal thyroid disease. The physiological adaptations include an increased activity of the thyroid gland, an increase in the levels of binding proteins, and a suppression of the immune system which implies that biochemical test results should be interpreted in the context of pregnancy. This narrative review will discuss the biochemical assessment of thyroid function and thyroid autoantibodies in pregnancy with a focus on the biochemical methods used and the interpretation of results including strategies for establishment of reference intervals. A key implication is that biochemical results obtained in pregnancy should be considered according to the timing of the blood sampling and the biochemical method used. This is reflected by recommendations on the use of method- and trimester-specific reference intervals as part of clinical care, but similar considerations apply when thyroid function tests and thyroid autoantibodies are evaluated as part of population monitoring and used for definition of exposure in scientific outcome studies. Future research is encouraged to support the biochemical assessment and interpretation of thyroid function tests and thyroid autoantibodies in pregnancy. Future perspectives include advancements in the biochemical methods and in the methodology applied for establishment of reference intervals or clinical decision limits.

Hypercalcaemia is a recognised complication of thyrotoxicosis usually related to increased bone resorption. However, coexistent hyperphosphataemia is uncommon and may create diagnostic uncertainty. It is postulated that serum calcium and phosphate levels rise due to high bone turnover and increased renal reabsorption of phosphate in response to excess thyroxine. Hypercalcaemia may also alter the clinical presentation of thyrotoxicosis, making both diagnosis and management challenging. We report two patients with this unusual biochemical presentation. The first patient was a 69-year-old woman who presented with body aches, lethargy, low mood, constipation, polyuria, and proximal muscle weakness for 2 months. The second was a 56-year-old woman who presented with palpitations, anxiety, tremulousness, dyspnoea, dysphagia, and headache for 4 months. Both had multinodular goitres (MNGs) without eye disease. Their TSH levels were undetectably low with extremely high free T4 levels. Serum calcium and phosphate levels were high in both patients. ALP levels were mildly elevated, vitamin D levels were deficient or insufficient, and parathyroid hormone (PTH) levels were low-normal. DXA scans revealed severe osteoporosis. Both patients improved clinically and biochemically with adequate intravenous hydration, frusemide, carbimazole, propranolol, and bisphosphonates. The second patient underwent a successful left thyroid lobectomy, while the first patient remained well on medical treatment. Unexplained hypercalcaemia and hyperphosphataemia should alert the clinicians to the possibility of underlying thyrotoxicosis. Prompt recognition and management is essential to prevent bone loss, correct metabolic abnormalities, and avoid complications. Clinicians should also consider the possibility of hypercalcaemia associated with thyroid dysfunction in patients presenting with nonspecific symptoms such as fatigue, constipation, proximal weakness, polyuria, or mood changes.

Hyperprolactinemia (HPRL) is a common adverse reaction induced by antipsychotic therapy in patients with schizophrenia, which greatly undermines medication adherence and impairs physiological functions of multiple body systems. In this real-world study, we analyzed retrospective prolactin testing data to compare the incidence of HPRL between schizophrenia patients and patients with other psychiatric disorders, so as to identify clinical high-risk factors. Meanwhile, hormones including thyroid-stimulating hormone (TSH), free tetraiodothyronine (FT4), free triiodothyronine (FT3), tetraiodothyronine (T4), Triiodothyronine (T3), and estradiol that closely correlated with prolactin metabolism were also included in the analysis. The results indicated that female patients with schizophrenia had the highest risk of HPRL (19.31%, n = 2009), and women during the prime reproductive (25-40 years) showed the highest average prolactin concentration (1,389.22 ± 50.138 mIU/L, n = 966). Distinct antipsychotics usage rates were observed among different clinical subgroups. Risperidone, paliperidone and sulpiride showed an increasing trend with elevated PRL levels, whereas quetiapine and aripiprazole were more frequently prescribed in the low-risk HPRL group. Antipsychotics showed divergent dopamine D2/D3 and 5-HT2A receptor-binding affinities (Ki values), and we constructed a weighted multi-receptor affinity index that demonstrated a strong linear correlation with the PRL risk score (R[2] = 0.878). Additionally, the average incidence of extrapyramidal symptoms (EPS) increased with rising PRL levels (P = 2.24E-10). Further analysis of EPS risk revealed distinct safety profiles across antipsychotics, with aripiprazole-characterized by low HPRL liability-demonstrating a higher EPS risk. The severe HPRL group presented a tendency of decreased thyroid function (TSH, P = 0.0027; FT4, P = 0.000031; FT3, P = 0.0076; T4, P = 0.0025) and a significant reduction in estradiol levels (P = 0.000049). Based on homogeneous clinical real-world data, this study comprehensively evaluated multiple antipsychotic medications simultaneously. It provides empirical clinical evidence for individualized medication strategies in patients with comorbid HPRL and EPS, and offers real-world evidence for the clinical early risk recognition, and long-term medication decision-making among patients with multiple adverse reactions concurrently.

The global incidence of thyroid cancer (TC), particularly differentiated thyroid cancer (DTC), has increased substantially over recent decades, while cardiovascular disease (CVD) remains the leading cause of death globally. As advances in diagnosis and treatment have significantly improved long-term survival in thyroid cancer patients, attention has increasingly shifted toward non-cancer complications, especially cardiovascular morbidity and mortality. Current evidence indicates that TC survivors have a higher risk of atrial fibrillation (AF), coronary artery disease (CAD), stroke, heart failure, and other cardiovascular complications than the general population. This association appears to result from a complex interaction between shared cardiometabolic risk factors and biological pathways. Obesity, metabolic syndrome, diabetes, hypertension, and dyslipidemia promote chronic inflammation, endothelial dysfunction, and insulin/IGF signaling, which contribute to atherosclerosis and tumor progression. Thyroid hormone dysregulation provides an additional link between thyroid cancer management and cardiovascular risk. Long-term thyroid-stimulating hormone (TSH) suppression therapy may induce subclinical hyperthyroidism and increase susceptibility to atrial fibrillation, ischemic heart disease, cardiac remodeling, and vascular dysfunction. Treatment-related factors, including thyroidectomy, radioactive iodine therapy, and targeted therapies, may also contribute to cardiovascular toxicity and influence long-term cardiovascular outcomes. Importantly, cardiovascular risk is heterogeneous among thyroid cancer survivors and may vary according to thyroid cancer risk category and current disease status, the intensity and duration of TSH suppression, radioactive iodine exposure, and patient-level characteristics such as age, sex, and baseline cardiovascular risk. This review synthesizes epidemiological and mechanistic evidence linking TC and CVD, with particular emphasis on shared metabolic and inflammatory pathways, hormonal and treatment-related factors, and changes in cardiovascular risk across different phases of thyroid cancer survivorship. Recognizing these determinants may support individualized cardiovascular risk assessment and help balance the oncologic benefits of thyroid cancer treatment against its potential long-term cardiovascular consequences.

Thyroid dysfunction and diabetes mellitus (DM) are two common endocrine disorders that share overlapping metabolic pathways. While several studies have explored the association between thyroid function and DM, findings have been inconsistent. Specifically, both elevated and suppressed thyroid-stimulating hormone (TSH) have been variably reported as risk or protective factors for diabetes, and the contribution of thyroid autoimmunity (thyroid peroxides antibody, TPOAb) to diabetes risk remains particularly contested across study populations. This study aimed to evaluate the relationship between thyroid function markers-TSH, free thyroxine (free T4), and TPOAb - and the presence of diabetes in Korean adults. This cross-sectional study analyzed data from 4910 adults aged 19 years or older who participated in the Korea National Health and Nutrition Examination Survey (KNHANES VI) from 2013 to 2015. Serum levels of TSH, free T4, and TPOAb were measured, and DM was defined based on fasting glucose levels, use of antidiabetic medication, or self-reported diagnosis. As KNHANES does not classify diabetes by etiological subtype, the DM group predominantly reflects type 2 diabetes, consistent with its overwhelming predominance among Korean adults; type 1 diabetes could not be separately identified. Multivariable logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for diabetes across thyroid function categories, with subgroup analyses by age and sex. High TSH levels were significantly associated with an increased risk of diabetes (OR = 2.82; 95% CI: 1.26-6.32), especially in men under 65 years (OR = 5.10; 95% CI: 1.65-15.77). Low TSH levels were inversely associated with diabetes risk (OR = 0.35; 95% CI: 0.15-0.86). Low free T4 levels were also linked to an increased risk (OR = 2.08; 95% CI: 1.16-3.75), particularly in younger men. TPOAb positivity showed no significant overall association with diabetes, although a potential protective trend was observed in older men. Altered thyroid function, especially high TSH and low free T4 levels, is associated with increased diabetes risk in Korean adults. These findings suggest the clinical utility of thyroid function screening in diabetes risk assessment and highlight the need for further longitudinal research.

This cross-sectional study investigated the association between central thyroid hormone resistance and chronic kidney disease (CKD) in patients with type 2 diabetes mellitus (T2DM) who have normal peripheral thyroid hormones. The study included 2,759 T2DM patients with normal serum free triiodothyronine (FT3) and free thyroxine (FT4) levels. Central thyroid sensitivity was quantified using the Thyroid Feedback Quantile-based Index (TFQI), thyrotrophic thyroxine resistance index (TT4RI), TSH Index (TSHI), and FT3/FT4 ratio. Utilizing multivariable logistic regression and restricted cubic splines (RCS), we found that elevated TSH levels and increased central thyroid hormone resistance (indicated by higher TFQI, TT4RI, and TSHI) were independently associated with an increased risk of CKD. Notably, RCS analysis revealed a significant non-linear relationship (p < 0.001). Participants in the highest TSH quartile exhibited a 1.5-fold increased risk of CKD in multivariable regression (OR 1.50, 95% CI 1.08-2.07). Crucially, this association remained robust after propensity score-matched analyses (n = 684 pairs, OR 1.66, 95% CI 1.21-2.27). In conclusion, for T2DM patients with normal peripheral thyroid hormones, elevated TSH and reduced central thyroid hormone sensitivity are independently associated with a heightened risk of eGFR-defined CKD. These easily calculated indices may serve as valuable clinical biomarkers for early renal risk stratification.