The contribution of post-transcriptional regulation remains largely unexplored in thyrotropin-secreting pituitary tumors (TSHomas), a rare endocrine pathology responsible for inappropriate TSH secretion and central hyperthyroidism. We investigated the TSHoma post-transcriptional regulatory landscape by analyzing components of molecular machineries controlling RNA metabolism [spliceosome/RNA-exosome/nonsense-mediated decay (NMD)], their associations with clinical parameters, and the impact of their pharmacological inhibition in TSHoma cells. A drastic dysregulation of multiple components of spliceosome [spliceosome (SF3B2/U2AF35/PRPF40A) and splicing factors (e.g., SRP30C/EIF4A3/DDX1/TRA2B/HNR NN F…)], RNA-Exosome (e.g., DIS3/DIS3L/PABPN1), and NMD [e.g., PABPC1, and NMD-canonical targets (DDIT3/GADD45B/MAFF/PDRG1/ATF4/ATF3)] was found in TSHomas vs. non-tumor pituitaries with some of these alterations associated with relevant clinical features (e.g., tumor size, TSHB/fT4-levels). Moreover, we demonstrate a clear antiproliferative action of spliceosome/RNA-Exosome/NMD inhibitors in primary patient-derived TSHoma cells. Overall, a clinically relevant spliceosome/RNA-Exosome/NMD-associated molecular dysregulation and antiproliferative actions of these machineries' inhibition are demonstrated in TSHomas, highlighting a potential source of novel diagnostic/prognostic biomarkers and therapeutic tools in TSHomas.

Acute mesenteric ischemia remains one of the most lethal abdominal emergencies, particularly when bowel necrosis has already occurred at the time of diagnosis. Embolic occlusion of the superior mesenteric artery is most commonly associated with atrial fibrillation. Although hyperthyroidism is a recognized trigger for atrial fibrillation, widespread systemic arterial embolization in this setting is rarely reported. We describe a 77-year-old woman with biochemical thyrotoxicosis and new-onset atrial fibrillation who developed simultaneous superior mesenteric and peripheral arterial occlusions, resulting in near-total small bowel necrosis that was not surgically survivable. Her rapid clinical deterioration underscores the aggressive nature of embolic mesenteric ischemia and the narrow window available for intervention.

Thyrotoxic periodic paralysis (TPP) is a rare complication of hyperthyroidism characterized by acute weakness and hypokalemia due to intracellular potassium shift. Clinical management of TPP consists of cautious potassium replacement, non-selective β-blockade, and prompt treatment of the underlying thyrotoxicosis. Definitive control of hyperthyroidism, combined with avoidance of known precipitants, is essential to prevent recurrent attacks. Failure to recognize the syndrome can result in repeated admissions, unnecessary evaluations, and life-threatening complications. We report the case of a 30-year-old Samoan man with Graves' disease who experienced recurrent episodes of paralysis over several months before the correct diagnosis was established. His initial presentations with severe hypokalemia and weakness were attributed to gastrointestinal and spinal disease, leading to repeated misdiagnoses despite multiple admissions. Alcohol intake, a less common but clinically important trigger, frequently precipitated his episodes; despite counseling, he was unable to achieve complete abstinence. He ultimately developed paralysis complicated by cardiac arrest, after which thyroid testing confirmed Graves' disease and TPP. Despite medical therapy, relapses continued due to lack of definitive thyroid treatment, intermittent methimazole lapses, ongoing alcohol use, and barriers to specialty follow-up. This case underscores the diagnostic challenges of TPP, the importance of recognizing it in Asian and Latino populations where prevalence is higher, and the need for early thyroid evaluation in patients with recurrent hypokalemic paralysis to prevent fatal outcomes.

Overt maternal hypothyroidism during pregnancy has been associated with cognitive impairment in offspring, but less is known about effects of subclinical hypothyroidism and other maternal thyroid conditions on autism spectrum disorder (ASD). This study examined the relationships between maternal thyroid dysfunction during pregnancy and child neurodevelopmental outcomes. Participants were from a high ASD likelihood pregnancy cohort (MARBLES). Maternal thyroid dysfunction (hypothyroid or hyperthyroid compared to euthyroid) was measured in up to one blood sample per trimester. Thyroid stimulating hormone (TSH) and free thyroxine (FT4) were also examined as exposures. Outcomes were child ASD diagnosis, non-typical development (non-TD), typical development and standardized scores from the Social Responsiveness Scale (SRS). Outcomes were confirmed by study psychometricians. Multinomial logistic and quintile regressions were used to examine associations of maternal thyroid dysfunction (using trimester-specific reference ranges) with developmental outcomes and SRS scores. Among 285 pregnancies, 83.9% were categorized as euthyroid, 9.5% hypothyroid, and 6.7% hyperthyroid. Of 285 children included in analyses, 28.8% were diagnosed with ASD (n = 82; female = 27) and 14.7% with non-TD (n = 42; female = 19). Maternal hypothyroid conditions were associated with increased ASD:TD odds (adjusted RRR = 3.40, 95% CI: 1.22, 9.45; p = 0.02). Significant relationships were also found between hypothyroid conditions and non-TD, and between first trimester TSH and ASD. There was no evidence of a relationship between either TSH or FT4 and preschool SRS scores. Findings suggest that maternal hypothyroid conditions during pregnancy are associated with greater chances of their children developing ASD and other neurodevelopmental differences among children with high familial likelihood of ASD.

Pruritus is a known but uncommon symptom of hyperthyroidism that can be misinterpreted or overlooked in a patient presentation. This is a case report of a 40-year-old female who presents with a 3-month history of severe, worsening pruritus. Further history demonstrated potential signs of hyperthyroidism, and laboratory values demonstrated low TSH levels, high T4 levels, and positive TSH receptor antibodies. A thyroid scan was performed, and increased uptake confirmed the diagnosis of Graves' disease in this patient. After discovering that the patient was pregnant, treatment with propylthiouracil was begun for the first 12 weeks of her pregnancy, with a switch to methimazole after the first 12 weeks. Graves' disease must be considered in the differential diagnosis of generalized pruritus, with thorough history and analysis of symptoms essential to determine if underlying hyperthyroidism may be present.

This study aims to investigate the associative relationships between thyroid dysfunction, dyslipidemia, and other metabolic risks among people undergoing health examinations. 305 individuals undergoing routine health examinations were enrolled (June 2023-December 2025). After exclusions, 300 participants were included in the final analysis. Core observation indicators included the thyroid function indices thyroid-stimulating hormone (TSH), free triiodothyronine (FT3) and free thyroxine (FT4); lipid profile parameters covering total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C); and metabolic markers such as fasting blood glucose (FBG), waist circumference (WC) and blood pressure (BP). Participants were grouped into euthyroid, hyperthyroid, and hypothyroid cohorts by standard thyroid diagnostic criteria. Pearson correlation and multivariate logistic regression analyses were performed to examine the associations between indicators and risk factors for thyroid dysfunction. Of 300 participants, 224 (74.67%) were euthyroid, 32 (10.67%) hyperthyroid, and 44 (14.66%) hypothyroid. One-way ANOVA demonstrated that participants with hyperthyroidism had lower TSH, higher FT3/FT4, reduced TC/TG/LDL-C, elevated HDL-C, higher FBG, lower WC/diastolic blood pressure (DBP), and mild systolic blood pressure (SBP) rise (all p < 0.05) than euthyroidism; hypothyroidism showed the opposite (all p. < 0.05). Pearson correlation analysis showed TSH positively correlated with TC, TG, LDL-C, FBG, WC, SBP, and DBP, and negatively correlated with HDL-C. FT3 and FT4 were negatively correlated with TC, TG, LDL-C, and positively correlated with HDL-C. Both markers had negative correlations with WC and DBP, with FT4 showing a moderate correlation with WC. Multivariate logistic regression confirmed independent associations of dyslipidemia and metabolic abnormalities with thyroid dysfunction in health examination populations. Thyroid dysfunction is closely associated with lipid and metabolic disturbances, and these indicators provide a valuable reference for population screening for chronic diseases. This study was limited by its single-center cross-sectional design, small sample size, and insufficient stratification of thyroid dysfunction subtypes.