The coexistence of hyperparathyroidism and thyroid cancer presents important diagnostic and management challenges. With minimally invasive parathyroid surgery trending, preoperative thyroid imaging becomes more important as concomitant thyroid and parathyroid lesions are reported. The aim of the study was to evaluate the rate of thyroid cancer in patients operated for either primary (PHPT) or secondary hyperparathyroidism (SHPT). Our retrospective study included PHPT and SHPT patients submitted to parathyroidectomy and, when indicated, concomitant thyroid surgery between 2010 and 2017. Parathyroidectomy was performed in 217 patients: 140 (64.5%) for PHPT and 77 (35.5%) for SHPT. Concomitant thyroid surgery was performed in 75 patients with PHPT (53.6%), and 19 papillary thyroid carcinomas (PTC) were found, accounting for 13.6% from all cases with PHPT and 25.3% from PHPT cases with concomitant thyroid surgery. Thirty-one of operated SHPT patients (40.3%) also underwent thyroid surgery and 9 PTC cases were diagnosed (11.7% of all SHPT patients and 29% of patients with concomitant thyroid surgery). We found differences between PHPT and SHPT patients (p < 0.001) with respect to age (54.6 ± 13y versus 48.8 ± 12y), female-to-male ratio (8:1 versus ~ 1:1), surgical technique (single gland parathyroidectomy in 82.8% PHPT cases; versus subtotal parathyroidectomy in 85.7% SHPT cases) and presurgical PTH (357.51 ± 38.11 pg/ml versus 1020 ± 161.38 pg/ml). Morphopathological particularities, TNM classification and multifocality incidence of PTC were similar in the two groups. All PTC from patients with SHPT were thyroid microcarcinomas (TMC, i.e. tumors with a diameter smaller than 1 cm), whereas seven out of the 19 cases with PTC and PHPT were larger than 1 cm. PTC was frequently and similarly associated with both PHPT and SHPT irrespective of presurgical PTH levels. Thyroid tumors above 1 cm were found only in patients with PHPT. Investigators should focus also on associated thyroid nodular pathology in patients with PHPT.

Pulmonary fibrosis, a critical outcome of chronic inflammatory diseases, has gained prominence in the context of post-coronavirus (post-COVID-19) complications. This review delves into the multifaceted landscape of post-COVID-19 pulmonary fibrosis, elucidating the intricate molecular mechanisms underlying its pathogenesis and highlighting promising therapeutic avenues. Examining the aftermath of severe acute respiratory syndrome-2 (SARS-CoV-2) infection, the review reveals key signaling pathways implicated in the fibrotic cascade. Drawing parallels with previous coronavirus outbreaks enhances our understanding of the distinctive features of post-COVID-19 fibrosis. Antifibrotic drugs, like pirfenidone and nintedanib, take center stage; their mechanisms of action and potential applications in post-COVID-19 cases are thoroughly explored. Beyond the established treatments, this review investigates emerging therapeutic modalities, including anti-interleukin agents, immunosuppressants, and experimental compounds, like buloxybutide, saracatinib, sirolimus, and resveratrol. Emphasizing the critical importance of early intervention, this review highlights the dynamic nature of post-COVID-19 pulmonary fibrosis research. In conclusion, the synthesis of current knowledge offers a foundation for advancing our approaches to the prevention and treatment of these consequential sequelae of COVID-19.

Excess iodine may induce and exacerbate autoimmune thyroiditis (AIT) in humans and animals. In order to assess the potential protective mechanisms of selenium (Se) in thyroid autoimmunity, the effects of inorganic Se (sodium selenite) administration on thyroid morphology and follicular cytology were investigated in adult Wistar rats with iodine-induced AIT. A total of 48 adult Wistar rats (24 females, 24 males) were allocated to one of four dietary regimens: C0, control; C1, only potassium iodine (KI); C2, concomitant KI and Se; C3, only KI initially, followed by Se administration. For AIT induction the rats were fed with 0.05% KI for 56 days. Se-treated rats received 0.3 mg/l sodium selenite in drinking water. Thyroid tissues were collected for pathologic diagnosis after 7 days in C0 group, 56 days in C1 and C2 groups, and 112 days in C3 group. In C1 group, moderate to severe thyroiditis was observed in 83% of males and 50% of female rats (P=0.223). In C3 group 16.7% of male rats developed moderate thyroiditis and none in C2 group, whereas no females were identified with moderate to severe thyroiditis in C2 or C3 group. Thus, the administration of Se was proven to have protective effects against thyroiditis cytology in both male and female Wistar rats.

To evaluate the effect of Selenium (Se) supplementation on: thyroid stimulating hormone (TSH), antiperoxidase antibodies (TPOAb) and glutathione peroxidise 1 (GPx1) in euthyroid subjects with autoimmune thyroiditis. 100 euthyroid women with autoimmune thyroiditis, from the same region, were randomized to receive daily 100 mg selenomethionine (n=50) or placebo (n=50) for 3 months. Serum concentrations of Se, TPOAb and TSH were performed in all patients at baseline and after 3 months. GPx1 activity was measured only in the interventional group before and after Se supplementation. At 3 months TSH presented a significant increase both in treated (2.49 vs. 2.09 UI/mL; p=0.001) and untreated groups (2.38 vs. 1.91 UI/mL; p=0.008). TPOAb decreased by 15.2% in patients treated with Se (p=0.002) and were not modified in untreated patients. At the end of the study Se and TPOAb were in direct insignificant correlation (r=+0.267, p=0.105). GPx1 did not show significant changes after Se supplementation. After 3 months of Se supplementation results showed a mild decrease of TPOAb and a weak negative correlation of these antibodies with Se levels. This suggests that Se treatment may improve the course of thyroid autoimmunity.

Obesity can conceal nutritional impairment and compromised muscle health in metabolic dysfunction-associated steatotic liver disease (MASLD). This critical narrative review examines the potential role of eating behaviors in nutritional impairment and muscle health in MASLD, focusing on adults with overweight or obesity while considering the limited findings in lean MASLD and, separately, pediatric evidence. Altered eating behaviors are associated with prevalent MASLD, but their contribution to malnutrition, myosteatosis, and sarcopenic obesity remains unproven. Nutritionally adverse dietary patterns and appetite loss may increase vulnerability, although evidence linking these factors to muscle outcomes derives predominantly from aging and general obesity populations. Total daily protein intake is better supported than specific meal-level distribution targets, while resistance exercise offers more consistent functional benefits than protein supplementation alone in the limited direct MASLD evidence. Restricting eating windows has not demonstrated additional hepatic benefit over usual care. Incretin-associated lean-mass loss does not by itself establish sarcopenia or disproportionate muscle harm and requires interpretation alongside muscle strength and function. Physical inactivity, socioeconomic circumstances, multimorbidity, and reverse causation complicate attribution to eating behavior. These findings support assessment beyond body mass index, integrating eating behaviors, nutritional risk, and muscle health. We propose an adult assessment framework; however, prospective studies are needed to validate it and clarify the independent contribution of eating behaviors to nutritional and muscle deterioration in MASLD.