A macro-thyroid-stimulating hormone (macro-TSH) is an infrequent yet noteworthy phenomenon in the thyroid field. A 69-year-old patient presented with persistently elevated thyroid-stimulating hormone (TSH) levels ranging from 30 to 50 mIU/L, paradoxically accompanied by normal thyroid hormone levels and normal thyroid ultrasound, with no findings on pituitary magnetic resonance. Laboratory studies were conducted to investigate potential interferences impacting the accuracy of TSH measurements. After excluding other potential causes, polyethylene glycol (PEG) precipitation technique was used, which led us to the diagnosis of macro-TSH. This result was confirmed through chromatography. Macro-TSH, although rare, emerged as the key contributor to the patient’s unexplained increase in TSH levels. This case highlights the importance of considering macro-TSH as a potential etiology in cases characterized by unexplained TSH elevation, offering insights into diagnostic protocols and expanding our understanding of thyroid function anomalies.

Introduction: Visualizing normal parathyroid glands (PTGs) using ultrasound (US) has historically been challenging. This study aims to assess the detection rate of normal PTGs in thyroid patients and evaluate their echostructure, anatomical location and their relation with the underlying thyroid pathology.Methods: A retrospective observational study was conducted over four weeks (September–October 2024) at the Thyroid Unit of Ente Ospedaliero Cantonale (EOC). Consecutive thyroid patients undergoing US for any thyroid indication were included, while those with a history of parathyroid disease, chronic kidney disease, or recent thyroid surgery were excluded. The primary outcome was the detection rate of normal PTGs. Secondary outcomes included PTG echostructure, anatomical location, and correlations with patient characteristics (age, gender, BMI, thyroid volume, and underlying thyroid pathology).Results: Normal PTGs were identified in 45.1% of patients (n=51). Most PTGs were located near the lower pole of the thyroid lobes and appeared mildly hyperechoic. Thyroid volume was inversely associated with PTG detection (p=0.001), while underlying thyroid pathology (e.g., thyroiditis, nodular disease) had no significant impact on detection rates.Conclusion: Normal PTGs can be visualized using US, particularly near the lower thyroid poles. Detection rates decrease in patients with larger thyroid volumes or athyreotic status. These findings confirm and expand on recent studies, challenging the historical belief that normal PTGs are undetectable, with potential implications for endocrine imaging and surgical planning.

Adding/removing text In the published article, there was an error in the Discussion section regarding the citation of the article by Marchand et al. Our article incorrectly referred to "64 intra-thyroid parathyroids" instead of "infrathyroid." Accordingly, the authors have removed this citation from the relevant passage (while keeping it elsewhere as it is cited multiple times), since the citation was no longer appropriate.A correction has been made to the section Discussion, Paragraph 2: "In our study, PTGs were visible in 51 out of 113 patients, representing a detection rate of 45%. This is lower than detection rates reported in some other studies (2, 3, 6, 7), which may be partially explained by our decision to exclude intra-thyroid PTGs to minimize bias. This exclusion was necessary because differentiating a PTG from thyroid tissue in this region is nearly impossible and would require FNA for confirmation. Table 3 provides a comparison of various studies in literature (2, 3, 6-9), highlighting differences in PTG detection rates, gland sizes, thyroid disorders of patients, and PTG locations."The original version of this article has been updated.

Hypoparathyroidism management has advanced in recent decades, particularly for patients unresponsive to conventional therapy. Several parathyroid hormone–based agents have been developed to better imitate physiologic hormone replacement. Recombinant human parathyroid hormone (1-84) [rhPTH(1-84), Natpar®] was approved as an adjunct to calcium and vitamin D for chronic hypoparathyroidism but was later withdrawn, with global production ceasing in 2024. Palopegteriparatide (Yorvipath®; TransCon PTH), a long-acting parathyroid hormone (1-34) prodrug recently approved, represents a new-generation replacement therapy. Transitioning patients from rhPTH(1-84) to palopegteriparatide is increasingly relevant but remains scarcely documented, with only a single real-world report available. We describe a patient with chronic postsurgical hypoparathyroidism after total thyroidectomy who continued to experience symptoms despite conventional therapy. rhPTH(1-84) initially improved symptoms and stabilized calcium levels, but additional supplementation became necessary over time. In September 2024, ahead of rhPTH(1-84) withdrawal, therapy was switched to palopegteriparatide, allowing gradual dose titration and complete withdrawal of calcium and magnesium supplements. The patient maintained stable biochemical values and reported improved well-being, with no adverse events. This case supports the effective transition from rhPTH(1-84) to palopegteriparatide, restoring biochemical stability and independence from conventional therapy.