Incidental parathyroidectomy (IP) is a complication seen at varying rates after thyroid surgery, and its relationship with postoperative hypocalcemia has not been clarified. In this study, our goal was to identify the frequency and risk factors for IP in a large patient cohort and assess its correlation with postoperative hypocalcemia. A total of 4052 patients who underwent thyroid surgery between 2008 and 2020 were reviewed retrospectively. The patients were divided into two groups, the IP and non-IP groups, and compared in terms of demographics, surgical procedures, pathological diagnosis, and specimen weight. The relationships between IP and hypocalcemia were also evaluated. There were 587 (14.5%) IPs out of 4052 cases. In these patients, mostly one gland was removed (84.6%), and 23.2% of these glands were intrathyroidal. The rate of transient hypocalcemia was 39.9%, and that of permanent hypocalcemia was 1.7%. Female gender, malignancy, lower preoperative thyroid volume, presence of central lymph node dissection, lower specimen weight, presence of autotransplantation and capsule invasion in malignant cases were determined to be risk factors for IP. After excluding hemithyroidectomy and autotransplantation, transient and permanent hypocalcemia were found to be significantly higher in cases with IP (p < 0.001). Multivariate analysis showed that female sex, no multinodular goiter, central dissection, and low thyroid volume were risk-adjusted independent variables. Our findings highlight the significant role of IP in postoperative hypocalcemia. Given that most IPs are located in the perithyroidal region, precise surgical dissection is vital to preserve parathyroid gland function and prevent IP and subsequent hypocalcemia.

Familial Hypocalciuria Hypercalcemia (FHH) is an inherited disease with autosomal dominant transmission characterized by the presence of usually mild-to-moderate hypercalcemia, hypophosphatemia, hypocalciuria, and normal or moderately increased PTH values. Generally, FFH is asymptomatic although symptoms related to elevated plasma calcium values such as asthenia, intense thirst, polyuria, polydipsia or confusional state may occur. Three types of FHH, which differ in the genetic alterations underlying the condition, are described. The majority of FHH cases are classified as type 1 (about 65 percent of cases), due to mutation in the gene for the calcium-sensitive receptor CASR, expressed on chromosome (Chr) 3q13.3-21, which encodes for a calcium-sensitive receptor G-protein-coupled protein of the plasma membrane. FHH types 2 and 3 are due to GNA11 and AP2S1 mutations, respectively, and other genes involved in the pathogenesis of the disease have likely yet to be identified. Rarely, familial hypocalciuric hypercalcemia may not recognize a genetic cause but be caused by autoantibodies directed against CASR. The frequency of the disease is not known and is estimated, probably by default, because of paucisymptomatic presentation of the disease, to be around 1:80000 cases. Recognition of FHH is especially important for differential diagnosis with primary hyperparathyroidism, which has a much higher incidence, about 1:1000 cases. This allows for the identification of patients at risk for chondrocalcinosis and/or pancreatitis. Clinical suspicion must be raised in cases of hypercalcaemia associated with hypocalciuria, and genetic analysis is fundamental in the differential diagnosis toward forms of primary hyperparathyroidism that might result in unnecessary surgical interventions. We describe a clinical case in which a novel inactivating mutation of CASR leading to FHH type 1 was found.

BACKGROUND: There has been a shift in recent years toward same-day parathyroidectomies due to the decrease in mutual costs with few significant differences in postoperative morbidity or mortality. We sought to determine if demographics, preoperative patient risk factors, or comorbidities were associated with a patient\'s likelihood of having same-day or inpatient surgery.
METHODS: A prospective database of parathyroid operations from 2001 to 2022 (n = 2948 patients) was reviewed for surgeries completed for primary hyperparathyroidism. Patients were categorized as same-day or inpatient surgery; demographics, risk factors, and co-morbidities were examined and differences across practice patterns during the 21-year period were studied and also analyzed in a subset of patients from 2013 to 2022.
RESULTS: In a recent subset of patients from 2013 to 2022, patients having inpatient surgery were more likely to be Black and use anticoagulation or antiplatelet therapy. Multivariable regression confirmed increased odds of aging and black patients requiring inpatient parathyroidectomy. Compared to 2001-2003, there was a significantly increased proportion of patients undergoing same-day surgery; compared to 2010-2012, there was a similar proportion of patients undergoing outpatient surgery between 2013 and 2018, and there was an increased proportion from 2019 through 2022.
CONCLUSIONS: Same-day parathyroidectomies have been shown to be safe and has become the typical practice for high-volume parathyroid surgeons over the last decade. Complications such as postoperative hematoma or hypocalcemia were previously shown to be incompletely mitigated by increased LOS or inpatient surgery, although demographics are considered to increase the odds of inpatient parathyroidectomy.

OBJECTIVE: To evaluate the potential benefit of adding a low frequency vascular probe to the conventional pre-operative ultrasound examination of patients with primary hyperparathyroidism.
METHODS: A prospective cohort of 136 patients with primary hyperparathyroidism underwent a conventional ultrasound examination of the neck with a high frequency ( > 10 MHz) linear ultrasound probe, followed by an add-on examination with a low frequency vascular probe. For each ultrasound probe, and for every potential parathyroid lesion, the presence of a feeding vessel, a polar placement of the feeding vessel, and the presence of a vascular arch was recorded.
RESULTS: A total of 146 ultrasound lesions were evaluated for vascularity by each probe. For both ultrasound probes, the odds of a hyperfunctioning parathyroid gland being correctly identified increased with the number of visible vascular features. The vascular probe identified a significantly higher number of vascular features among ultrasound true positive glands compared with the conventional probe (p < 0.0001). Among histopathologically verified pathological parathyroid glands, the vascular probe identified 20% more feeding vessels, 27% more polar placements of the feeding vessel, and 65% more vascular arches than the high frequency probe. However, the diagnostic confidence score for true positive glands did not differ significantly between the probes (p = 0.11).
CONCLUSIONS: The addition of a low frequency vascular probe increases the number of visible vascular features in hyperfunctioning parathyroid glands, which facilitates their preoperative detection. Whether or not this can increase the diagnostic confidence of ultrasound examiners has yet to be substantiated.

A 51-year-old woman with a history of primary hyperparathyroidism (PHPT) with prior parathyroidectomy, osteoporosis, and learning disability was referred for hypercalcemia discovered after a fall. Family history was negative for PHPT, pituitary, enteropancreatic neuroendocrine, or jaw tumors. Dysmorphic facies, multiple cutaneous melanocytic nevi, café au lait macules, long fingers, and scoliosis were observed. Laboratory evaluation showed an elevated parathyroid hormone (PTH) level, hypercalcemia, and hypophosphatemia, all consistent with PHPT. Preoperative imaging revealed a right inferior candidate parathyroid lesion. The patient underwent right inferior parathyroidectomy with normalization of PTH, calcium, and phosphorus. Genetic testing showed a likely pathogenic de novo heterozygous germline missense variant p.R764W in the ZFX gene that encodes a zinc-finger transcription factor previously shown to harbor somatic missense variants in a subset of sporadic parathyroid tumors. Germline variants in ZFX have been reported in patients with an X-linked intellectual disability syndrome with an increased risk for congenital anomalies and PHPT. Further research may determine if genetic testing for ZFX could be of potential benefit for patients with PHPT and developmental anomalies, even in the absence of a family history of parathyroid disease.

Normocalcemic primary hyperparathyroidism (NPHPT), a variant of primary hyperparathyroidism (PHPT) characterized by persistently elevated parathyroid hormone (PTH) levels and normal serum calcium, has gained recognition as a substantial subset of PHPT cases. Despite its increasing prevalence, the precise pathophysiology and natural progression of NPHPT remain enigmatic. This in-depth literature review explores recent advancements in our understanding of NPHPT, encompassing pathophysiology, clinical presentation, diagnostic approaches, medical and surgical management options. By synthesizing this wealth of information, this review aims to contribute to a more nuanced and informed approach to the treatment of patients grappling with NPHPT. As our understanding of the condition continues to evolve, the knowledge gathered from this review has the potential to significantly enhance the quality of care and outcomes for individuals afflicted with NPHPT, ultimately improving their overall well-being and prognosis.

Brown tumors, an exceptional bone complication of severe primary (PHP) or renal (secondary) hyperparathyroidism (RHP), are caused by long-standing, elevated parathormone (PTH)-induced osteoclast activation causing multinucleated giant cell conglomerates with hemosiderin deposits in addition to the local production of cytokines and growth factors. We aim to present an adult case series including two females displaying this complication as part of a multidisciplinary complex panel in high PTH-related ailments. The approach was different since they had distinct medical backgrounds and posed a wide area of challenges amid real-life settings, namely, a 38-year-old lady with PHP and long-term uncontrolled hypercalcemia (with a history of pregnancy-associated PHP, the removal of a cystic jaw tumor, as well as a family and personal positive diagnosis of polycystic kidney disease, probably a PHP-jaw tumor syndrome), as well as, a 26-year-old woman with congenital single kidney and chronic renal disease-associated RHP who was poorly controlled under dialysis and developed severe anemia and episodes of metabolic acidosis (including one presentation that required emergency hemodialysis and was complicated with convulsive seizures, followed by resuscitated respiratory arrest). Both subjects displayed a severe picture of PHP/RHP with PTH levels of >1000 pg/mL and >2000 pg/mL and elevated serum bone turnover markers. Additionally, they had multiple brown tumors at the level of the ribs and pelvis (asymptomatically) and the spine, skull, and pelvis (complicated with a spontaneous cervical fracture). As an endocrine approach, the control of the underlying parathyroid disease was provided via surgery in PHP (for the postparathyroidectomy hungry bone syndrome) via medical intervention (with vitamin D analogs) in RHP. Additionally, in this case, since the diagnosis was not clear, a multidisciplinary decision to perform a biopsy was taken (which proved inconclusive), and the resection of the skull tumor to confirm the histological traits. This series highlights the importance of addressing the entire multidisciplinary panel of co-morbidities for a better outcome in patients with PHP/RHP-related brown tumors. However, in the instance of real-life medicine, poor compliance and reduced adherence to recommendations might impair the overall health status. Thus, sometimes, a direct approach at the level of cystic lesion is taken into consideration; this stands for a narrow frame of decision, and it is a matter of personalized decision. As seen here, brown tumors represent the hidden face of PHP/RHP, primarily the complex and severe forms, and awareness is essential even in the modern era.

The most recent WHO classification of endocrine and neuroendocrine tumours has brought about significant changes in the diagnosis and grading of these lesions. For instance, pathologists now have the ability to stratify subsets of thyroid and adrenal neoplasms using various histological features and composite risk assessment models. Moreover, novel recommendations on how to approach endocrine neoplasia involve additional immunohistochemical analyses, and the recognition and implementation of these key markers is essential for modernising diagnostic capabilities. Additionally, an improved understanding of tumour origin has led to the renaming of several entities, resulting in the emergence of terminology not yet universally recognised. The adjustments in nomenclature and prognostication may pose a challenge for the clinical team, and care providers might be eager to engage in a dialogue with the diagnosing pathologist, as treatment guidelines have not fully caught up with these recent changes. Therefore, it is crucial for a surgical pathologist to be aware of the knowledge behind the implementation of changes in the WHO classification scheme. This review article will delve into the most significant diagnostic and prognostic changes related to lesions in the parathyroid, thyroid, adrenal glands and the gastroenteropancreatic neuroendocrine system. Additionally, the author will briefly share his personal reflections on the clinical implementation, drawing from a couple of years of experience with these new algorithms.

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