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Tc-99m sestamibi single-photon emission computed tomography/computed tomography (SPECT/CT) has been used to help surgeons explore the location of parathyroid diseases, but quantitative parameters have not been systemically investigated for this purpose. We aimed to establish objective criteria for adenoma and hyperplasia using the standardized uptake value (SUV) in patients with hyperparathyroidism.Thirty-nine hyperparathyroid patients (male/female: 17/22, age: 58.33 ± 11.69 years) with at least 1 uptake-positive lesion of any degree by visual assessment in preoperative Tc-99m sestamibi quantitative SPECT/CT were included from Oct 2015 to Oct 2017. Pathologically, 44 lesions (32 adenomas and 12 hyperplasia) were identified. All patients experienced normalized levels of intact parathyroid hormone immediately after surgery. Quantitative SPECT/CT was performed at 10 minute and 2 hour post injection of Tc-99m sestabmibi (dose = 740 MBq), and maximum SUV (SUVmax) was measured for the parathyroid lesions. Experienced pathologists evaluated the percentage cellular proportions of chief cells, oxyphil cells, and clear cells.SUVmax (g/mL) of adenomas, hyperplasia, and reference thyroid tissue were 12.92 ± 6.68, 7.90 ± 5.49, and 7.01 ± 2.62 at 10min (early phase), decreasing to 7.46 ± 5.66, 4.65 ± 3.14, and 2.21 ± 1.07 at 2 hour (delayed phase), respectively. The adenomas showed significantly higher SUVmax than both the hyperplasia (P = .0131) and reference thyroid tissue (P < .0001) along the early and delayed phases, but the SUVmax of the hyperplasia did not differ from that of the reference thyroid tissue (P = .4196). The adenomas and hyperplasia were discriminated from the reference thyroid tissue using a cutoff SUVmax of 3.26 at the delayed phase. The adenomas had lower %proportions of oxyphil cells than the hyperplasia (P = .0054), but its SUVmax at the delayed phase was positively correlated with the %proportions of mitochondria-abundant oxyphil cells (rho = 0.418, P = .0173). The hyperplasia showed no correlation between SUVmax and cellular proportions.SUVmax at the delayed phase in the Tc-99m sestamibi quantitative SPECT/CT was useful for the identification and differentiation of parathyroid lesions causing hyperparathyroidism.

A 77-year-old man with a history of hypertension, prostate hyperplasia, and urolithiasis was admitted for acute kidney injury caused by hypercalcemia. Neck ultrasonography showed a large cyst adjacent to the right lower thyroid lobe. Although a 99m technetium sestamibi scan was negative, an extremely high intracystic intact parathyroid hormone level suggested that the cyst had a parathyroid origin and that a functional parathyroid cyst was present. Immunohistochemical staining for the calcium-sensing receptor (CaSR) after right lower parathyroidectomy revealed CaSR-positive cells lining the cyst, indicating that the functional parathyroid cyst had originated from the hemorrhagic degeneration of a parathyroid adenoma.

Background: Secondary hyperparathyroidism is a common complication in patients with chronic kidney disease that requires vigilant treatment due to its high mortality rate. Pharmacologic therapy is recommended as an initial treatment; if there is no response, a total parathyroidectomy is performed. In some cases, surgery is accompanied by auto-transplantation of parathyroid tissue., Case Presentation: The patient was diagnosed with chronic kidney disease and received a kidney transplant. However, due to rejection of the transplanted kidney, medical nephrectomy was carried out and routine hemodialysis was initiated and observed. At this time, secondary hyperparathyroidism with elevated parathyroid hormone and hyperphosphatemia developed and pharmacologic treatment was applied. However, there was no response to pharmacologic treatment; therefore, total parathyroidectomy with auto-transplantation was performed. Eight years after surgery, a growing mass was observed in the transplantation site, accompanied by an elevation of parathyroid hormone. A complete resection of the mass was performed, and the patient was diagnosed with parathyroid carcinoma. Additional adjuvant radiation therapy was ordered, and the patient is being monitored., Conclusions: This is a rare but remarkable case of parathyroid carcinoma arising from auto-transplanted parathyroid tissue after total parathyroidectomy in a patient with secondary hyperparathyroidism. We suggest caution should be taken when choosing to auto- transplant parathyroid tissue and that careful postoperative observation should be performed.

The article describes two clinical cases of severe primary hyperparathyroidism (PHPT) caused by parathyroid carcinoma in young female patients who underwent molecular genetic testing to rule out the hereditary forms of PHPT. In both patients, heterozygous germline nonsense mutations of tumor suppressor gene CDC73 encoding parafibromin (p.R91X and p.Q166X) were identified using next-generation sequencing with Ion Torrent Personal Genome Machine (Thermo Fisher Scientific - Life Technologies, USA). It is the first description of CDC73 mutations in Russia, one of the mutations is described for the first time in the world. Identification of germline mutations in the CDC73 gene in patients with PHPT necessitates regular lifelong screening for other manifestations of hyperparathyroidism-jaw tumor syndrome (HPT-JT), PHPT recurrence due to parathyroid carcinoma as well, and identification of mutation carriers among first-degree relatives.

Purpose: 25-OH D3 (D3) deficiency causes secondary hyperparathyroidism. Asymmetric gland hypertrophy may also lead to unnecessary parathyroid gland resection by mistaking these glands for parathyroid incidentalomas. We tested the hypothesis that D3 deficiency causes parathyroid gland hypertrophy., Method: This is a prospective study of 100 consecutive patients undergoing total thyroidectomy. Pre-operative D3 measurement was made at first presentation and on the day after surgery. During thyroidectomy, the parathyroid glands were searched for and measured. Using an ellipsoid volume calculator, the gland volume was calculated. This was correlated with D3 and other possible confounding factors., Results: Normal parathyroid volume is 25.1 mm(3). Parathyroid gland size correlated with D3 levels, p < 0.001. There is a greater asymmetry in gland volume in those patients with the lowest levels of D3 (Spearman's rank correlation coefficient r = -0.51). There was a significant difference in individual gland volume between D3 levels >30 ng/ml and those <30 ng/ml. However, there was no difference in mean gland volume between these groups. There was no difference in correlation according to pathology or thyroid specimen weight., Conclusion: There is a significant difference in both individual gland volume and variation in parathyroid gland volume according to D3 levels. Patients with a D3 level <30 ng/ml have a more asymmetrical hyperplasia corresponding with parathyroid incidentalomas. D3 levels should be measured pre-operatively in all patients undergoing total thyroidectomy to avoid unnecessary parathyroid resection.

Primary hyperparathyroidism is the most common manifestation of MEN 1 syndrome. The management of these patients is complex due to the underlying disease process, which predisposes patients to persistent and recurrent disease. The surgical treatment of patients with MEN 1 and hyperparathyroidism can therefore be considered to be palliative in nature. The basic principles of surgery include (1) obtaining and maintaining normocalcaemia for the longest time possible, avoiding persistent/recurrent hypercalcaemia, (2) avoiding surgically induced hypocalcaemia, and (3) facilitating future surgery for recurrent disease. Two approaches have been described as the best practice for patients with hyperparathyroidism in MEN 1: subtotal parathyroidectomy, leaving a remnant of no more than 60 mg in the neck, and total parathyroidectomy with immediate autotransplantation of 10-20 1 mm(3) pieces of parathyroid tissue. Both approaches should be combined with efforts to exclude supernumerary glands and ectopic parathyroid tissue by including resection of fatty tissue from the central neck compartment and thymectomy in all patients. Cryopreservation of parathyroid tissue should be performed whenever facilities are available. In patients with persistent or recurrent disease, an attempt to obtain total elimination of cervical parathyroid tissue is justified, combined with cryopreservation of parathyroid tissue. As radical as surgery is for hyperparathyroidism in MEN 1, the surgeon must take steps to avoid permanent hypoparathyroidism, which in young patients may be worse than the disease itself.

A 51-year-old male patient with chronic renal failure, who had required dialysis for 22 years, presented with a cervical mass. Laboratory data were consistent with secondary hyperparathyroidism due to chronic renal failure. Cervical exploration was performed with excision of four parathyroid glands and autotransplantation of the normal gland into the forearm. The cervical tumor of the right inferior gland demonstrated parathyroid carcinoma histologically. Adenoma of the right superior gland and hyperplasia of the left superior gland were also recognized. The left inferior gland was normal. A few cases of parathyroid carcinoma in patients on maintenance hemodialysis have been previously reported. However, this is the first report in which all four parathyroid glands revealed different pathological findings: carcinoma, adenoma, hyperplasia and normal gland. Chronic stimulation of the parathyroid glands to release parathyroid hormone might have caused the variety of findings in the four parathyroid glands.

Total parathyroidectomy with autotransplantation of parathyroid tissue into the forearm musculature has been recommended as surgical treatment for renal hyperparathyroidism. Five of 41 patients, in whom this procedure was performed, developed hyperparathyroidism 7 to 33 months after surgery due to graft hyperplasia. Grafts had to be removed. Whereas about 20--25mg were implanted, the removed grafts weighed 0.9--3.1g. Morphological examination showed signs of accelerated growth, infiltration of adjacent structures and invasion of blood vessels. For total removal, repeated and extensive surgery was necessary. Conservative treatment failed to prevent tumour-like growth of autografts. We no longer recommend parathyroidectomy with autotransplantation of parathyroid tissue as the method of choice for the surgical treatment of renal hyperparathyroidism.

Neonatal inbred Wistar albino rats were given either 5 or 10 microCi radioiodine (131I) within 24 hours of birth. After weaning, animals were placed on diets high, normal, or deficient in vitamin D3 (cholecalciferol) for periods up to 2 years. In animals aged 12 months and older, adenomas were found in 0 of 67 unirradiated controls, in 22 of 67 given 5 microCi 131I, and in 25 of 67 given to microCi 131I. The incidence of tumors in irradiated animals was highest (55%) in those on a low-vitamin D diet and lowest (20%) in those on a high-vitamin D diet. Plasma calcium levels were significantly increased by the high-vitamin D diet, but the low-vitamin D diet did not lead to any significant decrease as compared to the calcium levels of the normal vitamin D diet group. Small but significant calcium increases were found in tumor-bearing animals. These findings indicate that parathyroid tumors in the rat can be induced by radiation and that their incidence is strongly influenced by dietary vitamin D content. The possibility that metabolites of vitamin D3 may influence parathyroid growth and tumor formation directly is discussed.

The results of clinical and morphologic studies performed in 41 patients with chronic, renal failure and secondary hyperparathyroidism, who had total parathyroidectomy and autotransplantation of parathyroid tissue into the forearm muscle are presented. In five cases, 7--33 months after autotransplantation we found transplantation tumors developing in the forearm. Explanted grafts showed invasive growth of parathyroid tissue in the adjacent structures, into the musculature and blood vessels. The increased incidence of mitosis otherwise seen as evidence of malignant neoplasia of parathyroid tumors, indicated atypical focal proliferation of the transplanted tissue. This is justification for not performing transplantations any more in the treatment of renal osteodystrophy.

The parathyroid glands of 14 deceased diabetics were investigated as well as nine control non-diabetics. Various in character and degree histological alterations were observed during the morphological investigations of those glands: mild or better manifested hyperplastic alterations (six cases), microadenoma (one case), focal vasculary determined atrophia (two cases, total atrophia of involutive type (two cases), close to the control alterations (three cases). Hyperplastic alterations are established most frequently in the presence of diabetic nephropathia and azotemia. They could be explained with the development of a secondary hyperparathyroidism, associated with chronic renal insufficiency. In single cases, an effect of the disturbance of the calcium-phosphorus metabolism in diabetes is admitted. Changes in the parathyroid glands, from the type of generalized diabetic microangiopathy, is suspected in one of the deceased patients. Two microadenomas were found in another case, predominantly with dark basic cells. No dependence was established between the morphological alterations and the severity, diabetes form, nor with the presence of pyelonephritis. Certain dependence was established between the age of the deceased and the stage of the azotemia.