Large Parathyroid Adenoma Research Articles

Parathyroid adenoma: Ultrasonography, Doppler, and elastography imaging

Symptomatic primary hyperparathyroidism due to parathyroid adenoma is still prominent in developing countries. We are presenting a case report of a young patient who presented with bone pain and a fracture. When investigated further, a large parathyroid adenoma was seen in the lower pole of the right thyroid gland.

Ectopic parathyroid adenoma in the carotid sheath

Parathyroid adenomas can be found in various ectopic positions including the carotid sheath. We report a 52-year-old Libyan woman who presented with neck mass and a fragility fracture. Her serum Calcium was elevated (14.3 mg/dl), as well as her parathyroid hormone (1202 pg/ml). Technetium-99m-sestamibi scan showed a large localized parathyroid adenoma at the upper lateral left aspect of the neck just below the left submandibular gland. The patient underwent surgical resection, and the histopathology confirmed the diagnosis of parathyroid adenoma. The rarity of the ectopic parathyroid adenoma in the carotid sheath led to a delayed diagnosis of this case. Therefore, ectopic parathyroid adenoma should be considered in the differential diagnosis of masses that arise from the carotid sheath.

Facial Dysmorphism Due to Multiple Brown Tumors Secondary to Large Parathyroid Adenoma, Diagnosed on 99mTc-Sestamibi Parathyroid Scintigraphy.

Brown tumors are an uncommon entity associated with hyperparathyroidism. Initially described with primary hyperparathyroidism, with the widespread use of dialysis, they were also seen to be associated with secondary and tertiary hyperparathyroidism. These are lytic, expansile lesions causing bony pains, and depending on the size and extent, skeletal dysmorphism. The present case illustrates the detection of parathyroid adenoma with multiple brown tumors on 99mTc-sestamibi parathyroid scintigraphy in a patient presenting with facial dysmorphism and multiple bony pains.

Hypercalcaemic crisis secondary to a large cystic parathyroid adenoma

Hypercalcaemic crisis secondary to a large cystic parathyroid adenoma

Molecular Characteristics of Large Parathyroid Adenomas

The clinical entity of large parathyroid adenomas (LPTAs) has not been well defined. It is speculated that LPTAs would have biochemical, histological, and molecular characteristics different from small adenomas. Our study aimed to find out occurrence of atypia and carcinomas in large parathyroid lesions and the presence of distinct molecular abnormalities in LPTAs. We divided the parathyroid lesions into large (>7 g, i.e., LPTAs) and small (<7 g) adenomas. We performed parafibromin, APC (adenomatous polyposis coli), galectin 3, and PGP9.5 (protein gene product 9.5) analysis by immunohistochemistry in adenomas without atypia, atypical adenomas, and carcinomas. Mean serum calcium, alkaline phosphatase, and intact PTH were significantly higher in large parathyroid tumor group. The presence of both atypical adenoma and carcinoma was higher in large parathyroid tumor group. There was higher percentage of atypia in patients with LPTAs >10 g (33%), and 68% of tumors showed at least one marker suggestive of malignancy in this group. Detailed analysis of immunohistochemical features of LPTA >10 g revealed that six patients showed complete loss of parafibromin immunoreactivity (out of these four showed atypia), while seven showed partial loss. In histopathologically proven malignancy (n = 9), six patients showed complete loss of parafibromin staining, 5 (55%) APC negativity, and 45% showed both galectin 3 and PGP9.5 positivity. Three out of these showed all IHC markers s/o malignancy, and all of them had evidence of metastases or recurrence. 32% of atypical adenoma and 13% of atypical adenoma showed complete loss of parafibromin staining, however none developed metastases or recurrence in follow-up (median follow-up 40 months). Loss of parafibromin staining (complete or partial) was higher in LPTA group (56%) than that in small adenoma (39%); however, it was not statistically significant. APC, galectin 3, and PGP9.5 markers suggestive were higher in LPTA group but were not significant. LPTAs may show some morphological and immunohistochemical features suggestive of malignancy and can be considered a separate entity. However, the immunohistochemical markers are unable to clearly segregate those LPTAs that may show premalignant potential. Further, we would like to recommend that LPTAs showing complete parafibromin loss together with atypia should be kept under close follow-up.

A large parathyroid adenoma presenting with pathological fractures in a young male

&lt;p class="abstract"&gt;&lt;span lang="EN-US"&gt;Parathyroid adenoma is the common cause of primary hyperparathyroidism and usually presents with features of hypercalcaemia. In the present case report, we describe a case of a large adenoma of the parathyroid gland presenting with pathological fractures. A 42 year old Male presented with bony pains and fracture of the left humerus after a trivial trauma. A detailed clinical examination and laboratory studies revealed hypercalcaemia secondary to hyperparathyroidism. The patient underwent targeted parathyroidectomy of the involved gland after appropriate preoperative localization. Histopathology of the resected specimen was consistent with parathyroid adenoma. Conclusion&lt;strong&gt; &lt;/strong&gt;is a common cause of primary hyperparathyroidism is a common endocrine disorder occurring as a result of Parathyroid adenoma in 80-85% cases. Patients usually present with symptoms related to hypercalcaemia. A high index of suspicion, careful preoperative workup, localization of the affected gland(s) and surgical excision ensures a successful cure.&lt;/span&gt;&lt;/p&gt;

Parathyroid Crisis Caused by a Large Parathyroid Adenoma

Parathyroid Crisis Caused by a Large Parathyroid Adenoma

A Case of Primary Hyperparathyroidism due to Ectopic Parathyroid Adenoma in the Thymus, Accompanied With Vitamin D Deficiency

Primary hyperparathyroidism (PHPT) caused by ectopic parathyroid adenoma (EPA) is not rare, whereas the concurrence of PHPT and vitamin D deficiency (VDD) in youth is uncommon. We reported a case of PHPT with EPA in the thymus, accompanied by a very low level of 25-hydroxyvitamin D. A 20-year-old man suffered from bilateral hip fractures under slight force or no force. Biochemical findings were consistent with PHPT and VDD. Examination results showed severe osteoporosis; both technetium-99m-sestamibi scintigraphy and computed tomography showed an abnormal nodule in the mediastinum, which was resected with a thoracoscope and confirmed pathologically as an EPA in the thymus. Hypocalcemia due to hungry bone syndrome (HBS) occurred after surgery and was resolved quickly with large-dose calcium and alfacalcidol supplementation. PHPT is usually a sporadic disease, and VDD is unfortunately a common global problem. Negative family history and no concomitant illness seemed to rule out familiar hyperparathyroidism. VDD with no gastrointestinal symptom and nutritional anemia was caused by long-term inadequate sun exposure before the first fracture and a 2-year absence of sun exposure due to immobilization. Both PHPT and VDD contributed to severe osteoporosis, which could be exacerbated by not attaining his peak bone mass and by immobilization because of a fragile fracture with delayed healing. Large parathyroid adenoma, VDD, overt bone disease, and PTH resistance in the patient were related to postoperative hungry bone syndrome. Any fracture in young adults that has not healed within 3 months should alert physicians to search for some factors or underlying diseases.

Large parathyroid adenoma presenting as a femoral fracture in a young male

Parathyroid adenoma classically presents symptoms of hypercalcaemia. Here, we present a case of a rare presentation of a parathyroid adenoma in a young male patient with a pathological fracture.

Maxillary brown tumor as initial presentation of parathyroid adenoma: A case report

Brown tumor is a rare late-stage skeletal change caused by long-term stimulation of excess parathyroid hormone. It is not neoplastic, but a reparative cellular process. Common sites of brown tumor are the ribs, clavicle, long bones and pelvic girdle. Solitary maxillary brown tumor as initial presentation of primary hyperparathyroidism is rare; it is often accompanied by brown tumors of the other facial bones. Here, we present the first case of solitary maxillary brown tumor in a 29-year-old ethnic Chinese woman with initial presentation of a large tumor filling the left maxillary sinus. Underlying long-standing primary hyperparathyroidism caused by a large parathyroid adenoma was finally diagnosed. Brown tumor tends to be misdiagnosed as malignancy, and delayed diagnosis of the underlying hyperparathyroidism is common. Our case validates the suggestion that young women have a higher probability of brown tumor. Biopsy of the suspicious bone tumor and blood tests for calcium and parathyroid hormone level are crucial and essential to reach the correct diagnosis. Most brown tumors show spontaneous regression after parathyroidectomy. However, direct excision of the brown tumor may be indicated to avoid the risk of facial deformity and orbital compression at a special anatomical site, as in our case.

Genetic characterization of large parathyroid adenomas

In this study, we genetically characterized parathyroid adenomas with large glandular weights, for which independent observations suggest pronounced clinical manifestations. Large parathyroid adenomas (LPTAs) were defined as the 5% largest sporadic parathyroid adenomas identified among the 590 cases operated in our institution during 2005–2009. The LPTA group showed a higher relative number of male cases and significantly higher levels of total plasma and ionized serum calcium (P<0.001). Further analysis of 21 LPTAs revealed low MIB1 proliferation index (0.1–1.5%), MEN1 mutations in five cases, and one HRPT2 (CDC73) mutation. Total or partial loss of parafibromin expression was observed in ten tumors, two of which also showed loss of APC expression. Using array CGH, we demonstrated recurrent copy number alterations most frequently involving loss in 1p (29%), gain in 5 (38%), and loss in 11q (33%). Totally, 21 minimal overlapping regions were defined for losses in 1p, 7q, 9p, 11, and 15q and gains in 3q, 5, 7p, 8p, 16q, 17p, and 19q. In addition, 12 tumors showed gross alterations of entire or almost entire chromosomes most frequently gain of 5 and loss of chromosome 11. While gain of 5 was the most frequent alteration observed in LPTAs, it was only detected in a small proportion (4/58 cases, 7%) of parathyroid adenomas. A significant positive correlation was observed between parathyroid hormone level and total copy number gain (r=0.48, P=0.031). These results support that LPTAs represent a group of patients with pronounced parathyroid hyperfunction and associated with specific genomic features.

Two cases of primary hyperparathyroidism caused by large parathyroid adenomas resembling thyroid tumor

Two cases of primary hyperparathyroidism caused by large parathyroid adenomas resembling thyroid tumor

Prevalence of cardiovascular risk factors in male and female patients with primary hyperparathyroidism.

To investigate the prevalence of cardiovascular risk factors in patients with primary hyperparathyroidism (PHPT) and to determine if they are gender specific. This was a retrospective case control study. Three hundred and sixty-three men and women with PHPT and 363 age-, sex-, and body mass index (BMI)-matched controls with benign goiter were included in the study. We documented each patient's laboratory results along with the presence of any cardiovascular risk factors. Intra-operatively, the resected parathyroid adenomas were weighed and recorded. The data are expressed as the number of patients in each category and percentage of total patients in that group and the mean±SD. The prevalence of obesity, hypertension, hyperlipidemia, Type 2 diabetes, and coronary artery disease (CAD) is higher in PHPT patients compared to the general New Jersey population and age-, sex-, and BMI-matched goiter patients. Male PHPT patients tended to be more obese and were found to have heavier parathyroid adenomas compared to female patients (p<0.05). Additionally, a higher percentage of male PHPT patients were found to have higher rates of CAD (11.5%) and Type 2 diabetes (23.0%) compared to female patients (5.80% and 10.9%, respectively, p<0.05). There is a higher prevalence of metabolic disorders and CAD in PHPT patients. Male PHPT patients had larger parathyroid adenomas at the time of surgery and had a higher prevalence of obesity, Type 2 diabetes and CAD compared to female PHPT patients.

Intrathymic parathyroid adenoma

Intrathymic parathyroid adenoma is a rare cause of persistent primary hyperparathyroidism. We encountered a case of intrathymic parathyroid adenoma, detected by computed tomographic scan and confirmed by Technetium-99 (Tc-99) Sestamibi scan and histology. The surgical approach included a median sternotomy and a large intrathymic parathyroid adenoma was identified and excised through the sternotomy. In this case, Tc-99 Sestamibi scan successfully localized a persistant abnormal tracer uptake in the mediastinum suggestive of mediastinal parathyroid adenoma. Although not recommended for routine preoperative evaluation, scintigraphy can be useful in the preoperative localization of ectopic parathyroid adenomas.

Large parathyroid adenoma: report of one case

患者 男，57岁，1年前治疗输尿管结石住院期间B超发现右侧颈部肿块，无临床特殊症状表现。2个月前出现全身骨痛，以下肢、腰部、肩部为主，无厌食、恶心、呕吐、多饮、多尿等症状。因“全身骨痛、肾结石、可疑甲状旁腺功能亢进”于2009年12月入我院。入院后体检右侧颈部可触及直径4.0cm大小的肿块，质地中等，边界清楚，肿块活动，无触痛，表面光滑。

A homozygous inactivating calcium‐sensing receptor mutation, Pro339Thr, is associated with isolated primary hyperparathyroidism: correlation between location of mutations and severity of hypercalcaemia

Inactivating mutations of the calcium-sensing receptor (CaSR), a G-protein-coupled receptor with extracellular (ECD), transmembrane (TMD) and intracellular (ICD) domains, cause familial hypocalciuric hypercalcaemia, neonatal severe primary hyperparathyroidism and occasionally primary hyperparathyroidism in adults. To investigate a patient with typical symptomatic primary hyperparathyroidism for CaSR abnormalities. PATIENT AND DESIGN: A 51-year-old woman with primary hyperparathyroidism was investigated for CaSR abnormalities as her severe hypercalcaemia (3·75 mm) persisted after the removal of two large parathyroid adenomas and she was the daughter of normocalcaemic consanguineous parents. Following informed consent, CASR mutational analysis was undertaken using leucocyte DNA. Wild-type and mutant CaSR constructs were expressed in human embryonic kidney (HEK) 293 cells and assessed by measuring their intracellular calcium responses to changes in extracellular calcium. Clinical data were pooled with previous studies to search for genotype-phenotype correlations. The proband was homozygous for a Pro339Thr CaSR missense mutation, located in the ECD, and her normocalcaemic relatives were heterozygous. The mutant Thr339 CaSR had a rightward shift in its dose-response curve with a significantly higher EC(50) = 3·18 mm ± 0·19 compared to the wild-type EC(50) = 2·16 mm ± 0·1 (P < 0·01), consistent with a loss-of-function mutation. An analysis of CaSR mutations in patients with primary hyperparathyroidism revealed that those of the ECD were associated with a significantly greater hypercalcaemia that was less likely to be corrected after removal of the parathyroid tumours. A CaSR missense mutation causing a loss-of-receptor-function can cause symptomatic primary hyperparathyroidism in adulthood.

The utility of 99mTc-sestamibi scintigraphy in the localisation of parathyroid adenomas in primary hyperparathyroidism

There are conflicting data in the literature about the sensitivity of sestamibi scintigraphy in parathyroid tumour localisation in primary hyperparathyroidism (PHPT). We aimed to evaluate the overall sensitivity of this modality in parathyroid tumour localisation and to determine clinical and biochemical factors which influence sensitivity of this method. We performed a retrospective review of 57 patients with a biochemical diagnosis of PHPT who had sestamibi scintigraphy performed. The sensitivity of sestamibi scanning was 56% in whole group and 63% in those without nodular thyroid disease. Among the patients with confirmed single gland disease (biochemical cure after surgical removal of a single adenoma), sensitivity was 71%. A positive scan was associated with younger age, greater adenoma weight and higher pre-operative serum calcium. Concordance between the sestamibi and neck ultrasonography was 92% accurate in pre-operative tumour localisation. Sestamibi scintigraphy was more likely to be positive in younger patients without nodular thyroid disease who have larger parathyroid adenomas with more severe hyperparathyroidism.

Hyperparathyroidism with hypercalcaemia in chronic kidney disease: primary or tertiary?

Objective. This study aims to highlight the challenges in the diagnosis of hyperparathyroidism (HPT) in patients with advanced chronic kidney disease (CKD).Methods. In this report, we describe a middle-aged Filipino gentleman with underlying CKD who presented with intractable nausea, vomiting, severe and medically refractory hypercalcaemia and parathyroid hormone (PTH) concentrations in excess of 2400 pg/mL. The underlying pathophysiology as well as the aetiologies and current relevant literature are discussed. We also suggest an appropriate diagnostic approach to identify and promptly treat patients with CKD, HPT and hypercalcaemia.Results. Evaluation confirmed the presence of a large parathyroid adenoma; HPT and hypercalcaemia resolved rapidly following resection.Conclusion. This case report is remarkable for its severe hypercalcaemia requiring haemodialysis, large adenoma size, acute-on-chronic kidney injury and markedly elevated PTH concentration in association with primary HPT in CKD.

Successful removal of intrathyroidal parathyroid adenoma diagnosed and accurately located preoperatively by parathyroid scintigraphy (SPECT-CT)

We describe the case of a large intrathyroidal parathyroid adenoma in a 46-year-old woman who had a history of recently diagnosed hypercalcaemia and a 2-year history of an asymptomatic enlargement of the right lobe of the thyroid. This rare case highlights the potential difficulties that can arise in the evaluation of hyperparathyroidism, especially in cases of multinodular goiter. In some cases, including this one, even a thorough preoperative evaluation that includes radiological studies (ultrasonography and computed tomography [CT]) may not allow for a definitive preoperative diagnosis due to limited sensitivity, especially in multinodular goiter. The overlapping histological features between thyroid and parathyroid lesions can also be problematic at the time of the intraoperative frozen-section evaluation. We present a case in which, with parathyroid scintigraphy and combination of structural and functional imaging (SPECT-CT), we could accurately locate the intrathyroidal parathyroid adenoma in a patient with multinodular goiter.

Scintigraphic findings in hungry bone syndrome following parathyroidectomy

Prolonged hypocalcemia following parathyroidectomy, called hungry bone syndrome, is a common complication of parathyroid surgery seen in 13–30% of cases. In this article, we report the case of a 48-year-old woman with bone pain and multiple brown tumors as the first manifestation of primary hyperparathyroidism due to a large parathyroid adenoma. After parathyroidectomy, the patient presented clinical signs of hypocalcemia consistent with hungry bone syndrome. Scintigraphic and radiographic modifications following parathyroidectomy are described.