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PubMed1996

Cyclin D1/PRAD1 expression in parathyroid adenomas: an immunohistochemical study.

The cyclin D1 (PRAD1) oncogene is rearranged with the PTH gene and is transcriptionally activated in a subset of parathyroid adenomas. Because of heterogeneity in rearrangement breakpoints, the true percentage of adenomas with cyclin D1 deregulation is unknown. Overexpression of the cyclin D1 protein in parathyroid adenomas appears to be a unifying consequence of all cyclin D1 gene rearrangements and can, therefore, be examined to more comprehensively identify adenomas in which cyclin D1 is pathogenetically important. We studied cyclin D1 expression in 65 parathyroid adenomas (from 64 patients), 51 normal parathyroid glands (from the same patients), and 4 parathyroid carcinoma specimens (from 3 patients) using a microwave-enhanced immunohistochemical method and affinity-purified cyclin D1 polyclonal antiserum. When available, data on adenoma mass, intact PTH level, and concurrent serum calcium level were also collected. Twelve of the 65 adenomas (18%) showed diffuse nuclear staining of approximately 30-70% of the tumor cells. All 51 normal glands were negative, except 1 gland that showed scattered cells ( < 10%) with positive nuclear staining. In addition, scattered positive cells were seen in the compressed rim of histologically normal parathyroid tissue surrounding 2 adenomas that were cyclin D1 negative. No significant differences in adenoma mass, intact PTH levels, or concurrent calcium levels were found between positive and negative tumors. Two of 4 parathyroid carcinoma specimens from 2 of 3 patients showed strong nuclear staining for cyclin D1. Overexpression of the cyclin D1 oncogene in 18% of our cases, due to the cyclin D1/PTH translocation and/or other mechanisms, suggests that overexpressed cyclin D1 plays a role in the pathogenesis of a much larger proportion of parathyroid adenomas than previously appreciated. Cyclin D1 overexpression is a feature of typical parathyroid adenomas and is not confined to unusually large, symptom-causing adenomas as had been suggested by early DNA studies. Although only three patients with parathyroid carcinoma were studied, two of the patients' tumors stained for cyclin D1, raising the possibility that the frequency of cyclin D1 overexpression may be even greater in carcinomas. Cyclin D1 overexpression appears to highlight a central pathway in parathyroid neoplasia.

Adenoma↗

PubMed2000

[Use of SPECT with (99m)Tc-Sestamibi in a patient affected by laryngeal carcinoma and parathyroid adenoma].

We report the case of a patient with a laryngeal carcinoma in whom asymptomatic hyperparathyroidism was also detected during the preoperative work-up. A planar (201)Thallium/(99m)Tc-pertecnetate subtraction scintigraphy was performed in order to locate the suspected parathyroid adenoma. The study showed a single area of increased (201)Thallium uptake just above the thyroid isthmus, likely due to the laryngeal tumor. The scintigraphic study was repeated using (99m)Tc-Sestamibi and (99m)Tc-pertechnetate and employing the SPECT technique. Both SPECT studies made it possible to identify correctly the parathyroid adenoma, located inferiorly and in a posterior position to the lower third of the right thyroid lobe. The laryngeal tumor and parathyroid adenoma could be excised in a single surgery session. This case is of interest due to the rarity of the coexistence of two neck tumors and the clear advantage shown by the SPECT technique with (99m)Tc-Sestamibi over the planar technique with 201Thallium.

Adenoma↗

PubMed2000

Hypercalcemia in a patient with renal cell carcinoma producing parathyroid hormone-related protein and interleukin-6.

A patient with renal cell carcinoma who developed humoral hypercalcemia of malignancy is reported. A 52-year-old male patient was diagnosed with renal cell carcinoma and multiple lung metastases. A cell line isolated from the surgical specimen exhibited continuous production of parathyroid hormone-related protein (PTHrP) in vitro. The production of PTHrP from the cancer cells was confirmed by RT-PCR and immunoradiometric assay. The serum calcium level was not enhanced, whereas the lung lesion was developing and producing interleukin-6, a possible modulator of osteoclastic resorption. Hypercalcemia was induced when the PTHrP concentration increased up to 3.3 pmol/L.

Carcinoma, Renal Cell↗

PubMed1993

[Primary hyperparathyroidism in intrathyroid parathyroid cancer].

Parathyroid carcinoma is a rare cause of hyperparathyroidism. Histological differentiation from parathyroid adenoma may be difficult and is rarely achieved intraoperatively. Parathyroid carcinomas are sometimes localized heterotopically. We report a case of parathyroid cancer in the left thyroid lobe. Surgical therapy should include en bloc resection of the tumor, the thyroid lobe and the parathyroid tissue.

Adenoma↗

PubMed1998

Role of interleukin-6 in uncoupling of bone in vivo in a human squamous carcinoma coproducing parathyroid hormone-related peptide and interleukin-6.

OCC tumor has been established from a human squamous carcinoma associated with humoral hypercalcemia of malignancy (HHM) and shown to overproduce parathyroid hormone-related peptide (PTHrP) and cause aggressive hypercalcemia when implanted into nude rats. In the present study, we have demonstrated by reverse transcription-polymerase chain reaction and Northern blot analysis that OCC tumor also overexpressed interleukin 6 (IL-6) mRNA and that tumor-bearing animals exhibited a marked increase in plasma IL-6 as well as PTHrP concentrations. When a monoclonal antibody against human IL-6 was injected to block the activities of tumor-derived IL-6, bone loss in tumor-bearing animals was significantly prevented. Quantitative bone histomorphometric analysis revealed that treatment with anti-IL-6 antibody caused a substantial decrease in both osteoclast number and eroded surface (as parameters of bone resorption) and also a significant increase in the mineral apposition rate, but little effect on the osteoblastic surface. These results provide in vivo evidence suggesting that in tumors coproducing IL-6 and PTHrP, IL-6 is involved not only in the acceleration of osteoclastic bone resorption but also, at least in part, in the suppression of osteoblastic functions in HHM syndrome.

Animals↗

PubMed2006

Genetic analyses in patients with familial isolated hyperparathyroidism and hyperparathyroidism-jaw tumour syndrome.

BACKGROUND: A subset of familial isolated primary hyperparathyroidism (FIHP) is a variant of hyperparathyroidism-jaw tumour syndrome (HPT-JT). AIM/PATIENTS AND METHODS: We investigated the involvement of the HRPT2, MEN1 and CASR genes in 11 provisional FIHP families and two HPT-JT families. RESULTS: Germline mutations of HRPT2 were found in two of the 11 FIHP families and one of the two HPT-JT families. One FIHP family with parathyroid carcinoma and atypical adenomas and another FIHP family with cystic parathyroid adenoma had novel frameshift mutations of 518-521del and 62-66del, respectively. In a patient with HPT-JT, a de novo germline mutation of 39delC was detected. Novel somatic HRPT2 mutations of 70-73del and 95-102del were found in two of five parathyroid tumours in a family with a 518-521del mutation. Biallelic inactivation of HRPT2 by a combination of germline and somatic mutation was confirmed in the parathyroid tumours. The finding that two families diagnosed with FIHP carried HRPT2 mutations suggests that they have occult HPT-JT. In the remaining 10 families, one family had a missense MEN1 mutation. No mutations of CASR were detected. CONCLUSION: Our results confirm the need to test for HRPT2 in FIHP families, especially those with parathyroid carcinomas, atypical adenomas or adenomas with cystic change.

Adenoma↗

PubMed1998

Somatic mutations of multiple endocrine neoplasia type 1 gene in the sporadic endocrine tumors.

Endocrine tumors of the parathyroid and pancreas are encountered either as sporadic type or as part of multiple endocrine neoplasia type 1 (MEN 1). A high frequency of the loss of heterozygosity (LOH) has been observed in tumors of the sporadic type in the locus of the MEN 1 gene, which has recently been cloned and designated the menin gene. It would be of great interest to determine whether somatic mutations in the menin gene are responsible for the sporadic endocrine tumors. For this purpose, we have investigated the menin gene mutations in 21 sporadic parathyroid adenomas, 2 parathyroid carcinomas, 4 sporadic insulinomas, and 1 malignant VIP (vasoactive intestinal polypeptide)oma with WDHA (watery diarrhea, hypokalemia, and achlorhydria) syndrome, using PCR-single strand conformation polymorphism analysis and DNA sequencing. In none of these cases did the patient have a family history or other possible association with MEN 1. We have discovered somatic point mutations in two parathyroid adenomas (A340T and A541T), in one insulinoma (T429K), and in the malignant VIPoma (W198X). In addition, we have found two polymorphisms (D418D and V367V) in two parathyroid carcinomas and two parathyroid adenomas. Of these mutations and polymorphisms, three (A340T, T429K, and V367V) are first reported here, in the present article. Our results indicate that somatic mutations of the menin gene are responsible for a proportion of the sporadic parathyroid adenomas and pancreatic islet cell tumors.

Adenoma↗

PubMed1989

The intrathyroidal hyperfunctioning parathyroid gland.

Six cases of primary hyperparathyroidism due to hyperfunctioning intrathyroidal parathyroid glands are reported. In five cases, hyperparathyroidism was due to an intrathyroidal parathyroid adenoma; in the sixth case, hyperparathyroidism resulted from an intrathyroidal parathyroid carcinoma. All five patients with adenoma were female with ages ranging from 40 to 70 yr. The patient with carcinoma was a 55-yr-old male. In all five patients with intrathyroidal parathyroid adenoma, thyroidectomy was performed when an abnormal parathyroid gland could not be located in the neck during surgery for hyperparathyroidism. The patient with intrathyroidal parathyroid carcinoma presented with hypercalcemia and a palpable right thyroid mass. The differential diagnosis of intrathyroidal parathyroid adenoma includes thyroid follicular adenoma. In some cases, the possibility of medullary carcinoma of thyroid might also be considered. Immunocytochemical staining for parathormone (PTH), thyroglobulin, and calcitonin is valuable in establishing the correct diagnosis.

Adenoma↗

PubMed1998

Familial isolated hyperparathyroidism maps to the hyperparathyroidism-jaw tumor locus in 1q21-q32 in a subset of families.

Approximately 70 families with familial isolated hyperparathyroidism (FIHP) have been reported. Whether it is a separate entity or a variant of multiple endocrine neoplasia type 1 (MEN1 at 11q13) or hyperparathyroidism-jaw tumor (HPT-JT or HRPT2 at 1q21-32) syndrome is not known. We describe here 3 unreported families with familial primary hyperparathyroidism and evaluate their clinical, pathological, and genetic profiles. Biochemical and radiological screenings for MEN1 were negative for all families. In 2 families with a total of 10 affected cases and 3 female obligate carriers, there is no evidence of jaw or renal lesions despite careful radiological investigations. In both families the disease was linked to the 1q21-q32 region with the maximum logarithm of the odds (lod) scores of 3.10 and 3.43 for markers D1S222 and D1S249 respectively, at recombination fraction of 0. In 1 family 2 types of parathyroid pathology were found: 3 of chief cell type and 1 of oxyphil/oncocytic cell type. Two chief cell tumors and 1 oxyphil tumor were found to have loss of heterozygosity (LOH) involving loss of the wild-type alleles for chromosome 1q markers. In the third family, with 4 affected siblings, a parathyroid carcinoma and 2 cases of polycystic kidney disease were found. The parathyroid carcinoma also showed loss of heterozygosity in the 1q region. In conclusion, we found that the hyperparathyroidism traits in a subset of FIHP families are linked to the 1q21-32 markers in the HRPT2 region. We describe the spectrum of parathyroid disease in 1q-linked families involving 3 different types of pathology and demonstrate for the first time loss of wild-type alleles in these parathyroid tumors. Taken together, the results suggest that some of the FIHP are a variant of HPT-JT and that the gene involved is a tumor suppressor gene.

Adult↗

PubMed2006

Diagnosis of parathyroid tumors in familial isolated hyperparathyroidism with HRPT2 mutation: implications for cancer surveillance.

CONTEXT: Mutations of the HRPT2 gene have recently been implicated in the development of parathyroid carcinoma. OBJECTIVE: The objective of this study was early diagnosis of parathyroid tumor in a family with germline HRPT2 mutation. PATIENTS, METHODS, AND RESULTS: In a 40-yr-old male previously treated for parathyroid atypical adenoma, we screened the 17 translated HRPT2 exons and their exon-intron boundaries and found a germline frameshift mutation in exon 7 (685delAGAG) predicting a premature stop codon at nucleotides 767-769. Nine family members (age, 33.9 +/- 19.8 yr, mean +/- SD) also carry the mutation, but eight have had normal serum calcium. Biochemical and ultrasonographic evaluation uncovered a 27-yr-old hypercalcemic carrier niece with an atypical parathyroid adenoma, and a 43-yr-old normocalcemic carrier sister was found by ultrasonography to have an extrathyroidal nodule, which proved to be parathyroid carcinoma. The index case, 12 yr after surgery, was normocalcemic, but ultrasonography revealed an extrathyroidal nodule in the contralateral hemithyroid tissue that proved to be atypical adenoma. CONCLUSIONS: Our report confirms that germline mutations of HRPT2 gene may be associated with multiple parathyroid neoplasms. Our experience suggests that longitudinal surveillance by serum biochemistry alone may not be 100% sensitive, and addition of routine neck ultrasonography is a readily accepted adjunct that may facilitate earlier disease detection in some families.

Adenoma↗

PubMedDate not supplied

Regional body FDG-PET in postoperative recurrent hyperparathyroidism.

PURPOSE: The use of preoperative imaging studies in patients with persistent or recurrent hyperparathyroidism after initial operation is generally accepted to improve the success rate and minimize the morbidity from reoperative surgery. The purpose of this study was to define the performance of FDG-PET for the localization of hyperfunctioning parathyroid tissue prior to reoperation. METHOD: Twenty patients with biochemical evidence of recurrent or persistent hyperparathyroidism following previous neck surgery were investigated. Regional body PET imaging of the neck and upper chest (axial field of view 27.5 cm) was acquired 45 min after 5-10 mCi FDG was given intravenously. RESULTS: Subsequent surgery revealed solitary parathyroid adenomas in 14 patients, seven hyperplastic glands in 2 patients, and parathyroid carcinoma in 1 patients. FDG-PET correctly identified 79% (11/14) of the parathyroid adenomas, 29% (2/7) of the hyperplastic glands, and the parathyroid carcinoma. FDG-PET was negative in 79% (30/38) of the surgically identified normal parathyroid glands. Eight false-positive findings led to a positive predictive value of 64%. CONCLUSION: These preliminary data suggest that regional body FDG-PET is a promising procedure in the evaluation of patients with persistent or recurrent postoperative hyperparathyroidism.

Adenoma↗

PubMed1990

The mutation for medullary thyroid carcinoma with parathyroid tumors (MTC with PTs) is closely linked to the centromeric region of chromosome 10.

Two new morphs (F and G) detected by the centromeric alpha satellite probe p alpha 10RP8 and D10Z1 in HinfI digests are linked to the PstI polymorphisms of D10Z1, confirming their chromosome 10 location. The F and G morphs were in strong linkage disequilibrium with each other but were in weak linkage disequilibrium with the A and B morphs defined in PstI digests. Data for haplotypes formed by using the A and F morphs improved the lod score for linkage between the disease locus for multiple endocrine neoplasia type 2A (MEN2A) and D10Z1 (Z = 14.06 at theta = 0) in the six large families studied by Wu et al. Furthermore, the locus that codes for a distinct phenotype, medullary thyroid carcinoma (MTC) with parathyroid tumors (PTs) and no pheochromocytomas (PHEOs) (referred to as MTC with PTs), in one of the families was closely linked to two markers, D10Z1 and RBP3, with lodscores of 2.86 and 3.54, respectively, at theta = 0. A possible allelic association was noted between disease phenotypes and centromeric haplotypes. The phenotype MTC and PHEOs with and without PTs was associated with the same relatively common centromeric haplotype (A + B-F-G-) in the four families in which all four morphs could be determined, while the phenotype MTC with PTs was associated with the rare centromeric haplotype (A-B-F-G+) in one family.

Adrenal Gland Neoplasms↗

PubMed1995

[Familial hyperparathyroidism].

Recently, not only the multiple endocrine adenomatosis (MEN)-associated type but also the type which can be isolated from MEN syndrome have been widely accepted in the classification of familial hyperparathyroidism. Analysis of gene markers specific to MEN syndrome contributed markedly to the establishment of isolated familial hyperparathyroidism. We attempted an analysis of 15 pedigrees in the report of familial hyperparathyroidism in which MEN syndrome was actively ruled out. In 7 pedigrees, adenoma alone was seen while in 2 pedigrees was hyperplasia alone seen. In 6 pedigrees parathyroid carcinoma was also admitted (other members of the pedigree were affected with parathyroid adenoma or hyperplasia). There were 5 pedigrees in which cementifying fibroma or ossifying fibroma of the jaw was associated with familial hyperparathyroidism. The association of parathyroid carcinomas or benign jaw tumors should be paid attention.

Fibroma↗

PubMed2000

Different pathological findings in each of four parathyroid glands in a long-standing hemodialysis patient.

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.

Adenoma↗

PubMed2006

Does Hurthle cell lesion/neoplasm predict malignancy more than follicular lesion/neoplasm on thyroid fine-needle aspiration?

Thyroid fine-needle aspiration (FNA) is a standard procedure for the clinical triage of thyroid nodules. The diagnosis of an adequately sampled thyroid FNA is generally grouped into three categories: benign, malignant, and indeterminate. The latter group usually includes follicular neoplasm, follicular lesion, and sometimes a more specific diagnosis such as Hurthle cell neoplasm or follicular lesion/neoplasm with Hurthle cell change. Whether a FNA diagnosis of Hurthle cell lesion/neoplasm (HLN) denotes a worse clinical outcome than follicular lesion/neoplasm (FLN) remains controversial. A cohort of 303 thyroid FNA cases with follow-up thyroidectomy in our institutes was identified, with the follow-up excision diagnosis compared to the FNA diagnosis in order to address this issue. Of this cohort, 87 cases had an FNA diagnosis of HLN while 216 cases had a diagnosis of FLN. Upon excision, the FNA diagnosis of HLN group had 14 cases of goiter/nodular hyperplasia (16%), 46 cases of adenoma (12 follicular adenoma (14%) and 34 cases of Hurthle cell adenoma (39%)), and 27 cases of carcinoma (31%, 12 papillary carcinoma and 15 Hurthle cell carcinoma). The FLN group had 74 cases of goiter/nodular hyperplasia (34.3%), 8 cases of Hashimoto thyroiditis (3.7%), 73 cases of follicular adenoma (33.8%), one case of granular cell tumor, and 60 cases of carcinoma (27.8%, 46 papillary carcinoma, 12 follicular carcinoma, and 1 Hurthle cell carcinoma and 1 parathyroid carcinoma) upon excision. There is no significant difference in predicting cancer between the two cytology diagnosis groups (HLN versus FLN, 31% versus 27.8%, P = 0.5771). When sorting all the cases by the surgical diagnosis, while comparable for age at diagnosis, the cancer group having the higher proportion of male patients than the non-cancer group (28.7% versus 16.7%, P = 0.0259). Hurthle cell carcinoma patients are typically older than patients with other cancer diagnoses (59 versus 44, P = 0.0077). Our results suggest that an FNA diagnosis of HLN does not predict more malignancy than FLN. Males and older patients with a HLN FNA diagnosis carry a higher risk of Hurthle cell carcinoma upon thyroidectomy.

Adenocarcinoma, Follicular↗

PubMed1996

Obvious mRNA and protein expression but absence of mutations of the RET proto-oncogene in parathyroid tumors.

The study on the expression of the RET proto-oncogene in parathyroid tumors disclosed obvious mRNA expression by the reverse transcription (RT)-polymerase chain reaction (PCR) method and protein expression by Western blotting. To find out whether mutations in the cysteine-rich regions or tyrosine kinase domain of the RET proto-oncogene are etiological for parathyroid tumorigenesis, sporadic parathyroid adenomas and carcinomas, parathyroid tumors from multiple endocrine neoplasia 1, familial isolated hyperparathyroidism or hereditary hyperparathyroidism-jaw tumor syndrome were screened by PCR-single strand conformation polymorphism and PCR restriction fragment length polymorphism. Missense mutations in the cysteine-rich region, or codons 768 or 918 in the tyrosine kinase domain of the RET proto-oncogene, were not detected in any of the examined cases of parathyroid tumors. These results suggest that mutations of the RET proto-oncogene do not represent a frequent mechanism of tumorigenesis for parathyroid tumors.

Adult↗

PubMed1999

[Retrosternal parathyroid gland cystic neoplasm as a cause of primary hyperparathyroidism].

Parathyroid carcinoma is a rare cause of primary hyperparathyroidism (1-2%). In this paper a case of parathyroid cancer of the right inferior parathyroid gland cyst (5 cm in diameter) localised mostly retrosternally is presented in a patient suffering from severe hypercalcaemia (Ca--3.7 mmol/l, Ca(++)--1.8 mmol/l), severe bone pains and weakness, huge osteoporosis with following L5 compression fracture and recurrent nephrolithiasis. PTH blood level before surgical treatment was 1243 pg/ml (Norm: 10-60 pg/ml). In the preoperative ultrasonography of the neck, a lesion was found, but it was considered to be a cyst in the inferior pole of the right thyroid lobe. In a fine-needle biopsy from the lesion-colloid mass without any cells was found. In a 99mTc-MIBI scintigraphy of the neck a suspicion of focus lesion in the right superior parathyroid gland was made, which was not confirmed intra-operatively. Parathyroid carcinoma was diagnosed intraoperatively in histological examination. 'En block' resection of the retrosternal parathyroid tumor and right thyroid lobe was performed from the jugular incision. Any enlarged jugular lymph nodes were not found. In a postoperative period a transient hypocalcaemia was present, which disappeared after pharmacological treatment. During 32 months of follow-up neither no features of local recurrence nor distant metastases were found. Calcium level in blood was normal, PTH 216.0 pg/ml, severity of bone pains and weakness lessened, osteoporosis in a course of pharmacological treatment--with no further progress.

Diagnosis, Differential↗

PubMed2002

Recurrent or persistent hyperparathyroidism.

Approximately 90% of patients with primary hyperparathyroidism (PHPT) are cured by parathyroidectomy at the initial neck exploration. Those not cured either remain hypercalcemic in the immediate postoperative period or develop hypercalcemia after a long period of normocalcemia. Almost all cases of hypercalcemia after neck exploration for PHPT are evident early in the postoperative period and are caused either by an overlooked parathyroid adenoma or an incomplete resection of hyperplastic parathyroid tissue. Less commonly, the surgeon has failed to recognize, and adequately treat, parathyroid carcinoma, or the diagnosis of PHPT was incorrect and there is another cause of the hypercalcemia. A successful neck exploration for PHPT is primarily dependent on the experience of the operating surgeon, the anatomic location of the parathyroid glands, either in "normal" or "ectopic" sites, and the presence of a single enlarged parathyroid gland as opposed to multiglandular disease or parathyroid carcinoma. In cases where an enlarged parathyroid gland is not identified at operation, noninvasive or invasive radiographic imaging procedures are useful in localizing the gland. Currently, the most reliable and practical procedure is technetium 99m sestamibi scanning. This technique identifies an enlarged parathyroid gland in 65-80% of cases. Single photon emission computed tomography (SPECT) in association with sestamibi scanning increases the sensitivity of the procedure to 85%. These imaging procedures are least reliable in patients with multiglandular disease. Ultrasound and computed tomographic scanning are less sensitive; however, they are commonly used as confirmatory tests in association with sestamibi scanning. When noninvasive imaging procedures fail to identify an enlarged parathyroid gland, invasive procedures, such as selective arteriography, are performed. Whereas invasive procedures are useful, they are associated with significant morbidity. Reoperations for persistent or recurrent hyperparathyroidism, compared with the initial operations, are associated with higher complication rates. In 90% of cases, the abnormal pathology can be reached through a cervical incision. The success rate of the reoperation depends primarily on the results of the localization procedure and whether the patient has a single enlarged parathyroid gland or multiglandular disease. Resection of a single enlarged gland is curative in virtually all patients. If, however, the patient has multiple gland disease, the operation is successful less often, especially in those with certain familial endocrinopathies.

Choristoma↗