National Cancer Institute®
Last Modified: August 1, 2002
UI - 12092283
AU - Brown JJ; Mohamed H; Williams-Smith L; Osborne R; Coker J; Yee B
TI - Primary hyperparathyroidism secondary to simultaneous bilateral parathyroid carcinoma.
SO - Ear Nose Throat J 2002 Jun;81(6):395-8, 400-1
AD - Department of Otolaryngology-Head and Neck Surgery, Charles R. Drew University School of Medicine and Science, Martin Luther King Jr. Drew Medical Center, Los Angeles, CA, USA. firstname.lastname@example.org
Parathyroid carcinoma is a rare malignancy, and experience with its management is limited. It is generally accepted that surgery is the treatment of choice, and the initial operative intervention might represent the only chance for long-term success. At the time of surgery, a high index of suspicion for carcinoma is vital to performing the appropriate surgical procedures, because frozen-section diagnosis of parathyroid carcinoma is notoriously unreliable. In this article, we describe our experience with this rare entity.
UI - 12146987
AU - Lee NC; Norton JA
TI - Multiple-gland disease in primary hyperparathyroidism: a function of operative approach?
SO - Arch Surg 2002 Aug;137(8):896-9; discussion 899-900
AD - Department of Surgery, University of California, San Francisco, USA.
HYPOTHESIS: The approach to surgery for primary hyperparathyroidism (PHPT) is controversial. To determine whether routine bilateral neck exploration increases the detection of multiple-gland disease compared with a focused unilateral approach, we compared the incidence of single vs multiple-gland disease in patients undergoing surgical treatment for PHPT as a function of unilateral or bilateral exploration. DATA SOURCES: From 1993 through 1997, 214 consecutive patients underwent initial bilateral neck exploration for PHPT by a single surgeon. Each patient underwent the surgical procedure without prior localizing studies. Four parathyroid glands were identified, and abnormal glands were excised. The results were compared with published studies of patients who underwent either bilateral neck exploration or focused unilateral neck exploration for PHPT. STUDY SELECTION: All reported studies from 1995 through 2001 in a MEDLINE search using the terms "parathyroidectomy" or "primary hyperparathyroidism and surgery" and either "bilateral" or "conventional" or "minimally invasive," "selective," or "unilateral." DATA EXTRACTION: The studies were analyzed for numbers of patients and a final diagnosis of either a single adenoma or multiple-gland disease (double adenoma or hyperplasia). Proportions were compared statistically with a chi(2) test. DATA SYNTHESIS: In our series of 214 patients who underwent bilateral neck exploration, 79.4% had a single adenoma, and 20.6% had multiple-gland disease. Of 2166 patients in 14 studies who underwent bilateral neck exploration, 79.7% had a single adenoma, and 19.3% had multiple-gland disease. Of 2095 patients in 31 studies with a focused unilateral approach, 92.5% had a single adenoma, whereas only 5.3% had multiple-gland disease. The incidence of multiple-gland disease was significantly lower among patients treated with a focused unilateral approach compared with a bilateral approach as used in our series and the literature (P<.001). CONCLUSION: The data suggest that a focused unilateral surgical approach for PHPT may underestimate the incidence of multiple-gland disease.
UI - 12173721
AU - Dionisi S; Minisola S; Pepe J; De Geronimo S; Paglia F; Memeo L;
TI - Fitzpatrick LA Concurrent parathyroid adenomas and carcinoma in the setting of multiple endocrine neoplasia type 1: presentation as hypercalcemic crisis.
SO - Mayo Clin Proc 2002 Aug;77(8):866-9
AD - Department of Clinical Sciences, University of Rome La Sapienza, Italy.
We describe a patient with multiple endocrine neoplasia type 1 characterized by the simultaneous occurrence of parathyroid cancer, parathyroid adenomas, and pancreatic gastrinoma, who presented with an episode of acute hypercalcemia. The rapid parathyroid hormone assay provided a basis for the diagnosis of parathyroid hyperfunction. Mediastinal metastasis of the parathyroid carcinoma was found at autopsy. However, the staining of pancreatic and gastric tissue for parathyroid hormone-related protein does not make it possible to exclude completely the contribution of this peptide in mediating the hypercalcemia. To our knowledge, this is the first reported case of parathyroid carcinoma as part of the multiple endocrine neoplasia type 1 syndrome.
UI - 12053214
AU - Vestergaard H; OStergaard Kristensen L
TI - Normocalcemia and persistent elevated serum concentrations of 1-84 parathyroid hormone after operation for sporadic parathyroid adenoma: evidence of increased morbidity from cardiovascular disease.
SO - World J Surg 2002 Jun;26(6):657-60
AD - Department of Endocrinology, Herlev Hospital, University of Copenhagen, DK-2730 Herlev, Denmark. email@example.com
Elevated serum concentrations of 1-84 parathyroid hormone (PTH) after operation for sporadic parathyroid adenoma have been reported in previous studies, years after operation for primary hyperparathyroidism (pHPT). The cause and significance of this finding have not been elucidated. Primary hyperparathyroidism was diagnosed in 195 patients 124 patients. To evaluate long-term effects of elevated serum 1-84 PTH, biochemical variables and pre- and postoperative diseases were investigated from hospital case records. Of the 124 patients operated on, 103 had a solitary adenoma. Among these patients, 60 had normal serum concentrations of 1-84 PTH and calcium postoperatively, 38 patients had follow-up for more than 12 months (range 12-207 months-group A). Persistent elevated serum concentrations of 1-84 PTH and normocalcemia were found in 23 patients. Fourteen patients had follow-up for more than 12 months (range 15-76 months-group B). Two patients had persistent pHPT, and 18 were normocalcemic, but in this retrospective study data on serum 1-84 PTH were not available. No significant differences were found between groups A and B at the time of diagnosis concerning clinical characteristics. More that 12 months after operation for pHPT, the patients in group B, with persistent elevated serum concentrations of 1-84 PTH, had a significantly (c2 = 11, p = 0.005, and power of test 0.66) higher frequency of cardiovascular diseases from ischemic heart disease and hypertension. Persistent elevated serum concentrations of 1-84 PTH after operation for sporadic parathyroid adenoma may be associated with development of cardiovascular disease. This group of patients therefore needs lifelong control and, possibly, medical intervention.
UI - 12161532
AU - Shattuck TM; Costa J; Bernstein M; Jensen RT; Chung DC; Arnold A
TI - Mutational analysis of Smad3, a candidate tumor suppressor implicated in TGF-beta and menin pathways, in parathyroid adenomas and enteropancreatic endocrine tumors.
SO - J Clin Endocrinol Metab 2002 Aug;87(8):3911-4
AD - Center for Molecular Medicine and Division of Endocrinology and Metabolism, University of Connecticut School of Medicine, Farmington, Connecticut 06030, USA.
Based upon molecular allelotyping and comparative genomic hybridization studies, chromosome 15q is the likely location of a tumor suppressor gene important in the pathogeneses of sporadic enteropancreatic endocrine tumors and parathyroid adenomas. Interest has focused on Smad3 as a candidate endocrine tumor suppressor gene because 1) it is localized to 15q and 2) it encodes a TGF beta signaling molecule that has been identified as a binding partner of the multiple endocrine neoplasm type 1 gene product menin, itself involved in enteropancreatic and parathyroid neoplasia. To determine whether Smad3 plays a primary role in development of these tumors, 20 enteropancreatic tumors and 67 parathyroid adenomas were investigated for loss of heterozygosity at DNA markers surrounding Smad3. Twenty percent of enteropancreatic tumors and 24% of parathyroid adenomas showed loss. All 9 coding exons and intron-exon boundaries of the Smad3 gene were then sequenced in genomic DNA from all 20 enteropancreatic and 25 parathyroid tumors, including every case with loss of heterozygosity. No acquired clonal mutations, insertions, or microdeletions in Smad3 were detected in any tumors. Because inactivating somatic mutation is the hallmark of an authentic tumor suppressor, Smad3 is unlikely to function as a classical tumor suppressor gene in the pathogenesis of sporadic parathyroid or enteropancreatic endocrine tumors.
The above citations and abstracts reflect those newly added to CANCERLIT for the month and topic listed in the title. The citations have been retrieved from CANCERLIT using a predefined search strategy of indexed subject terms. Although the search strategy has been refined as best as possible, citations may appear that are not directly related to the topic, and occasionally relevant references may be omitted.