Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary hyperparathyroidism is a rare occurrence in pregnancy with significant risks to the mother and the foetus, witch is related to the level of serum calcium. A 41-year-old women, gravida 2, para 1, presented at 22 weeks gestation with nausea, vomiting and mild cognitive dysfunction associated with hypercalcemic crisis. The hypercalcemia was observed to be related to parathyroid hyperplasia that was surgically removed. Complete resolution of her symptomatology and hypercalcemia occurred postoperatively. The pregnancy was complicated with transient hypertension. A small for gestational age healthy male infant was delivered at term with no neonatal complications related with this pathology.
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PMID:[Hypercalcemic crisis associated with primary hyperparathyroidism during pregnancy]. 1661 44

Primary hyperparathyroidism is the most frequent cause of hypercalcemia in ambulatory patients. Elevated serum parathyroid hormone in the presence of persistent hypercalcemia is the diagnostic sine qua non for primary hyperthyroidism. Since examination of serum calcium became a routine diagnostic test, most patients with primary hyperparathyroidism are asymptomatic at the time of diagnosis. Primary hyperparathyroidism in most of patients is caused by parathyroid adenoma, and parathyroid hyperplasia and cancer are rare causes of the disorder. Parathyroidectomy is the primary treatment of choice for primary hyperparathyroidism by any cause. Parathyroidectomy should be performed in most of patients with primary hyperparathyroidism, but asymptomatic or only mildly hypercalcemic patients are treated according to the guidelines for surgical treatment established by the NIH Consensus Development Conference in 2002. For patients with osteoporosis who are not indicated for or decline surgical procedures can be treated with bisphosphonates.
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PMID:[Primary hyperparathyroidism]. 1697 86

In 80% to 90% of patients with primary hyperparathyroidism, a single parathyroid adenoma will be identified as the culprit, whereas the remaining 10% to 20% are caused by multiple adenomas, parathyroid hyperplasia, and rarely, parathyroid carcinoma. At the 2002 National Institute of Health consensus meeting, minimally invasive parathyroidectomy was endorsed as a promising and attractive alternative to total parathyroidectomy. Therefore, preoperative localization of the adenoma is critical in the clinical evaluation of the patient before surgical resection. Although adenomas less than 1 cm may be difficult to visualize sonographically, knowledge of typical imaging characteristics of parathyroid adenomas and use of special sonographic techniques will facilitate identification in most patients. Typical imaging characteristics of parathyroid adenomas include homogeneously hypoechoic echotexture on gray scale with an enlarged feeding artery and peripheral arc of vascularity seen on color and power Doppler. Proper neck extension, unilateral graded compression techniques, and patient swallowing will improve visualization of adenomas.
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PMID:Sonography of the abnormal parathyroid gland. 1714 33

Preoperative imaging has proved its use successful in the localization of solitary parathyroid adenomas in patients with suspected primary hyperparathyroidism. However, due to multiglandular disease at presentation patients with renal hyperparathyroidism need to be analyzed separately, making the usefulness of imaging techniques controversial. Recently, improved methods of functional imaging like parathyroid scan with 99mTc-sestamibi or positron emission tomography, especially when combined with computed tomography, can provide additional quantitative and qualitative information that has yet to be assessed. Nuclear medicine procedures could prove useful not only in preoperative diagnosis, but also in the selection of medical or surgical therapeutic alternatives in secondary hyperparathyroidism patients. There is evidence that 99mTc-sestamibi uptake in parathyroid hyperplasia or adenoma is related to biochemical markers of parathyroid function. We are only beginning to identify the factors involved in radiotracer uptake by parathyroid cells and how it can be modulated to obtain more accurate results. This review analyzes the current use of non-invasive imaging modalities in patients with secondary hyperparathyroidism, taking into account the latest trends in the field combining anatomic and functional modalities and the relevant factors linked to radiotracer uptake in abnormal hyperfunctioning parathyroid glands.
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PMID:Localising imaging in secondary hyperparathyroidism. 1884 26

Whereas the sensitivity of the membrane calcium receptors is decreased in parathyroid adenoma, extracellular calcium may reduce parathyroid hormone (PTH) secretion through the protein kinase C pathway in parathyroid hyperplasia. The aim of this study was to determine the role of a preoperative oral calcium loading test in the differential diagnosis between adenoma and hyperplasia. Twenty-two subjects with adenoma (group A, age +/- standard error 56 +/-2 years, female/male 15/7), 10 individuals with hyperplasia (group H, age 54 +/-3, female/male 8/2), and 32 age and gender pair-matched controls (group C) underwent the test. Calcium and PTH were measured before and 60, 120, and 180 min after oral administration of 1 g of calcium (as gluconolactate). Product P was defined as minimal PTH concentration (pg/mL) x maximal calcium concentration (mg/dL) during the test. Ratio R was defined as relative PTH decline/relative calcium increase. The PTH decline during the test in group H was comparable to that of the controls. PTH decline <30%, Product P > 1,100, and Ratio R < 4 diagnosed adenoma with specificity of 100%, 90%, and 100%, respectively. PTH decline >60% diagnosed hyperplasia with specificity of 100%. The total accuracy of the test (65%) was comparable to that of technetium-99 m sestamibi scintigraphy (66%) and better than that of ultrasonography (58%). The test may discriminate patients with sporadic diffuse hyperplasia from individuals with solitary adenoma in cases of primary hyperparathyroidism with an indication for surgery.
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PMID:Primary hyperparathyroidism: role of the preoperative oral calcium loading test in the differential diagnosis between adenoma and hyperplasia. 1902 Jul 89

We report a 13 year-old mate with a history of multiple fractures and kidney stones. The laboratory showed a hypercalcemia of 11.5 mg/dl, a PTH of 112.6 pg/ml and 24 hour urinary calcium of 571 mg. Bone densitometry showed spine and femur Z scores of -2.9 and -1.6, respectively, kidney ultrasound showed nephrocalcinosis and a MIBI-SPECT scintigram showed a higher uptake in the right lower parathyroid gland. The diagnosis of primary hyperparathyroidism was made and the patient was operated, excising the right lower parathyroid gland. After surgery, serum calcium and PTH levels returned to normal values. In children, the proportion of cases with parathyroid hyperplasia is higher than in adults. Therefore, during surgery all four parathyroid glands must be explored. There is also a higher frequency of ectopic adenomas. Family history must be explored to discard the presence of a multiple endocrine neoplasia (MEN I or II), a familial hyperparathyroidism or a syndrome of primary hyperparathyroidism associated to mandibular tumor.
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PMID:[Primary hyperparathyroidism in an adolescent. Report of one case]. 1919 27

Establishing a diagnosis of multiple endocrine neoplasia type 1 (MEN1) especially in children, adolescents, and young adults can be challenging because of phenotypic heterogeneity even among family members. We report an adolescent girl diagnosed to have MEN1 following presentation with multiple collagenomas. Histological evaluation of her cutaneous lesions revealed >70 collagenomas. Hormonal evaluation included calcium, phosphate, and parathormone measurements. Exons 2-10 of the MEN1 gene and flanking intron-exon borders were sequenced and revealed a novel nonsense mutation, Y222X. Following the identification of the cutaneous lesions as collagenomas by the pathologist, the patient was referred for an endocrine evaluation which revealed asymptomatic primary hyperparathyroidism. The patient elected to have surgery at which time she was found to have parathyroid hyperplasia. This case emphasizes the usefulness of cutaneous findings for the diagnosis and management of MEN1.
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PMID:Reverse referral: from pathology to endocrinology. 1920 29

Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant hereditary disease. Primary hyperparathyroidism is known to occur at an early age in MEN1 patients. In MEN1 patients, special care regarding not only surgery for hyperparathyroidism but also other MEN1-related tumors is required. Between 1998 and 2007, 482 patients, including 16 whose hyperparathyroidism was discovered by family screening for MEN1, underwent surgical therapy for primary hyperparathyroidism at our institution. We recommended MEN1 gene analysis for patients having one of the following clinicopathological features: 1) age younger than 30 years old; 2) enlargement of multiple glands; 3) coexistence or presence of past history of MEN1-related tumors; or 4) family history of hyperparathyroidism or MEN1-related tumors. Sixty patients had at least one of the above features and were recommended for genetic analysis. Thirty-nine of these patients consented to undergo MEN1 genetic analysis and 16 (41%) showed MEN1 mutation. Pathological examination confirmed multiglandular parathyroid hyperplasia in 15 cases. Subject to this strategy, MEN1 index patients in Japan could be detected efficiently and selected for appropriate therapies for hyperparathyroidism and MEN1-related tumors.
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PMID:MEN1 gene analysis in patients with primary hyperparathyroidism: 10-year experience of a single institution for thyroid and parathyroid care in Japan. 1946 Nov 64

In patients with primary hyperparathyroidism (pHPT), positive preoperative localization studies enable to perform a minimally invasive approach for parathyroid surgery. However, current imaging techniques are not always successful. We therefore conducted a study to determine the sensitivity of C-11 methionine positron emission tomography/computed tomography (Met-PET/CT) in localizing parathyroid adenomas in pHPT. Met-PET/CT scans of the neck and mediastinum of 33 patients undergoing parathyroidectomy for primary HPT were compared with intraoperative and histological findings. Primary HPT was caused by a single gland adenoma in 30 patients, while another 3 patients had multiglandular disease. Met-PET/CT scan correctly located a single gland adenoma in 25 out of 30 (83%) patients with pHPT, among them 2 patients with persistent disease, 7 patients with prior neck surgery, and 8 patients with concomitant thyroid nodules. In 3 patients with multiglandular disease, Met-PET/CT showed only one enlarged parathyroid gland in two individuals and was negative in the third patient. Statistical analysis found a significant correlation between true-positive results and the weight (2.42+/-4.05 g) and diameter (2.0+/-1.18 cm) of parathyroid adenomas while the subgroup with false negative findings had significantly smaller (0.98+/-0.54 cm) and lighter (0.5+/-0.38 g) glands. Sensitivity was 83% for single gland adenomas and 67% for multiglandular disease. Met-PET/CT correctly localized 83% of single gland parathyroid adenomas in patients with pHPT. However, preoperative localization of multiglandular disease due to double adenomas or parathyroid hyperplasia remained difficult.
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PMID:C-11 methionine positron emission tomography/computed tomography localizes parathyroid adenomas in primary hyperparathyroidism. 2001 49

We are reporting a case of a capillary haemangioma-like proliferation arising within a parathyroid gland adenoma, associated with primary hyperparathyroidism. The vessel proliferation bearing a close resemblance to a capillary haemangioma consisted of tightly packed capillaries, endothelial buds and occasional small caliber muscle-containing vessels. The observation expands the spectrum of tumour-associated vascular proliferations by adding an exuberant haemangioma-like pattern to its extreme end. These are a heterogeneous group of lesions reportedly induced by aberrant production of angiogenic factors. We investigated expression of VEGF, pKDR, FGF2, HIF1alpha and HIF2alpha and only VEGF gave a strong positive reaction in the adenoma cells entrapped in the vascular meshwork. Although this does not constitute a proof that aberrant VEGF production was a causative agent, unexpected supportive evidence for its pathogenic role emerged from a failure to detect chromogranin A. Chromogranin A is a precursor of several regulatory proteins, including vasostatin I, a multilevel suppressor of VEGF. The production of vasostatin I may have been reduced in a chromogranin A-negative adenoma which could lead to a loss of its opposing effect on VEGF-regulated processes. The only two other published cases of haemangioma of the parathyroid gland were reported in patients diagnosed with primary parathyroid hyperplasia with hyperparathyroidism, a pathophysiologic condition similar to our case. Therefore we raise the question whether these tumours could also represent a reactive phenomenon.
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PMID:Haemangioma of the parathyroid gland. Does it really exist? 2006 87


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