View clinical trials related to Hyperparathyroidism, Primary.
Filter by:The biological diagnosis of the primary hyperparathyroidism is now facilitated by the reliability of the balance of phosphate and calcium and the dosage of parathyroid hormone (PTH). This diagnosis of preoperative localization is important as surgery are now targeted to the responsible lesion. The "gold standard" for this localization is the cervical ultrasound exploring the usual sites of adenomas and a MIBI scintigraphy (the parathyroid adenoma significantly concentrating this cell marker). However, the diagnosis of preoperative localization remains a subject of discussion as to the most appropriate tests. Indeed, the morphological diagnosis is performed at the ultrasound stage in more than half the cases. It is the new performance of this morphological examination that makes it possible to obtain these results.
The primary objective of this study is to estimate the percent change in baseline bone mineral density (BMD) starting at one year after parathyroidectomy and all the following available dates in patients presenting with primary hyperparathyroidism. The secondary objective is to identify patient factors associated with change in BMD.
This trial studies molecular and immunohistochemical profiling of tumors in patients with parathyroid tumors. Studying molecular and immunohistochemical profiling of tumors may help doctors avoid inconsistencies in diagnosis, unnecessary or incomplete surgery, surgical morbidity, psychological stress, and inadequate follow up.
The goal of this study is to assess the performance of parathyroid imaging on a cardiac-dedicated CZT camera, compared to planar pinhole imaging, in patients referred for primary hyperparathyroidism.
The overall sensitivity and specificity of 11C-MET PET/CT is superior to 18F-FDG PET/CT and conventional SPECT-CT for the detection of abnormal parathyroid glands.
Primary hyperparathyroidism (PHPT) is one of the common endocrine disorders. The major clinical symptoms involve stones, bones, abdominal groans and psychiatric moans. Increased parathyroid cell proliferation and decreased calcium-mediated control of the PTH secretion are characteristic findings. The most common cause of PHPT is adenoma followed by hyperplasia and carcinoma.The molecular mechanisms involved in parathyroid tumorigenesis are partially known. Few genes have been identified and their roles are under study. The genes which are under study by different groups are unable to give a definite direction towards the understanding of parathyroid tumorigenesis and the mechanism involved in overgrowth of parathyroid tissue. So identifying different proteins and their regulation pattern from adenomas to carcinomas will be the initial steps towards understanding the proteins involved in tumorigenesis of parathyroid tissues. By using proteomics approach one can generate protein level information. In this study, using a combined approach based on 2 D gel electrophoresis and mass spectrometry (MS), the investigators propose to study a comparative proteomics to examine the changes of protein profiles in parathyroid tumor tissues with normal and hyperplasic parathyroid tissues. This work plan will help us to understand differentially expressed proteins in patients with PHPT. This will help in understanding the disease and identifying better diagnostic and curative measures of the disease. The investigators are also planning to access nuclear morphometry changes in sporadic parathyroid tumors. It will help in establishing cellular and nuclear change pattern variations from normal to parathyroid tumors.
The present study is designed to examine the expression of VDR, CaSR, PTH, Cyclin D1, Ki67 and PCNA and to find out its relationship with clinical parameters in parathyroid adenomas. Examination of the contribution of genes expression can elucidate the critical link between proliferation and functional abnormalities in parathyroid adenomas. Alternative to DNA and RNA, protein expression can provide a better understanding of this disease.
Primary Hyperparathyroidism (pHPT) increases bone turnover and resorption and thus calcium efflux out of bone. After successful surgical treatment of pHPT, bone takes up calcium again which may result in secondary hyperparathyroidism or even "hungry bone syndrome". Until today there are no studies about this problem helping to develop recommendations or guidelines how to prevent these symptoms. Study hypothesis: Calcium and vitamin D intake after surgery for PHPT protects the bone by keeping PTH in the normal range (less secondary, reactive hyperparathyroidism), prevents hungry bone- syndrome and improve bone-turnover markers (osteoporosis protection).