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Kidney International. Supplement Dec 1999Secondary hyperparathyroidism is a universal complication in patients with chronic renal failure. Hyperplasia of the parathyroid glands is typically seen in these... (Review)
Review
Secondary hyperparathyroidism is a universal complication in patients with chronic renal failure. Hyperplasia of the parathyroid glands is typically seen in these patients. In early renal failure, alteration in vitamin metabolism, decreased levels of calcitriol and moderate decreases in ionized calcium may allow greater synthesis and secretion of PTH. As the disease progresses, there is a decrease in the number of vitamin D receptors (VDR) and calcium receptors (CaR). The decreased number of VDR and CaR makes the parathyroid glands more resistant to calcitriol and calcium. Phosphorus induces hyperplasia of the parathyroid glands independent of calcium and calcitriol, and by a post-transcriptional mechanism increases PTH synthesis and secretion. Experimental work in uremic rats demonstrated that if the animals are fed a high-phosphorus diet, they not only developed secondary hyperparathyroidism but parathyroid cell hyperplasia. If the diet is then reduced in phosphorus, the levels of PTH return to normal. However, the parathyroid cell hyperplasia persists and no apoptosis is seen. Thus, the control of the three most important factors, calcium, calcitriol and phosphorus, is critical to prevent the development of secondary hyperparathyroidism and hyperplasia of the parathyroid glands.
Topics: Animals; Calcium; Humans; Hyperparathyroidism, Secondary; Parathyroid Hormone; Phosphorus; Receptors, Calcitriol; Renal Insufficiency; Vitamin D
PubMed: 10633458
DOI: 10.1046/j.1523-1755.1999.07304.x -
American Journal of Physiology.... Oct 2016Secondary hyperparathyroidism is a well-known complication of end-stage renal disease (ESRD). Both nodular and diffuse parathyroid hyperplasia occur in ESRD patients....
Secondary hyperparathyroidism is a well-known complication of end-stage renal disease (ESRD). Both nodular and diffuse parathyroid hyperplasia occur in ESRD patients. However, their distinct molecular mechanisms remain poorly understood. Parathyroid tissue obtained from ESRD patients who had undergone parathyroidectomy was used for Illumina transcriptome screening and subsequently for discriminatory gene analysis, pathway mapping, and gene annotation enrichment analysis. Results were further validated using quantitative RT-PCR on the independent larger cohort. Microarray screening proved homogeneity of gene transcripts in hemodialysis patients compared with the transplant cohort and primary hyperparathyroidism; therefore, further experiments were performed in hemodialysis patients only. Enrichment analysis conducted on 485 differentially expressed genes between nodular and diffuse parathyroid hyperplasia revealed highly significant differences in Gene Ontology terms and the Kyoto Encyclopedia of Genes and Genomes database in ribosome structure (P = 3.70 × 10). Next, quantitative RT-PCR validation of the top differently expressed genes from microarray analysis proved higher expression of RAN guanine nucleotide release factor (RANGRF; P < 0.001), calcyclin-binding protein (CACYBP; P < 0.05), and exocyst complex component 8 (EXOC8; P < 0.05) and lower expression of peptidylprolyl cis/trans-isomerase and NIMA-interacting 1 (PIN1; P < 0.01) mRNA in nodular hyperplasia. Multivariate analysis revealed higher RANGRF and lower PIN1 expression along with parathyroid weight to be associated with nodular hyperplasia. In conclusion, our study suggests the RANGRF transcript, which controls RNA metabolism, to be likely involved in pathways associated with the switch to nodular parathyroid growth. This transcript, along with PIN1 transcript, which influences parathyroid hormone secretion, may represent new therapeutical targets to cure secondary hyperparathyroidism.
Topics: Adult; Aged; Female; Focal Nodular Hyperplasia; Gene Expression Profiling; Gene Expression Regulation; Humans; Hyperparathyroidism, Primary; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Male; Middle Aged; Multigene Family; Parathyroid Glands; Parathyroid Hormone; Parathyroidectomy; RNA, Messenger; Renal Dialysis; Transcriptome
PubMed: 27600827
DOI: 10.1152/ajpendo.00517.2015 -
International Journal of Hyperthermia :... 2022Hyperparathyroidism (HPT) is classified into primary HPT (PHPT), secondary HPT (SHPT), tertiary HPT (THPT), and pseudohyperparathyroidism. Parathyroid surgery is... (Review)
Review
BACKGROUND
Hyperparathyroidism (HPT) is classified into primary HPT (PHPT), secondary HPT (SHPT), tertiary HPT (THPT), and pseudohyperparathyroidism. Parathyroid surgery is generally reserved for patients with symptomatic PHPT and asymptomatic patients who meet the surgical guideline criteria. However, the risk of complications and mortality after parathyroid gland surgery increases with increasing patient age.
AIM
This study aimed to review existing research on laser ablation, radiofrequency ablation, microwave ablation, and high-intensity focused ultrasound in the treatment of HPT and analyze its application prospects.
CONCLUSIONS
Thermal ablation is a good alternative treatment for patients with parathyroid hyperplasia who do not meet the criteria or decline surgery. Being a type of minimally invasive treatment, ultrasound-guided thermal ablation has the advantages of easy operation, rapid recovery, and reusability and is used widely.
Topics: Humans; Hyperparathyroidism, Primary; Hyperparathyroidism, Secondary; Parathyroid Glands; Ultrasonography; Ultrasonography, Interventional
PubMed: 35271788
DOI: 10.1080/02656736.2022.2028907 -
Seminars in Ultrasound, CT, and MR Dec 1996Primary hyperparathyroidism resulting in hypercalcemia is the most common presentation of parathyroid pathology and usually is related to a parathyroid adenoma and, less... (Review)
Review
Primary hyperparathyroidism resulting in hypercalcemia is the most common presentation of parathyroid pathology and usually is related to a parathyroid adenoma and, less commonly, to hyperplasia. Imaging of the parathyroid glands focuses on the detection of adenomas in patients with primary hyperparathyroidism. The role of imaging (as well as the modality used) for preoperative localization of the parathyroid glands continues to be controversial. The embryology, anatomy, and physiology of the parathyroid glands are reviewed. The diagnostic utility of radiological imaging-including ultrasonography, CT, MR imaging, and nuclear scintigraphy-are discussed, particularly as it pertains to the evaluation of primary hyperparathyroidism.
Topics: Diagnostic Imaging; Humans; Parathyroid Diseases; Parathyroid Glands
PubMed: 9023868
DOI: 10.1016/s0887-2171(96)90004-9 -
Archives of Pathology & Laboratory... Aug 2008Primary hyperparathyroidism (P-HPT) is one of the most common of all endocrine disorders. Eighty percent to 85% of cases are due to parathyroid adenomas while... (Review)
Review
CONTEXT
Primary hyperparathyroidism (P-HPT) is one of the most common of all endocrine disorders. Eighty percent to 85% of cases are due to parathyroid adenomas while hyperplasia and carcinoma account for 10% to 15% and less than 1%, of cases, respectively. The past decade has witnessed remarkable advances in the understanding of the molecular basis of parathyroid hyperplasia and neoplasia. Additionally, imaging studies and the development of the intraoperative assay for parathyroid hormone have transformed the diagnosis and management of patients with these disorders.
OBJECTIVE
To review the pathology of parathyroid lesions associated with P-HPT, their molecular and genetic bases, including heritable hyperparathyroidism syndromes, and their clinical diagnosis and management.
DATA SOURCES
Review of pertinent epidemiology, pathology, radiology, and surgery literature on the diagnosis, classification, and treatment of P-HPT.
CONCLUSIONS
Although heritable causes of P-HPT including multiple endocrine neoplasia 1 and 2A and hyperparathyroidism-jaw tumor syndrome account for a minority of cases of P-HPT, advances in the characterization of the affected genes have provided insights into the genetic basis of sporadic parathyroid neoplasms. Alterations in cyclin D1 and loss of heterozygosity of chromosome 11q in adenomas and hyperplasias have provided support for clonality of these lesions. Parafibromin, the protein product of the HRPT2 gene responsible for hyperparathyroidism-jaw tumor syndrome, has been implicated in the development of sporadic parathyroid carcinomas and loss of immunohistochemical expression of this protein has been suggested to be of value in making the diagnosis of parathyroid carcinoma. Sestamibi scanning and ultrasound have revolutionized the planning of surgical approaches and the intraoperative parathyroid hormone assay has become the standard in guiding completion or extension of surgery.
Topics: Adenoma; Carcinoma; Humans; Hyperparathyroidism, Primary; Hyperplasia; Incidence; Parathyroid Glands; Parathyroid Neoplasms; Syndrome
PubMed: 18684024
DOI: 10.5858/2008-132-1251-PHACP -
The Journal of International Medical... Feb 2013This retrospective study investigated the characteristics of secondary hyperparathyroidism (SHPT) by examining the presence of the calcium-sensing receptor (CaSR) and...
OBJECTIVE
This retrospective study investigated the characteristics of secondary hyperparathyroidism (SHPT) by examining the presence of the calcium-sensing receptor (CaSR) and the rate of cell proliferation and apoptosis in parathyroid glands.
METHODS
Eighteen diffuse and 57 nodular hyperplastic parathyroid glands from 24 patients with SHPT were compared with 14 primary adenomas and 33 normal parathyroid glands using immunohistochemical staining of CaSR and a marker of proliferative activity (Ki67 antigen). Apoptosis was measured using the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labelling assay.
RESULTS
The mean ± SE labelling index (LI) of CaSR (12.8% ± 1.5%) in nodular hyperplasia was significantly lower than that in normal parathyroid glands (26.8% ± 0.8%), whereas the mean ± SE LI of CaSR in diffuse hyperplasia was similar to that in normal parathyroid glands (23.3% ± 1.8%). The mean ± SE LI of Ki67 antigen was significantly higher in primary adenoma and nodular hyperplasia than in normal parathyroid glands.
CONCLUSION
These results indicate that downregulation of CaSR, and a higher rate of proliferation over apoptosis, could contribute to the pathological progression of SHPT.
Topics: Adenoma; Adult; Apoptosis; Demography; Humans; Hyperparathyroidism, Secondary; Hyperplasia; Immunohistochemistry; In Situ Nick-End Labeling; Middle Aged; Parathyroid Glands; Receptors, Calcium-Sensing
PubMed: 23569134
DOI: 10.1177/0300060513476600 -
Endocrine-related Cancer Jan 2016Five syndromes share predominantly hyperplastic glands with a primary excess of hormones: neonatal severe primary hyperparathyroidism, from homozygous mutated CASR,... (Review)
Review
Five syndromes share predominantly hyperplastic glands with a primary excess of hormones: neonatal severe primary hyperparathyroidism, from homozygous mutated CASR, begins severely in utero; congenital non-autoimmune thyrotoxicosis, from mutated TSHR, varies from severe with fetal onset to mild with adult onset; familial male-limited precocious puberty, from mutated LHR, expresses testosterone oversecretion in young boys; hereditary ovarian hyperstimulation syndrome, from mutated FSHR, expresses symptomatic systemic vascular permeabilities during pregnancy; and familial hyperaldosteronism type IIIA, from mutated KCNJ5, presents in young children with hypertension and hypokalemia. The grouping of these five syndromes highlights predominant hyperplasia as a stable tissue endpoint and as their tissue stage for all of the hormone excess. Comparisons were made among this and two other groups of syndromes, forming a continuum of gland staging: predominant oversecretions express little or no hyperplasia; predominant hyperplasias express little or no neoplasia; and predominant neoplasias express nodules, adenomas, or cancers. Hyperplasias may progress (5 of 5) to neoplastic stages while predominant oversecretions rarely do (1 of 6; frequencies differ P<0.02). Hyperplasias do not show tumor multiplicity (0 of 5) unlike neoplasias that do (13 of 19; P<0.02). Hyperplasias express mutation of a plasma membrane-bound sensor (5 of 5), while neoplasias rarely do (3 of 14; P<0.002). In conclusion, the multiple distinguishing themes within the hyperplasias establish a robust pathophysiology. It has the shared and novel feature of mutant sensors in the plasma membrane, suggesting that these are major contributors to hyperplasia.
Topics: Adenoma; Adult; Child; Endocrine Glands; Female; Hormones, Ectopic; Humans; Hyperplasia; Hyperthyroidism; Male; Parathyroid Glands; Parathyroid Neoplasms; Pregnancy; Puberty, Precocious
PubMed: 26407873
DOI: 10.1530/ERC-15-0171 -
International Journal of Molecular... May 2022Parathyroid tumors are very prevalent conditions among endocrine tumors, being the second most common behind thyroid tumors. Secondary hyperplasia can occur beyond... (Review)
Review
Parathyroid tumors are very prevalent conditions among endocrine tumors, being the second most common behind thyroid tumors. Secondary hyperplasia can occur beyond benign and malignant neoplasia in parathyroid glands. Adenomas are the leading cause of hyperparathyroidism, while carcinomas represent less than 1% of the cases. Tumor suppressor gene mutations such as and were demonstrated to be involved in tumor development in both familiar and sporadic types; however, the epigenetic features of the parathyroid tumors are still a little-explored subject. We present a review of epigenetic mechanisms related to parathyroid tumors, emphasizing advances in histone modification and its perspective of becoming a promising area in parathyroid tumor research.
Topics: Epigenesis, Genetic; Epigenomics; Histone Code; Humans; Hyperparathyroidism; Parathyroid Neoplasms
PubMed: 35628190
DOI: 10.3390/ijms23105378 -
Canadian Association of Radiologists... Aug 2013Accurate preoperative localization is the key to successful parathyroid surgery in the era of minimally invasive parathyroid surgery. This article presents and discusses... (Review)
Review
Accurate preoperative localization is the key to successful parathyroid surgery in the era of minimally invasive parathyroid surgery. This article presents and discusses the embryologic basis of parathyroid gland and ectopic location and different imaging modalities helpful in diagnosing and localizing parathyroid adenomas and/or hyperplasia. We also aim to review the current surgical concepts in treatment of parathyroid adenomas and/or hyperplasia, the utility of 4-dimensional computed tomography for accurate preoperative localization of hyperfunctioning parathyroid glands, imaging classification of adenomas and/or hyperplasia, and, finally, present some of the limitations of 4-dimensional computed tomography.
Topics: Adenoma; Adult; Aged; Contrast Media; Female; Four-Dimensional Computed Tomography; Humans; Hyperplasia; Male; Middle Aged; Parathyroid Glands; Parathyroid Neoplasms; Preoperative Care; Radiographic Image Enhancement; Reproducibility of Results; Triiodobenzoic Acids
PubMed: 23260861
DOI: 10.1016/j.carj.2012.03.002 -
BMC Endocrine Disorders Nov 2012Thyroid hemiagenesis is a rare anomaly, more commonly seen on the left side (ratio 4:1) and in females (ratio 3:1). The first to describe this anomaly was Handfield...
BACKGROUND
Thyroid hemiagenesis is a rare anomaly, more commonly seen on the left side (ratio 4:1) and in females (ratio 3:1). The first to describe this anomaly was Handfield Jones in 1852.
CASE PRESENTATION
We present a 66 year old female patient with right thyroid hemiagenesis, parathyroid adenoma on the side of hemiagenesis and parathyroid hyperplasia on the contralateral side. The patient had neck pain and was diagnosed as Hashimto thyroiditis with hyperparathyroidism. Parathyroid hormone, thyroglobulin antibodies (Tg-Ab) and thyroid peroxidase antibodies (TPO-Ab) were elevated. Neck ultrasound and technetium 99mTc-methoxyisobutyl isonitrile (MIBI) scintigraphy confirmed the right thyroid hemiagenesis, but not adenoma of parathyroid glands. Intraoperatively, right thyroid hemiagenesis was confirmed and left loboistmectomy was performed with removal of left inferior hyperplastic parathyroid gland. Postoperative PTH (parathyroid hormone) levels were within normal range. Five months after the operation PTH level was elevated again with calcium values at the upper limit. MIBI scintigraphy was performed again which showed increased accumulation of MIBI in the projection of the right parathyroid gland. Surgical reexploration of the neck and excision of the right upper parathyroid adenoma was performed which was located behind cricoid laryngeal cartilage. After surgery a normalization of calcium and PTH occured.
CONCLUSION
From available literature we have not found the case that described parathyroid adenoma on the side of thyroid hemiagenesis,with parathyroid hyperplasia on the contralateral side.
PubMed: 23148717
DOI: 10.1186/1472-6823-12-29