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)

In parathyroid glands removed from patients with primary hyperparathyroidism (pHPT), hyperplasias and adenomas cannot be distinguished from one another by light microscopy when only one gland is available for examination. When a second gland is available, it is necessary to establish whether it is normal, suppressed, or hyperplastic. This distinction may be difficult, and the main criterion is the amount of cytoplasmic lipid in the parenchymal cells. If the lipid is abundant, the gland is considered normal or suppressed, and if it is scanty, the gland is interpreted as hyperplastic. We have performed a morphometric ultrastructural study to test the reliability of this criterion. Twenty-five adenomatous glands removed from patients with pHPT, when compared with glands of normal size from euparathyroid patients, showed a significant increase in the parameters indicative of metabolic activity, namely the size of the Golgi apparatus, the amount of rough endoplasmic reticulum, and the length of plasmalemmas. In addition, the amount of cytoplasmic lipid was significantly reduced. Furthermore, 25 glands of normal size removed from the same patients with pHPT showed an amount of lipid similar to that of normal glands from euparathyroid patients. However, all the parameters indicative of metabolic activity were significantly higher than those in glands from euparathyroid patients and comparable to those found in adenomatous glands. These results suggest that in pHPT, normal-size glands are as active as adenomatous glands, regardless of a higher lipid content.
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PMID:Parathyroid glands in primary hyperparathyroidism: an ultrastructural morphometric study of 25 cases. 138 34

Immunohistochemical and ultrastructural studies were performed on cases with hyperparathyroidism. The relationship between histology and cell activity in hyperfunctioning parathyroid glands was studied. Furthermore, the synthesis-secretion process of parathyroid hormone (PTH), which has been more or less elucidated biochemically, was studies by a morphological means. The subjects employed in the present study were 23 cases of primary hyperparathyroidism (PHPT) and 31 cases of secondary hyperparathyroidism (SHPT). Based on the results of the immunohistochemical study using anti-PTH antibody, the histology of the parathyroid gland was classified into 4 types: type A; sporadic cells showing intense yellowish brown staining in their cytoplasm, type B; glandular cells showing intense yellowish brown staining specifically in their cytoplasm, type C; as a whole the cells were weakly stained, but intensely stained cells were absent, and type D; only the cytoplasm of large cells showed uniform and intense yellowish brown staining. In both PHPT and SHPT, type C constituted about 80%. On the other hand, all water clear cell hyperplasia in SHPT showed type D staining. Electron microscopic studies performed on the hyperparathyroidism revealed that the rough endoplasmic reticulum and Golgi apparatus, which are related to the synthesis of PTH, were well developed. Immunoelectron microscopy revealed that only the secretory granules were specifically stained with the anti-PTH antibody. This finding suggests that PTH becomes active once it reaches the secretory granule.
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PMID:[Immunohistochemical classification and ultrastructural study of hyperparathyroidism]. 147 49

The relationship between tissue morphology and cellular activity in hyperparathyroidism was investigated by 2-color flowcytometry and an immunohistochemical technique using anti-parathyroid hormone (PTH) antibody. A total of 21 cases were employed, which included 8 cases of primary hyperparathyroidism (PHPT) and 13 cases of secondary hyperparathyroidism (SHPT). The results of 2-color flowcytometry on DNA ploidy pattern revealed that all the 8 PHPT cases were diploids. In SHPT, however, there were 9 diploids (69.2%), 2 tetraploids (15.4%) and 2 aneuploids (15.4%). Electron microscopic studies were performed on the diploid 2c and 4c peak cells, which were obtained by individually sorting the cells from each cycle. As a result, these cells were found to possess well developed rough endoplasmic reticulum and Golgi apparatus. These cells in general showed weak immunostaining. Furthermore, numerous secretory granules were found in the cells obtained from abnormal peak of aneuploid when compared to diploid cells. In tetraploids and aneuploids, the darkly stained cells and glandular cells showed intense immunostaining. These cells contained numerous secretory granules and they were thought to possess high cellular activity.
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PMID:[The relationship between morphology and cell activity in hyperparathyroidism]. 147 50

Primary hyperparathyroidism may be caused by one or two benign tumors in separate glands, adenoma, a malignant tumor of one gland, carcinoma or hyperplasia of all four glands. Pathologically, the main problem lies in distinguishing between primary chief cell hyperplasia and adenoma, it is impossible from pathological findings of only one gland. Parathyroid adenomas and chief cell hyperplasias contain large numbers of active chief cells. The cells contain aggregated arrays of rough endoplasmic reticulum and large, complex Golgi apparatus with numerous vacuoles and vesicles. Secretory granules are often present in these cells. Most of the cells are generally interpreted to be in the more active phases of parathyroid hormone synthesis and secretion.
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PMID:[Primary hyperparathyroidism--pathological findings and ultrastructure]. 775 73

Parathyroid glands (n = 271) removed from 130 patients were examined by light and electron microscopy. A standardized method of tissue processing was employed and morphometry was performed. The aim of the paper is to provide a description of the human parathyroid chief cell ultrastructure in health and disease, with quantitative evaluation of structures involved in secretion of parathyroid hormone in a large case series, and to discuss their role in current diagnostic histopathology. The patients were euparathyroid (n = 10), or affected by primary (n = 97), secondary (n = 8), or tertiary (n = 15) hyperparathyroidism. In normal glands, solid parenchyma was composed of chief cells, large clear cells, transitional-oxyphil cells, and oxyphil cells. Chief cell hyperplasia, pseudo-adenomatous hyperplasia, adenoma, water-clear cell hyperplasia, and carcinoma were the most usual forms of parathyroid disease responsible for primary hyperparathyroidism. In chief cell hyperplasia, all the parathyroid glands were enlarged and the chief cells were in an active state of hormone secretion, with a large Golgi complex, abundant rough endoplasmic reticulum (RER), small lipid droplets, and tortuous plasma membrane. In pseudo-adenomatous hyperplasia, one gland was enlarged and the others displayed a normal size; however, electron microscopic examination and morphometric analysis showed that all the glands had active cells. Adenomas displayed a pattern similar to those of pseudo-adenomatous hyperplasia, with one gland enlarged and the others of normal size. However, ultrastructural examination and morphometry showed that the normal-size glands were hypo-active. Water-clear cell hyperplasia showed cells filled with cytoplasmic vacuoles. In these cells, structures with intermediate features between secretory granules and vacuoles were visible. Nucleo-cytoplasmic atypias were frequently visible in parathyroid carcinoma cells. In secondary and tertiary hyperplasia, active chief cells were regularly mixed with oxyphil or transitional-oxyphil cells. The tertiary hyperplasia was characterized by RER-associated structures that were not found in the normal or other pathological conditions. These results demonstrate that electron microscopy and morphometry represent useful tools in parathyroid histopathology.
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PMID:Ultrastructure of human parathyroid cells in health and disease. 858 May 10

Parathyroid adenoma is the main cause of primary hyperparathyroidism, which is characterized by enlarged parathyroid glands and excessive parathyroid hormone secretion. Here, we performed transcriptome analysis, comparing parathyroid adenomas with normal parathyroid gland tissue. RNA extracted from ten parathyroid adenoma and five normal parathyroid samples was sequenced, and differentially expressed genes (DEGs) were identified using strict cut-off criteria. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed using DEGs as the input, and protein-protein interaction (PPI) networks were constructed using Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) and visualized in Cytoscape. Among DEGs identified in parathyroid adenomas (n = 247; 45 up-regulated, 202 down-regulated), the top five GO terms for up-regulated genes were nucleoplasm, nucleus, transcription DNA-template, regulation of mRNA processing, and nucleic acid binding, while those for down-regulated genes were extracellular exosome, membrane endoplasmic reticulum (ER), membrane, ER, and melanosome. KEGG enrichment analysis revealed significant enrichment of five pathways: protein processing in ER, protein export, RNA transport, glycosylphosphatidylinositol-anchor biosynthesis, and pyrimidine metabolism. Further, PPI network analysis identified a densely connected sub-module, comprising eight hub molecules: SPCS2, RPL23, RPL26, RPN1, SEC11C, SEC11A, RPS25, and SEC61G. These findings may be helpful in further analysis of the mechanisms underlying parathyroid adenoma development.
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PMID:Comparative Gene Expression Profiles in Parathyroid Adenoma and Normal Parathyroid Tissue. 3083 48