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)

Recently, parathyroid hormone (PTH) was shown to support survival of progenitor cells in bone marrow. The release of progenitor cells occurs in physiological and pathological conditions and was shown to contribute to neovascularization in tumors and ischemic tissues. In the present study we sought to investigate prospectively the effect of primary hyperparathyroidism (PHPT) on mobilization of bone marrow-derived progenitor cells. In 22 patients with PHPT and 10 controls, defined subpopulations of circulating bone marrow-derived progenitor cells (BMCs) were analyzed by flow cytometry (CD45(+)/CD34(+)/CD31(+) cells indicating endothelial progenitor cells, CD45(+)/CD34(+)/c-kit(+) cells indicating hematopoietic stem cells, and CD45(+)/CD34(+)/CXCR4(+) cells indicating progenitor cells with the homing receptor CXCR4). Cytokine serum levels (SCF, SDF-1, VEGF, EPO, and G-CSF) were assessed using ELISA. Levels of PTH and thyroid hormone as well as serum electrolytes, renal and liver parameters, and blood count were analyzed. Our data show for the first time a significant increase of circulating BMCs and an upregulation of SDF-1 and VEGF serum levels in patients with PHPT. The number of circulating BMCs returned to control levels measured 16.7 +/- 2.3 mo after surgery. There was a positive correlation of PTH levels with the number of CD45(+)/CD34(+)/CD31(+), CD45(+)/CD34(+)/c-kit(+), and CD45(+)/CD34(+)/CXCR4(+) cells. However, there was no correlation between cytokine serum concentrations (SDF-1, VEGF) and circulating BMCs. Serum levels of G-CSF, EPO, and SCF known to mobilize BMCs were even decreased or remained unchanged, suggesting a direct effect of PTH on stem cell mobilization. Our data suggest a new function of PTH mobilizing BMCs into peripheral blood.
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PMID:Primary hyperparathyroidism is associated with increased circulating bone marrow-derived progenitor cells. 1791 47

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