Myelofibrosis Secondary to Hyperparathyroidism

Kumbasar, Abdülbaki; Taylan, Ismail; Kazancıoğlu, Rümeyza; Agan, Mehmet; Yenigün, Mustafa; Sar, Fuat

doi:10.1055/s-2004-817820

Cited by 19 publications

(17 citation statements)

References 17 publications

(31 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…(30–32) Chronic HPT results in severe metabolic bone disease. In addition to the bone abnormalities described herein, HPT patients are anemic, have disturbed immune function,(33–36) and show a marked accumulation of hematopoietic-derived mast cells in their bone marrow. 37 Mast cells play a key role in innate immunity.…”

Section: Discussionmentioning

confidence: 77%

The role of mast cells in parathyroid bone disease

Turner

Iwaniec

Marley

et al. 2010

Journal of Bone and Mineral Research

View full text Add to dashboard Cite

Chronic hyperparathyroidism (HPT) is a common cause of metabolic bone disease. These studies investigated the underlying cellular and molecular mechanisms responsible for the detrimental actions of elevated parathyroid hormone (PTH) on the skeleton. Bone biopsies from hyperparathyroid patients revealed an association between parathyroid bone disease and increased numbers of bone marrow mast cells. We therefore evaluated the role of mast cells in the etiology of parathyroid bone disease in a rat model for chronic HPT. In rats, mature mast cells were preferentially located at sites undergoing bone turnover, and the number of mast cells at the bone–bone marrow interface was greatly increased following treatment with PTH. Time-course studies and studies employing parathyroid hormone–related peptide (PTHrP), as well as inhibitors of platelet-derived growth factor-A (PDGF-A, trapidil), kit (gleevec), and PI3K (wortmannin) signaling revealed that mature mast cell redistribution from bone marrow to bone surfaces precedes and is associated with osteitis fibrosa, a hallmark of parathyroid bone disease. Importantly, mature mast cells were not observed in the bone marrow of mice. Mice, in turn, were resistant to the development of PTH-induced bone marrow fibrosis. These findings suggest that the mast cell may be a novel target for treatment of metabolic bone disease. © 2010 American Society for Bone and Mineral Research.

show abstract

Section: Discussionmentioning

confidence: 77%

The role of mast cells in parathyroid bone disease

Turner

Iwaniec

Marley

et al. 2010

Journal of Bone and Mineral Research

View full text Add to dashboard Cite

show abstract

“…Bone pathology shows spicules of woven bone and undermineralized bone matrix embedded in a mass of connective tissue made of abnormal, poorly differentiated stromal cells (Marie, et al 1997; Riminucci, et al 1997; Riminucci, et al 1999). This fibrosis is reminiscent of that seen in patients with severe primary or secondary hyperparathyroidism (Kumbasar, et al 2004). Likewise, mice expressing a constitutively active PTH1R mutant also display significant accumulation of fibroblastoid cells in the bone marrow (Calvi et al 2001), indicating a major role for enhanced PTH actions in the pathogenesis of fibrous dysplasia.…”

Section: Human Disorders Caused By Mutations In the Gene Encoding Gsαmentioning

confidence: 78%

Heterotrimeric G proteins in the control of parathyroid hormone actions

Baştepe

Turan

2017

Journal of Molecular Endocrinology

View full text Add to dashboard Cite

Parathyroid hormone (PTH) is a key regulator of skeletal physiology and calcium and phosphate homeostasis. It acts on bone and kidney to stimulate bone turnover, increase the circulating levels of 1,25 dihydroxyvitamin D and calcium, and inhibit the reabsorption of phosphate from the glomerular filtrate. Dysregulated PTH actions contribute to or are the cause of several endocrine disorders. This calciotropic hormone exerts its actions via binding to the PTH/PTH-related peptide receptor (PTH1R), which couples to multiple heterotrimeric G proteins, including Gs and Gq/11. Genetic mutations affecting the activity or expression of the alpha-subunit of Gs, encoded by the GNAS complex locus, are responsible for several human diseases for which the clinical findings result, at least partly, from aberrant PTH signaling. Here we review the bone and renal actions of PTH with respect to the different signaling pathways downstream of these G proteins, as well as the disorders caused by GNAS mutations.

show abstract

“…There have been only a few reports of a primary HP accompanied by myelofibrosis. Kumbasar et al. (2004) reported a patient with parathyroid adenoma, anemia and myelofibrosis, which improved after parathyroidectomy.…”

Section: Discussionmentioning

confidence: 93%

“…Myelofibrosis, in association with anemia, has been identified in some studies (Yetgin et al, 1989;Rao, Shih & Mohini, 1993;Komatsuda et al, 1998;Duarte et al, 2002;Kumbasar et al, 2004;Lotinun, Sibonga & Turner, 2006). It has been suggested that elevated levels of PTH stimulate marrow fibroblasts, resulting in myelofibrosis (Rao, Shih & Mohini, 1993;Nomura et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Pancytopenia and secondary myelofibrosis could be induced by primary hyperparathyroidism

Lim

Park

et al. 2007

Int J Lab Hematology

View full text Add to dashboard Cite

Hyperparathyroidism may be a precipitating factor important to the development of myelofibrosis: however, there has been only a few reports regarding myelofibrosis secondary to primary hyperparathyroidism. Recently, a rare case of pancytopenia caused by myelofibrosis in a 41-year-old woman who complained of general weakness and arthralgia presented to our clinical service. The patient was diagnosed with primary hyperparathyroidism with pancytopenia. Bone marrow biopsy revealed myelofibrosis. Right parathyroidectomy was performed and a parathyroid adenoma was totally excised. After surgery, the CBC counts and other clinical abnormalities gradually improved without further intervention. We concluded that the pancytopenia was because of bone marrow fibrosis resulting from primary hyperparathyroidism. Therefore, physicians should consider myelofibrosis secondary to primary hyperparathyroidism as a cause of pancytopenia in hypercalcemic patients, even though it is rare.

show abstract

Myelofibrosis Secondary to Hyperparathyroidism

Cited by 19 publications

References 17 publications

The role of mast cells in parathyroid bone disease

The role of mast cells in parathyroid bone disease

Heterotrimeric G proteins in the control of parathyroid hormone actions

Pancytopenia and secondary myelofibrosis could be induced by primary hyperparathyroidism

Contact Info

Product

Resources

About