Recurrent hypercalcemia and elevated 1,25-dihydroxyvitamin D levels in hodgkin's disease

Mercier, Richard J.; Thompson, James; Harman, G. S.; Messerschmidt, Gerald L.

doi:10.1016/0002-9343(88)90028-9

Cited by 24 publications

(7 citation statements)

References 22 publications

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“…( 1–4 , 12–21 ) However, to date, studies have failed to fully define the precise basis for this abnormality. On the one hand, a significant number of reports have described an association with raised circulating levels of 1,25(OH) 2 D 3 , ( 4 , 12–18 ) similar to that observed with granulomatous diseases such as sarcoidosis. ( 3 ) On the other hand, several reports have highlighted a role for PTHrP as a lymphoma product that may or may not be linked to the vitamin D status of the host.…”

Section: Discussionmentioning

confidence: 99%

Vitamin D-Mediated Hypercalcemia in Lymphoma: Evidence for Hormone Production by Tumor-Adjacent Macrophages

Hewison

Kantorovich

Liker

et al. 2003

Journal of Bone and Mineral Research

122

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Section: Discussionmentioning

confidence: 99%

Vitamin D-Mediated Hypercalcemia in Lymphoma: Evidence for Hormone Production by Tumor-Adjacent Macrophages

Hewison

Kantorovich

Liker

et al. 2003

Journal of Bone and Mineral Research

122

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“…None of the reported patients with 1,25-(OH) 2 D 3 -mediated hypercalcaemia had concomitant granulomatous disease, and hypercalcaemia often improved with medical or surgical therapy that resulted in a decrease in serum 1,25-(OH) 2 D 3 concentration. Recurrence of hypercalcaemia and increased plasma 1,25-(OH) 2 D 3 concentrations have been documented with recurrence of disease (Mercier et al 1988).…”

Section: Hhm Vsmentioning

confidence: 99%

Hypercalcaemia of malignancy and basic research on mechanisms responsible for osteolytic and osteoblastic metastasis to bone

Clines

Guise²

2005

Endocr Relat Cancer

229

211

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Calcium homeostasis is a tightly regulated process involving the co-ordinated efforts of the skeleton, kidney, parathyroid glands and intestine. Neoplasms can alter this homeostasis indirectly through the production of endocrine factors resulting in humoral hypercalcaemia of malignancy. Relatively common with breast and lung cancer, this paraneoplastic condition is most often due to tumour production of parathyroid hormone-related protein and ensuing increased osteoclastic bone resorption. Although control of hypercalcaemia is generally successful, the development of this complication is associated with a poor prognosis. The metastasis of tumour cells to bone represents another skeletal complication of malignancy. As explained in the 'seed and soil' hypothesis, bone represents a fertile ground for cancer cells to flourish. The molecular mechanisms of this mutually beneficial relationship between bone and cancer cells are beginning to be understood. In the case of osteolytic bone disease, tumour-produced parathyroid hormone-related protein stimulates osteoclasts that in turn secrete tumour-activating transforming growth factor-b that further stimulates local cancer cells. This 'vicious cycle' of bone metastases represents reciprocal bone/ cancer cellular signals that likely modulate osteoblastic bone metastatic lesions as well. The development of targeted therapies to either block initial cancer cell chemotaxis, invasion and adhesion or to break the 'vicious cycle' is dependent on a more complete understanding of bone metastases. Although bisphosphonates delay progression of skeletal metastases, it is clear that more effective therapies are needed. Cancer-associated bone morbidity remains a major public health problem, and to improve therapy and prevention it is important to understand the pathophysiology of the effects of cancer on bone. This review will detail scientific advances regarding this area.

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“…Additionally, many of the reported patients had altered renal function, a finding that suggests that impaired renal calcium clearance may also be contributing to the hypercalcemia in certain patients. Recurrence of hypercalcemia and increased plasma 1,25-(OH) 2 D 3 concentrations has been documented with recurrence of disease (207). Prostaglandins, when measured, have been low, and selected patients had no calcium-lowering effect from indomethacin therapy (199).…”

mentioning

confidence: 99%

Cancer and Bone*

1998

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Recurrent hypercalcemia and elevated 1,25-dihydroxyvitamin D levels in hodgkin's disease

Cited by 24 publications

References 22 publications

Vitamin D-Mediated Hypercalcemia in Lymphoma: Evidence for Hormone Production by Tumor-Adjacent Macrophages

Vitamin D-Mediated Hypercalcemia in Lymphoma: Evidence for Hormone Production by Tumor-Adjacent Macrophages

Hypercalcaemia of malignancy and basic research on mechanisms responsible for osteolytic and osteoblastic metastasis to bone

Cancer and Bone*

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