Evidence for parathyroid hormone-related peptide as a cause of hypercalcemia in myeloma [letter]

Tamura, Kazuo; Koyama, Koji; Kurabayashi, Hitoshi; Take, Hirohiko; Shirakura, Takuo; Shibata, Harumichi; Kojima, Itaru

doi:10.1182/blood.v84.5.1692.1692

Cited by 11 publications

(5 citation statements)

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“…Indirect evidence of an association between PTHrP and hypercalcaemia in myeloma has been provided by detection of PTHrP in the supernatant of cultures of myeloma cell lines (Suzuki et al, 1994). m-RNA for PTHrP has also been demonstrated by RT-PCR in bone marrow containing myeloma cells from one patient, although the specific cell source of the m-RNA could not be identified by such an approach, and circulating PTHrP was not detected in the patient (Tamura et al, 1994). In the present study, PTHrP has thus been shown for the first time to behave as a humoral mediator of hypercalcaemia in this disorder.…”

Section: Discussionmentioning

confidence: 99%

“…Anecdotal reports have suggested that excess 1,25(OH) 2 vitamin D production is the most common humorallymediated cause of hypercalcaemia in Hodgkin's disease, and to a lesser extent in NHL, but accounts for only a proportion of PTHrP in Hypercalcaemia due to Haematological Neoplasia # 1996 Blackwell Science Ltd, British Journal of Haematology 94: [486][487][488][489][490][491][492] some hypercalcaemic patients with T and B cell NHL (Motokura et al, 1989;Wada et al, 1992;Ikeda et al, 1994), myeloma (Budayr et al, 1989;Tamura et al, 1994) and chronic lymphatic leukaemia (Fain et al, 1994;Seymour & Keating, 1995).…”

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confidence: 99%

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Parathyroid hormone‐related protein in hypercalcaemia associated with haematological malignancy

et al. 1996

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The incidence of hypercalcaemia and its association with humoral mechanisms involving parathyroid hormone-related protein (PTHrP), parathyroid hormone (PTH), or 1.25(OH)2 vitamin D were assessed in a prospective study of patients admitted to a clinical haematology unit. Hypercalcaemia was detected in 18/165 patients, and was due to primary hyperparathyroidism in 3/17 patients in whom results of humoral mediator assessments were obtained. In the other patients, hypercalcaemia was associated in nine instances with myeloma, in five with B-cell non-Hodgkin's lymphoma (NHL), and in one with myeloid neoplasia. No evidence was obtained of a humoral mechanism involving 1.25(OH)2 vitamin D, but elevated circulating levels of PTHrP, comparable with those in humoral hypercalcaemia of malignancy, were present in 2/4 patients with NHL, and in 3/9 with myeloma. The relationship between presence or absence of elevated circulating PTHrP, and presence or absence of hypercalcaemia during the course of treatment, indicated PTHrP was involved in the production of hypercalcaemia. Such an association raises the possibility that PTHrP released by neoplastic cells in these disorders acts in a paracrine manner to produce local bone resorption, and when produced in greater amounts causes elevated circulating levels which make an additional humorally-mediated contribution to the development of hypercalcaemia.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Parathyroid hormone‐related protein in hypercalcaemia associated with haematological malignancy

et al. 1996

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“…Hypercalcemia of malignancy occurs most commonly with solid tumours, especially squamous cell malignancy of any origin, and breast and renal cell carcinoma (3). In these situations, a humoral secretion of PTHrP has been implicated as the most likely etiology, while the intact PTH is usually sup- pressed (14). Because this condition may occasionally mimic hyperparathyroidism, a PTH level is commonly required for the diagnosis.…”

Section: Discussionmentioning

confidence: 99%

“…Other endogenously secreted mediators, however, have been postulated, including transformin growth factor alpha, interleukin-1-alpha, tumour necrosis factor, prostaglandin E and 1,25 dihydroxyvitamin D (11,14).…”

Section: Discussionmentioning

confidence: 99%

Severe Hypercalcemia as an Initial Presenting Manifestation of Hepatocellular Carcinoma

Ghobrial

George

Mannam

et al. 2002

Canadian Journal of Gastroenterology

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An 80-year-old white woman who presented with fatigue, weakness, weight loss, constipation and polydipsia is reported. The patient was given a diagnosis of severe hypercalcemia and was subsequently found to have clinical, roentgenographic and pathological evidence of hepatocellular carcinoma. Further studies revealed a low parathyroid hormone level, excluding the possibility of primary hyperparathyroidism, and a negative bone survey, precluding metastatic bone disease. The patient's hypercalcemia was believed to emanate from the humoral secretion of a parathyroid hormone-related peptide, which was found to be elevated, and was abated with conservative management while her cancer was being treated with chemotherapy. The details of this rarely documented presentation, which can easily be mistaken for hepatic encephalopathy, are provided.

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“…It has been reported that PTHrP is implicated in hypercalcemia of other hematological disease preceding ATL (3). The expression of PTHrPin a myelomacase was demonstrated in a 72-year-old Japanese woman (4) and in a 70-year-old Australian man (5).…”

Section: Introductionmentioning

confidence: 89%

Hypercalcemia Induced with the Plasma Levels of Parathyroid Hormone-Related Peptide in Multiple Myeloma.

et al. 2000

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A 69-year-old man visited our department of neurology with symptomsof paresthesia on the lower extremities and lumbago. Biochemical examination of serum samples showed hypercalcemia (serum concentration 15.6 mg/dl). The levels of intact parathyroid hormone (i-PTH) and 1,25dihydroxyvitamin D were suppressed, whereas parathyroid hormone-related peptide (PTHrP) was elevated up to 5.4 pM (normal range: below 0.6 pM). Additionally, bone survey revealed a punched-out lesion in radiological examinations of the skull. Bonemarrowaspiration demonstrated manyatypical plasma cells suggesting multiple myeloma. Nephrogenouscyclic adenosine monophosphate(CAMP), urinary deoxypyridinoline, plasma interleukin 6 (IL-6) and transforming growth factor p (TGFP) concentrations were elevated, whereas %of renal tubular reabsorption of phosphate ( % TRP) was decreased. The immunohistochemical results demonstrated the expression of PTHrPin atypical plasma cells. These data indicated that hypercalcemia complicating multiple myelomacauses an elevation of renal calcium reabsorption and an increase of bone resorption mediated by PTHrP action.

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Evidence for parathyroid hormone-related peptide as a cause of hypercalcemia in myeloma [letter]

Cited by 11 publications

References 0 publications

Parathyroid hormone‐related protein in hypercalcaemia associated with haematological malignancy

Parathyroid hormone‐related protein in hypercalcaemia associated with haematological malignancy

Severe Hypercalcemia as an Initial Presenting Manifestation of Hepatocellular Carcinoma

Hypercalcemia Induced with the Plasma Levels of Parathyroid Hormone-Related Peptide in Multiple Myeloma.

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