Cisplatin-Induced Hypocalcemia and Hypomagnesemia

Lyman, Neil; Hemalatha, C.; Viscuso, Ronald; Jacobs, Martin

doi:10.1001/archinte.1980.00330220069024

Cited by 36 publications

(12 citation statements)

References 7 publications

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“…These findings suggest that previously reported variances in serum immunoreactive PTHlevels are due to differences in the degree (and duration to some extent) of hypomagnesemiaand hypocalcemia. Magnesium supplementation induced a striking increase in mid-region PTHand intact PTHin the present patient as in the previous reports (1 [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17] in which serum values ofPTHwere measured with traditional assays. This increase indicates that the stimulating drive for PTHsecretion in response to severe hypocalcemia was suppressed by magnesium depletion.…”

Section: Discussionsupporting

confidence: 83%

“…Both cisplatin (1)(2)(3)(4) and doxorubicin (3,5,6) have already been shown to cause hypomagnesemia due to magnesiumleaking from the kidney.…”

Section: Discussionmentioning

confidence: 99%

“…(cis-diamminedichloroplatinum)-induced tiypomagnesemia and hypocalcemia have been reported in several patients (1)(2)(3), and the renal magnesium wasting due to its nephrotoxic effect is suggested to be pathogenic (4). Doxorubicin hydrochloride is also thought to possess a similar Lowering effect on serum magnesium (3,5,6), although its sole effect has not been fully evaluated.…”

Section: Cisplatinmentioning

confidence: 99%

“…Doxorubicin hydrochloride is also thought to possess a similar Lowering effect on serum magnesium (3,5,6), although its sole effect has not been fully evaluated. Regarding the mechanisms involved in the development of hypocalcemia in magnesium deficiency, several conflicting data have been reported in various conditions (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19).…”

Section: Cisplatinmentioning

confidence: 99%

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Tetany due to Hypomagnesemia Induced by Cisplatin and Doxorubicin Treatment for Synovial Sarcoma.

et al. 1993

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Hypocalcemiccrisis developed in a patient with monophasicsynovial sarcoma after amputation of the right leg, followed by long-term treatment with cisplatin and doxorubicin. Laboratory data revealed severe hypomagnesemia and hypocalcemia. High normal intact parathyroid hormone (PTH), elevated mid-region PTHand undetectable osteocalcin levels had already been found before the appearance of obvious symptomsconcomitantly associated with moderate hypomagnesemia and hypocalcemia. Further, both PTHlevels measured by two different methods gradually decreased until the initiation of magnesium supplementation. The magnesiumsupplement immediately relieved the tetany, and induced striking increases in both intact and mid-region PTHlevels transiently and continuous elevations of osteocalcin levels. These results suggest that magnesiumdepletion has dual effects on PTHsecretion, from stimulation to inhibition, as hypomagnesemiaprogresses. Both relative hypoparathyroidism and refractoriness of bone to PTH were thought to be responsible for hypocalcemia due to hypomagnesemia.

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Section: Discussionsupporting

confidence: 83%

“…Both cisplatin (1)(2)(3)(4) and doxorubicin (3,5,6) have already been shown to cause hypomagnesemia due to magnesiumleaking from the kidney.…”

Section: Discussionmentioning

confidence: 99%

Section: Cisplatinmentioning

confidence: 99%

Section: Cisplatinmentioning

confidence: 99%

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Tetany due to Hypomagnesemia Induced by Cisplatin and Doxorubicin Treatment for Synovial Sarcoma.

et al. 1993

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“…This chemotherapeutic agent is associated with nephrotoxicity which appears to be dose-dependent [4]. Hypomagnesemia with renal magnesium wasting [5,6], impaired water metabolism [7], hypocalcemia and hypo kalemia [8][9][10] are among the nephrotoxic effects that have been reported following cisplatin administration.…”

Section: Introductionmentioning

confidence: 99%

Effect of Chronic Cisplatin Administration on Phosphate and Glucose Transport by the Renal Brush Border Membrane

Halabe

Wong²,

Sutton³

1991

Nephron

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Cisplatin (CIS-diamine dichloroplatinum) is a highly nephrotoxic antineoplastic agent which may cause acute renal failure and renal tubular dysfunction. In the present study we have examined the effect of chronic cisplatin administration on sodium-dependent ³²P-phosphate and ³H glucose transport by the renal brush border membrane vesicles (BBMV). Our results indicate that both transport mechanisms were significantly reduced at the BBMV following cisplatin therapy due to an increased K_m (0.13 ± 0.09 vs. 0.34 ± 0.09 mM; p= < 0.01) without significant change in Vmax (56 ± 18 vs. 44 ± 17 pM/mg/s). The results of these studies indicate that cisplatin causes a diffuse renal injury in the proximal segment of the nephron altering both transport mechanisms. Possible mechanisms of cisplatin nephrotoxicity are discussed.

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Mitomycin-induced hemolytic-uremic syndrome. Successful treatment with corticosteroids and intense plasma exchange

Lyman¹

1983

Archives of Internal Medicine

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Mitomycin has been associated with microangiopathic hemolytic anemia and renal failure. We describe a patient with the adult hemolytic-uremic syndrome due to mitomycin who was successfully treated with intense plasma exchange therapy and corticosteroid therapy. Patients receiving mitomycin should have their conditions monitored closely for acute renal failure, thrombocytopenia, and hemolytic anemia.

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Cisplatin-Induced Hypocalcemia and Hypomagnesemia

Cited by 36 publications

References 7 publications

Tetany due to Hypomagnesemia Induced by Cisplatin and Doxorubicin Treatment for Synovial Sarcoma.

Tetany due to Hypomagnesemia Induced by Cisplatin and Doxorubicin Treatment for Synovial Sarcoma.

Effect of Chronic Cisplatin Administration on Phosphate and Glucose Transport by the Renal Brush Border Membrane

Mitomycin-induced hemolytic-uremic syndrome. Successful treatment with corticosteroids and intense plasma exchange

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