The Interrelationships among Prolactin, 1,25-Dihydroxyvitamin D, and Parathyroid Hormone in Humans*

1979 ◽  
Vol 49 (4) ◽  
pp. 628-630 ◽  
Author(s):  
NANCY D. ADAMS ◽  
THOMAS L. GARTHWAITE ◽  
RICHARD W. GRAY ◽  
THAD C. HAGEN ◽  
JACOB LEMANN
PLoS ONE ◽  
2014 ◽  
Vol 9 (8) ◽  
pp. e104825 ◽  
Author(s):  
Lisa A. Houghton ◽  
Andrew R. Gray ◽  
Michelle J. Harper ◽  
Pattanee Winichagoon ◽  
Tippawan Pongcharoen ◽  
...  

Endocrinology ◽  
1984 ◽  
Vol 114 (3) ◽  
pp. 897-903 ◽  
Author(s):  
KNUT HOVE ◽  
RONALD L. HORST ◽  
E. TRAVIS LITTLEDIKE ◽  
DONALD C. BEITZ

2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Takunori Ogawa ◽  
Jun Miyata ◽  
Koichi Fukunaga ◽  
Akihiko Kawana ◽  
Takashi Inoue

Hypercalcemia of malignancy frequently manifests as paraneoplastic syndrome in patients with solid tumors. A 71-year-old man was diagnosed with stage IIIB lung squamous cell carcinoma. Laboratory examination revealed high serum calcium concentration with elevated serum parathyroid hormone-related protein (PTHrP) and 1,25-dihydroxyvitamin D3 levels. As the patient did not respond to the initial treatment with calcitonin, extracellular fluid infusion, and chemotherapy, systemic prednisolone was administered additionally. Thus, the levels of serum calcium normalized and PTHrP and 1,25-dihydroxyvitamin D3 decreased simultaneously. To our knowledge, this is the first case report on the successful treatment of hypercalcemia of malignancy caused by PTHrP and 1,25-dihydroxyvitamin D3 cosecretion in a patient with lung cancer.


2020 ◽  
Vol 13 (8) ◽  
pp. e235209
Author(s):  
Filip Ionescu ◽  
Ioana Petrescu ◽  
Maria Marin

Hypercalcaemia in malignancy is most commonly caused by paraneoplastic secretion of parathyroid hormone-related protein or osteolytic metastases. Very rarely (<1% of cases), the mechanism behind increased serum calcium is increased production of calcitriol (1,25-dihydroxyvitamin D) and even rarer is the occurrence of this phenomenon in solid malignancies, with few such instances reported in the literature. We present a case of a neuroendocrine malignancy originating in the oesophagus associated with calcitriol-induced hypercalcaemia, a phenomenon that has not been previously described. We review the pathophysiology of calcitriol-induced hypercalcaemia and previously reported cases of solid tumours with this presentation.


1989 ◽  
Vol 257 (6) ◽  
pp. E903-E908
Author(s):  
A. Goulding ◽  
E. Gold

To examine the abilities of estrogens and progestogens to slow bone resorption and conserve bone in ovariectomized rats deficient in calcitonin (CT) or parathyroid hormone (PTH), nine groups of animals with 45Ca-labeled bones were studied for 12 wk. Rats were thyroidectomized (TX), parathyroidectomized (PTX), or given sham neck operations (Sham) and treated orally with either estrogen, 300 micrograms 17 beta-estradiol.kg body wt-1.wk-1; progestogen, 500 micrograms norethisterone acetate.kg body wt-1.wk-1; or placebo (Plac). The TX rats had parathyroid autografts and thyroxine replacement. In all surgical groups, estradiol (E2) and norethindrone (Nor) slowed urinary 45Ca excretion and conserved bone (P less than 0.001). However E2 lowered urinary hydroxyproline more than Nor. Total body Ca values (mg +/- SD) were Sham + Plac, 3,079 +/- 201; Sham + E2, 3,886 +/- 335; Sham + Nor, 3,567 +/- 459; TX + Plac, 3,123 +/- 159; TX + E2, 3,869 +/- 235; TX + Nor, 3,540 +/- 422; PTX + Sham, 3,067 +/- 249; PTX + E2, 3,775 +/- 414; PTX + Nor, 3,635 +/- 467. Importantly, E2 and Nor conserved bone as effectively in TX and PTX groups as in Sham rats, although the PTX rats had slower bone resorption and lower plasma 1,25-dihydroxyvitamin D values (P less than 0.001) than groups with intact parathyroids. We conclude that the effects of estrogens and progestogens to slow bone resorption and conserve bone are independent of CT and PTH. These findings appear relevant to the pathogenesis and treatment of postmenopausal osteoporosis.


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