<i>In vitro</i> Stability of Endogenous Parathyroid Hormone-Related Protein in Blood and Plasma

Hutchesson, A. C. J.; Hughes, Sarah M.; Bowden, Sarah; Ratcliffe, W. A.

doi:10.1177/000456329403100106

Cited by 10 publications

(4 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, the results indicate an instability of PTHrP when stored for longer periods ( 1 10 years). Due to the risk of degradation, it is recommended that PTHrP should be assessed in plasma [20,21] . There are, however, several reports on the analysis of PTHrP in serum [9,12,22] , including the present study.…”

Section: Discussionmentioning

confidence: 99%

Parathyroid Hormone-Related Protein and Serum Calcium in Patients with Renal Cell Carcinoma

Papworth¹,

Grankvist²,

Ljungberg³

et al. 2005

Tumor Biol

View full text Add to dashboard Cite

Objective: To evaluate serum parathyroid hormone-related protein (PTHrP) in relation to serum calcium and clinical outcome of patients with renal cell carcinoma.Methods: Sera from 243 patients with renal cell carcinoma were collected prior to therapy. Serum PTHrP was analyzed using an immunoradiometric assay. Tumour stage, nuclear grade, corrected serum calcium, and survival were assessed. Results: Serum PTHrP was detectable in 37/243 sera (15%) and hypercalcaemia (≧2.60 mmol/l) in 32/220 (15%). A positive correlation between serum PTHrP and serum calcium was found (r = 0.326; p < 0.01). Following subdivision of the material, based on storage time, the frequency of detectable serum PTHrP seemed to decrease with time. Serum calcium, but not serum PTHrP, was correlated to tumour stage (p < 0.001). Survival was similar for patients with detectable and undetectable PTHrP, but those with hypercalcaemia had a significantly shorter survival time compared to those with normal serum calcium (p < 0.001). A multivariate analysis showed that tumour stage and serum calcium were independent prognostic factors, but not grade or PTHrP. Conclusions: A positive relation of serum PTHrP to serum calcium was demonstrated in patients with renal cell carcinoma. Hypercalcaemia but not serum PTHrP predicted a worse prognosis.

show abstract

Section: Discussionmentioning

confidence: 99%

Parathyroid Hormone-Related Protein and Serum Calcium in Patients with Renal Cell Carcinoma

Papworth¹,

Grankvist²,

Ljungberg³

et al. 2005

Tumor Biol

View full text Add to dashboard Cite

show abstract

“…Appropriate samples for PTHrP measurement should be collected as EDTA plasma in a chilled tube that also contains a protease inhibitor (such as aprotinin), kept chilled on ice during transport to the laboratory, and (within 15 min) spun in a refrigerated centrifuge, separated, and frozen. Even with these rigorous steps taken to reduce proteolytic cleavage, PTHrP begins to degrade in EDTA-aprotinin plasma within 15 min of sample collection (423). In contrast to this ideal sample collection and processing, many studies used stored sera that had been allowed to clot at room temperature for 60 min before routine processing (925).…”

Section: Parathyroid Hormone-related Proteinmentioning

confidence: 99%

Maternal Mineral and Bone Metabolism During Pregnancy, Lactation, and Post-Weaning Recovery

Kovacs

2016

Physiological Reviews

384

524

View full text Add to dashboard Cite

During pregnancy and lactation, female physiology adapts to meet the added nutritional demands of fetuses and neonates. An average full-term fetus contains ϳ30 g calcium, 20 g phosphorus, and 0.8 g magnesium. About 80% of mineral is accreted during the third trimester; calcium transfers at 300-350 mg/day during the final 6 wk. The neonate requires 200 mg calcium daily from milk during the first 6 mo, and 120 mg calcium from milk during the second 6 mo (additional calcium comes from solid foods). Calcium transfers can be more than double and triple these values, respectively, in women who nurse twins and triplets. About 25% of dietary calcium is normally absorbed in healthy adults. Average maternal calcium intakes in American and Canadian women are insufficient to meet the fetal and neonatal calcium requirements if normal efficiency of intestinal calcium absorption is relied upon. However, several adaptations are invoked to meet the fetal and neonatal demands for mineral without requiring increased intakes by the mother. During pregnancy the efficiency of intestinal calcium absorption doubles, whereas during lactation the maternal skeleton is resorbed to provide calcium for milk. This review addresses our current knowledge regarding maternal adaptations in mineral and skeletal homeostasis that occur during pregnancy, lactation, and post-weaning recovery. Also considered are the impacts that these adaptations have on biochemical and hormonal parameters of mineral homeostasis, the consequences for long-term skeletal health, and the presentation and management of disorders of mineral and bone metabolism.

show abstract

“…First, PTHrP is subject to rapid cleavage and degradation in serum; consequently, blood samples are optimally collected as EDTA plasma with aprotinin (a protease inhibitor), kept chilled on ice, and promptly (within 15 min) centrifuged, separated, and frozen. Even when optimally collected as EDTA-aprotinin plasma and kept chilled on ice, PTHrP begins to degrade within 15 min of sample collection (275). Many studies did not approach this rigor of sample collection and preparation, and it is common to see use of stored sera that had been allowed to clot at room temperature for up to 60 min (678).…”

Section: Pthrpmentioning

confidence: 99%

Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

Kovacs

2014

Physiological Reviews

211

188

View full text Add to dashboard Cite

Mineral and bone metabolism are regulated differently in utero compared with the adult. The fetal kidneys, intestines, and skeleton are not dominant sources of mineral supply for the fetus. Instead, the placenta meets the fetal need for mineral by actively transporting calcium, phosphorus, and magnesium from the maternal circulation. These minerals are maintained in the fetal circulation at higher concentrations than in the mother and normal adult, and such high levels appear necessary for the developing skeleton to accrete a normal amount of mineral by term. Parathyroid hormone (PTH) and calcitriol circulate at low concentrations in the fetal circulation. Fetal bone development and the regulation of serum minerals are critically dependent on PTH and PTH-related protein, but not vitamin D/calcitriol, fibroblast growth factor-23, calcitonin, or the sex steroids. After birth, the serum calcium falls and phosphorus rises before gradually reaching adult values over the subsequent 24 -48 h. The intestines are the main source of mineral for the neonate, while the kidneys reabsorb mineral, and bone turnover contributes mineral to the circulation. This switch in the regulation of mineral homeostasis is triggered by loss of the placenta and a postnatal fall in serum calcium, and is followed in sequence by a rise in PTH and then an increase in calcitriol. Intestinal calcium absorption is initially a passive process facilitated by lactose, but later becomes active and calcitriol-dependent. However, calcitriol's role can be bypassed by increasing the calcium content of the diet, or by parenteral administration of calcium.

show abstract

In vitro Stability of Endogenous Parathyroid Hormone-Related Protein in Blood and Plasma

Cited by 10 publications

References 13 publications

Parathyroid Hormone-Related Protein and Serum Calcium in Patients with Renal Cell Carcinoma

Parathyroid Hormone-Related Protein and Serum Calcium in Patients with Renal Cell Carcinoma

Maternal Mineral and Bone Metabolism During Pregnancy, Lactation, and Post-Weaning Recovery

Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

Contact Info

Product

Resources

About