Evaluation of calcium and phosphate metabolism and musculoskeletal system in patients with chronic pancreatitis - preliminary report

Pancreatology ◽  
2021 ◽  
Vol 21 ◽  
pp. S27
Author(s):  
M. Rakowska ◽  
A. Mianowska ◽  
M. Jaworski ◽  
M. Wojcik ◽  
P. Pludowski ◽  
...  
PEDIATRICS ◽  
1983 ◽  
Vol 72 (2) ◽  
pp. 225-233
Author(s):  
James C. M. Chan ◽  
Reuben B. Young ◽  
Uri Alon ◽  
Peter Mamunes

Forty-two children received 1,25-dihydroxy-vitamin-D3 for treatment of disorders in calcium and phosphate metabolism secondary to chronic renal insufficiency (n = 29), sex-linked dominant hypophosphatemic rickets (n = 9), hypoparathyroidism (n = 2), and pseudohypoparathyroidism (n = 2). Serum calcium, phosphate, and creatinine concentrations were measured monthly for a mean of 26 months and a total of 1,079.5 patient-months. Patients with renal osteodystrophy manifested hypercalcemia (>11 mg/dL) once in every 13 months of treatment on the average. Of three children with hypophosphatemic rickets who experienced hypercalcemia, two proved to have tertiary hyperparathyroidism. Among children with hypoparathyroidism and pseudohypoparathyroidism, three episodes of hypercalcemia were observed during 124.5 patient-months, an incidence of one hypercalcemic episode per 39 treatment months. Renal function, as represented by reciprocals of serum creatinine determined retrospectively for a mean of 22 months before and prospectively for a mean of 26 months after initiation of 1,25-dihydroxyvitamin-D3 treatment, underwent no significant changes except in seven of 29 children with chronic renal insufficiency, six of whose rate of renal function deterioration increased on the treatment and one whose rate decreased. With one exception, hypercalcemia was associated in all cases with accelerated renal function deterioration. Before and after initiation of treatment with 1,25-dihydroxyvitamin-D3 the mean calcium x phosphate solubility products were 42.9 and 47.2, respectively. Values less than 60 are accepted as normal. Hypercalcemia is an occasional concomitant of such treatment and a more rapid deterioration of renal function may occur in some of the patients treated with 1,25-dihydroxyvitamin-D3. Thus, careful monitoring of concentrations of serum calcium, phosphate, and creatinine must accompany 1,25-dihydroxy-vitamin-D3 therapy.


1986 ◽  
Vol 6 (1) ◽  
pp. 131-133 ◽  
Author(s):  
Fabio Malberti ◽  
Maurizio Surian ◽  
Giacomo Colussi ◽  
Pablo Cosci ◽  
Bruno Corradi ◽  
...  

Bone Research ◽  
2020 ◽  
Vol 8 (1) ◽  
Author(s):  
Lei Qin ◽  
Wen Liu ◽  
Huiling Cao ◽  
Guozhi Xiao

Abstract Osteocytes, the most abundant and long-lived cells in bone, are the master regulators of bone remodeling. In addition to their functions in endocrine regulation and calcium and phosphate metabolism, osteocytes are the major responsive cells in force adaptation due to mechanical stimulation. Mechanically induced bone formation and adaptation, disuse-induced bone loss and skeletal fragility are mediated by osteocytes, which sense local mechanical cues and respond to these cues in both direct and indirect ways. The mechanotransduction process in osteocytes is a complex but exquisite regulatory process between cells and their environment, between neighboring cells, and between different functional mechanosensors in individual cells. Over the past two decades, great efforts have focused on finding various mechanosensors in osteocytes that transmit extracellular mechanical signals into osteocytes and regulate responsive gene expression. The osteocyte cytoskeleton, dendritic processes, Integrin-based focal adhesions, connexin-based intercellular junctions, primary cilium, ion channels, and extracellular matrix are the major mechanosensors in osteocytes reported so far with evidence from both in vitro and in vitro studies. This review aims to give a systematic introduction to osteocyte mechanobiology, provide details of osteocyte mechanosensors, and discuss the roles of osteocyte mechanosensitive signaling pathways in the regulation of bone homeostasis.


1988 ◽  
Vol 138 (1) ◽  
pp. 57-61 ◽  
Author(s):  
John H. Toogood ◽  
Richard G. Crilly ◽  
Glenville Jones ◽  
John Nadeau ◽  
George A. Wells

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