Fluoride Therapy and Parathyroid Hormone Activity in Osteoporosis

1990 ◽  
Vol 79 (3) ◽  
pp. 233-238 ◽  
Author(s):  
T. C. B. Stamp ◽  
P. W. Saphier ◽  
N. Loveridge ◽  
C. R. Kelsey ◽  
A. J. Goldstein ◽  
...  
Keyword(s):  
Alkaline Phosphatase ◽  
Parathyroid Hormone ◽  
Sodium Fluoride ◽  
Serum Alkaline Phosphatase ◽  
Biologically Active ◽  
Calcium Balance ◽  
Hormone Activity ◽  
Cross Sectional ◽  
Parathyroid Hormone Activity

1. To determine the relationships between parathyroid hormone activity and long-term sodium fluoride therapy in osteoporosis, cytochemical bioassays (for biologically active parathyroid hormone) were performed in 22 osteoporotic control patients and in 18 patients after 15 ± 10 months of treatment (60 mg of sodium fluoride daily). Ten patients were studied longitudinally by repeated metabolic balances and were therefore common to both groups. All patients were receiving mineral supplements. 2. Cross-sectional data showed a fourfold mean increase in biologically active parathyroid hormone on fluoride treatment (P < 0.005) together with a 51% increase in serum alkaline phosphatase (P < 0.005). Longitudinal data showed, in addition, a significant increase in the calcium balance of 2.4 ± 1.2 (sem) mmol daily (P < 0.05) and the development of a positive phosphorus balance (P < 0.02). 3. Fluoride-treated patients were then analysed in two groups according to the level of biologically active parathyroid hormone. Thirty-two per cent of values were above the upper limit of normal (18 pg/ml). The mean serum alkaline phosphatase level in this group showed no elevation above that of the control patients, the overall rise being accounted for entirely by patients with normal levels of biologically active parathyroid hormone. High levels of biologically active parathyroid hormone were also associated with relative hypophosphataemia (P < 0.01), relative hypercalciuria (P < 0.05) and an increased urine/faecal calcium ratio (P < 0.025). 4. Results show that long-term fluoride and calcium therapy increase biologically active parathyroid hormone in osteoporosis and that excessive parathyroid hormone activity may account for certain features of the refractory state.

Fluoride therapy in osteoporosis: Acute effects on parathyroid and mineral homoeostasis

1988 ◽  
Vol 75 (2) ◽  
pp. 143-146 ◽  
Author(s):  
Trevor C. B. Stamp ◽  
Michael V. Jenkins ◽  
Nigel Loveridge ◽  
Peter W. Saphier ◽  
Monica Katakity ◽  
...  
Keyword(s):  
Sodium Fluoride ◽  
Serum Levels ◽  
Biologically Active ◽  
Metabolic Effects ◽  
Calcium Balance ◽  
Acute Effects ◽  
Phosphorus Absorption ◽  
Therapeutic Results ◽  
Calcium And Phosphorus

1. Acute metabolic effects of sodium fluoride therapy were analysed among 41 osteoporotic patients already receiving large calcium supplements, 33 of whom underwent simultaneous metabolic balance studies. 2. Mean serum calcium fell transiently within 24–48 h by 0.03 ±0.07 (sd) mmol/l (P < 0.01) and phosphorus by 0.06±0.08 (sd) mmol/l (P < 0.001). In a subgroup, ionized calcium fell and biologically active parathyroid hormone (bio-PTH) rose more than fivefold (P < 0.01). Urine calcium rose after an insignificant fall. 3. Pretreatment calcium and phosphorus balances were significantly positive and did not change overall during the first 8 days of treatment. However, on analysing balances in two groups relative to serum changes, in patients whose serum levels changed least sodium fluoride increased faecal calcium (P < 0.025) and phosphorus (P < 0.01) and reduced calcium balance (P < 0.01), giving a mean balance difference between the two groups of 2.1 mmol daily (P < 0.001). 4. Very small changes in serum levels therefore indicate well-marked metabolic responses: sodium fluoride acutely stimulates bio-PTH activity and must also enhance mineral uptake from circulation into tissue(s). By separate and opposing action(s) it inhibits intestinal calcium and phosphorus absorption, predominantly in those whose serum levels remain stable. All these effects may be relevant to long-term therapeutic results.

The Effect of Long-Term Mestranol Administration on Calcium and Phosphorus Homeostasis in Oophorectomized Women

1971 ◽  
Vol 41 (3) ◽  
pp. 233-236 ◽  
Author(s):  
J. M. Aitken ◽  
D. McKay Hart ◽  
D. A. Smith
Keyword(s):  
Parathyroid Hormone ◽  
Serum Calcium ◽  
Urinary Calcium ◽  
Calcium Excretion ◽  
Hormone Activity ◽  
Phosphorus Excretion ◽  
Calcium And Phosphorus ◽  
Urinary Phosphorus Excretion ◽  
Parathyroid Hormone Activity

1. A group of women who had undergone hysterectomy and bilateral salpingooophorectomy were studied and subsequently given either 20–40 μg of mestranol per day or a placebo for 1 year. 2. The administration of mestranol to these oophorectomized women for 1 year was associated with significant falls in serum calcium and phosphorus concentrations, a fall in urinary calcium excretion and a rise in relative urinary phosphorus excretion. 3. It is suggested that these results are consistent with an increase in sensitivity to calcitonin and that the relative hyperphosphaturia reflects a compensatory rise in parathyroid hormone activity.

Increased serum alkaline phosphatase as a predictor of long-term mortality after stroke

Neurology ◽  
2010 ◽  
Vol 75 (22) ◽  
pp. 1995-2002 ◽  
Author(s):  
W.- S. Ryu ◽  
S.- H. Lee ◽  
C. K. Kim ◽  
B. J. Kim ◽  
B.- W. Yoon
Keyword(s):  
Alkaline Phosphatase ◽  
Serum Alkaline Phosphatase ◽  
Long Term Mortality

Skeletal Blood Flow in Paget's Disease of Bone and its Response to Calcitonin Therapy

1978 ◽  
Vol 54 (1) ◽  
pp. 69-74 ◽  
Author(s):  
R. Wootton ◽  
J. Reeve ◽  
E. Spellacy ◽  
M. Tellez-Yudilevich
Keyword(s):  
Alkaline Phosphatase ◽  
Blood Flow ◽  
Serum Alkaline Phosphatase ◽  
Paget’S Disease ◽  
Paget's Disease ◽  
Short Term ◽  
Urinary Hydroxyproline ◽  
Rapid Fall ◽  
Hydroxyproline Excretion

1. Blood flow to the skeleton was measured by the 18F clearance method of Wootton, Reeve & Veall (1976) in 24 patients with untreated Paget's disease. In every patient but one, resting skeletal blood flow was increased. There was a significant positive correlation between skeletal blood flow and serum alkaline phosphatase and between skeletal blood flow and urinary total hydroxyproline excretion. 2. Fourteen patients were re-studied after they had received short-term (7 days or less) or long-term (7 weeks or more) calcitonin. Skeletal blood flow, alkaline phosphatase and urinary hydroxyproline excretion fell towards normal in every case. There was some evidence from the short-term studies that calcitonin produced a more rapid fall in skeletal blood flow than in alkaline phosphatase. 3. Glomerular filtration rate appeared to increase transiently in response to calcitonin.

Rickets Associated With Long-Term Anticonvulsant Therapy in a Pediatric Outpatient Population

PEDIATRICS ◽  
1975 ◽  
Vol 56 (1) ◽  
pp. 52-57 ◽  
Author(s):  
Carl J. Crosley ◽  
Claire Chee ◽  
Peter H. Berman
Keyword(s):  
Alkaline Phosphatase ◽  
Alkaline Phosphatase Activity ◽  
Serum Alkaline Phosphatase ◽  
Pediatric Population ◽  
Anticonvulsant Therapy ◽  
Control Population ◽  
Serum Alkaline Phosphatase Activity ◽  
Calcium And Phosphorus ◽  
And Control

Over a 12-month period, an ambulatory pediatric population receiving long-term anticonvulsants was surveyed for the presence of biochemical and radiologic rickets. There were 74 treated children and 95 matched controls. Elevations of serum alkaline phosphatase activity occurred in 31 of the 74 (42%) treated children (23 of 47 children between 2 and 10 years and 8 of 21 children between 10 and 16 years). This frequency of abnormal values was significantly greater than that which occurred in our control population. Calcium and phosphorus abnormalities were minimal in both treated and control populations. Radiologic rickets occurred in 6 of the 74 (8%) of the treated children and in none of the control population. Neither the severity of the rickets nor the degree of hyperalkaline phosphatasemia were correlated with age of the patient, duration, and/or dose of anticonvulsant therapy.

Long-Term Follow-up of Hypophosphatemic Bone Disease Associated With Elemental Formula Use: Sustained Correction of Bone Disease After Formula Change or Phosphate Supplementation

2020 ◽  
Vol 59 (12) ◽  
pp. 1080-1085
Author(s):  
Abigail S. Eswarakumar ◽  
Nina S. Ma ◽  
Leanne M. Ward ◽  
Philippe Backeljauw ◽  
Halley Wasserman ◽  
...  
Keyword(s):  
Alkaline Phosphatase ◽  
Bone Disease ◽  
Serum Alkaline Phosphatase ◽  
Serum Phosphorus ◽  
Phosphorus Concentration ◽  
Disease Extent ◽  
Elemental Formula ◽  
Radiology Reports ◽  
Phosphate Supplementation

In this article, we describe the long-term outcomes of children who were previously reported to have developed hypophosphatemic bone disease in association with elemental formula use. An extended chart review allowed for an updated report of 34 children with regard to severity/duration of bone disease, extent of recovery, and time to correction using radiology reports and biochemical data. After implementation of formula change and/or phosphate supplementation, we found that serum phosphorus concentration increased and serum alkaline phosphatase activity decreased in all patients, normalizing by 6.6 ± 4.0 (mean ± SD) months following diagnosis. The decrease in serum alkaline phosphatase from diagnosis to the time of correction was moderately correlated with the concurrent increase in serum phosphorus ( R = 0.48, P < .05). Age at diagnosis significantly correlated with time to resolution ( R = 0.51, P = .01). This study supports the earlier report that bone disease associated with hypophosphatemia during elemental formula use responds to formula change and/or phosphate supplementation.

Abnormal Bone Mineral Metabolism after Long-Term Anticonvulsant Treatment

1994 ◽  
Vol 28 (1) ◽  
pp. 47-48 ◽  
Author(s):  
Christopher P. Alderman ◽  
Catherine L. Hill
Keyword(s):  
Alkaline Phosphatase ◽  
Serum Concentration ◽  
Bone Mineral ◽  
Serum Alkaline Phosphatase ◽  
Mineral Metabolism ◽  
Bone Mineral Metabolism ◽  
Hepatic Microsomal Enzyme ◽  
Grand Mal ◽  
Anticonvulsant Treatment

OBJECTIVE: To present a case of anticonvulsant-induced disturbances of bone mineral metabolism associated with long-term phenytoin treatment. CASE SUMMARY: An 87-year-old woman was hospitalized with generalized acroparesthesia. Her medical history was significant for grand mal epilepsy, which had been treated with phenytoin for more than ten years. On admission she was found to be hypocalcemic, and her alkaline phosphatase concentration was markedly elevated. DISCUSSION: Further investigations revealed that the patient's serum concentration of 25-hydroxycalciferol was well below the expected range. Phenytoin treatment was withdrawn, and calcitriol supplementation commenced. Ten weeks later she was normocalcemic, and the calcitriol dosage was reduced. Radiologic investigations at this time revealed an ununited hip fracture, as well as widespread evidence of bone demineralization. CONCLUSIONS: Minor elevations of liver enzymes observed in association with anticonvulsant treatment may reflect hepatic microsomal enzyme induction. Marked elevation of serum alkaline phosphatase, particularly when seen in concert with hypocalcemia, may be markers of anticonvulsant-induced bone disease. Under these circumstances, further radiologic investigations and measurement of the vitamin D serum concentration should be undertaken.

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