PRIMARY HYPERPARATHYROIDISM AND THE RELATIONSHIP BETWEEN 25-VITAMIN D, 1,25 VITAMIN D AND PARATHYROID HORMONE: A PROSPECTIVE CASE SERIES
AACE ePoster Library. Hadwen T. 05/13/15; 97769; 726
Dr. Thomas Hadwen
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Abstract
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Introduction
Primary hyperparathyroidism is a common endocrinological disease with an evolving clinical presentation. Vitamin D deficiency is more common in PHPT than the general population, partly related to the elevated PTH converting 25-hydroxyvitaminD into 1,25-dihydroxyvitamin D. Observational studies have shown that a low 25-hydroxyvitamin D is associated with reduced BMD, post-op hypocalcaemia and elevated PTH. Small RCTs have shown that 25-hydroxyvitamin D replacement decreases PTH but has no significant effect on BMD post parathyroidectomy, calcium level, muscle strength or quality of life. The mechanism of vitamin D supplementation suppressing PTH secretion is unclear and there has been little research into the role of 1,25-dihydroxyvitamin D.
Aims/Objectives
To analyse the data of patients with PHPT looking for correlations between PTH, calcium, 25-hydroxyvitaminD, 1,25-dihydroxyvitaminD and 25-hydroxyvitaminD replacement.
Methods
We performed a prospective case series of all patients referred to the Cairns Hospital with primary hyperparathyroidism.
Results
52 patients were diagnosed with PHPT. Average corrected calcium, expressed as mmol/L above normal, was 0.19 and the average PTH, expressed as a multiple above upper limit of normal, was 1.86. The average 25-VitD was 60.5nmol/L (50-150) and the average 1,25-VitD was elevated at 190pmol/L (40-150) (22 patients). There was a statistically significant difference in average PTH level between 25-VitD deficient and replete groups, 2.28 and 1.61 times normal respectively (p=0.016) without a statistically significant difference in corrected calcium. The correlation factor of PTH and 25-VitD was -0.475 and the correlation factor of PTH and 1,25-VitD was +0.575. There was a negative correlation between 25-VitD and 1,25-VitD (-0.616) and replacing vitamin D did not alter the calcium level (13 patients).
Discussion
In our study a low 25-VitD is associated with increased PTH but not hypercalcaemia. Interestingly 25- and 1,25-VitD are inversely related and there is conflicting evidence about this relationship in the literature. The proposed mechanism for 25-VitD replacement suppressing PTH is by increasing the level of plasma 1,25-VitD but our findings of elevated 1,25-VitD in the vitamin D deficient and positive correlation between 1,25VitD and PTH does not support this. 25-VitD may regulate PTH via intra-parathyroid gland 1α-hydroxylase conversion of 25- to 1,25-VitD, dependant on plasma 25-VitD but independent of plasma 1,25-VitD. There is limited evidence that vitamin D replacement has any clinical benefit for the patient. Our study is limited by the small number of patients.
Conclusion
25-Vitamin D deficiency is common in PHPT and associated with an increased PTH. Our study found an inverse relationship between 25- and 1,25-VitD but a direct relationship between 1,25-VitD and PTH. The current guidelines are to replace Vitamin D but whilst replacement likely suppresses PTH there is little evidence to show that replacement has any clinical benefit. The mechanism for the suppression of PTH with vitamin D supplementation is unclear and further research is needed. Large RCT are required to assess the efficacy of Vitamin D replacement.
Primary hyperparathyroidism is a common endocrinological disease with an evolving clinical presentation. Vitamin D deficiency is more common in PHPT than the general population, partly related to the elevated PTH converting 25-hydroxyvitaminD into 1,25-dihydroxyvitamin D. Observational studies have shown that a low 25-hydroxyvitamin D is associated with reduced BMD, post-op hypocalcaemia and elevated PTH. Small RCTs have shown that 25-hydroxyvitamin D replacement decreases PTH but has no significant effect on BMD post parathyroidectomy, calcium level, muscle strength or quality of life. The mechanism of vitamin D supplementation suppressing PTH secretion is unclear and there has been little research into the role of 1,25-dihydroxyvitamin D.
Aims/Objectives
To analyse the data of patients with PHPT looking for correlations between PTH, calcium, 25-hydroxyvitaminD, 1,25-dihydroxyvitaminD and 25-hydroxyvitaminD replacement.
Methods
We performed a prospective case series of all patients referred to the Cairns Hospital with primary hyperparathyroidism.
Results
52 patients were diagnosed with PHPT. Average corrected calcium, expressed as mmol/L above normal, was 0.19 and the average PTH, expressed as a multiple above upper limit of normal, was 1.86. The average 25-VitD was 60.5nmol/L (50-150) and the average 1,25-VitD was elevated at 190pmol/L (40-150) (22 patients). There was a statistically significant difference in average PTH level between 25-VitD deficient and replete groups, 2.28 and 1.61 times normal respectively (p=0.016) without a statistically significant difference in corrected calcium. The correlation factor of PTH and 25-VitD was -0.475 and the correlation factor of PTH and 1,25-VitD was +0.575. There was a negative correlation between 25-VitD and 1,25-VitD (-0.616) and replacing vitamin D did not alter the calcium level (13 patients).
Discussion
In our study a low 25-VitD is associated with increased PTH but not hypercalcaemia. Interestingly 25- and 1,25-VitD are inversely related and there is conflicting evidence about this relationship in the literature. The proposed mechanism for 25-VitD replacement suppressing PTH is by increasing the level of plasma 1,25-VitD but our findings of elevated 1,25-VitD in the vitamin D deficient and positive correlation between 1,25VitD and PTH does not support this. 25-VitD may regulate PTH via intra-parathyroid gland 1α-hydroxylase conversion of 25- to 1,25-VitD, dependant on plasma 25-VitD but independent of plasma 1,25-VitD. There is limited evidence that vitamin D replacement has any clinical benefit for the patient. Our study is limited by the small number of patients.
Conclusion
25-Vitamin D deficiency is common in PHPT and associated with an increased PTH. Our study found an inverse relationship between 25- and 1,25-VitD but a direct relationship between 1,25-VitD and PTH. The current guidelines are to replace Vitamin D but whilst replacement likely suppresses PTH there is little evidence to show that replacement has any clinical benefit. The mechanism for the suppression of PTH with vitamin D supplementation is unclear and further research is needed. Large RCT are required to assess the efficacy of Vitamin D replacement.
Introduction
Primary hyperparathyroidism is a common endocrinological disease with an evolving clinical presentation. Vitamin D deficiency is more common in PHPT than the general population, partly related to the elevated PTH converting 25-hydroxyvitaminD into 1,25-dihydroxyvitamin D. Observational studies have shown that a low 25-hydroxyvitamin D is associated with reduced BMD, post-op hypocalcaemia and elevated PTH. Small RCTs have shown that 25-hydroxyvitamin D replacement decreases PTH but has no significant effect on BMD post parathyroidectomy, calcium level, muscle strength or quality of life. The mechanism of vitamin D supplementation suppressing PTH secretion is unclear and there has been little research into the role of 1,25-dihydroxyvitamin D.
Aims/Objectives
To analyse the data of patients with PHPT looking for correlations between PTH, calcium, 25-hydroxyvitaminD, 1,25-dihydroxyvitaminD and 25-hydroxyvitaminD replacement.
Methods
We performed a prospective case series of all patients referred to the Cairns Hospital with primary hyperparathyroidism.
Results
52 patients were diagnosed with PHPT. Average corrected calcium, expressed as mmol/L above normal, was 0.19 and the average PTH, expressed as a multiple above upper limit of normal, was 1.86. The average 25-VitD was 60.5nmol/L (50-150) and the average 1,25-VitD was elevated at 190pmol/L (40-150) (22 patients). There was a statistically significant difference in average PTH level between 25-VitD deficient and replete groups, 2.28 and 1.61 times normal respectively (p=0.016) without a statistically significant difference in corrected calcium. The correlation factor of PTH and 25-VitD was -0.475 and the correlation factor of PTH and 1,25-VitD was +0.575. There was a negative correlation between 25-VitD and 1,25-VitD (-0.616) and replacing vitamin D did not alter the calcium level (13 patients).
Discussion
In our study a low 25-VitD is associated with increased PTH but not hypercalcaemia. Interestingly 25- and 1,25-VitD are inversely related and there is conflicting evidence about this relationship in the literature. The proposed mechanism for 25-VitD replacement suppressing PTH is by increasing the level of plasma 1,25-VitD but our findings of elevated 1,25-VitD in the vitamin D deficient and positive correlation between 1,25VitD and PTH does not support this. 25-VitD may regulate PTH via intra-parathyroid gland 1α-hydroxylase conversion of 25- to 1,25-VitD, dependant on plasma 25-VitD but independent of plasma 1,25-VitD. There is limited evidence that vitamin D replacement has any clinical benefit for the patient. Our study is limited by the small number of patients.
Conclusion
25-Vitamin D deficiency is common in PHPT and associated with an increased PTH. Our study found an inverse relationship between 25- and 1,25-VitD but a direct relationship between 1,25-VitD and PTH. The current guidelines are to replace Vitamin D but whilst replacement likely suppresses PTH there is little evidence to show that replacement has any clinical benefit. The mechanism for the suppression of PTH with vitamin D supplementation is unclear and further research is needed. Large RCT are required to assess the efficacy of Vitamin D replacement.
Primary hyperparathyroidism is a common endocrinological disease with an evolving clinical presentation. Vitamin D deficiency is more common in PHPT than the general population, partly related to the elevated PTH converting 25-hydroxyvitaminD into 1,25-dihydroxyvitamin D. Observational studies have shown that a low 25-hydroxyvitamin D is associated with reduced BMD, post-op hypocalcaemia and elevated PTH. Small RCTs have shown that 25-hydroxyvitamin D replacement decreases PTH but has no significant effect on BMD post parathyroidectomy, calcium level, muscle strength or quality of life. The mechanism of vitamin D supplementation suppressing PTH secretion is unclear and there has been little research into the role of 1,25-dihydroxyvitamin D.
Aims/Objectives
To analyse the data of patients with PHPT looking for correlations between PTH, calcium, 25-hydroxyvitaminD, 1,25-dihydroxyvitaminD and 25-hydroxyvitaminD replacement.
Methods
We performed a prospective case series of all patients referred to the Cairns Hospital with primary hyperparathyroidism.
Results
52 patients were diagnosed with PHPT. Average corrected calcium, expressed as mmol/L above normal, was 0.19 and the average PTH, expressed as a multiple above upper limit of normal, was 1.86. The average 25-VitD was 60.5nmol/L (50-150) and the average 1,25-VitD was elevated at 190pmol/L (40-150) (22 patients). There was a statistically significant difference in average PTH level between 25-VitD deficient and replete groups, 2.28 and 1.61 times normal respectively (p=0.016) without a statistically significant difference in corrected calcium. The correlation factor of PTH and 25-VitD was -0.475 and the correlation factor of PTH and 1,25-VitD was +0.575. There was a negative correlation between 25-VitD and 1,25-VitD (-0.616) and replacing vitamin D did not alter the calcium level (13 patients).
Discussion
In our study a low 25-VitD is associated with increased PTH but not hypercalcaemia. Interestingly 25- and 1,25-VitD are inversely related and there is conflicting evidence about this relationship in the literature. The proposed mechanism for 25-VitD replacement suppressing PTH is by increasing the level of plasma 1,25-VitD but our findings of elevated 1,25-VitD in the vitamin D deficient and positive correlation between 1,25VitD and PTH does not support this. 25-VitD may regulate PTH via intra-parathyroid gland 1α-hydroxylase conversion of 25- to 1,25-VitD, dependant on plasma 25-VitD but independent of plasma 1,25-VitD. There is limited evidence that vitamin D replacement has any clinical benefit for the patient. Our study is limited by the small number of patients.
Conclusion
25-Vitamin D deficiency is common in PHPT and associated with an increased PTH. Our study found an inverse relationship between 25- and 1,25-VitD but a direct relationship between 1,25-VitD and PTH. The current guidelines are to replace Vitamin D but whilst replacement likely suppresses PTH there is little evidence to show that replacement has any clinical benefit. The mechanism for the suppression of PTH with vitamin D supplementation is unclear and further research is needed. Large RCT are required to assess the efficacy of Vitamin D replacement.
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