scholarly journals Hypercalcaemia in Cleveland: A Hospital-Based Survey

1984 ◽  
Vol 77 (9) ◽  
pp. 742-746 ◽  
Author(s):  
A Rajathurai ◽  
R Cove-Smith
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Primary Hyperparathyroidism ◽  
General Practitioners ◽  
Serum Calcium ◽  
Screening Test ◽  
Patient Records ◽  
Biochemical Profiles ◽  
Hospital Doctors

Over a period of six months all reports in the South Tees Health District of serum calcium levels greater than 2.70 mmol/1 were extracted and patient records examined to establish the associated diseases and patterns of management. A total of 235 reports were evaluated, and after exclusion of doubtful cases 196 patients were included in the study. No cause had been identified in 57 (29%). Many of these were elderly females in whom hypercalcaemia may have been due to primary hyperparathyroidism, but parathyroid hormone levels had not been measured. Of those in whom a diagnosis had been made, 62 (45%) were associated with malignancy and 50 (36%) with chronic renal failure. 72% of cases of hypercalcaemia reported to general practitioners and 13% of those reported to hospital doctors were not investigated further. Despite the inclusion of serum calcium estimation on routine biochemical profiles, many cases of hypercalcaemia are being ignored or not investigated further. The study emphasizes the need for a reliable screening test for primary hyperparathyroidism.

Effects of hypercalcemia and parathyroid hormone on blood pressure in normal and renal-failure rats

1986 ◽  
Vol 250 (5) ◽  
pp. F924-F929 ◽  
Author(s):  
K. Iseki ◽  
S. G. Massry ◽  
V. M. Campese
Keyword(s):  
Blood Pressure ◽  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Mean Arterial Pressure ◽  
Primary Hyperparathyroidism ◽  
Serum Calcium ◽  
Induced Hypertension ◽  
Calcium Infusion ◽  
Permissive Role

Hypertension is common in primary hyperparathyroidism, but the mechanisms are not clear. Significant hypercalcemia induces elevation in blood pressure (BP), whereas excessive parathyroid hormone (PTH) lowers BP. However, in chronic renal failure (CRF) and secondary hyperparathyroidism, the hypercalcemia-induced hypertension is more severe. We examined the interaction between PTH and calcium on BP in normal rats and in those with CRF. Calcium caused a dose-related rise in serum calcium and a rise in mean arterial pressure (MAP). For a comparable rise in serum calcium, the increment in MAP in parathyroidectomized (PTX) rats (7 +/- 3 mmHg) was significantly lower (P less than 0.05) than in sham PTX rats (19 +/- 7.3 mmHg). In PTX rats receiving PTH, the MAP response to calcium infusion (17 +/- 2.4 mmHg) was similar to that in the sham PTX rats. The infusion of similar amounts of calcium in CRF rats caused a greater rise in serum calcium. In CRF-PTX rats, the changes in MAP during calcium infusion were significantly lower (P less than 0.05) than in CRF-sham PTX animals, despite similar rise in serum calcium. For a comparable rise in serum calcium, the rise in MAP in CRF rats was greater than in normal rats. These data suggest that the presence of PTH plays an important permissive role for the hypertensive action of the hypercalcemia.

Renal adenylate cyclase assay for biologically active parathyroid hormone: clinical utility and physiological significance

1986 ◽  
Vol 108 (1) ◽  
pp. 9-15 ◽  
Author(s):  
B. Auf'mkolk ◽  
R.-D. Hesch
Keyword(s):  
Renal Failure ◽  
Alkaline Phosphatase ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Primary Hyperparathyroidism ◽  
Serum Calcium ◽  
Renal Stones ◽  
Biologically Active ◽  
Bone Lesions ◽  
Simple Relationship

ABSTRACT The stimulation of cyclic AMP production by human renal cortical membranes in the presence of the GTP analogue 5′-guanylimidodiphosphate and a calcium chelator represents a homologous assay system for the evaluation of biologically active parathyroid hormone (bioPTH) in human serum. Bioactive PTH was raised above normal (normal range: undetectable to 4·6 pmol human PTH(1–34) per 1) in 13/17 (76%) patients with primary hyperparathyroidism, in 5/6 (83%) patients with surgically proven hyperparathyroidism secondary to chronic renal failure, in 4/5 (80%) patients with hyperparathyroidism secondary to hypocalcaemia, in all three patients with pseudohypoparathyroidism, in 5/17 (29%) patients with osteoporosis and in 1/9 (11%) patients with renal stones and/or hypercalciuria. Bioactive PTH correlated positively with immunoreactive PTH (iPTH) measured with a radioimmunoassay predominantly recognizing the middleand carboxyl-terminal region of the PTH molecule (r = 0·503, P<0·001). A positive correlation (r = 0·572, P<0·05) was found between values of serum calcium and bioPTH in the group with primary hyperparathyroidism. Immunoreactive PTH did not correlate significantly with calcium in this group. In the other patients except those who had chronic renal failure, a negative correlation between serum calcium and both bioPTH and iPTH was observed (P<0·01). When alkaline phosphatase was compared with bioPTH in all patients, the correlation was positive (r = 0·390, P<0·01); no significant correlation existed between iPTH and alkaline phosphatase in the patients studied. When comparing the metabolic status of the bones with bioPTH, there was a higher incidence of severe bone lesions in those patients with primary hyperparathyroidism who had extremely raised levels of bioPTH. In osteoporosis no simple relationship was apparent. J. Endocr. (1986) 108, 9–15

scholarly journals Study of prevalence of secondary hyperparathyroidism in chronic renal failure in hadoti region

2019 ◽  
Vol 7 (8) ◽  
pp. 2903
Author(s):  
Chiranjee Lal Dayma ◽  
Devendra Ajmera ◽  
Shiv Charan Jelia ◽  
Pankaj Jain
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Secondary Hyperparathyroidism ◽  
Serum Calcium ◽  
Calcium Level ◽  
Serum Calcium Level ◽  
Hormone Level ◽  
Serum Parathyroid Hormone ◽  
The Difference

Background: Secondary hyperparathyroidism is known and early complication of chronic renal failure patients. Aim of this study was to assess the prevalence of secondary hyperparathyroidism and correlation between serum parathyroid hormone level with biochemical parameters in renal failure patients in tertiary care hospital in Kota, Rajasthan.Methods: A cross sectional observational study was carried out in 50 patients who had creatinine clearance of 30ml/min/1.73m2 or less for greater than 6 weeks attended the OPD of department of General Medicine, New Medical College hospital, Kota, Rajasthan from May 2018 to November 2018. Investigations like complete blood count, renal function test, urine routine microscopy and USG abdomen with serum parathyroid hormone, serum phosphorus, serum calcium levels were done. Serum parathyroid hormone level was done by calorimetric method.Results: The prevalence of secondary hyperparathyroidism in our study was 72%.In hyperparathyroidism patient’s serum calcium level was low and the difference was highly significant (p<0.001). There is negative correlation between S.PTH and S. calcium level (r=-0.536). Mean serum calcium level in our study is 1.6mmol/l. In hyperparathyroidism patient’s serum phosphate level was high and the difference was highly significant (p<0.001). There was positive correlation between S.PTH and S.PO4 level (r=0.402). Mean serum phosphorus level in our study is 5.7 mg/dl. Prevalence of hyperparathyroidism was high among CRF patients with normal BP than hypertensive patients and with normal sugar than diabetics but the difference in proportion was not significant (p=0.87, p=0.98 respectively). 90% patients were on haemodialysis while 10% patients were on conservative management.Conclusions: Early detection of secondary hyperparathyroidism in chronic renal failure patients can reduce its complications like bone fracture and cardiovascular complications.

scholarly journals Parathyroid hormone: what are we measuring and does it matter?

2002 ◽  
Vol 39 (3) ◽  
pp. 169-172 ◽  
Author(s):  
Aubrey Blumsohn ◽  
Amna Al Hadari
Keyword(s):  
Vitamin D ◽  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Primary Hyperparathyroidism ◽  
Intact Parathyroid Hormone ◽  
Intact Pth ◽  
Improve Outcome ◽  
Shed Light ◽  
Improved Outcome

Immunometric assays claiming to determine intact parathyroid hormone (PTH) generally cross-react with N-truncated forms such as PTH(7-84). Laboratories need to examine the relevance of new assays with probable PTH(1-84) specificity. It is logical that assays should measure what they state they do. However, it seems unlikely that use of older 'intact' PTH assays will affect the clinical interpretation of results in primary hyperparathyroidism or vitamin D deficiency. It is plausible that appropriate application of new PTH assays could improve outcome in chronic renal failure. However, it has never been suggested that straightforward replacement of existing assays with new PTH(1-84) assays will lead to this improved outcome. A better understanding of PTH fragments and their interaction with PTH receptors may shed light on the relevance of different PTH assays. In the meantime, older technologies will continue to work well for the vast majority of patients.

Distribution of Circulating Immunoreactive Components of Parathyroid Hormone in Normal Subjects and in Patients with Primary and Secondary Hyperparathyroidism: The Role of the Kidney and of the Serum Calcium Concentration

1979 ◽  
Vol 57 (5) ◽  
pp. 435-443 ◽  
Author(s):  
M. A. Dambacher ◽  
J. A. Fischer ◽  
W. H. Hunziker ◽  
W. Born ◽  
J. Moran ◽  
...  
Keyword(s):  
Vitamin D ◽  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Primary Hyperparathyroidism ◽  
Vitamin D Deficiency ◽  
Normal Subjects ◽  
Dependent Manner ◽  
Intact Pth ◽  
Calcium Dependent

1. The distribution of intact parathyroid hormone-(1–84) [PTH-(1–84)] and of its COOH-terminal fragments was determined in human serum by column chromatography. In addition to PTH-(1–84) (peak I), COOH-terminal fragments having molecular weights of approximately 4000–7000 (peak II) and immunoreactive components co-eluting with human PTH-(1–12) (peak III) were observed. 2. Mean concentrations of intact PTH-(1–84) and of its COOH-terminal fragments were significantly raised in chronic renal failure as compared with those of normal subjects. Mean amounts of peak II were higher in patients with chronic renal insufficiency than in nutritional vitamin D deficiency, in pseudohypoparathyroidism and in primary hyperparathyroidism, despite comparable amounts of PTH-(1–84). 3. In chronic renal failure as well as in a group of patients with vitamin D deficiency, pseudohypoparathyroidism and primary hyperparathyroidism and in controls, significant linear relations were found between the serum concentrations of calcium and log (peak II/peak I). Our findings suggest that the conversion of intact PTH-(1–84) into COOH-terminal fragments by the parathyroid glands (resulting in a raised secretion of fragments) and/or in peripheral organs may be directly related to the serum concentration of calcium. However, the degradation of the fragments may also be suppressed in a calcium-dependent manner.

scholarly journals P114 Effect of vitamin D on parathyroid hormone, serum calcium and bone mineral density in patients with primary hyperparathyroidism being managed conservatively

Rheumatology ◽  
2021 ◽  
Vol 60 (Supplement_1) ◽  
Author(s):  
Mahrukh Khalid ◽  
Vismay Deshani ◽  
Khalid Jadoon
Keyword(s):  
Bone Mineral Density ◽  
Vitamin D ◽  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Bone Mineral ◽  
Serum Calcium ◽  
Mineral Density ◽  
Neck Of Femur ◽  
Vitamin D Levels ◽  
Significant Difference

Abstract Background/Aims  Vitamin D deficiency is associated with more severe presentation of primary hyperparathyroidism (PTHP) with high parathyroid hormone (PTH) levels and reduced bone mineral density (BMD). We analyzed data to determine if vitamin D levels had any impact on PTH, serum calcium and BMD at diagnosis and 3 years, in patients being managed conservatively. Methods  Retrospective analysis of patients presenting with PHPT. Based on vitamin D level at diagnosis, patients were divided into two groups; vitamin D sufficient (≥ 50 nmol/L) and vitamin D insufficient (≤ 50 nmol/L). The two groups were compared for age, serum calcium and PTH levels at diagnosis and after mean follow up of 3 years. BMD at forearm and neck of femur (NOF) was only analyzed in the two groups at diagnosis, due to lack of 3 year’s data. Results  There were a total of 93 patients, 17 males, mean age 70; range 38-90. Mean vitamin D level was 73.39 nmol/L in sufficient group (n = 42) and 34.48 nmol/L in insufficient group (n = 40), (difference between means -38.91, 95% confidence interval -45.49 to -32.33, p &lt; 0.0001). There was no significant difference in age, serum calcium and PTH at the time of diagnosis. After three years, there was no significant difference in vitamin D levels between the two groups (mean vitamin D 72.17 nmol/L in sufficient group and 61.48 nmol/L in insufficient group). Despite rise in vitamin D level in insufficient group, no significant change was observed in this group in PTH and serum calcium levels. BMD was lower at both sites in vitamin D sufficient group and difference was statistically significant at NOF. Data were analyzed using unpaired t test and presented as mean ± SEM. Conclusion  50% of patients presenting with PHPT were vitamin D insufficient at diagnosis. Vitamin D was adequately replaced so that at 3 years there was no significant difference in vitamin D status in the two groups. Serum calcium and PTH were no different in the two groups at diagnosis and at three years, despite rise in vitamin D levels in the insufficient group. Interestingly, BMD was lower at forearm and neck of femur in those with sufficient vitamin D levels and the difference was statistically significant at neck of femur. Our data show that vitamin D insufficiency does not have any significant impact on PTH and calcium levels and that vitamin D replacement is safe in PHPT and does not impact serum calcium and PTH levels in the short term. Lower BMD in those with adequate vitamin D levels is difficult to explain and needs further research. Disclosure  M. Khalid: None. V. Deshani: None. K. Jadoon: None.

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