Decline In Parathyroid Hormone Levels Research Articles

Improved Clinical Outcomes Associated With Hungry Bone Syndrome Following Parathyroidectomy in Dialysis Patients

ObjectiveHungry bone syndrome (HBS) is a common complication after parathyroidectomy in dialysis patients with severe secondary hyperparathyroidism. The rapid decline in parathyroid hormone (PTH) levels diminishes bone resorption and accelerates bone formation. This causes a significant influx of calcium and phosphate into the bone, resulting in severe and prolonged hypocalcemia. While previous studies have established risk factors for HBS, the outcomes beyond the reduced recurrence rate of hyperparathyroidism have been largely unexplored. MethodsThis single-center retrospective study analyzed 322 cases in 314 dialysis patients who underwent parathyroidectomy between 2012 and 2022. The study examined baseline factors associated with HBS, adverse events, and clinical outcomes, including changes in blood pressure and hematologic and nutritional parameters over 3-12 months of follow-up, stratified by HBS status. ResultsTotal parathyroidectomy was performed in 28 cases (8.7%), total parathyroidectomy with implantation in 98 cases (30.4%), and subtotal parathyroidectomy in 196 cases (60.9%). HBS occurred in 207 cases (64%). Independent predictors of HBS included male sex, lower serum calcium levels, higher PTH levels, and lack of active vitamin D treatment at baseline. Patients with HBS had longer hospital stays but did not experience an increase in other adverse events. Following parathyroidectomy, the HBS group showed a greater reduction in blood pressure and more significant increases in hemoglobin, total lymphocyte count, and serum creatinine. This group also saw a more substantial decrease in the proportions of patients with hemoglobin <11 g/dL and serum creatinine/body surface area <380 μmol/L/m2. Although the HBS group showed a more significant decline in PTH levels from baseline, similar proportions achieved the target PTH level by the end of the study. Serum calcium levels remained substantially lower in the HBS group throughout the follow-up, while serum phosphate and PTH levels were comparable. ConclusionHBS was associated with more pronounced improvements in blood pressure, anemia, and nutritional parameters. The presence of HBS could indicate greater achievement in controlling hyperparathyroidism following parathyroidectomy.

PTH levels, sleep quality, and cognitive function in primary hyperparathyroidism.

Cognitive function in patients with primary hyperparathyroidism (PHPT) may be affected and be identified to have been linked to the level of parathyroid hormone (PTH). Previous studies have suggested that patients with PHPT present poor sleep quality, which might interact with cognitive decline. The purpose of this study was to determine whether sleep quality mediates the association between PTH level and cognitive function and investigate whether surgery improves sleep quality and cognition in PHPT patients. Between June 2019 and August 2022, we recruited 146 patients diagnosed with PHPT (n = 146). We collected clinical data from medical records and evaluated sleep quality and cognition preoperatively and 2 months postoperatively by using the Pittsburgh Sleep Quality Index and Min-Mental State Examination. We examined the mediation effects of sleep disturbance and latency on correlations between PTH level and cognitive impairment by using the Bootstrap method. The sleep quality and cognitive function were correlated with PTH level before surgery. Sleep latency or sleep disturbance exhibited a partial mediating effect on the association between PTH level and MMSE scores in PHPT patients (p < 0.05). In PHPT patients, there was a significant decline in PTH levels and an improvement in cognitive function post-surgery compared to pre-surgery, but no significant differences in sleep quality. Sleep disturbance and sleep latency may mediate the association between PTH level and cognitive impairment in PHPT before surgery. The surgery could reduce PTH levels and improve cognition, but might not improve sleep quality in PHPT patients.

Racial differences in the relationship between high-normal 25-hydroxy vitamin d and parathyroid hormone levels in early stage chronic kidney disease.

ABSTRACTAim:Current guidelines do not address between-person variability in markers of bone and mineral metabolism across subgroups of patients, nor delineate treatment strategies based upon such factors.Methods:A cross sectional study was carried out to analyze data from 20,494 United States Veterans and verify the variability of Vitamin D (25(OH)D) and parathyroid hormone (PTH) levels across race and stage of chronic kidney disease.Results:PTH levels were higher in Black Americans (BA) than White Americans (WA) at all levels of 25(OH)D and across eGFR strata. There was a progressive decline in PTH levels from the lowest (25(OH)D < 20) to highest quartile (25(OH)D >=40) in both BA (134.4 v 90 pg/mL, respectively) and WA (112.5 v 71.62 pg/mL) (p<0.001 for all comparisons).Conclusion:In this analysis, higher than normal 25(OH)D levels were well tolerated and associated with lower parathyroid hormone values in both blacks and whites. Black Americans had higher PTH values at every level of eGFR and 25(OH)D levels suggesting a single PTH target is not appropriate.

Vitamin D Status and its correlation with Parathyroid Hormone level among population in Riyadh, Saudi Arabia

This study aimed to assess the relationship between vitamin D [25(OH)D] status and parathyroid hormone (PTH) in Saudi adults to determine the optimum 25(OH)D cut-off in the Saudi adult population. A total of 1093 apparently healthy Saudi subjects (720 women and 373 men) aged 50.7 ± 13.9 years were included in this cross-sectional study. Serum 25(OH)D, PTH, calcium and albumin levels were determined. The over-all prevalence of 25(OH)D deficiency (<50 nmol/) was 42.5% (N = 464). The overall prevalence of severe 25(OH)D deficiency (<25 nmol/L) was 24% (N = 262). In all subjects, there is a significant inverse relationship between serum PTH and 25(OH)D (r = − 0.40; p < 0.0001), but no distinct plateau for serum PTH with rising of serum 25(OH)D levels were observed. Despite the lack of threshold, the rising trend in serum 25(OH)D levels had an equivalent gradual decline in PTH levels in both males and females (p < 0.001). In conclusion, the lack of optimum 25(OH)D cut-off in the present study may suggest a lower threshold for the Saudi population and the current definitions for vitamin D status overestimate the true prevalence of vitamin D deficiency in Saudi Arabia.

Switching tenofovir disoproxil fumarate to tenofovir alafenamide results in a significant decline in parathyroid hormone levels: uncovering the mechanism of tenofovir disoproxil fumarate-related bone loss?

: An increasing number of patients have been switched from tenofovir disoproxil fumarate (TDF) to tenofovir alafenamide because of its improved bone safety profile, although the pathophysiological mechanism is not fully understood. We show that serum parathyroid hormone levels drop significantly after the switch from TDF to tenofovir alafenamide. This observation supports the theories that TDF-related bone loss is parathyroid hormone-driven and that this effect is dose-dependent.

The Necessity and Reliability of Intraoperative Parathyroid Hormone (PTH) Testing in Patients with Mild Hyperparathyroidism and PTH Levels in the Normal Range

Intraoperative parathyroid hormone (IoPTH) testing is useful in the management of hyperparathyroidism. The successful removal of hypersecreting parathyroids is indicated by a decrease in PTH levels >50% within 15 min. A subset of patients with mild hyperparathyroidism will actually have starting PTH levels in the normal range. We sought to determine if IoPTH testing is necessary in these patients and if the 50% rule delineating surgical cure is reliable. A retrospective review was performed on all patients who underwent parathyroidectomy for hyperparathyroidism at a single institution from 3/2001 to 8/2008. Of the 1,001 patients, 142 (14%) had mild hyperparathyroidism and normal baseline PTH levels (<65 pg/ml). Their mean PTH was 59 ± 1 pg/ml. During surgery, 105 (74%) had a >50% decline in PTH levels after resection of hyperfunctioning parathyroid glands, and their operations were terminated. In contrast, 37 (26%) patients did not have a >50% decline in PTH levels leading to further surgical exploration. In these 37 patients, the PTH levels fell by >50% after the removal of the additional glands in 25 patients (17.6%) and dropped after 20 min in 7 patients (4.9%). In 5 patients (3.5%) the IoPTH did not drop. Of the 142 total patients, 91 had single adenomas and 51 patients had multi-gland disease. All patients (100%) were cured (normal serum calcium after 6 months). Intraoperative PTH testing plays an important role in the operative management in 14% of patients with mild hyperparathyroidism. Importantly, a 50% decline in IoPTH level within 15 min of parathyroidectomy is 96.5% reliable in predicting cure in these patients with PTH starting in the normal range.

Vitamin D supplementation in chronic kidney disease: a systematic review and meta-analysis of observational studies and randomized controlled trials.

Vitamin D deficiency is highly prevalent among patients with chronic kidney disease (CKD). The benefits and harms of vitamin D supplementation (ergocalciferol or cholecalciferol) were assessed in patients with nondialysis-dependent CKD, dialysis-dependent CKD, and renal transplant recipients. MEDLINE (1966 to September 2009), SCOPUS (September 2009), and nephrology conference proceedings were searched for relevant observational and randomized controlled trials (RCTs). Treatment effects were summarized as mean differences (MDs) with 95% confidence intervals (CIs) using a random effects model. Separate analyses were conducted for observational studies and RCTs. Twenty-two studies (17 observational and 5 RCTs) were included. There was a significant improvement in 25-hydroxyvitamin D (MD 24.1 ng/ml, 95% CI 19.6 to 28.6) and an associated decline in parathyroid hormone (PTH) levels (MD -41.7 pg/ml, 95% CI -55.8 to -27.7) among observational studies. PTH reduction was higher in dialysis patients. Among RCTs, there was a significant improvement in 25-hydroxyvitamin D (MD 14 ng/ml, 95% CI 5.6 to 22.4) and an associated decline in PTH levels (MD -31.5 pg/ml, 95% CI -57 to -6.1). A low incidence of hypercalcemia and hyperphosphatemia was reported with vitamin D supplementation. Cardiovascular and skeletal effects of vitamin D supplementation have not been studied. Included studies were mostly of low to moderate quality. Available evidence from low-to-moderate quality observational studies and fewer RCTs suggests that vitamin D supplementation improves biochemical endpoints. However, whether such improvements translate into clinically significant outcomes is yet to be determined.

Secondary hyperparathyroidism in children with chronic renal failure: pathogenesis and treatment.

Despite advances in the management of patients with chronic renal failure, histologic features associated with secondary hyperparathyroidism remain the predominant skeletal findings; however, over the last decade the prevalence of adynamic bone has increased in both adult and pediatric patients with chronic renal failure. The management of children with secondary hyperparathyroidism and mild to moderate chronic renal failure should be started early, and should include correction of hypocalcemia and metabolic acidosis, maintenance of age-appropriate serum phosphorus levels, and institution of vitamin D therapy when serum intact parathyroid hormone (PTH) measurements are elevated to maintain the blood levels within normal limits; however, in children undergoing chronic dialysis therapy, the current recommendation is to maintain the serum intact PTH levels at least 2-4 times the upper limits of normal to prevent the development of low bone turnover disease. Serum calcium, phosphorus, alkaline phosphatase, and PTH levels should be monitored frequently, especially in infants and very young children. Discontinuation or reduction of vitamin D should be considered when there is a rapid decline in PTH levels, persistent elevation in serum calcium and serum phosphorus levels, and a significant diminution in alkaline phosphatase levels. In addition, a reduction in the calcium concentration of the dialysis fluid, and judicious use of calcium-containing salts as phosphate binding agents should also be performed in these patients. Although not yet extensively used in pediatric patients with secondary hyperparathyroidism, several therapeutic alternatives, such as the less calcemic vitamin D analogs, including paricalcitol [19-nor-1,25-(OH)(2)D(2)] and doxercalciferol [1-alpha-(OH)(2)D(2)], calcimimetics, and the availability of a calcium-free, aluminum-free phosphate binder such as sevelamer hydrochloride and lanthanum carbonate, may play significant roles in the future management of children with secondary hyperparathyroidism to promote linear growth, prevent parathyroid gland hyperplasia, avoid calciphylaxis and, in the long run, avert vascular calcifications.

Parathyroid hormone suppression by intravenous 1,25-dihydroxyvitamin D. A role for increased sensitivity to calcium.

Numerous in vitro studies in experimental animals have demonstrated a direct suppressive effect of 1,25-dihydroxyvitamin D (1,25(OH)2D) on parathyroid hormone (PTH) synthesis. We therefore sought to determine whether such an effect could be demonstrated in uremic patients undergoing maneuvers designed to avoid changes in serum calcium concentrations. In addition, the response of the parathyroid gland in patients undergoing hypercalcemic suppression (protocol I) and hypocalcemic stimulation (protocol II) before and after 2 wk of intravenous 1,25(OH)2D was evaluated. In those enlisted in protocol I, PTH values fell from 375 +/- 66 to 294 +/- 50 pg (P less than 0.01) after 1,25(OH)2D administration. During hypercalcemic suppression, the "set point" (PTH max + PTH min/2) for PTH suppression by calcium fell from 5.24 +/- 0.14 to 5.06 +/- 0.15 mg/dl (P less than 0.05) with 1,25(OH)2D. A similar decline in PTH levels after giving intravenous 1,25(OH)2D was noted in protocol II patients. During hypocalcemic stimulation, the parathyroid response was attenuated by 1,25(OH)2D. We conclude that intravenous 1,25(OH)2D directly suppresses PTH secretion in uremic patients. This suppression, in part, appears to be due to increased sensitivity of the gland to ambient calcium levels.

The effects of intraperitoneal calcitriol on calcium and parathyroid hormone

Parathyroid suppression by intraperitoneal calcitriol (1,25(OH)2D3) during peritoneal dialysis. The purpose of this study was to determine if parathyroid hormone (PTH) suppression could be achieved by increasing calcium mass transfer (Ca MT) with high dialysate Ca (4 mEq/liter) or via intraperitoneal (i.p.) 1,25(OH)2D3 in patients undergoing continuous ambulatory peritoneal dialysis. Eleven patients were dialyzed for two months with standard Ca dialysate (3.5 mEq/liter) followed by two months with 4.0 mEq/liter Ca, then by three months of i.p. 1,25(OH)2D3. During the latter period, patients were randomized to groups whose dialysate contained either 3.5 mEq/liter or 4.0 mEq/liter Ca. We found that 4.0 mEq/liter Ca dialysate more than doubled Ca MT (37 +/- 17 mg/day to 84 +/- 6 mg/day) leading to a modest fall (P less than 0.05) in PTH levels (84 +/- 5.5% of controls). Ionized calcium levels did not change. With i.p. 1,25(OH)2D3, however, ionized calcium rose significantly (P less than 0.001) leading to a decline in PTH levels to 53.9 +/- 7.9% of control values. Serum 1,25(OH)2D3 levels rose from undetectable to 47.7 +/- 7.2 pg/dl (normal range 20 to 35). These studies indicate that increasing Ca MT using a 4.0 mEq/liter Ca dialysate leads to a small reduction in PTH concentrations. On the other hand, i.p. 1,25(OH)2D3 is well absorbed into the systemic circulation, raises ionized calcium levels, and leads to a marked suppression of PTH. Thus, i.p. 1,25(OH)2D3 may be a simple and effective means to suppress secondary hyperparathyroidism in patients undergoing CAPD.