Effect Of Parathyroidectomy Research Articles

Effect of parathyroidectomy on anemia and erythropoietin dosing in end-stage renal disease patients with hyperparathyroidism

It has been suggested that parathyroidectomy for hyperparathyroidism (HPT) in end-stage renal disease (ESRD) may result in improvement in anemia and the response to erythropoiesis-stimulating drugs. This study examines the effect parathyroidectomy had on erythropoietin (EPO) dosing requirements and anemia in ESRD. A retrospective review was conducted. Patients were included if pre-operative and 12 month postoperative hemoglobin (Hg) and hematocrit (Hct) levels were available and they did not receive a kidney transplant or have failure of parathyroidectomy during the follow-up. Erythropoietin (EPO) dose and serum levels of calcium, phosphorus, alkaline phosphatase, albumin, and parathyroid hormone (PTH) were also obtained. Other data collections were at 1 and 2 mos. postoperatively. Thirty-seven patients met inclusion criteria. Parathyroidectomy resulted in decreased PTH from 1,871 +/- 236 (mean +/- SEM) to 172 +/- 29 pg/mL (P < .001) at 1 year. EPO dosing requirement showed a profound decrease from 10,086 +/- 1,721 to 3,514 +/- 620 units/week (P < .05). Hb and Hct levels followed an upward trend at 12 mos (11.4 +/- 0.3 to 12.1 +/- 0.2 g/dL and 35.7 +/- 1.0 to 37.1 +/- 0.6%, respectively). In ESRD, parathyroidectomy for HPT improves anemia and decreases requirements for exogenous erythropoietin suggesting either increased endogenous EPO production or improved response. As a result, we propose refractory ESRD-associated anemia as a secondary indication for parathyroidectomy resection in this population.

Parathyroid and bone. Indication for parathyroidectomy in primary hyperparathyroidisms

Primary hyperparathyroidism is a disease in which somatic chromosomal defects such as activations of oncogenes or inactivations of tumor suppressor genes enhance chromosomal parathyroid cell growth. Decreased calcium-sensing receptor causes oversecretion of PTH from abnormal parathyroid cells. Oversecreted PTH enhances bone turnover and finally exhibits bone fragility. In this review, the indications of parathyroidectomy and the effects of parathyroidectomy on bone in primary hyperparathyroidism are discussed.

Parathyroidectomy reduces cardiovascular events and mortality in renal hyperparathyroidism

Secondary hyperparathyroidism (SHPT) and its associated abnormalities in mineral metabolism increase the risk of cardiovascular morbidity and death in chronic renal failure (CRF). The effect of parathyroidectomy (PTX) on the incidence of major cardiovascular events in CRF patients with SHPT is unknown. We tested the hypothesis that PTX reduces the incidence of cardiovascular complications and death in CRF patients with severe SHPT scheduled for PTX, comparing the outcome of patients treated or not treated by PTX. The study comprised 118 CRF patients with SHPT on maintenance hemodialysis, unresponsive to medical treatment and scheduled for PTX. Patients underwent comprehensive cardiovascular evaluations at baseline. They were followed up until death, occurrence of major cardiovascular events, or kidney transplantation. No deaths related to PTX occurred. After a median follow-up of 30 months, 50 patients (42%) had undergone PTX whereas 68 (58%) had not. The groups were comparable in terms of age, sex, race, serum parathyroid hormone, calcium or phosphate, calcium x phosphate product, and all major cardiovascular variables, except diastolic blood pressure. PTX was associated with a reduced incidence of major cardiovascular events (P = .02) and overall mortality (P </= .001). Cox proportional multivariate analysis showed that variables associated independently with events were No-PTX (RR = 2.36, CI 1.11-6.32, P = .02) and age (RR = 1.07, IC 1.02-1.14, P = .009). All-cause mortality was related to No-PTX (RR = 2.34, CI 1.25-5.14, P = .007) and hematocrit (RR = 1.15, CI 1.03-1.29, P = .01). PTX confers protection against future major cardiovascular events and death in select CRF patients with severe refractory SHPT.

Abstract 967: Parathyroidectomy Reduces Cardiovascular Events And All-cause Mortality In Renal Hyperparathyroidism

Background: Secondary hyperparathyroidism (SHPT) and its associated abnormalities in mineral metabolism increase the risk of cardiovascular morbidity and death in chronic kidney disease (CKD). The effect of parathyroidectomy (PTX) on the incidence of major cardiovascular events in CKD patients with SHPT is unknown. We tested the hypothesis that PTX reduces the incidence of cardiovascular complications and death in CKD patients with severe SHPT scheduled for PTX, comparing the outcome of patients treated or not treated by surgery. Methods: The study comprised 118 CKD patients with SHPT on maintenance hemodialysis, unresponsive to medical treatment, and scheduled for PTX. Patients underwent comprehensive cardiovascular evaluations at baseline. They were followed up until death, occurrence of major cardiovascular events, or kidney transplantation. Results: No deaths related to surgery occurred. After a median follow-up of 30 months, 50 patients (42.4%) had undergone PTX while 68 (57.9%) had not. The groups were comparable in terms of age, sex, race, parathyroid hormone (PTH), calcium, phosphate, calcium x phosphate product, and all major cardiovascular variables, except diastolic blood pressure. PTX was associated with a reduced incidence of major cardiovascular events (log-rank= 0.02) and overall mortality (log-rank= 0.001). Cox proportional multivariate analysis showed that variables significantly and independently associated with events were PTX (RR=2.36, CI 1.11–6.32, p=0.02) and age (RR=1.07, IC 1.02–1.14, p=0.009). All-cause mortality was related to PTX (RR=2.34, CI 1.25–5.14, p=0.007) and hematocrit (RR=1.15, CI 1.03–1.29, p=0.01). Conclusion: PTX confers protection against future major cardiovascular events and death in select CKD patients with severe refractory SHPT.

Effects of parathyroidectomy on bone remodeling markers and vitamin D status in patients with chronic kidney disease–mineral and bone disorder

Chronic renal failure (CRF) is often associated with bone disorders including chronic kidney disease-mineral and bone disorder (CKD-MBD). Parathyroid hormone (PTH) has a relationship to bone remodeling, and so this study was undertaken to evaluate changes in bone remodeling markers after parathyroidectomy (PTX). Twelve adult patients, mean age 43.4 +/- 12.7 years, of both genders, were evaluated, prior to and six months after PTX. Analysis of biochemical markers of bone metabolism, such as total and ionized calcium, phosphorus, 25(OH)D(3), total alkaline phosphatase (TAP), bone-specific alkaline phosphatase (BAP), intact PTH, osteoprotegerin (OPG), and tartrate-resistant acid phosphatase isoform 5b (TRAP), were measured. No changes were observed after PTX in the serum total and ionized calcium, TAP, BAP, and 25(OH)D(3). After surgery there was a significant decrease in serum phosphorus, iPTH, and TRAP (P < 0.001). No significant change was observed in OPG; however there was a positive correlation between OPG and 25(OH)D(3) before and after surgery (r = 0.774, P = 0.014; and r = 0.706, P = 0.01, respectively). The percentage of patients with vitamin D deficiency decreased from 16.7% to 8.3%, while those with sufficient levels increased from 41.7% to 58.3%. The small number of patients in the study notwithstanding, the present study is unique because it provides information on bone metabolism and vitamin D status six months after PTX. The removal of parathyroid glands significantly decreased bone resorption and indicated a tendency of 25(OH)D(3) concentration to increase. However, the precise role of OPG and BAP in the improvement in bone remodeling in patients with CKD-MBD requires further study.

Effect of parathyroidectomy on osteoporosis and bone metabolism

The presentation of patients with hyperparathyroidism has changed over the past decades with the routine use of multichannel serum electrolyte analyzers. Serum calcium abnormalities rather than overt symptoms prompt the evaluation for suspected hyperparathyroidism. It is rare to see a patient with cystic bone changes; instead it is more common to have subtle bone loss identified in the evaluation of bone mineral density. Parathyroidectomy is recommended in patients with osteoporosis. Since the effect of parathyroid hormone on bone is complex, the changes in bone metabolism following parathyroidectomy and the effect of parathyroidectomy on fracture risk are important factors to consider. Studies have yielded conflicting results regarding the questions of bone density and fracture risk, limited by small sample size and short follow-up periods. Recent investigations describe a subset of patients with bone disease that may benefit from early surgical intervention.

Effect of Parathyroidectomy on Quality of Life and Neuropsychological Symptoms in Primary Hyperparathyroidism

Neuropsychological symptoms are found in a certain number of patients with primary hyperparathyroidism (PHPT). Preoperative and postoperative quality of life, anxiety, and depression are measured to analyze the impact of parathyroidectomy on these symptoms. In this prospective study, 66 patients underwent parathyroidectomy for PHPT and were evaluated pre- and postoperatively with two validated psychometric instruments (HADS, PHQ-9). Health-related quality of life was measured with a 12-item short-form health survey (SF-12). Preoperatively, the median physical component score (SF-12) of 43.0 and mental component score of 43.5 were lower than those of the general population (52.8 and 54.2 points, respectively). One year postoperatively the mental component score increased to 48.6 (p = 0.011), whereas the physical functioning scale scored 45.3 and therefore did not change significantly (p = 0.585). Preoperatively, symptoms of depression were found in 23.4% of the patients, and 15.6% of the patients displayed symptoms of anxiety (HADS). The prevalence of depression was significantly higher in patients with preoperative serum calcium levels > 11.2 mg/dl (2.8 mmol/L) (p = 0.015). Twelve months postoperatively, the overall proportion of patients with anxiety and depression decreased to 7.8% and 15.7%, respectively (p = NS). The severity of depression as measured with the PHQ-9 declined postoperatively as well. In this study, preoperative neuropsychological symptoms were related to the serum calcium levels. Postoperative health-related quality of life improved significantly. Among patients with preoperative symptoms of depression and anxiety, both symptoms were alleviated significantly at the 12-month follow-up. Therefore, surgery for PHPT seems to be effective in reducing neuropsychological morbidity associated with PHPT.

The Effect of Parathyroidectomy on Bone Fracture Risk in Patients With Primary Hyperparathyroidism

The Effect of Parathyroidectomy on Bone Fracture Risk in Patients With Primary Hyperparathyroidism

Effect of parathyroidectomy on fluctuations in calcium transport between the blood and mineralized tissues of rats

Parathyroidectomy increases the degree of(45)Ca fluctuations between the blood and mineralized tissues (bones and teeth) in rats, which is associated with a decrease in 14C-glycine incorporation into bone proteins. Disturbances in Ca(2+)metabolism and transport during hyperparathyroidism are partly prevented by parathyroidectomy. It is mainly related to variations in the interaction of parathyroid hormone, calcitonin, 1.25(OH)2D3, and other bioactive substances, but not to initiation of mineralization with protein matrixes.

The Effect of Parathyroidectomy on Bone Fracture Risk in Patients With Primary Hyperparathyroidism

Parathyroidectomy may increase bone density in primary hyperparathyroidism (PHPT), but it is unclear whether fracture risk is decreased. Parathyroidectomy decreases fracture risk. Retrospective cohort study with median follow-up of 6.5 years. Twelve regional hospitals in California. One thousand five hundred sixty-nine patients with PHPT. Parathyroidectomy or observation. Main Outcome Measure Fracture-free survival. Mean initial calcium, parathyroid hormone, and creatinine levels were 11.2 mg/dL (2.8 mmol/L), 123.0 pg/mL, and 0.9 mg/dL (79.6 micromol/L), respectively. Parathyroidectomy was performed in 452 (28.8%) patients, and 1117 (71.2%) were observed. The 10-year fracture-free survival after PHPT diagnosis was 73% in patients treated with parathyroidectomy compared with 59% in those observed (hazard ratio [HR], 0.53; 95% confidence interval [CI], 0.38-0.73; P < .001). Parathyroidectomy decreased the 10-year hip fracture rate by 8% (P = .001) and the upper extremity fracture rate by 3% (P = .02). Parathyroidectomy was independently associated with a decreased fracture risk (HR, 0.68; 95% CI, 0.47-0.98), whereas female sex (HR, 1.82; 95% CI, 1.19-2.80) and increased creatinine level (HR per 1-mg/dL [88.4-micromol/L] increment, 2.05; 95% CI, 1.22-3.46) remained independently associated with an increased fracture risk. Age of 50 years or older (HR, 1.62; 95% CI, 0.99-2.66), initial parathyroid hormone level (HR, 1.00; 95% CI, 0.99-1.02), and calcium level (HR, 1.02; 95% CI, 0.75-1.37) were not independently associated with fracture risk after adjusting for all other variables. Parathyroidectomy is associated with a decreased risk of fracture in PHPT. The largest decrease was in hip fractures. Parathyroidectomy should be considered for all patients with PHPT to reduce fracture risk, regardless of age or calcium or parathyroid hormone levels.

Metabolic abnormalities in patients with normocalcemic hyperparathyroidism detected at a population-based screening

Dyslipidemia, hypertension, diabetes mellitus and also primary hyperparathyroidism (pHPT) are associated with an increased risk of cardiovascular diseases. Metabolic abnormalities in mild pHPT have been reported, but never in cases with normal calcium and high parathyroid hormone (PTH) levels, i.e. suffering from 'normocalcemic pHPT'. Our aim was to explore the occurrence of these metabolic abnormalities in individuals with normocalcemic pHPT identified in a population-based screening, and the effects of parathyroidectomy vs conservative treatment on metabolic variables. A population-based screening of 5202 post-menopausal women identified 30 patients with normal calcium, inappropriately high PTH and normal creatinine. A 5-year follow-up included 15 parathyroidectomized (PTx) and nine conservatively followed cases, in a non-randomized setting, together with age-matched controls. Biochemical variables and body mass index (BMI) were investigated. At study entry, cases had higher calcium, PTH, glucose, low-density lipoprotein (LDL)/high-density lipoprotein (HDL)-cholesterol, very low-density lipoprotein (VLDL)-cholesterol, total triglycerides, and BMI compared to controls (P = < 0.0001-0.035). The cases had a lower HDL-cholesterol value (P = 0.013) and one third of the cases had hypertriglyceridemia. During follow-up, the PTx cases decreased in calcium, PTH, LDL/HDL-cholesterol, total and LDL-cholesterol (P = 0.0076-0.022). Investigated biochemical variables remained adverse in conservatively followed cases during follow-up except a decreased LDL-cholesterol value. All surgically treated patients had parathyroid adenoma. Cases with normocalcemic pHPT have increased proatherogenic lipoprotein levels, BMI and glucose levels compared to age-matched controls. Parathyroidectomy has positive effects on some of these variables and reverses them to the same level as the controls, while conservative treatment fails to normalize the investigated metabolic variables.

Changes in Cardiovascular Calcification After Parathyroidectomy in Patients With ESRD

The effect of parathyroidectomy on vascular calcification in patients with end-stage renal disease has been a subject of interest for many years, although studies in this area have not been definitive. The purpose of this investigation is to determine changes in vascular calcification after subtotal parathyroidectomy by using fast-gated helical computed axial tomographic imaging to measure coronary and carotid artery calcification. Computed tomographic imaging was performed at baseline and in follow-up on 10 patients who had undergone subtotal parathyroidectomy and 10 reference patients who had not undergone parathyroidectomy. Patients who underwent subtotal parathyroidectomy had a mean change in coronary calcification of -92.3 +/- 469/y, and reference patients had a mean change of +479 +/- 630/y (P = 0.03). The 2 parathyroidectomy patients with the highest baseline scores had significant declines in both coronary and carotid calcification. In this study, subtotal parathyroidectomy is associated with a significant decrease in vascular calcification in 2 of 10 dialysis patients with high coronary artery calcium scores and stabilization in 7 of 10 patients with low baseline scores.

Effect of Parathyroidectomy on Renal Graft Function

Some authors have reported acute impairment of renal transplant function after parathyroidectomy (PTx). Since 1996 PTx has been performed in 22 renal transplant recipients (follow-up, 24.2 ± 15 months; serum creatinine concentration (SCr) pre-PTx, 1.26 ± 0.4 mg/dL). We analyzed the serum levels of immunoreactive parathyroid hormone, calcitriol, calcium, phosphate, alkaline phosphatase, SCr, and hemoglobin, as well as proteinuria, blood pressure, and immunosuppressive treatment at several times: before PTx and at 7 days, 1 month, and then every 3 months post-PTx. After PTx we observed acute renal function deterioration until the third post-PTx month, when SCr levels returned to baseline values. We found no changes in blood pressure, although there was a trend toward a reduced dosage of antihypertensive drugs. We compared the patients who showed more significant increases (>30% from baseline) in SCr (group A, n = 7) with those who did not (group B, n = 15). Group A had higher SCr levels pre-PTx. We observed no other significant differences, either pre-PTx or post-PTx. In 2 patients in group A, SCr returned to baseline at the third month after PTx, but in the other 5 the renal function impairment persisted. Taking into account this risk and that severe hyperparathyroidism does not revert after transplantation, it would seem more appropriate in such cases to perform PTx while the patient is on the waiting list. The causes of this renal functional impairment are not clear, but the patients who showed worse deterioration also had a worse renal function pre-PTx.

A controlled, prospective study of neuropsychological outcomes post parathyroidectomy in primary hyperparathyroid patients

There is an increasing number of primary hyperparathyroidism (PHPT) patients with neuropsychological or psychiatric symptoms. Many of these patients do not have osseous or renal complications to satisfy the criteria for parathyroidectomy according to the NIH guidelines. To assess whether there is any improvement in neuropsychological and mood symptoms following parathyroidectomy. Twenty PHPT patients undergoing parathyroidectomy and 20 orthopaedic controls matched for age, gender and estimated intelligence were subjects to pre and postoperative assessment of cognition and mood with a mean surgery-retest interval of 3 months. Using two tests of attentional flexibility [the Stroop test, the Digit symbol test of the Wechsler Adult Intelligence Scale-Revised (WAIS-R)], and two memory tests for prose and nonverbal material, no significant change was found between the groups when comparing scores before and after surgery. There was no improvement between pre and postoperative measures of verbal (dominant hemisphere) as opposed to visuo-spatial (nondominant hemisphere) function when compared to controls. There was no relationship between the reduction in serum calcium and the change in the neuropsychological measures postoperatively. This controlled, prospective study demonstrates no significant improvement in neuropsychological indices using objective, validated psychometric tools in an unselected cohort of PHPT patients. No relationship was found between serum calcium level and the degree of neuropsychological deficit. More studies are needed to assess whether the effect of parathyroidectomy is beneficial and sustainable in PHPT patients with neuropsychological symptoms alone.

Effects of parathyroidectomy on lead mobilization from bone in patients with primary hyperparathyroidism

Since lead (Pb) accrued from environmental exposure accumulates in bone with a half life time between 6 and 10 years, a release of bone Pb into the circulation and/or urine (PbU) should be expected in diseases with increased bone metabolism such as hyperparathyroidism. We studied 60 patients with primary hyperparathyroidism (pHPT, 50 women, 10 men, aged 61.4 ± 10.6 and 64.1 ± 9.9 years, respectively) (a) before, (b) 1–6 months, and (c) 6–12 months after parathyroidectomy. Besides lead in blood (PbB) and lead in 24-h urine samples (PbU), parathyroid hormone (PTH), serum Ca 2+, osteocalcin (OC), phosphate (PO 4), and serum pyridinoline cross-linked telopeptide (cTP) were determined. Control data were determined in 20 healthy age-matched subjects. As expected, Ca 2+ decreased after parathyroidectomy. Mean PbB in patients with pHPT was in the same range as in controls. A decrease of PbB after parathyroidectomy was found in the interval beyond 6 months. In contrast, mean PbU initially increased after surgery (3.05 ± 1.94 vs. 4.25 ± 2.65 μg/l, P = 0.004) and was not different beyond 6 months in comparison with preoperative values at (c). Investigating only patients with PTH < 150 ng/l, no significant PbB or PbU alterations were detected before and after parathyroidectomy. In patients with PTH > 150 ng/l, the decrease of PbB at (c) was more pronounced as was the increase of PbU at (b). In these patients, PbB and OC as well as PbB and cTP were correlated preoperatively. In conclusion, our data show that in environmentally lead-exposed (by food or by pollution) hyperparathyroid individuals, there is no hazardous PbB release from bone. The preoperative correlation between PbB and OC in pHPT patients with PTH > 150 ng/l provides evidence that in fact there is a Pb release from bone into the blood-pool by bone remodeling. The increase of PbU after parathyroidectomy is suspected to be caused by PTH-dependent Pb accumulation in the kidney, which seems to be restored with decreasing PTH. Moreover, our data confirm prior findings that bone remodeling seems to be normalized 6 months after parathyroidectomy.

Skeletal changes in osteoprotegerin and receptor activator of nuclear factor-κb ligand mRNA levels in primary hyperparathyroidism: effect of parathyroidectomy and association with bone metabolism

The effect of parathyroid hormone (PTH) on the production of osteoprotegerin (OPG) and ligand of receptor activator of NF-κB (RANKL) in human bone is incompletely understood. Most in vitro studies indicate that PTH decreases OPG and increases RANKL production. In primary hyperparathyroidism (PHPT), hypersecretion of PTH leads to enhanced bone resorption and formation with increased risk of fracture. Decreasing PTH levels by surgery normalizes bone metabolism, but the effects on skeletal OPG and RANKL production are unknown. In this study, 24 patients referred to our clinic for evaluation, and treatment of PHPT were included. A transiliac bone biopsy was done before ( n = 24) and 12 months after parathyroidectomy (PTX) ( n = 21). Biopsies were frozen in liquid nitrogen and RNA extracted using Trizol. A competitive RT-PCR assay for RANKL and OPG mRNA using artificial cDNA standards was developed and used for quantification. Results were normalized for GAPDH mRNA content. Before surgery, the RANKL/GAPDH gene expression ratio showed positive correlations with serum osteocalcin ( r = 0.42, P < 0.05) and urinary NTX ( r = 0.43, P < 0.05). The OPG/GAPDH mRNA levels in iliac bone before surgery correlated with serum osteocalcin ( r = 0.52, P < 0.01), but not with bone resorption markers. The mRNA ratio of RANKL/OPG decreased significantly ( P < 0.05) after surgery. In conclusion, RANKL and OPG gene expression within the human bone microenvironment are influenced by PTH, as the ratio RANKL/OPG decreased upon PTX. In addition, locally produced RANKL appears to affect bone turnover in the hyperparathyroid state.

Effects of Parathyroidectomy on Renal Allograft Survival

Background: Hyperparathyroidism is a common problem secondary to renal insufficiency and is often not entirely resolved after renal transplantation (TX). Methods: In this retrospective analysis, the effects of parathyroidectomy (PTX) on allograft function were evaluated and the risk factors involved in allograft deterioration in patients after PTX will be discussed. Results: The rise in creatinine was steeper 1 year after PTX compared to 2 years before PTX in the majority (13 of 22) of patients. Compared to a cohort without PTX, graft survival was significantly decreased by 60% in 6 years (p < 0.0001). After multivariate adjustment, risk factors attributed to graft function included baseline creatinine (p = 0.02), baseline systolic blood pressure (p = 0.04) and time between TX and PTX, but not PTX itself. The peri-PTX drop in serum calcium was significantly more accentuated in patients exhibiting a worsening of graft function after PTX (p = 0.04). Conclusions: In patients requiring PTX, graft function is in danger of worsening. Since many factors contribute to this negative correlation and no association with parathyroid hormone (PTH) levels before PTX has been observed, we do not recommend prophylactic PTX on the basis of PTH levels only. However, appropriate management of peri-PTX risk factors is highly important. If the clinical situation, e.g. progressive renal osteodystrophy, requires removal of parathyroid glands, the procedure should be performed, if possible, in the presence of stable graft function.

Osteoprotegerin levels in primary hyperparathyroidism: effect of parathyroidectomy and association with bone metabolism.

The effect of parathyroid hormone (PTH) on the production of osteoprotegerin (OPG) remains controversial. Most in vitro studies indicate that PTH decreases OPG secretion by the osteoblast, but in vivo observations are conflicting. In primary hyperparathyroidism (PHPT), hypersecretion of PTH leads to enhanced bone resorption and formation with increased risk of fracture. Patients with PHPT are cured by surgery, resulting in normalization of PTH levels and bone metabolism, but the concomitant effects on OPG production are not known. The hypothesis of the present study was that the circulating level of OPG is diminished in patients with PHPT and increases with successful parathyroidectomy. We also speculated that serum OPG may determine the magnitude of bone loss up to the time of surgery. In the present study, 20 patients (17 women and 3 men, mean age 62 y) with PHPT who were candidates for surgical cure were examined before and 12 months after surgery. Bone turnover markers decreased and BMD increased significantly after surgery. Serum OPG did not correlate with PTH before surgery (r = 0.07, P = 0.77) and was not affected by parathyroidectomy (P = 0.79). After normalization of PTH, bone formation markers showed significant (P1NP) and near-significant (osteocalcin) correlations with serum OPG. In conclusion, serum OPG is not decreased in patients with PHPT, nor is serum OPG to any demonstrable extent regulated by PTH pre- or postoperatively.

Clinical effect of parathyroidectomy for advanced renal hyperparathyroidism

Advanced renal hyperparathyroidism induced not only osteitis fibrosa but also vessel and valvular calcification which affect high mortality due to cardiovascular disease. Parathyroidectomy usually promises dramatic clinical improvement of hyperparathyroidism. However, ectopic calcification except for tumor calcinosis is irreversible by parathyroidectomy. Then the surgery should be indicated at right time. Total parathyroidectomy with forearm autograft is suitable operative method for renal hyperparathyroidism, because removal of autograft can be less invasively performed at recurrence which is not negligible after the internal operation.

Evolving concepts of pathogenesis of cardiovascular disease in chronic uremia: Role of hyperparathyroidism, calcium-phosphate metabolism, and their therapy

W hemodialysis was introduced for the treatment of end-stage renal disease (ESRD), nephrologists were faced with the development of several new complications. Bone alterations and secondary hyperparathyroidism were between those complications and gave rise to major interest in experimental and clinical research. Although disturbances of calcium and phosphate metabolism were considered principally as factors controlling secretion of parathyroid hormone, PTH was considered as a major uremic toxin associated with bone disease and many nonskeletal disorders including cardiovascular complications. In in vitro studies, PTH was shown to have chronotropic and inotropic effects on isolated cardiomyocytes. These changes were associated with increased intracellular calcium content; disturbed lipoprotein metabolism; and altered mitochondrial energy production, storage, and utilization. These experimental studies were certainly interesting, but the clinical relevance was uncertain. Indeed, in ESRD patients, the secondary hyperparathyroidism was not associated with uniform cardiovascular abnormalities, the cardiovascular effects of parathyroidectomy or nonsurgical control of PTH levels were minimal or absent, and skeletal complications were rarely the cause of death. The role of PTH and associated calciumphosphate disorders on pathogenesis of cardiovascular disorders were recently reanalyzed. Several reports in the literature have suggested that hyperphosphatemia, in association with hyperparathyroidism or hypoparathyroidism and vitamin D3 or calcium overload, was an independent predictor of death and the possible culprit associated with cardiovascular complications in dialysis patients. Cardiovascular disease is the major cause of mortality and morbidity in patients suffering from ESRD. Atherosclerosis and aortic stiffening are the major vascular compliactions observed. Atheromatous plaques of ESRD patients are more frequently and more intensively calcified than those of nonuremic subjects, and several recent studies have shown the presence of extensive and almost generalized vascular calcifications in patients undergoing hemodialysis. Moreover, the extent of calcifications as such is an independent factor to cardiovascular mortality. These calcifications concern not only plaques (intimal calcifications) but also diffuse medial calcifications. Although the arterial calcifications are associated with nonspecific classical factors such as age, diabetes, or smoking habits, there is a growing body of evidence that alterations of phosphate and calcium metabolism play a predominant role. For many years, calcifications were considered to be caused by passive mineral precipitation associated with elevated calcium x phosphate product. Recent studies have shown that this process may be active involving mechanisms normally found in bone. Phosphate seems to be of primary importance in the initiation of cardiovascular calcification through the change of the vascular smooth muscle phenotype and induction of the expression by vascular smooth muscle cells of osteocalcin abd Cbfa-1, which are markers of osteoblastic differention. The pathogenic role of PTH as such is less clear than previously suspected, and extensive calcifications are frequently observed in patients with low bone activity and adynamic bone disease. Of note, in the general population, the cardiovascular calcifications are inversely correlated with bone density in osteoporotic