Outcomes of Limited Parathyroidectomy in Secondary Hyperparathyroidism
0
Citation
17
Reference
10
Related Paper
Abstract:
To determine the outcomes of unintended limited parathyroidectomy (LPTX; three or less than three glands removed) in patients with secondary hyperparathyroidism (SHPT).Retrospective cohort study.Jiangmen Central Hospital, China, from January 2012 and December 2019.The operative and biochemical outcomes of LPTX with total parathyroidectomy plus auto-transplantation (PTX+AT) among patients with SHPT were compared. Primary outcomes were persistence and time to recurrence. Secondary outcomes were all-cause death and levels of serum parathyroid hormone (PTH), calcium, alkaline phosphatase (ALP), and phosphate measured pre-surgery, on postoperative day 1 (POD1), and one-year post-PTX in patients cured after the initial surgery.Forty-three patients received LPTX, and 78 underwent PTX-AT. Persistent SHPT was more frequent in the LPTX group (p = 0.001). The area under the receiver operating characteristic curve was 0.89 for POD1 PTH (p <0.001). The frequencies of SHPT recurrence and all-cause mortality were not significantly different. One-year postsurgery, PTH, calcium, ALP, and phosphate levels were significantly decreased in both groups, compared with the respective preoperative values (p <0.001, each).LPTX resulted in a higher proportion of persistent SHPT. However, more than half of the patients could be cured and achieved satisfactory outcomes. Cured patients who underwent LPTX can be identified according to PTH levels on POD1.Limited parathyroidectomy, Secondary hyperparathyroidism, Recurrence, Persistence, All-cause death.In order to evaluate the effect of dietary phosphorus (P) restriction on the pathogenesis of secondary hyperparathyroidism (2°HPT) in chronic renal failure (CRF), we studied parathyroid function and parathyroid cell proliferation in 5/6 nephrectomized rats (CRF rats) fed with three different dietary P contents (0.6, 0.3 and 0.1%). Four weeks after 5/6 nephrectomy, serum immuno-reactive parathyroid hormone (PTH) concentration, PTH mRNA level in parathyroid glands and the size of parathyroid glands were increased in CRF rats compared to those of sham-operated rats when both groups of rats were fed with normal P (0.6%) diet. These changes were not accompanied by any detectable changes of serum concentrations of calcium (Ca), inorganic phosphate (Pi) or calcitriol. In contrast, such evidence of 2°HPT was obliterated in CRF rats fed with 0.3 or 0.1% P diet. In rats fed with 0.3% P diet, serum concentrations of Ca, Pi, and calcitriol were not different from those of sham-operated rats or from CRF rats fed with normal P diet. In contrast, serum Ca and calcitriol concentrations increased and serum Pi decreased in CRF rats fed with 0.1% P diet. These data suggest that 2°HPT can be completely prevented at the levels of PTH secretion, synthesis and parathyroid cell proliferation by mild dietary P restriction (0.3%) alone, and that such effects may not depend upon the changes in serum concentrations of Ca, Pi or calcitriol, but may depend on reduced dietary P content per se. Thus, mild dietary P restriction from the early stage of CRF may be clinically effective for the prevention of 2°HPT.
Parathyroid chief cell
Cite
Citations (85)
The serum levels of 1,25-dihydroxycholecalciferol [1,25(OH)2D3] were increased in five patients with primary hyperparathyroidism [60 ± 13(SD) pg/ml; normal value, 33 ±15 (SD) pg/ml] but fell rapidly after parathyroidectomy to values of 23 ±9 (SD) pg/ml. This was accompanied by parallel decreases in the serum concentrations of calcium and immunoreactive parathyroid hormone. Over the following 5–35 days, the serum (l,25(OH)2D3 concentrations increased markedly to levels of 59±17 (SD) pg/ml, which could most likely be explained by a stimulatory effect of the hypocalcemia per se on the renal production of (1,25(OH)2(D)3.(J Clin Endocrinol Metab50: 480, 1980)
Cite
Citations (49)
The present studies were designed to explore the mechanism underlying skeletal refractoriness to PTH in a vitamin D-deficient animal by assessment of PTH-stimulated cAMP release from isolated perfused bone. In vitamin D-deficient (−D) rats both basal and PTH-stimulated cAMP release were markedly diminished, compared with that in vitamin Dreplete (+D) rats. Isolated perfused bones from −D rats that had undergone parathyroidectomy 2 days before death still showed reduced cAMP release in response to PTH, compared with +D bones. To investigate which factors in terms of Ca, endogenous PTH, or vitamin D might primarily be responsible for the impaired PTH-stimulated cAMP release from −D bones, some −D rats were switched to a diet identical to the vitamin D-deficient diet but with high Ca content (4%) for 2 or 5 weeks before death. This schedule maintained normocalcemia despite vitamin D deficiency. PTH-stimulated cAMP release in these rats was increased to a level intermediate between that in −D rats and +D rats, indicating partial restoration of the impaired response to PTH in −D rats. These data indicate that skeletal refractoriness to PTH in vitamin D-deficient animals might, in part, be due to the impaired activation of adenylate cyclase, which cannot be explained entirely by hypocalcemia or associated secondary hyperparathyroidism. Vitamin D deficiency per se, therefore, may play a key role in the impaired cAMP response to PTH. (Endocrinology118: 1808–1813, 1986)
Basal (medicine)
Cyclic adenosine monophosphate
Cite
Citations (7)
Cite
Citations (71)
Cite
Citations (0)
Plasma parathyroid hormone (PTH) was measured in adult, age-matched, intact normal mice and Hyp male mice (n = 11/genotype). Hyp mice are an animal model for the human disease X-linked hypophosphatemia. A RIA was used which detects intact and carboxyl-terminal fragments of PTH. Hyp mice were found to have significantly higher plasma PTH levels (0.21 ± 0.03 ng bovine PTH eq/ml) than normal mice (0.04 ± 0.03 ng/ml; P < 0.01). This hyperparathyroidism in the slightly hypocalcemic, osteomalacic Hyp mice may be the result of skeletal resistance to endogenous PTH and may contribute to their characteristically elevated renal excretion of phosphate and urinary cAMP.
Hypophosphatemia
Cite
Citations (42)
The aim of the present work was to characterize at the molecular level the mechanism of PTH resistance in a rat model of secondary hyperparathyroidism resulting from vitamin D deprivation. PTH/PTH-related protein (PTHrp) receptor messenger RNA (mRNA) expression, assayed by ribonuclease protection analysis, was studied in the kidney, femoral epi/metaphysis, and diaphysis. In addition, in the kidney, PTH/PTHrp receptor mRNA expression was correlated to receptor function by measuring adenyl cyclase activity in crude renal membranes after stimulation by PTH (10(-10) - 10(-6) M), forskolin (0.1 and 0.2 mM), NaF (5 and 10 mM), and isoproterenol (1 and 10 microM). Four groups of rats were studied to investigate the effects of calcium, PTH, and/or vitamin D status. The first group received a control diet (D+D+). The second group received a diet deficient in vitamin D until death (D-D-). In the two other groups that also received a vitamin D-deficient diet, the hypocalcemia and the hyperparathyroidism were later corrected, by either vitamin D supplementation (D-D+) or lactose and high calcium diet (D-Ca+), 1 week before death. The results revealed a 2-fold decrease in the PTH-induced adenyl cyclase activity of the renal membranes in the D-D- rats compared to those in the three other groups. There was no significant difference in the four groups in adenyl cyclase activity stimulated by forskolin, NaF, and isoproterenol. The decrease in PTH-induced adenyl cyclase activity was associated with an approximately 2-fold increase in PTH/PTHrp receptor mRNA expression in the kidneys of the D-D- rats compared to controls. Normalization of PTH/PTHrp receptor mRNA expression was observed after vitamin D supplementation (D-D+ rats), but not after correction of the hypocalcemia and secondary hyperparathyroidism by oral lactose and calcium supplementation. In the epi/metaphysis, an approximately 2-fold increase in PTH/PTHrp receptor mRNA was also observed in the D-D- rats compared to the controls; this increase was partially corrected upon normalization of the calcemia and PTH levels with either vitamin D (D-D+ group) or lactose/calcium (D-Ca+ group). In the diaphysis, no change in the expression of PTH/PTHrp receptor mRNA was observed in any group.
Parathyroid hormone receptor
Cite
Citations (7)
The aim of the present work was to characterize at the molecular level the mechanism of PTH resistance in a rat model of secondary hyperparathyroidism resulting from vitamin D deprivation. PTH/PTH-related protein (PTHrp) receptor messenger RNA (mRNA) expression, assayed by ribonuclease protection analysis, was studied in the kidney, femoral epi/metaphysis, and diaphysis. In addition, in the kidney, PTH/PTHrp receptor mRNA expression was correlated to receptor function by measuring adenyl cyclase activity in crude renal membranes after stimulation by PTH (10(-10) - 10(-6) M), forskolin (0.1 and 0.2 mM), NaF (5 and 10 mM), and isoproterenol (1 and 10 microM). Four groups of rats were studied to investigate the effects of calcium, PTH, and/or vitamin D status. The first group received a control diet (D+D+). The second group received a diet deficient in vitamin D until death (D-D-). In the two other groups that also received a vitamin D-deficient diet, the hypocalcemia and the hyperparathyroidism were later corrected, by either vitamin D supplementation (D-D+) or lactose and high calcium diet (D-Ca+), 1 week before death. The results revealed a 2-fold decrease in the PTH-induced adenyl cyclase activity of the renal membranes in the D-D- rats compared to those in the three other groups. There was no significant difference in the four groups in adenyl cyclase activity stimulated by forskolin, NaF, and isoproterenol. The decrease in PTH-induced adenyl cyclase activity was associated with an approximately 2-fold increase in PTH/PTHrp receptor mRNA expression in the kidneys of the D-D- rats compared to controls. Normalization of PTH/PTHrp receptor mRNA expression was observed after vitamin D supplementation (D-D+ rats), but not after correction of the hypocalcemia and secondary hyperparathyroidism by oral lactose and calcium supplementation. In the epi/metaphysis, an approximately 2-fold increase in PTH/PTHrp receptor mRNA was also observed in the D-D- rats compared to the controls; this increase was partially corrected upon normalization of the calcemia and PTH levels with either vitamin D (D-D+ group) or lactose/calcium (D-Ca+ group). In the diaphysis, no change in the expression of PTH/PTHrp receptor mRNA was observed in any group.(ABSTRACT TRUNCATED AT 400 WORDS)
Parathyroid hormone receptor
Cite
Citations (36)
Pseudohypoparathyroidism
Parathyroid hormone receptor
Osteodystrophy
Cite
Citations (1)
Forty patients with hypocalcemia and/or Albright/s hereditary osteodystrophy were studied. Based on the estimation of serum calcium and parathyroid hormone (PTH) levels as well as the urinary cAMP response to infusions with parathyroid extract, it was possible to classify all of the patients studied as cases with idiopathic hypoparathyroidism (n = 6, low PTH, normal cAMP response), pseudohypoparathyroidism (PHP) type I (n = 18, high PTH, low cAMP response) and type II (n = 2, high PTH, normal cAMP response), as well as pseudopseudohypoparathyroidism (n = 14, normal PTH, normal cAMP response). In three cases studied at the age of 12, 17, and 23 yr, the signs of Albright's hereditary osteodystrophy were not observed. PTH levels were unusually high for a given serum calcium concentration in some patients with PHP, the increased PTH levels were, however, normalized during iv calcium infusions. In two young children with PHP, a gradual increase of serum PTH levels occurred despite persistent normocalcemia over a period of 3 yr. This suggests that factors other than hypocalcemia or frequent small unobservable falls of the serum calcium concentration, such as a deficient formation of 1,25- dihydroxyvitamin D3, secretion of an abnormal PTH, or an abnormal metabolism of the hormone, may contribute to the secondary hyperparathyroidism in PHP.
Pseudohypoparathyroidism
Hypoparathyroidism
Osteodystrophy
Cite
Citations (76)