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PubMed1997

Intraoperative parathyroid hormone monitoring during parathyroidectomy for secondary hyperparathyroidism.

BACKGROUND: The surgical management of secondary hyperparathyroidism by experienced surgeons is associated with excellent results. The presence of supernumerary glands and inadequate initial parathyroidectomy can lead to reoperations for recurrence. Intraoperative parathyroid hormone monitoring (qPTH), which has been described during parathyroidectomy for primary hyperparathyroidism, may be helpful in preventing or predicting the need for reoperation. This report describes the use of qPTH assays during parathyroidectomy in patients with secondary hyperparathyroidism. METHODS: Intraoperative parathyroid hormone (PTH) levels were determined in 13 patients with secondary hyperparathyroidism undergoing total parathyroidectomy with autotransplantation (n = 3) or subtotal parathyroidectomy (n = 10). Levels were determined using a modified immunochemiluminometric assay (qPTH). RESULTS: The average PTH levels before and after parathyroidectomy were 1599 pg/ml (620 to 2486 pg/ml) and 230.3 pg/ml (129 to 345 pg/ml), respectively. All patients had significant decreases in PTH levels after parathyroidectomy (mean, 84.6%). Symptoms were improved in all patients after operation. PTH levels at early follow-up were consistently below intraoperative levels. CONCLUSIONS: Intraoperative PTH monitoring reproducibly demonstrates the clinically relevant decrease in PTH levels after parathyroidectomy for secondary hyperparathyroidism similar to those previously documented in patients with primary hyperparathyroidism. Long-term follow-up and increasing numbers of patients are crucial in defining the role of qPTH monitoring during parathyroidectomy for secondary hyperparathyroidism.

Adult↗
PubMed1978

Primary hyperparathyroidism in paraneoplastic hypercalcaemia.

Hypercalcaemia is often associated with malignant disease. Causes of elevated serum-calcium levels in the absence of bony metastases include parathyroid-hormone production by the tumour, osteolytic factors made by the tumour, and coexistent primary hyperparathyroidism. By measuring nephrogenous cyclic-A.M.P. excretion to assess parathyroid-hormone function, we have determined the mechanism of such hypercalcaemia in 15 patients. Nephrogenous cyclic A.M.P. ranges from 0.05 to 2.40 mumol/g of creatinine in normal subjects, from 2.27 to 8.45 mumol/g in patients with primary hyperparathyroidism, and from 0.50 to 1.30 mumol/g in patients with proven non-hyperparathyroid hypercalcaemia without malignancy. 9 patients (60%) with hypercalcaemia and malignancy had normal levels of nephrogenous cyclic A.M.P. (range 0.35-2.07 mumol/g creatinine). The other 6 (40%) had elevated nephrogenous cyclic A.M.P. (range 2.70-5.55 mumol/g) consistent with increased parathyroid-hormone secretion. Surgical exploration of the neck in these patients showed that the increased parathyroid-hormone secretion was secondary to primary hyperparathyroidism, not ectopic hyperparathyroidism. Thus, the data indicate that coexistent hyperparathyroidism may be common in patients with hypercalcaemia and malignancy and that the measurement of nephrogenous cyclic A.M.P. is very useful in identifying patients at risk for hyperparathyroidism.

Adenocarcinoma↗
PubMed2006

The diagnosis and management of asymptomatic primary hyperparathyroidism.

Classical primary hyperparathyroidism--a disease of 'bones, stones, and psychic groans'--is a rarity in the US, although it is still seen in some parts of the world. Today, most patients with primary hyperparathyroidism are asymptomatic. This change in clinical profile is not merely because of improved detection techniques, and patients with primary hyperparathyroidism who lack symptoms, if left untreated, rarely develop the 'classical' features that were common previously. Indeed, currently available data suggest that there is, today, a disorder with different, yet characteristic, effects on the end-organs of the hyperparathyroid process. In this review, the features of the skeletal, renal, neuropsychologic, cardiovascular, and gastrointestinal manifestations of 'asymptomatic' primary hyperparathyroidism will be discussed. The considerable body of data that has emerged since the recognition of the new clinical profile of primary hyperparathyroidism has allowed a reconsideration of standards of care for this disease. These data were reviewed and incorporated into new clinical guidelines at the 2002 NIH workshop on asymptomatic primary hyperparathyroidism. These recommendations highlight both what is known about the disease, and important areas that need investigation. Continued interest in the skeletal, cardiovascular, and neuropsychiatric manifestations of the disease, and therapeutic trials of medical approaches for its management, will further refine our current understanding, and could lead to additional modifications in the approach to patients with this common endocrine disorder.

Bone Diseases↗
PubMed1999

Genetic studies of a family with hereditary hyperparathyroidism-jaw tumour syndrome.

BACKGROUND AND OBJECTIVES: Familial hyperparathyroidism may occur as familial isolated hyperparathyroidism (FIHP) or as part of an inherited syndrome, in particular multiple endocrine neoplasia types 1 and 2A (MEN1, MEN2A) and hyperparathyroidism-jaw tumour (HPT-JT) syndrome. The localization of the genes responsible for these syndromes has enabled genetic screening of families with primary hyperparathyroidism (PHPT) to be carried out. This has important clinical implications in terms of individual follow-up and management. We previously reported a large FIHP family with an increased risk of parathyroid cancer and excluded its linkage to MEN1, MEN2 and PTH genes. Here we re-analysed this family and performed genetic linkage to the HPT-JT locus in chromosome 1q21-q32. Loss of heterozygosity studies of 1q21-q32, 11q13 and X chromosome were also performed. PATIENTS AND DESIGN: We studied 19 family members, aged 6-63 years. High molecular weight DNA was isolated from peripheral blood samples from 17 family members. For the two deceased individuals, DNA was extracted from normal paraffin embedded tissues. MEASUREMENTS: All individuals (except two deceased patients) had serum corrected calcium, inorganic phosphate, intact PTH, prolactin and various pancreatic hormones, measured on fasting blood samples. Twenty microsatellite markers were examined for the 1q21-q32 region, the locus for the HPT-JT gene. Genetic polymorphisms were determined by polymerase chain reaction amplification of genomic DNA and genetic linkage analysis was performed. Loss of heterozygosity studies were performed using paraffin-embedded parathyroid tissues from four affected members. RESULTS: Seven of the eight affected family members included in this study had biochemical evidence of PHPT and surgically proven parathyroid tumours. Indication of linkage of the disease to the HPT-JT locus was demonstrated with a maximum lod score of 2.32 by two-points linkage analysis. Linkage data were supported by multi-point analysis which gave a maximum lod score of 2.7. Meiotic recombinations detected in one affected individual narrowed the region to 26 cM. As a result of the genetic findings, we re-screened the living family members by orthopantomograph and renal ultrasound, and identified two jaw lesions in two gene carriers. One affected family member demonstrated polycystic kidney disease, thus establishing the association between the two conditions. A reduced penetrance of HPT in females was evident, in agreement with our previous study. No allelic deletion was detected in any tumour at 1q21-q32, 11q13 or X chromosome. CONCLUSIONS: This study illustrates the usefulness and importance of genetic studies in familial isolated hyperparathyroidism families. Our clinical and genetic findings indicate that this previously reported familial isolated hyperparathyroidism family has hyperparathyroidism-jaw tumour syndrome.

Adolescent↗
PubMed1996

Hyperparathyroidism and long-term lithium therapy--a cross-sectional study and the effect of lithium withdrawal.

OBJECTIVES: To assess in patients with long-term lithium treatment the incidence and prevalence of hypercalcaemia and hyperparathyroidism, and to evaluate the relationship between parathyroid function and renal function: also, to examine the effect of treatment discontinuation. DESIGN: Part 1. An epidemiological cross-sectional study covering defined catchment areas. Part 2. A lithium withdrawal study in a subgroup of the patients who were examined after a mean of 8.5 (4-16) weeks off lithium. Comparisons were made with a group of psychiatric non-lithium patients matched for sex and age. SETTING: Outpatient treatment at nine psychiatric departments in southern Sweden. SUBJECTS: Inclusion criterion was 15 years or more on lithium. Excluded from Part 2 were patients with a high risk of relapse. Out of 215 identified patients. 142 (66%) entered and completed Part 1, while 13 of the latter entered and completed Part 2. RESULTS: The point prevalence of persistent hypercalcaemia was 3.6% and of surgically verified hyperparathyroidism 2.7%. The observed incidence of hyperparathyroidism over 19 years was 6.3%. It was significantly higher than expected in females. In the withdrawal group serum calcium was significantly increased compared to controls, and did not change during 8.5 weeks without lithium. Isostenuria was significantly more common among patients with than without hyperparathyroidism. CONCLUSIONS: The point prevalence, and the 19-year incidence of hyperparathyroidism, were increased. The point prevalence of hypercalcaemia was also increased, and not reversible during 8.5 weeks off lithium. The findings support the hypothesis of a causal relationship between lithium treatment and hyperparathyroidism. Hypercalcaemia and hyperparathyroidism are sometimes aetiologically related to reduced renal function in long-term lithium patients.

Adult↗
PubMed2000

Bone mineral density and blood pressure in patients with asymptomatic hyperparathyroidism. The Tromsø Study.

OBJECTIVE: To evaluate bone mineral density and blood pressure in asymptomatic hyperparathyroidism. DESIGN: A case-control study. SETTING: The participants obtained from an epidemiological survey in Tromso 1994-95, that included more than 27 000 subjects. The re-examination in 1998 was performed at the University Hospital of Tromso, Norway. Participants. Thirty-nine subjects with hyperparathyroidism and 72 control subjects were studied. MAIN OUTCOME MEASURES: Bone mineral density measurements of the lumbar spine and the proximal femur (femoral neck, Ward's triangle, and trochanter). Systolic and diastolic blood pressure. RESULTS: In the hyperparathyroidism group bone mineral density was significantly lower measured at the lumbar spine (1.000 +/- 0.181 vs. 1.079 +/- 0. 194 g cm-2, mean +/- SD, P < 0.01) and at the femoral neck (0.806 +/- 0.121 vs. 0.852 +/- 0.141 g cm-2, P < 0.05). In the females, but not in the males, blood pressure was significantly higher in the hyperparathyroidism group than in the control group [systolic blood pressure 146.7 +/- 18.6 vs. 137.4 +/- 23.0 mmHg (P < 0.05) and diastolic blood pressure 88.1 +/- 11.8 vs. 82.2 +/- 10.6 mmHg (P < 0. 05)]. In the females the number of subjects on antihypertensive medication was significantly higher in the hyperparathyroidism group than in the control group (32.1% and 16.6%, respectively, P < 0.01). CONCLUSIONS: Subjects with asymptomatic hyperparathyroidism have moderately reduced bone mineral density. In females with hyperparathyroidism there is an increase in blood pressure.

Adult↗
PubMed1999

Coincidence of hot thyroid nodules and primary hyperparathyroidism.

Hyperthyroidism is frequently associated with hypercalcemia, which usually subsides after successful treatment of hyperthyroidism. Moreover, thyroid nodules are frequently detected by preoperative thyroid ultrasound in patients with primary hyperparathyroidism. Sensitised by the observation of a patient with coexisting hyperthyroidism and hyperparathyroidism we prospectively evaluated thyroid nodules in euthyroid patients with hyperparathyroidism by thyroid scintigraphy. Whereas the first patient with hyperparathyroidism was hyperthyroid the subsequent four patients with hyperparathyroidism and thyroid nodules had normal fT3 and fT4. Two patients had hypercalcemia and nephroureterolithiasis. Three patients suffered from hypercalcemia and bone pain due to osteoporosis. In the hyperthyroid patient hypercalcemia persisted after euthyroidism was achieved intact parathyroid hormone was found to be elevated. Subsequently, thyroid nodules, detected by preoperative ultrasound in four euthyroid patients with primary hyperparathyroidism, were identified as compensated hot nodules by thyroid scintigraphy. All patients underwent combined subtotal thyroidectomy and parathyroid resection. Histology showed hyperplastic parathyroid glands in one patient and a single parathyroid adenoma in four cases. Postoperatively calcium and PTH levels returned to normal and TSH levels increased in all patients. Persistence of hypercalcemia after successful treatment of hyperthyroidism should be reason for the determination of parathyroid hormone. Thyroid nodules detected by preoperative ultrasound in patients with hyperparathyroidism living in areas of iodine deficiency should be further evaluated by scintigraphy even if TSH is normal. In the case of hot thyroid nodules both parathyroid and partial thyroid resection should be performed.

Aged↗
PubMedDate not supplied

[Primary hyperparathyroidism in pregnancy--a case report].

BACKGROUND: Primary hyperparathyroidism during pregnancy is rare. The incidence of primary hyperparathyroidism in women of child-bearing age is estimated to be approximately 8 cases per 100,000 population per year. CASE REPORT: We provide a case report of a 33-year old pregnant woman, in whom primary hyperparathyroidism was diagnosed because of neonatal hypocalcemia two days after delivery. There was a history of recurrent urinary tract infections with hydronephrosis on the left side. The woman had been treated on an outpatient basis by an urologist, nephrostomy had been performed. After delivery, nephrolithiasis was diagnosed by x-ray and treated endoscopically. Parathyroid adenoma was found and removed successfully. DISCUSSION: Due to physiological changes of calcium metabolism primary hyperparathyroidism is often without symptoms during pregnancy. Operative elimination of adenoma as a frequent cause of primary hyperparathyroidism reduces maternal and fetal morbidity and mortality. CONCLUSIONS: In pregnant women with hydronephrosis on the left side primary hyperparathyroidism should be considered. If undetected, hyperparathyroidism causes considerable morbidity, not only for the mother but also for the child.

Adenoma↗
PubMed2001

Primary hyperparathyroidism in patients with multiple endocrine neoplasia type 1: comparison with sporadic parathyroid adenomas.

A prospective study on the natural course of primary hyperparathyroidism has recently been reported. Since hyperparathyroidism in multiple endocrine neoplasia type 1 (MEN 1) is genetically distinct from most forms of sporadic hyperparathyroidism, it is important to know the natural course of hyperparathyroidism in MEN 1 for better clinical management. For this purpose, we retrospectively reviewed clinical parameters of patients with MEN 1 when they were diagnosed as having hyperparathyroidism, and compared them with those of patients with sporadic primary hyperparathyroidism. In patients with MEN 1: 1) levels of intact PTH (i-PTH) gradually increased with age, which accelerated over 40 years; 2) compared to the steep rise in i-PTH levels in aged patients, increase in serum calcium or decrease of serum inorganic phosphate concentration was relatively mild, and 3) the high concentrations of i-PTH in aged patients were not due to renal insufficiency. These features were not observed in patients with sporadic primary parathyroid adenomas. Clinical features of untreated hyperparathyroidism in MEN 1 may be significantly affected by the age of the patient. The effect, if any, of age-dependent deterioration on recurrence rate after subtotal or total parathyroidectomy requires further elucidation.

Adenoma↗
PubMed2000

Reoperation for secondary uremic hyperparathyroidism: are technical difficulties influenced by initial surgical procedure?

BACKGROUND: Parathyroid surgery in patients with uremia and secondary hyperparathyroidism is performed either by subtotal parathyroidectomy or total parathyroidectomy with immediate reimplantation. The aim of this study was to compare the results of reoperation for persistent or recurrent hyperparathyroidism after parathyroidectomy according to which initial operative procedure was used. PATIENTS AND METHODS: Eighty-nine patients had reoperation for persistent (28 patients) or recurrent (61 patients) hyperparathyroidism after 53 subtotal parathyroidectomies and 36 total parathyroidectomies with immediate reimplantation. Results of the reoperation were assessed in terms of success rate, morbidity, and operative findings. RESULTS: The success rate of reoperation in patients with persistent hyperparathyroidism was 89% and was independent of the initial type of surgery. Success rates of reoperation for recurrent hyperparathyroidism after initial subtotal parathyroidectomy and total parathyroidectomy with immediate reimplantation were 87% and 70%, respectively (P = .02). Hypertrophy of the parathyroid remnant was the main cause of recurrence after subtotal parathyroidectomy. After total parathyroidectomy with immediate reimplantation, recurrence was located in the graft in half the patients, while hyperplastic tissue was found in the neck or the mediastinum in the other half. CONCLUSIONS: Subtotal parathyroidectomy provides the best conditions for successful reoperation in case of recurrent hyperparathyroidism and should become the surgical treatment of choice for secondary hyperparathyroidism.

Adult↗
PubMed2002

Primary hyperparathyroidism in pregnancy: evidence-based management.

UNLABELLED: Primary hyperparathyroidism during pregnancy poses significant risks to the mother and the fetus. Fortunately, prompt diagnosis and effective management can improve outcomes for both. There is controversy regarding appropriate management of these patients, especially late in gestation. The objective of this article, therefore, is to review the literature and to propose an evidence-based approach to managing these patients. The prevalence of primary hyperparathyroidism in the general population is 0.15%. This condition is more common in women and 25% of cases appear in women during the childbearing years. The true incidence during pregnancy, however, is not known. Because up to 80% of gravid patients with primary hyperparathyroidism are asymptomatic, diagnosing this condition is more difficult. Complications associated with primary hyperparathyroidism in pregnancy have been reported to occur in up to 67% of mothers and 80% of fetuses. In addition to many constitutional symptoms, maternal complications include nephrolithiasis, bone disease, pancreatitis, hyperemesis, muscle weakness, mental status changes, and hypercalcemic crisis. Reported fetal complications include intrauterine growth retardation, low birth weight, preterm delivery, intrauterine fetal demise, postpartum neonatal tetany, and permanent hypoparathyroidism. A four-fold decrease in perinatal complications may be achieved with appropriate therapy. Conservative intervention may be appropriate under certain circumstances, but excision of a parathyroid adenoma remains the only definitive treatment. Debate continues regarding the safety of surgery in the third trimester. However, several cases of successful surgery have been reported. TARGET AUDIENCE: Obstetricians & Gynecologists, Family Physicians. LEARNING OBJECTIVES: After completion of this article, the reader will be able to describe the typical presentation of a patient with hyperparathyroidism, summarize the work up and management of a patient with hyperparathyroidism, and list the treatment options for a pregnant patient with hyperparathyroidism.

Adenoma↗
PubMed2007

Psychiatric and cognitive aspects of primary hyperparathyroidism.

PURPOSE OF REVIEW: Clinical guidelines for the treatment of primary hyperparathyroidism have been established by the 2002 NIH workshop on asymptomatic primary hyperparathyroidism. The panel called for further study of the ill-defined psychiatric and cognitive changes often seen in patients with primary hyperparathyroidism. The present paper provides a rigorous, updated review of the most recent advances and studies that have measured health-related quality of life, neurocognitive and psychiatric changes, as well as neurophysiologic imaging in patients with primary hyperparathyroidism undergoing parathyroidectomy. RECENT FINDINGS: In studies conducted pre and postparathyroidectomy, six recent articles have described improvements in health-related quality of life. Five studies included evaluations with validated psychiatric and cognitive tests in prospective case-control trials, and showed varied improvements in depression, memory and concentration after parathyroidectomy. Two studies evaluated in a preliminary fashion the brains of patients with primary hyperparathyroidism with functional imaging studies, showing regional cerebral blood flow changes and prefrontal cortical activation with sleep improvement in postsurgical patients. SUMMARY: The studies described in this paper underline the benefits of surgical treatment on nontraditional symptoms in patients with primary hyperparathyroidism, and open the door to the continued study of the endocrine effects of primary hyperparathyroidism on brain function.

Cognition Disorders↗
PubMed1998

Genetic alterations in primary and secondary hyperparathyroidism.

Hyperparathyroidism refers to a term representing a wide spectrum of parathyroid disorders that are characterized by the increased production of parathyroid hormone. Hyperparathyroidism was once thought to be rare but is now more commonly recognized, affecting 1 in 500 women over 40 years of age. Yet the interpretation of parathyroid pathology is still controversial and confusing. Over the past 10 years, genetic changes (ret and menin genes) involved in the pathogenesis of MEN 2 and MEN 1 have been discovered in succession. Different mutations of the calcium-sensing receptor gene have been identified in neonatal severe hyperparathyroidism and familial hypocalciuric hypercalcemia, respectively. The HRPT 2 gene responsible for the development of hereditary hyperparathyroidism and jaw tumors has been localized on the 1q21-31 locus. Several genetic alterations have also been characterized in primary and secondary hyperparathyroidism. Different genetic alterations appear to involve the development of different types of hyperparathyroidism. These novel advances give us new insights into the pathogenesis of hyperparathyroidism and allow better differentiation between the different types of parathyroid disorders.

Adult↗
PubMedDate not supplied

The prevalence of diabetes mellitus in patients with primary hyperparathyroidism and among their relatives.

The prevalence of diabetes mellitus in a series of 205 patients with proven primary hyperparathyroidism was 7.8% (16 patients). Eight patients were known to have diabetes at first attendance (prevalence 3.9%), four were discovered at the time of diagnosis of hyperparathyroidism (combined prevalence 5.9%) and four subsequently. Diabetes had been diagnosed from age 39 yr onwards, and in those with diabetes hyperparathyroidism was diagnosed at age 44 yr or later. The prevalence of diabetes in primary hyperparathyroidism is significantly greater than in a series of 200 consecutive non-hyperparathyroid outpatients attending the same unit (3.0%, p less than 0.05), or in the general populations of Oxford and Poole, after matching for age and sex (p less than 0.05), or in the combined populations of Oxford, Poole, and Southall (white population) (p less than 0.05) after similar matching. However, the prevalence of diabetes in hyperparathyroidism did not differ significantly from that of the white population of Coventry, where the prevalence is higher than that of Oxford, Poole and Southall. For hyperparathyroid patients presenting at age 40 yr or over, the prevalence of known diabetes (4.7%) is significantly greater than in the general populations at similar age of Oxford, Poole, and Southall.

Adult↗
PubMed2005

Serum fibroblast growth factor-23 levels predict the future refractory hyperparathyroidism in dialysis patients.

BACKGROUND: Secondary hyperparathyroidism is a common complication among long-term dialysis patients. The method of predicting future parathyroid function has not yet been established. Fibroblast growth factor-23 (FGF-23) is a newly found humoral phosphaturic factor. METHODS: One hundred and three nondiabetic dialysis patients whose plasma intact parathyroid hormone (PTH) levels were below 300 pg/mL were included in the study. Blood samples were stored at -80 degrees C for 2 years. Meanwhile, each physician in charge decided upon the strategy of medical therapy for maintaining intact PTH levels between 150 and 300 pg/mL. Patients were judged 2 years after the sample collection with regard to whether the hyperparathyroidism responded to the medical therapy. The definition of refractory secondary hyperparathyroidism was either (1) retaining intact PTH levels greater than 300 pg/mL 2 years after sample collection, or (2) having received the parathyroid intervention therapy during the observation period. Serum FGF-23 levels were determined with a sandwich enzyme-linked immunosorbent assay system that detects biologically active human FGF-23. RESULTS: Seventeen patients with intact PTH levels greater than 300 pg/mL were judged as having secondary hyperparathyroidism refractory to medical therapy. A stepwise regression analysis revealed that only serum levels of FGF-23 were significantly related to the prognosis of parathyroid function. A receiver-operated characteristic analysis demonstrated that the area under the curves obtained from FGF-23 (7099.9) was significantly greater than that obtained from intact PTH (6306.4, P < .01) and Ca x Pi (5670.3, P <.0001). Although the plasma intact PTH levels at the beginning of the observation period were comparable to each other, the intact PTH levels at 2 years after the sample collection were significantly higher in the patients with FGF-23 >/=7500 ng/L than in those with FGF-23 <7500 ng/L (P < .0001). CONCLUSION: Serum FGF-23 level was found to be the most useful factor in predicting future development of refractory secondary hyperparathyroidism in long-term dialysis patients with mild secondary hyperparathyroidism. The measurement of serum FGF-23 levels is a promising laboratory examination that can be applied in the clinical practice of uremic secondary hyperparathyroidism.

Adult↗
PubMed1968

Tertiary hyperparathyroidism.

In our first 200 cases of primary hyperparathyroidism confirmed by operation 12 were also shown to have a long history either of a malabsorption syndrome or of chronic renal-glomerular failure. We consider that they first went through a phase of secondary hyperparathyroidism, during which one or more of the glands became autonomous adenamata. This then produced the biochemical changes of "primary" hyperparathyroidism, necessitating excision of the adenoma. This condition is best described as "tertiary" hyperparathyroidism. The transition from secondary to tertiary hyperparathyroidism occurred in four of the 12 patients while under our observation. We think the same process can be traced retrospectively in the other eight cases. The concept of tertiary hyperparathyroidism may help to explain the high incidence of other diseases in association with primary hyperparathyroidism.The behaviour of the parathyroid glands provides a valuable model for the investigation of tumour formation in man. All states occurred in our patients with primary hyperparathyroidism, from normal through hyperplasia to adenoma formation and finally to parathyroid carcinoma.

Adenoma↗
PubMed1997

Noradrenergic blood pressure dysregulation and cytosolic calcium in primary hyperparathyroidism.

The purpose of this study was to characterize the changes in noradrenergic blood pressure regulation and the causes of this dysregulation in patients with histologically proven primary hyperparathyroidism before and after parathyroidectomy. In untreated hypertensive patients with primary hyperparathyroidism slightly higher plasma levels of norepinephrine, enhanced cardiovascular reactivity to norepinephrine (p<0.05) and increased cytosolic free calcium concentration in platelets (p<0.05) were found. Parathyroidectomy resulted in the correction of noradrenergic blood pressure dysregulation and in the reduction of cytosolic free calcium and led to normotension. In vitro incubation of platelets from normal subjects with heterologous plasma ultrafiltrates from either hypertensive patients with primary hyperparathyroidism or normotensive uremic patients with secondary hyperparathyroidism led to raised platelet calcium in primary hyperparathyroidism but not in secondary hyperparathyroidism, although in both conditions intact parathormone levels were elevated equally. Furthermore, when platelets of normotensive subjects were preincubated with commercially available parathormone, no effect on resting platelet cytosolic calcium was observed. Our results suggest that hypertension in primary hyperparathyroidism may be caused in part by noradrenergic blood pressure dysregulation and seems to be causally linked to the secretion of a parathyroid hypertensive factor, which increases cytosolic calcium and alters vascular tone and reactivity.

Adult↗
PubMed1983

Effects of dietary-induced hyperparathyroidism on the parathyroid hormone-receptor-adenylate cyclase system of canine kidney. Evidence for postreceptor mechanism of desensitization.

The present studies were designed to examine the consequences of chronic mild elevations of endogenous parathyroid hormone (PTH) in vivo on the PTH receptor-adenylate cyclase system of canine kidney cortex. Hyperparathyroidism was induced in normal dogs by feeding a diet low in calcium, high in phosphorus to the animals for a period of 6-9 wk. This maneuver resulted in a two to threefold increase in the plasma levels of carboxy-terminal immunoreactive PTH. This degree of hyperparathyroidism is similar to that seen in patients with hyperparathyroidism and normal renal function. After 6-9 wk on the diet the animals were killed and basolateral renal cortical membranes prepared for the study of the PTH receptor-adenylate cyclase system in vitro. The dietary hyperparathyroidism resulted in desensitization of the PTH-responsive adenylate cyclase (Vmax 3,648 +/- 654 pmol cyclic (c)AMP/mg protein per 30 min in hyperparathyroid animals vs. 5,303 +/- 348 in normal controls). The Kact (concentration of PTH required for half-maximal enzyme activation) was unchanged. However, PTH receptor binding (125I-norleucyl8-norleucyl18-tyrosinyl34, 125I[Nle8, Nle18, Tyr34] bPTH (1-34) NH2 as radioligand) was not different in the two groups of animals. Thus, dietary hyperparathyroidism resulted in an uncoupling of the PTH receptor-adenylate cyclase system. This defect was not corrected by guanyl nucleotides in vitro, and the effects of guanyl nucleotides on PTH binding and enzyme activation appeared normal. NaF-stimulated enzyme activity was reduced in the hyperparathyroid animals (8,285 +/- 607 pmol cAMP/mg protein per 30 min vs. 10,851 +/- 247 in controls). These data indicate that desensitization of the PTH-responsive adenylate cyclase system of canine kidney as a result of mild chronic elevations of endogenous PTH is due to a postreceptor defect, demonstrable by NaF activation, not corrected by guanyl nucleotides, leading to abnormal PTH-receptor adenylate cyclase coupling.

Adenylyl Cyclases↗