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PubMed1999

Prospective evaluation of total parathyroidectomy and autotransplantation for the treatment of secondary hyperparathyroidism.

OBJECTIVE: To evaluate the clinical effectiveness of total parathyroidectomy with autotransplantation for the treatment of hyperparathyroidism and the recurrence rate of hyperparathyroidism after this procedure. DESIGN: A prospective study of total parathyroidectomy and autotransplantation in 19 consecutive patients with severe secondary (renal) hyperparathyroidism. SETTING: University hospital department of surgery. PATIENTS: Nineteen patients operated on for the treatment of secondary hyperparathyroidism between March 1993 and March 1996. Eighteen had been receiving longterm hemodialysis, and 1 had a functioning renal graft. INTERVENTION: Total parathyroidectomy and autotransplantation of excised parathyroid tissue into the brachioradialis muscle of the arm opposite that in which the arteriovenous fistula had been placed for dialysis. MAIN OUTCOME MEASURES: Clinical and biochemical improvement, morbidity, mortality, and recurrence rates of hyperparathyroidism after the procedure. RESULTS: The conditions of 13 (72%) of 18 patients followed up improved, and the clinical and laboratory variables indicating secondary hyperparathyroidism returned to normal. One patient died 50 days after surgery. In 2 patients (10%), mild hypoparathyroidism developed, and in 1 patient (5%), persistent hyperparathyroidism developed and required reoperation. In 2 patients (10%), recurrent hyperparathyroidism developed, and 1 (5%) required reoperation. CONCLUSIONS: Total parathyroidectomy with autotransplantation effectively relieves the symptoms of hyperparathyroidism, and the recurrence rate of hyperparathyroidism is low. Because all procedures used resulted in good control of clinical and biochemical variables, the method used for the surgical treatment of secondary hyperparathyroidism depends on the surgeon's preference.

Adult↗
PubMed1995

Fracture incidence in postmenopausal women with primary hyperparathyroidism.

BACKGROUND: The association of bone loss and increased fractures in postmenopausal women with minimally symptomatic hyperparathyroidism has not been clearly defined. This study was done to determine the frequency of fractures in postmenopausal women with hyperparathyroidism. METHODS: Forty-six postmenopausal women who had undergone parathyroidectomy for hyperparathyroidism during a 5-year period (1986 to 1991) were interviewed, and their medical records were examined to determine their fracture history. Forty-four postmenopausal women without hyperparathyroidism were contacted by random digit dialing and interviewed as controls. RESULTS: The groups were comparable with regard to age, weight, height, race, and age at menopause. Medical conditions and medication use were also similar, except for more reports of hypothyroidism in the hyperparathyroidism group (p = 0.05). Only 13% of women presented for treatment because of bone concerns, either fractures (9%) or low bone density (4%). However, on interview, 48% of the patients with hyperparathyroidism reported fractures compared with 25% of the controls (p = 0.02), a difference that remained even when those presenting with bone disease were excluded (p = 0.05). Of those with fractures, multiple fractures occurred in 36% of patients with hyperparathyroidism compared with 9% of controls and generally occurred after minor rather than major trauma (92% versus 45%, p = 0.002). Appendicular skeletal sites were reported for 86% of hyperparathyroidism group's and 92% of control group's fractures. Moreover, 50% of patients with hyperparathyroidism reported height loss compared with 27% of the control group (p = 0.05). CONCLUSIONS: This study shows that postmenopausal women with hyperparathyroidism reported more fractures and height loss than the control group, even when patients with hyperparathyroidism who presented because of bone disease were excluded.

Aged↗
PubMed1979

Pre- and postoperative studies of plasma calcitonin in primary hyperparathyroidism.

The importance of calcitonin in the homeostatic response to the chronic hypercalcemia of primary hyperparathyroidism is uncertain. To clarify this issue, we have used a new, sensitive radioimmunoassay for human calcitonin to measure basal plasma calcitonin concentrations in 50 patients with primary hyperparathyroidism (32 female, 18 male). We assayed calcium-stimulated calcitonin concentrations preoperatively in 22 of the patients (16 female, 6 male) and postoperatively in 6. Finally, we assayed pentagastrin-stimulated calcitonin concentrations preoperatively in eight of the patients (three female, five male). Plasma calcitonin values after an overnight fast were indistinguishable from those in normal subjects (mean+/-SE, males, 48+/-3 normal and 46+/-5 pg/ml hyperparathyroid, females, 31+/-2 normal and 37+/-3 pg/ml hyperparathyroid.) Among hyperparathyroid patients of both sexes, increases of calcitonin during Ca infusion (15 mg Ca/kg in 4 h) were within normal limits. However, the mean maximal increase of calcitonin was significantly lower in hyperparathyroid than in normal subjects (P < 0.05). In six patients normocalcemic 5-15 mo after parathyroid surgery, fasting plasma calcitonin values were not significantly different, but responses to Ca infusion were greater than preoperatively (Delta calcitonin +/-SE: 13+/-4 preoperatively and 53+/-35 pg/ml postoperatively). The mean maximal increase of calcitonin after pentagastrin (0.5 mug/kg i.v.) was slightly lower than normal in the patients (mean+/-SE, males, 45+/-8 normal and 38+/-10 pg/ml hyperparathyroid, females, 6+/-2 normal and 0 pg/ml hyperparathyroid). Thus, primary hyperparathyroidism is accompanied by normal steady-state concentrations of circulating calcitonin, and normal-to-blunted C-cell responses to pentagastrin or induced hypercalcemia, the response to calcium generally increasing after successful parathyroid surgery. These results clearly show that primary hyperparathyroidism is not characterized by hypercalcitoninemia. The seemingly paradoxical absence of elevated steady-state calcitonin concentrations may be accounted for partly by decreased secretory reserve. However, primary hyperparathyroidism may also be accompanied by an increase in the threshold of sensitivity for calcium stimulation of calcitonin secretion.

Adolescent↗
PubMed1992

[Pancreatic exocrine and endocrine functions stimulated with secretin and thyrotropin-releasing hormone in patients with hyperparathyroidism].

This study was designed to investigate pancreatic exocrine and endocrine secretion stimulated with secretin and thyrotropin-releasing hormone (TRH) in hyperparathyroidism. Pancreatic exocrine secretion during 30 min stimulated by constant secretin infusion of 1U/kg/hour was significantly increased in patients with secondary hyperparathyroidism compared with controls and patients with primary hyperparathyroidism. Intravenous administration of TRH at a dose of 20 micrograms/kg/hour, superimposed on secretin, produced a significant decrease of pancreatic exocrine secretion in both primary and secondary hyperparathyroidism but not in control. Serum insulin, glucagon and secretin levels were significantly higher in the subjects of both primary and secondary hyperparathyroidism than those of controls. Serum glucagon and secretin levels were significantly higher in secondary hyperparathyroidism than primary hyperparathyroidism. The pancreatic endocrine secretion was not influenced by TRH administration. Pancreatic exocrine secretion was not changed by parathyroidectomy in patients with primary hyperparathyroidism. As for endocrine secretion, however, only serum secretin level decreased to the level before parathyroidectomy. In this study, it was speculated that the increase of pancreatic secretion in secondary hyperparathyroidism may be due to hypersecretinemia, and the decrease of exocrine secretion by TRH in primary and secondary hyperparathyroidism may be resulted from the direct effect of TRH on the pancreatic acinar cells.

Adult↗
PubMed1995

Intracellular calcium and blood pressure: comparison between primary hyperparathyroidism and essential hypertension.

Intracellular calcium has been reported to be increased in essential hypertension, and thought to play a role in its genesis through facilitation of vascular smooth muscle contraction. Since hypertension is more prevalent in primary hyperparathyroidism, intracellular calcium may also be increased in this condition. To investigate whether the hyperparathyroid condition, i.e., hypercalcemia and increased PTH per se, could be associated with high intracellular calcium, we measured intracellular calcium in platelets with the Quin-2 AM fluorometric method in 11 normotensive patients with primary hyperparathyroidism, 15 patients with essential hypertension, and 18 normal controls, all matched for age and sex. We repeated the measurements in 9 of the hyperparathyroid patients after successful surgery. We found that intracellular calcium was higher in normotensive patients with primary hyperparathyroidism than in normal controls (198 +/- 24 vs 113 +/- 11 nM, p < 0.05), but lower than in patients with essential hypertension (198 +/- 24 vs 286 +/- 38 nM, p < 0.05). Successful removal of a parathyroid adenoma decreased intracellular calcium from 215 +/- 22 to 116 +/- 19 nM, (p < 0.01). In the patients with primary hyperparathyroidism, intracellular calcium was strongly correlated with the levels of PTH (r = 0.87, p < 0.01), but not with the total serum calcium levels (r = 0.04, NS). The decrease in intracellular calcium after parathyroidectomy was also strongly correlated with the decrease in PTH (r = 0.84, P < 0.01), but not with the decrease in total serum calcium (r = 0.16, NS). In the patients with essential hypertension, intracellular calcium correlated well with systolic (r = 0.69, p < 0.01), diastolic (r = 0.76, p < 0.01) and especially mean arterial pressure (r = 0.86, P < 0.01). There was no correlation between blood pressure and intracellular calcium in the patients with primary hyperparathyroidism. We conclude that normotensive patients with primary hyperparathyroidism, as well as patients with essential hypertension, can have increased concentrations of intracellular calcium in platelets. The correction of the hyperparathyroid condition normalizes intracellular calcium concentration. The close correlation between PTH and intracellular calcium suggests that PTH may act as a ionophore for calcium entry into cells. Whether the increased levels of intracellular calcium may reflect a pre-hypertensive condition in normotensive patients with primary hyperparathyroidism remains to be determined.

Adenoma↗
PubMed1990

Calcium oxalate crystal formation in patients with hyperparathyroidism and hyperthyroidism and related metabolic disturbances.

The crystallization of calcium oxalate in the urine of patients with hyperparathyroidism and hyperthyroidism was studied using a mixed suspension mixed product removal (MSMPR) system. In addition, calcium metabolism in hyperthyroidism and its relationship to urolithiasis was investigated. The urines from all the three groups (normal subjects, hyperparathyroid and hyperthyroid patients) showed reduced nucleation rates and increased growth rates in comparison with the control synthetic urine. The nucleation rate was not significantly different between the three human urine groups, while the growth rate was significantly higher in the hyperparathyroid group compared to the normal and hyperthyroid groups. Crystal volume (suspension density) in the hyperparathyroid group was approximately twice that in the other two groups. Serum and ionized calcium levels in hyperparathyroid patients were higher than in normal subjects, while hyperthyroid patients had levels only slightly higher than those in normal subjects. The hyperparathyroid and hyperthyroid groups differed significantly from the normal group in urinary calcium excretion. These two groups also showed significantly higher levels of serum alkaline phosphatase and urinary hydroxyproline than did the normal group. Although hyperthyroid patients have a calcium metabolism similar to hyperparathyroid patients, the incidence of urolithiasis is no different between hyperthyroid and normal subjects. The results of both crystallization and calcium metabolism in hyperparathyroid patients were not significantly different between those with and without urolithiasis. The result of crystallization was also not significantly different between hyperparathyroid patients with and without hypercalciuria. This study suggests that hypercalciuria alone does not produce urinary stones and that urine from hyperparathyroid patients may contain promotors of calcium oxalate crystallization and calcium stone formation.

Calcium Oxalate↗
PubMed1996

Accelerated bone loss in post-menopausal women with mild primary hyperparathyroidism.

OBJECTIVES: Osteopenia is regarded as an indication for parathyroidectomy in primary hyperparathyroidism. However, uncertainty exists as to the extent and degree of the skeletal effects in those with mild disease. We sought to determine whether mild primary hyperparathyroidism affects the rate of bone loss in postmenopausal women. DESIGN: Prospective 2-year comparison of rates of bone loss throughout the skeleton in 17 post-menopausal women with untreated mild asymptomatic primary hyperparathyroidism, and 48 age-matched, eucalcaemic controls. RESULTS: The women with primary hyperparathyroidism had a greater annual rate of loss of bone mineral density (BMD) of the total body (mean +/- SE, primary hyperparathyroidism -1.15 +/- 0.31%, controls -0.39 +/- 0.10%; P = 0.04) and its spine subregion (primary hyperparathyroidism -2.08 +/- 0.88%, controls 0.04 +/- 0.35%; P = 0.02). Lumbar spine BMD tended to decline in the primary hyperparathyroidism group (-0.35 +/- 0.33%) in contrast to the control group (+0.28 +/- 0.22%) (P = 0.10). There were no significant differences between the groups in rates of changes of BMD in the legs or the proximal femur. In the primary hyperparathyroidism group, the rate of total body bone loss in the eight women known at study entry to have had long-standing (> 5 years) primary hyperparathyroidism was -1.52 +/- 0.61%/year, similar to that of the whole group. CONCLUSION: Primary hyperparathyroidism is associated with an increased rate of loss of total body bone mineral density in post-menopausal women. Prolonged disease duration is therefore likely to be associated with an increasing risk of osteopenia, such that skeletal surveillance and interventions designed to reduce bone loss should be considered.

Aged↗
PubMed1990

Oral calcium load test: diagnostic and physiologic implications in hyperparathyroidism.

An oral calcium load test (CLT) (1 gm Ca/50 kg) was administered to 11 control subjects and 35 patients with overt hyperparathyroidism to assess its efficacy in diagnosis of hyperparathyroidism. All participants were placed on a low-calcium diet 3 days before the CLT. Intact parathormone and ionized calcium (Cai) levels were measured 0, 1, 2, and 3 hours after CLT. Initial Cai and parathormone (mean +/- SE) were 1.22 +/- 0.01 mmol/L and 2.94 +/- 0.03 pmol/L in the control group compared with 1.43 +/- 0.02 mmol/L and 10.6 +/- 2.2 pmol/L in the group with hyperparathyroidism. Both groups had a similar percent increase in Cai values (control, 5.9% +/- 0.8%; hyperparathyroidism, 6.3% +/- 0.6% (p greater than 0.1). A decline in parathormone levels of 47.6% +/- 2.8% in patients with hyperparathyroidism was significantly less than the 75.3% +/- 5.3% decline observed in control subjects (p less than 0.025). Three hours after CLT, parathormone was suppressed in control subjects, whereas a rebound occurred in patients with hyperparathyroidism. Postoperative CLT demonstrated a higher mean percent Cai increase and percent parathormone decline (Cai, 8.9% +/- 1.1%; parathormone, 67.9% +/- 1.8%) compared with preoperative values (Cai, 6.0% +/- 1.0%; PTH, 49.6% +/- 4.3%) (p less than 0.025), and 3 hours after calcium intake, parathormone remained suppressed, similar to control subjects. After surgery, three patients had elevated parathormone and low normal Cai levels and parathormone response to a CLT confirmed the diagnosis of secondary hyperparathyroidism. In conclusion, a CLT (1) can confirm the diagnosis of hyperparathyroidism and successful parathyroidectomy, (2) distinguished postoperative secondary from persistent primary hyperparathyroidism, (3) demonstrated nonautonomy of abnormal parathyroid glands with a parathormone response to a calcium load characterized by an earlier nadir, decreased suppressibility, and more rapid recovery, and (4) produced dynamic changes that did not distinguish patients with hyperparathyroidism from control subjects or hyperplasia from adenoma.

Administration, Oral↗
PubMed1989

Primary hyperparathyroidism.

Hyperparathyroidism was described initially in the mid 1920s in patients suffering from a rare and severe form of bone disease, osteitis fibrosa cystica. In the 1940s and 1950s renal stone disease was recognized as a far more frequent complication of primary hyperparathyroidism than bone disease, and approximately half of the patients with primary hyperparathyroidism in clinical series published through the 1970s presented with renal stones. The introduction of routine determination of serum calcium concentration in the mid 1970s has had a dramatic impact on the frequency with which primary hyperparathyroidism is diagnosed in the population, particularly in older individuals with predominantly nonspecific symptoms of the disease. Stone complications appear to occur in less than 10 per cent of such patients. Underlying primary hyperparathyroidism is diagnosed in approximately 1 to 5 per cent of the patients with calcium stone disease. The predominant risk factor for stone formation in primary hyperparathyroidism is hypercalciuria, and patients typically present with moderate to marked hypercalciuria but with only mild hypercalcemia, in the range of 11 mg. per dl. or less. Hypercalciuria in these patients is principally the result of 1,25-dihydroxyvitamin D-mediated hyperabsorption of calcium from the intestine. The pattern of hypercalciuria disproportionate to the degree of hypercalcemia that typifies patients with primary hyperparathyroidism and stone disease reaches an extreme degree in patients with so-called subtle or normocalcemic primary hyperparathyroidism, in whom diagnosis by routine techniques may be difficult. Parathyroid exploration remains the treatment of choice in patients with primary hyperparathyroidism and stone complications.

Adult↗
PubMed1996

Surgical management of hyperparathyroidism in patients with multiple endocrine neoplasia type 2A.

BACKGROUND: The surgical management of hyperparathyroidism in patients with multiple endocrine neoplasia type 2A (MEN 2A) is controversial. We report the long-term follow-up, mutational analysis, and surgical outcome in a large group of patients with MEN 2A and hyperparathyroidism. METHODS: Clinical and genetic data for MEN 2A patients with biochemically and pathologically confirmed hyperparathyroidism and a minimum of 5 years of follow-up were analyzed retrospectively, and outcomes after surgical management were compared. RESULTS: Thirty-five (29%) of 119 patients from 14 MEN 2A kindreds had biochemical and pathologic evidence of hyperparathyroidism, with a mean follow-up of 14.7 years. The phenotypic expression of hyperparathyroidism was associated with germline mutations of the RET protooncogene at codons 634 and 618. At initial operation, 21 (62%) patients had a selective resection, eight (24%) had a subtotal resection, five (14%) had total parathyroidectomy with autotransplantation, and one had an inadvertent total parathyroidectomy. Twenty-seven (77%) patients were cured by the first operation. Persistent hyperparathyroidism occurred in three (8.6%) patients, and recurrent hyperparathyroidism occurred in five (14.3%) patients; both occurred only in patients treated with selective or subtotal resection. Permanent postoperative hypoparathyroidism occurred in six (21%) of 29 patients after selective or subtotal resection, in the one patient with inadvertent total parathyroidectomy, and in one (20%) of 5 patients treated with total parathyroidectomy and autotransplantation. CONCLUSIONS: Recurrent or persistent hyperparathyroidism occurs after selective or subtotal parathyroidectomy, as a result of either missed glands or interval development of neoplasia in previously normal parathyroid glands left in situ. Therefore we advocate total parathyroidectomy and heterotopic autotransplantation for patients with hyperparathyroidism and MEN 2A.

Adolescent↗
PubMed1996

Oral calcium tolerance test in the early diagnosis of primary hyperparathyroidism and multiple endocrine neoplasia type 1 in patients with the Zollinger-Ellison syndrome. Groupe de Recherche et d'Etude du Syndrome de Zollinger-Ellison.

BACKGROUND: In patients with the Zollinger-Ellison syndrome, the exclusion of multiple endocrine neoplasia type 1 is of important clinical relevance. Its diagnosis often relies on the existence of primary hyperparathyroidism. AIM AND METHODS: To investigate the parathyroid function of patients with the Zollinger-Ellison syndrome by use of an oral calcium tolerance test to identify both hypercalcaemic and normocalcaemic primary hyperparathyroidism, and, accordingly, multiple endocrine neoplasia type 1. PATIENTS: Among 51 consecutive patients with the Zollinger-Ellison syndrome referred to us between 1988 and 1994, 28 had not been investigated for parathyroid function and were prospectively studied. RESULTS: The investigation of calcium metabolism was abnormal in nine patients. One displayed characteristic features of humoral hypercalcaemia of malignancy. The diagnosis of primary hyperparathyroidism was biologically established in eight patients (29%) and subsequently confirmed by the presence of hyperplasia of the parathyroid glands in the seven patients who underwent neck exploration. Three patients with primary hyperparathyroidism had fasting hyper-calcaemia but the other five had normal fasting serum total calcium concentration and the diagnosis of primary hyperparathyroidism was established by means of the oral calcium tolerance test. Primary hyperparathyroidism was demonstrated in the five patients in whom the diagnosis of multiple endocrine neoplasia type 1 had been previously established on other criteria than primary hyperparathyroidism. By contrast, in three patients, primary hyperparathyroidism, either hypercalcaemic (one patient) or normocalcaemic (two patients) was the sole criteria for the diagnosis of multiple endocrine neoplasia type 1. These results also suggest that primary hyperparathyroidism is present before or close to the time of Zollinger-Ellison syndrome diagnosis. CONCLUSION: Complete investigation of the parathyroid function with calcium calcium and parathyroid hormone concentrations.

Administration, Oral↗
PubMed2004

Association between primary hyperparathyroidism and increased body weight: a meta-analysis.

Although primary hyperparathyroidism is frequently asymptomatic, it has been associated with an increased prevalence of hypertension, insulin resistance, dyslipidemia, cardiovascular mortality, and cancer. Previously we reported that patients with primary hyperparathyroidism are heavier than age-matched controls. Increased body weight could contribute to the association between primary hyperparathyroidism and these extraskeletal complications. We searched MEDLINE for English language studies published between 1975 and 2003 that reported body weight or body mass index in subjects with primary hyperparathyroidism and a healthy age- and sex-comparable eucalcemic control group. Seventeen eligible studies were identified. Subjects with primary hyperparathyroidism were 3.34 kg (95% confidence interval, 1.97-4.71; P < 0.00001) heavier than controls in 13 studies reporting body weight. In four studies reporting body mass index, subjects with primary hyperparathyroidism had an increased body mass index of 1.13 kg/m(2) (-0.29 to 2.55; P = 0.12) compared with controls. Standard mean difference analysis showed that subjects with primary hyperparathyroidism had an increased weight or body mass index of 0.3 sd (0.19-0.40; P < 0.00001) compared with controls. We conclude that patients with primary hyperparathyroidism are heavier than their eucalcemic peers, and that increased body weight may contribute to the reported associations between primary hyperparathyroidism and some extraskeletal complications.

Body Weight↗
PubMed2005

Hyperparathyroidism in persons exposed to iodine-131 from the Hanford Nuclear Site.

CONTEXT: The risk of primary hyperparathyroidism from exposure to external radiation has been well documented in the last 20 yr. However, it remains unclear whether hyperparathyroidism might also be caused by internal exposure to radioactive iodine. OBJECTIVE: The objective of this study was to determine whether exposure to 131I from the Hanford Nuclear Site during 1944-1957 increased the risk of hyperparathyroidism among people living in the area. DESIGN: The Hanford Thyroid Disease Study was conducted as a retrospective cohort study. SETTING: The study setting was the general community in Washington State. PARTICIPANTS: The participants were 5199 persons born to mothers with usual residence in one of seven counties in eastern Washington State, randomly selected from birth records for the years 1940-1946. INTERVENTION: Of the 5199 selected, 3440 underwent a Hanford Thyroid Disease Study clinical evaluation, including an evaluation for hyperparathyroidism. Individual thyroid radiation dose, which could be estimated for 3191 study participants, ranged from 0.0029-2823 mGy (mean, 174 mGy). MAIN OUTCOME MEASURE: Hyperparathyroidism was the main outcome measure. RESULTS: Of 3440 evaluable participants, we confirmed 12 cases of primary hyperparathyroidism (0.35%). We found no evidence that the cumulative incidence of hyperparathyroidism increased with increasing radiation dose. CONCLUSION: In summary, this study shows no evidence that 131I, received at young ages and at the doses and exposure conditions experienced by this cohort, increased the risk of primary hyperparathyroidism. However, the effects of different doses and conditions of exposure to 131I on the risk of hyperparathyroidism remain to be defined.

Cohort Studies↗
PubMed1996

Circulating levels of interleukin-6 and tumor necrosis factor-alpha are elevated in primary hyperparathyroidism and correlate with markers of bone resorption--a clinical research center study.

The pathogenesis of PTH-induced bone loss is uncertain. Experimental evidence suggests that PTH induces the production by osteoblasts of the bone-resorbing cytokine, interleukin-6. We measured the circulating levels of interleukin-6, tumor necrosis factor-alpha, and interleukin-1 beta and examined their relationship to biochemical markers of bone turnover in 38 patients with primary hyperparathyroidism (7 of whom also were studied after successful parathyroid adenomectomy), 6 patients with hypoparathyroidism, and 12 subjects with normal parathyroid function. The patients with untreated primary hyperparathyroidism had mean serum levels of interleukin-6 that were 16-fold higher than control values (mean +/- SEM; primary hyperparathyroidism 18.6 +/- 2.1 pg/mL, controls 1.1 +/- 0.1; P < 0.001). Circulating levels of interleukin-6 soluble receptor (primary hyperparathyroidism 41.7 +/- 1.2 ng/ mL, controls 25.1 +/- 1.0; P < 0.001), and tumor necrosis factor-alpha (primary hyperparathyroidism 11.6 +/- 0.8 pg/mL, controls 2.5 +/- 0.2; P < 0.001) were also elevated. After successful parathyroid adenomectomy, levels of each of these cytokines fell into the normal range. The mean levels of interleukin-6, its soluble receptor, and tumor necrosis factor-alpha in the subjects with hypoparathyroidism were lower than control values (P < 0.001 for each variable). There was no difference between subjects with primary hyperparathyroidism and controls in the circulating level of interleukin-1 beta. In the subjects with untreated primary hyperparathyroidism, serum levels of interleukin-6 correlated strongly with those of intact PTH (r = 0.47, P = 0.003) and biochemical markers of bone resorption: serum deoxypyridinoline (r = 0.93, P < 0.001), serum type I collagen carboxyterminal telopeptide (r = 0.87, P < 0.001), urinary pyridinoline (r = 0.81, P < 0.001), and urinary deoxypyridinoline (r = 0.63, P = 0.005). Levels of tumor necrosis factor-alpha correlated less strongly with the same variables: PTH (r = 0.41, P = 0.01), serum deoxypyridinoline (r = 0.48, P = 0.002), serum type I collagen carboxyterminal telopeptide (r = 0.46, P = 0.004), urinary pyridinoline (r = 0.61, P = 0.008), and urinary deoxypyridinoline (r = 0.61, P = 0.007). Levels of interleukin-6 also correlated with those of tumor necrosis factor-alpha (r = 0.44, P = 0.005). Multiple regression analysis indicated that interleukin-6, but not tumor necrosis factor-alpha, was independently predictive of bone resorption. We conclude that serum levels of interleukin-6 and tumor necrosis factor-alpha are increased in patients with primary hyperparathyroidism and are normalized by successful surgical treatment. The finding that these cytokines correlate with biochemical markers of bone resorption suggests that they play a role in the pathogenesis of bone loss in primary hyperparathyroidism.

Adenoma↗
PubMedDate not supplied

Skeletal effects of primary hyperparathyroidism.

OBJECTIVE: To review the effect of primary hyperparathyroidism on bone mass and occurrence of fractures as well as the advances in medical management of this relatively common condition. METHODS: We conducted a MEDLINE search of peer-reviewed publications for the period from 1960 to 1999. Studies reviewed were those that evaluated bone mass and fracture risk in primary hyperparathyroidism in both male and female populations. Studies that assessed intervention with hormone replacement therapy, bisphosphonates, calcimimetic agents, and surgical treatment and their effect on bone mass and fracture were also reviewed. Preference was given to prospective studies, but retrospective, cross-sectional, and case-control studies were also evaluated. RESULTS: Most densitometry studies completed to date have been limited by their design. Some cross-sectional studies that used both single-photon absorptiometry and dual-energy x-ray absorptiometry have demonstrated preferential bone loss at cortical skeletal sites. Bone density seems to be relatively well preserved at cancellous bone sites. The absence of large prospective controlled trials makes it difficult to evaluate fracture incidence associated with hyperparathyroidism. Retrospective and case-control studies have found conflicting results relative to fracture incidence in patients with primary hyperparathyroidism. Parathyroidectomy has been shown to be of value in improving bone mineral density at both the lumbar spine and the femoral neck. Hormone replacement therapy in postmenopausal women with primary hyperparathyroidism has also been effective in improving bone mineral density and decreasing bone turnover. Bisphosphonates are currently being evaluated for effectiveness in improving bone mineral density and reducing the risk of fracture. Early results with alendronate treatment have demonstrated improvements in bone mass. Calcimimetic agents are a new treatment option that may become useful in the medical management of primary hyperparathyroidism. CONCLUSION: Although conflicting findings have been reported, bone loss has been noted in patients with primary hyperparathyroidism, especially at cortical skeletal sites. Medical management does not seem to be associated with increased morbidity or mortality in patients with asymptomatic primary hyperparathyroidism. Bone densitometry is advised, particularly for monitoring of bone mass at the midradius or femoral neck, in patients with primary hyperparathyroidism.

Bone Density↗
PubMed1986

Hyperparathyroid crisis reviewed: a role for parenteral cimetidine?

Hyperparathyroid crisis secondary to primary hyperparathyroidism has variously been described as hypercalcemic crisis, parathyroid storm, and parathyroid intoxication as well as other equally descriptive terms. Whatever the nomenclature, all emphasize the seriousness and urgency of the condition. Although fewer than 200 cases have been described since the first report by Hanes in 1939, it is generally agreed that hyperparathyroid crisis is more prevalent than commonly appreciated. The signs and symptoms of the syndrome are believed due not only to the presence of hypercalcemia, but to the toxic effects of parathormone as well. Its wide, but nonspecific clinical spectrum makes it easily confused with other causes of rapidly fatal cardiovascular or renal disease. The mortality in untreated cases is essentially 100 per cent. With combined medical-surgical treatment, it is still reported as high as 60 per cent. Three patients with severe hyperparathyroid syndrome are reported. Effective control of both hypercalcemia and the toxic effects of acute hyperparathyroid crisis was achieved with the use of parenteral cimetidine. Definitive surgical removal of a solitary parathyroid adenoma was performed in all three patients. The intimate relationship of the bioavailability of cimetidine and its effect in primary hyperparathyroidism is clearly demonstrated. An analogy to the use of cimetidine in Zollinger-Ellison syndrome is made. Both are endocrinopathies that require doses of cimetidine in excess of that normally considered therapeutic for peptic ulcer disease. The signs and symptoms of hyperparathyroid crisis as well as current modalities of treatment are reviewed. It is concluded that parenteral cimetidine is an important aid in the management of acute hyperparathyroid syndromes secondary to primary hyperparathyroidism.

Adult↗
PubMed1980

[Hyperparathyroidism and anemia: experimental study in the rat (author's transl)].

Red blood cell (RBC) production has been explored in hyperparathyroid as compared to normal rats. The hyperparathyroid state was obtained by feeding the rats a calcium-deficient diet during 30 days. A significant decrease (p less than 0.001) in reticulocyte count and in erythrocyte 59Fe incorporation was observed in hyperparathyroid rats when compared to control animals. A comparable inhibition of erythrocyte 59Fe incorporation in hyperparathyroid rats was found when the study was performed after stimulating bone marrow activity by acute arterial hemorrhage. These results of decreased RBC production using a model of endogenous hyperparathyroidism could be confirmed in additional experiments using a model of exogenous hyperparathyroidism. In this model, the rats received either parathyroid extract (3 x 10 USP/day during 8 days) or vehicle only. Again, a decrease in erythrocyte 59Fe incorporation was observed in hyperparathyroid animals when compared to control animals. It is concluded that the hyperparathyroid state is accompanied by a decrease of RBC production in the rat. It is probable that a similar pathogenesis underlies the anemia of patients with primary or secondary hyperparathyroidism.

Anemia↗
PubMed1999

[Definition of hyperparathyroidism and indication for surgical therapy].

Parathyroid excess may happen as a result of autonomous overactivity of the parathyroid glands (primary hyperparathyroidism). Secondary hyperparathyroidism is the consequence of chronic hypocalcemia, leading to parathyroid hyperplasia. Long-lasting secondary hyperparathyroidism may turn to autonomy in the sense of tertiary hyperparathyroidism. In primary hyperparathyroidism indications for surgical intervention are renal, intestinal or osseous organ manifestations, as well as relevant clinical symptoms of the so-called hypercalcemic syndrome. In truly asymptomatic primary hyperparathyroidism, observation is justified. However, the patients need regular supervision. If there is progression indicating health risk, the strategy must switch from observation to operation. Secondary hyperparathyroidism has must be treated by surgery if renal osteodystrophy progresses or tertiary hyperparathyroidism develops.

Chronic Kidney Disease-Mineral and Bone Disorder↗