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PubMed1997

Analysis of proliferative activity of the parathyroid glands using proliferating cell nuclear antigen in patients with hyperparathyroidism.

To elucidate the cellular proliferative kinetics of the parathyroidal gland in patients with hyperparathyroidism, we investigated the expression of proliferating cell nuclear antigen (PCNA) in parathyroidal tissues using an immunohistochemical procedure. The PCNA labeling index (LI; maximum LI, maximal stained area; average LI, evenly distributed stained area) indicating cellular proliferative activity was defined as the number of PCNA-positive cells per 1000 parathyroid cells in the region of interest. We used these indexes to compare and investigate the proliferative activity of parathyroid cells under various conditions. The specimens used for the study were 42 parathyroid glands from 21 patients with primary hyperparathyroidism (19 cases of adenoma and 2 cases of primary hyperplasia due to multiple endocrine neoplasia type 1) and 129 parathyroid glands from 32 patients with secondary hyperparathyroidism. An additional 40 parathyroid glands resected during thyroid surgery of 30 normocalcemic patients were used as normal controls. In normally functioning parathyroids, a small number of cells in the growth phase were found. In primary hyperparathyroidism, proliferative activity was highest in the adenoma followed by primary hyperplasia. In contrast, the PCNA LIs showed a low value in the normal rim of the adenoma and normal glands resected as biopsy specimens from adenoma patients. We, therefore, assumed that proliferative activity was suppressed in these cells compared with that in normally functioning glands. In secondary hyperparathyroidism, when the cell component of the parathyroid tissues was divided into five types, PCNA immunoreactivity was lowest in the dark chief cells. Proliferative activity in cells of the oxyphil series was the same or higher than that in the clear chief cells or vacuolated chief cells. When classified according to the structure of the parathyroid glands, cell proliferation was significantly higher in the nodular type than in the diffuse type (maximum LI, 176 +/- 231 vs. 38.3 +/- 55.7; average LI, 120 +/- 188 vs. 24.8 +/- 43.5; mean +/- SD; P < 0.001). More PCNA-immunoreactive cells were found in autotransplanted glands with recurrence than in glands resected during the initial surgery. To summarize the PCNA expression classified according to the pathological types of hyperparathyroidism, the PCNA LIs were highest in secondary hyperplasia (maximum LI, 144 +/- 212; average LI, 96.0 +/- 169) and adenoma (maximum LI, 102 +/- 81.7; average LI, 67.5 +/- 67.7), followed by primary hyperplasia (maximum LI, 25.0 +/- 25.4; average LI, 19.2 +/- 22.2) and normal glands (maximum LI, 13.6 +/- 23.9; average LI, 4.40 +/- 8.90). These findings suggest that the cellular proliferative kinetics of the parathyroid gland differ depending on the type of hyperparathyroidism, glandular structure, and cell components. As the detection method of intranuclear expression of PCNA in cells is too sensitive, we should be careful not to overestimate the number of cells in the proliferative cycle. However, these results could not have been obtained using a conventional method such as DNA analysis by flow cytometry.

Adenoma↗
PubMed2003

[Endocrine surgery: the tenth report. Diagnosis, surgical indications and operative strategy of renal hyperparathyroidism].

In Japan, there are many dialysis patients because of the successful development and wide application of dialysis techniques. Almost all patients require long-term hemodialysis treatment because kidney transplantation is performed rarely. Renal hyperparathyroidism is one of the serious complications for hemodialysis patients. According to the overview of regular dialysis treatment reported by the Japanese Society for Dialysis Therapy, parathyroidectomy is required in 9.2%of patients who remain on hemodialysis more than 10 years and in 33.5%of those who so remain for more than 25 years. In this paper, we will describe the diagnosis, surgical indications, and operative strategy of renal hyperparathyroidism. The symptoms and biochemical variables were high serum parathyroid hormone (PTH) level, hyperphosphatemia, bone and joints pain, itching, irritability, muscle weakness, severe skeletal deformity, progression of ectopic calcification, and anemia. The clinical indications for performing parathyroidectomy to treat renal hyperparathyroidism in our institute are based on the indications reported by Tominaga et al. These are 1) high serum PTH level, 2) detection of enlarged parathyroid glands, 3) detection of osteitis fibrosa cystica on radiography or detection of high bone turnover by bone metabolic markers or bone scintigram, 4) resistance of symptoms to medical treatment. The routine operative procedure for renal hyperparathyroidism is total parathyroidectomy with forearm autograft. For autotransplantation, 30 pieces sliced 1x1x3 mm of diffuse hyperplasia are implanted into 30 pockets in the forearm without arteriorvenous (A-V) fistula for hemodialysis. In any surgical procedure for renal hyperparathyroidism, it is crucial to identify all parathyroid glands, including supernumerary glands and ectopic glands. At the initial operation for renal hyperparathyroidism, the surgeon must remove all parathyroid glands to avoid persistent and recurrent hyperparathyroidism and choose proper and adequate parathyroid tissue for autograft.

Humans↗
PubMed2005

Incidence of primary hyperparathyroidism in Rochester, Minnesota, 1993-2001: an update on the changing epidemiology of the disease.

UNLABELLED: We updated the incidence of primary hyperparathyroidism in Rochester, Minnesota. The lower rates previously noted persisted, whereas parathyroidectomies at our institution remained high. These data suggest an etiologic factor may be responsible for the peak incidence in the 1970s. INTRODUCTION: Automated serum calcium measurements were associated with a dramatic rise in primary hyperparathyroidism in the early 1970s, but a progressive decline in the incidence thereafter was unexpected and suggested a fundamental change in the epidemiology of the disease. Our objective was to evaluate trends in the incidence of primary hyperparathyroidism since 1992. MATERIALS AND METHODS: In this population-based descriptive study, Rochester, MN, residents who met defined diagnostic criteria for primary hyperparathyroidism from January 1993 through December 2001 were identified through the medical record linkage system of the Rochester Epidemiology Project and the Mayo Clinic Laboratory Information System. Changes in incidence were evaluated by Poisson regression. RESULTS: Altogether, 136 Rochester residents (94 women and 42 men) were newly identified with primary hyperparathyroidism in 1993-2001. Their mean age was 56 years, and 93% had definite disease. The overall age- and sex-adjusted (to 2000 U.S. whites) rate during this period was 21.6 per 100,000 person-years, which was less than the annual rate of 29.1 per 100,000 observed in 1983-1992 and 82.5 per 100,000 in July 1974-1982. Although community incidence declined, the number of parathyroidectomies performed at our institution increased during the same period. Serum calcium was deleted from the automated chemistry panel in June 1996, but most subjects remained asymptomatic at diagnosis (95%) with mild hypercalcemia. The majority of subjects were observed without parathyroid surgery (75%), and there was minimal impact on patient management from the 1990 NIH consensus conference on asymptomatic primary hyperparathyroidism. CONCLUSIONS: The lower incidence of primary hyperparathyroidism noted through 1992 has persisted in our community through 2001, whereas parathyroidectomies at our institution remained high. These data suggest that some underlying etiologic factor, in addition to the introduction of automated serum calcium testing, may have been responsible for the peak incidence in the 1970s.

Calcium↗
PubMed1980

Urinary 3',5'-cyclic adenosine monophosphate in relation to serum and urinary calcium in acromegaly and primary hyperparathyroidism.

A comparison of the interrelations between serum and urinary calcium values and the urinary excretion of cAMP in acromegaly (No. of subjects: 26), patients with primary hyperparathyroidism (n = 18) and control subjects (n = 42) is presented. The cAMP excretion was greatest in primary hyperparathyroidism, but acromegalics also exhibited higher values for this parameter than controls. A positive correlation was found between serum calcium values and cAMP in primary hyperparathyroidism, while acromegalics showed no correlation between these parameters. In controls there was a negative correlation between serum calcium and cAMP. Serum calcium levels corrected for variations in total protein concentrations were elevated both in acromegaly and primary hyperparathyroidism, mostly in the latter. Acromegalics and patients with primary hyperparathyroidism exhibited an increase in 24 h calcium excretion. While there was a negative relationship between urinary calcium excretion and cAMP in acromegaly, a positive correlation between these parameters as found in primary hyperparathyroidism. Controls showed a negative correlation between urinary calcium values and cAMP. It is concluded that the role of the parathyroids in the regulation of calcium metabolism in acromegaly is different from that of both normal controls and primary hyperparathyroidism. It is postulated that an active form of Vitamin D plays a major role in the regulation of calcium metabolism in acromegaly.

Acromegaly↗
PubMed2002

Molecular pathogenesis of primary hyperparathyroidism.

This article will primarily focus on the molecular pathogenesis of common, sporadic (nonfamilial) parathyroid adenomas; two genes currently have established roles in the development of these tumors. The cyclin D1/PRAD1 gene was identified as a clonally activated oncogene in parathyroid adenomas and has subsequently been established as a major contributor to human neoplasia. Overexpression of cyclin D1, a key regulator of the cell cycle, has been implicated in the pathogenesis of 20-40% of sporadic parathyroid adenomas. That such cyclin D1 overexpression indeed constitutes a stimulus to excessive parathyroid cell proliferation has been confirmed experimentally by the development of a transgenic mouse model with parathyroid-targeted overexpression of cyclin D1. Parathyroid hormone (PTH)-cyclin D1 transgenic mice develop parathyroid hypercellularity, biochemical hyperparathyroidism, and a shifted in vivo parathyroid-calcium setpoint; these mice constitute an animal model of human hyperparathyroidism in which aspects of tumorigenesis, parathyroid secretory setpoint control, and the pathophysiology of the chronic hyperparathyroid state can be further investigated. The MEN1 tumor suppressor is the only other gene to date with an established role in the pathogenesis of sporadic parathyroid adenomatosis. Specific clonal alterations involving somatic mutation and/or deletion of both MEN1 alleles have been demonstrated in about 15-20% of sporadic parathyroid adenomas. Allelic losses on 11q occur in roughly twice this number of adenomas, raising the still-unresolved possibility that an additional tumor suppressor gene on 11q may be the functional target of many of these acquired deletions. A mouse model of MEN1 deficiency causes a phenotype that includes parathyroid hypercellularity albeit unaccompanied by biochemical hyperparathyroidism, and additional mouse models in which menin deficiency is targeted to the parathyroids will likely provide additional important insights. The MEN1 gene product menin may have a role in transcriptional regulation involving JunD; several other menin-interacting proteins have also been identified. The in vivo mechanism of menin's actions, with special attention to its role as a parathyroid oncosuppressor, will be important to establish, as will the potential interrelationships between these pathways and those involving cyclin D1. A number of genes, put forth as candidate tumor suppressors based on their genomic locations, roles in familial disease, and/or other relevant biological functions, have been examined for pathogenetic mutations in sporadic parathyroid tumors with negative results; these include the calcium-sensing receptor protein (CaR), vitamin-D receptor (VDR), and RET. However, the CaR, which when partially or markedly deficient because of germline mutation can cause familial hypocalciuric hypercalcemia or neonatal severe hyperparathyroidism, must still be considered as having a potentially important secondary role in the manifestations of sporadic parathyroid tumors. Future goals include identifying additional parathyroid oncogenes and tumor suppressor genes; exploiting tools of complex trait genetics to ascertain whether development of "sporadic" hyperparathyroidism might be influenced by predisposing polymorphic alleles in the population; obtaining molecular insights into the relationship between proliferative and hormone regulatory abnormalities of hyperparathyroidism; and obtaining molecular insights into the observed association of parathyroid neoplasia with exposure to ionizing irradiation and with the postmenopausal state.

Adenoma↗
PubMed2003

[Results of bone scintigraphy, densitometry and radiography in secondary hyperparathyroidism in patients with chronic renal failure].

UNLABELLED: Secondary hyperparathyroidism occurs frequently in patients with chronic renal failure (CRF). Cardinal manifestations in patients with secondary hyperparathyroidism involve also skeletal changes. Hence the aims of our studies were detailed investigations of bones using isotope scintigraphy (99mTc-MDP), densitometry (DEXA-Lunar) and radiography, in a group of 34 patients with advanced secondary hyperparathyroidism with very high PTH serum concentrations. Bone mineral density of radius amounted to 74.14 +/- 14%, and 29 cases had osteoporosis, and 5 cases osteopenia. Bone mineral density of vertebral bodies was 85.6 +/- 10.5% was within osteopenia range in 16 cases, osteoporosis in 11 cases and was normal in 6 cases. Bone scintigraphy revealed: excessive tracer uptake in cranial vault, mandible, spine and lateral parts of the sacral bone. Tracer accumulation was decreased in soft tissues and absent in kidneys. Roentgen studies revealed changes typical to secondary hyperparathyroidism: acroosteolysis in 60% of cases, subperiosteal resorption in 43% of cases, calcifications in 20% of cases, cortical fibrosis in 35% of cases and osteoporosis in 85% of cases. CONCLUSIONS: 1. Bone mineral density is markly decreased in the radius and to a lower extent in the vertebral bodies, hence DEXA studies of radius are most appropriate for evaluation of mineral bone density. The differences in BMD are characteristic of hyperparathyroidism, both primary and secondary. 2. In most patients bone scintigraphy shows characteristic abnormalities, thus scintigraphy is helpful in the diagnosis of advanced secondary hyperparathyroidism. 3. In x-ray studies osteoporosis is frequently observed, other signs of secondary hyperparathyroidism are not so common and appear in later stage of disease than decreased bone mineral density in densitometry.

Absorptiometry, Photon↗
PubMed1991

Total parathyroidectomy alone or with autograft for renal hyperparathyroidism?

Seventy-six patients underwent parathyroidectomy for renal hyperparathyroidism. There were 10 subtotal parathyroidectomies, 49 total parathyroidectomies with implantation of part of one gland as an autograft, nine total parathyroidectomies with no autograft, and eight patients in whom only three parathyroid glands were found. In 34 dialysis patients who underwent total parathyroidectomy with an autograft there was a high rate of recurrent hyperparathyroidism after 6 years in those remaining on dialysis. Fifty per cent had asymptomatic recurrent hyperparathyroidism and 30 per cent required partial autograft excision for symptomatic hyperparathyroidism. In contrast, recurrent hyperparathyroidism was rare in renal transplant recipients with good renal function. This favourable outcome did not depend upon whether parathyroid surgery was performed before or after transplantation, or on the type of parathyroidectomy. Total parathyroidectomy without an autograft was performed in nine dialysis patients without any short-term adverse effects, and with clinical and pathological improvement in bone disease. In summary, the results of surgery for renal hyperparathyroidism were excellent in patients who received a successful renal transplant. However, there was a high incidence of recurrent hyperparathyroidism in patients who remained on long-term dialysis. Total parathyroidectomy without an autograft may be the treatment of choice in patients unlikely to receive a renal transplant.

Adult↗
PubMed1977

Experience with the radioimmunoassay for parathyroid hormone in the diagnosis of primary hyperparathyroidism.

Our results with radioimmunoassay studies for parathyroid hormone performed during the last 6 years are compared retrospectively to results of the laboratory tests customarily secured when hyperparathyroidism is suspected. The results obtained in patients with known primary hyperparathyroidism and in patients with unconfirmed but presumptive hyperparathyroidism are compared to the results obtained from a group of normal controls. Despite the fact that certain discrepant results were noted in the earlier assay techniques the over-all results and, in particular, those of more recent years have been highly sensitive and reproducible corroboratives of the existence of primary hyperparathyroidism. About two-thirds of the patients with primary hyperparathyroidism will present to the urologist. All patients with calcium-containing stones should have at least 3 determinations of the serum calcium in screening for primary hyperparathyroidism. The radioimmunoassay for parathyroid hormone provides the most reliable confirmation. The patient with calculous disease, elevation of the immunoreactive parathyroid hormone level and hypercalcemia is virtually certain to have primary hyperparathyroidism.

Calcium↗
PubMed1995

Effects of parathyroidectomy on left ventricular mass in patients with hyperparathyroidism.

The effects of parathyroidectomy on left ventricular muscle volume and mechanical performance were evaluated echocardiographically in 24 patients with secondary hyperparathyroidism due to chronic renal failure and in 7 with primary hyperparathyroidism. Intraventricular septum and posterior wall thickness, left ventricular end-diastolic diameters, shortening fraction, ejection fraction, and left ventricular mass index were measured by M mode recording by the parasternal short axis view prior to parathyroidectomy as baseline and repeated 12 months after parathyroidectomy. Serum basal carboxyterminal parathyroid hormone levels in patients with secondary hyperparathyroidism (34.4 +/- 13.7 ng/ml) were significantly higher than in those with primary hyperparathyroidism (3.4 +/- 5.1 ng/ml; p < 0.0001). At 12 months after parathyroidectomy, intraventricular septum and posterior wall thickness, left ventricular end-diastolic diameter and left ventricular mass index were reduced from 11.8 +/- 3.1 mm, 10.9 +/- 1.7 mm, 53.8 +/- 6.3 mm, 200.8 +/- 57.1 g/m2 to 10.0 +/- 2.1 mm (p < 0.05), 9.8 +/- 1.9 mm (p < 0.05), 50.7 +/- 7.2 mm (p < 0.05), 149.6 +/- 38.7 g/m2 (p < 0.0001), in patients with secondary hyperparathyroidism. In patients with primary hyperparathyroidism, all echocardiographic parameters remained in the normal range and did not show any significant changes before or after parathyroidectomy. From this study, parathyroid hormone at extremely high concentrations as seen in secondary hyperparathyroidism appears to be a cardiotoxic substance. Therefore, all patients with secondary hyperthyroidism should be examined by echocardiography and parathyroidectomy should be considered if myocardial hypertrophy is present.

Adult↗
PubMedDate not supplied

[Hyperparathyroidism with lithium].

Lithium has proved to be a highly effective preventive measure in mood disorders and an increasing number of patients are receiving long-term lithium carbonate therapy. Among other biologically and clinically important effects of lithium, the possible induction of hyperparathyroidism was first suggested in 1973 by Garfinkel et al. About thirty other case reports have since been described, but they could simply have represented the coincidental occurrence of primary hyperparathyroidism and lithium carbonate treatment in the same patients. Eleven cross-sectional studies of calcium metabolism in patients treated with lithium carbonate have been reported. Evidence of a causal relationship of lithium to hyperparathyroidism can lead to a loss of effectiveness of lithium in controlling the affective symptoms. Interestingly, coexistence with hypothyroidism is not uncommon. Low serum phosphate, high serum chloride are also observed. Bone mineral content may decrease. In addition, several studies have shown that lithium treatment increases serum magnesium level. Unusual metabolic features are associated with hyperparathyroidism and long-term lithium treatment: low urinary calcium excretion, absence of nephrolithiasis, and normal urinary cyclic AMP excretion. Lithium inhibition of PTH sensitive adenylcyclase in the kidney would explain these features. In vitro studies suggested that lithium is a potent inhibitor of several hormone responsive adenylcyclase systems. It is possible that the tissue susceptibility to adenylcyclase inhibition in an individual may decide the nature of endocrine dysfunction seen during lithium treatment. Information about the time course with which abnormalities may develop is derived from longitudinal studies. Several months to several years are needed for lithium inducing primary hyperparathyroidism. In vitro studies provide strong evidence that lithium can induce a shift in the set-point for inhibition of PTH secretion by calcium and a direct stimulation of PTH secretion. The extent to which we can extrapolate these data to the clinical situation is discussed. In vivo data from Shen an Seely are compatible with these two mechanisms. These alterations should cause parathyroid hyperplasia. The possibility that a generalized parathyroid stimulus might lead to formation of a single adenima is not proved. Several recommendations regarding parathyroid function in patients receiving lithium have been suggested. Measurement of total calcium and serum proteins or of serum calcium ion values when available should be performed before therapy is begun. If elevated values are obtained, lithium treatment should be deferred and evaluation for hyperparathyroidism performed. Serum calcium should be monitored periodically during lithium treatment. Sustained hypercalcemia or true hyperparathyroidism require parathyroidectomy. If hypercalcemia is mild without complication and psychiatric symptoms well controlled, perhaps surgery should not be employed.

Adult↗
PubMedDate not supplied

Parathyroidectomy in the treatment of secondary hyperparathyroidism in chronic renal failure.

During the period 1983-1995, 200 chronic renal failure patients (115 males and 85 females) were parathyroidectomized for hyperparathyroidism in our Department. In all of them, the presenting clinical symptoms, physical signs, biochemical and radiological tests were typically those of hyperparathyroidism. One hundred ninety patients were operated for the first time whereas 10 were re-operated due to relapse of the disease; 3 of these cases were primary hyperparathyroidism, 182 secondary and 5 tertiary. All three primary hyperparathyroidism cases underwent removal of the adenoma; in the group of secondary hyperparathyroidism, 50 underwent removal of all the parathyroid glands found, 25 underwent total parathyroidectomy with forearm or deltoid autograft and 60 subtotal parathyroidectomy whereas in 39 and 8 patients only 3 and 2 parathyroid glands were found respectively. In the group of tertiary hyperparathyroidism, we removed only the hyperplastic gland detected as the operative detection of the rest was not possible. Ten cases were re-operated for removal of the remaining glands. No complications were noted postoperatively, apart from severe hypocalcemia in 20 cases, treated successfully by Calcium and Vitamin D administration. The highest relapse rate was noted among the 8 patients with only the 2 parathyroid glands removed. It seems that total or subtotal parathyroidectomy represents the most successful methods for surgical treatment of hyperparathyroidism complicating chronic renal failure.

Female↗
PubMed1976

Geriatric primary hyperparathyroidism.

Primary hyperparathyroidism occurs in a significant number of patients over 60 years of age; about one-third of the 182 patients we studied were in this age group. Primary hyperparathyroidism has been recognized with greater frequency in recent years, particularly in patients without manifestations of renal lithiasis or osteitis fibrosa cystica and in older patients. Age alone is not critical in the occurrence of serious complications from hypercalcemia, the presence of other life-endangering disease, or the development of major postoperative complications in the management of primary hyperparathyroidism. A liberal but selective policy is advocated in advising operation for primary hyperparathyroidism in the elderly. Different clinical patterns of primary hyperparathyroidism are recognized in all age groups. The operative procedure for primary hyperparathyroidism is determined primarily by the surgeons at the time of operation, on the basis of gross characteristics of the parathyroid glands. A precise correlation is not found between microscopic changes, gross changes, and clinical features of primary hyperparathyroidism.

Aged↗
PubMed1998

Primary and reoperative parathyroid operations in hyperparathyroidism of multiple endocrine neoplasia type 1.

BACKGROUND: Operation and reoperation for hyperparathyroidism in multiple endocrine neoplasia type 1 (MEN 1) is controversial regarding surgical strategy, preoperative localization, and biochemical indexes of recurrence. METHODS: Fifty patients with MEN 1 with hyperparathyroidism were followed up 2 to 27 years after subtotal (SPX; n = 35) or total parathyroidectomy with forearm autografiing (TPX; n = 15), including 24 who underwent 28 reoperations because of persistent or recurrent hyperparathyroidism. RESULTS: Persistent or recurrent hyperparathyroidism was seen in 66% and 20% of patients after SPX involving extirpation of at least 3 glands and TPX, respectively, and 100% after single-gland excision as a primary procedure. After reoperation, hypercalcemia was reversed in 33% of patients by SPX and 61% by intended TPX procedures. All patients received vitamin D substitution after TPX, but restricted thyroid function allowed withdrawal in all but 10 patients (36%). Intact serum parathyroid hormone levels in nongrafted and grafted arms rose with time, but only exceptional ratios localized graft recurrence. Localization of recurrent hyperparathyroidism was achieved with 11C-labeled methionine positron emission tomography. CONCLUSION: MEN 1 hyperparathyroidism has a high risk of recurrence, and operation may include primarily SPX of at least 3 glands or TPX, although the latter includes a higher risk of long-term hypoparathyroidism. Reoperation should involve TPX with recognition of the enhanced recurrence rate in individuals with postoperative hyperparathyroidism.

Adolescent↗
PubMed2003

Tc-99m MIBI parathyroid scintigraphy and intact parathyroid hormone levels in hyperparathyroidism.

Tc-99m MIBI has been widely used to evaluate hyperparathyroidism based on increased tracer uptake in hyperfunctioning parathyroid tissue. The functional status measurement of parathyroid glands with intact parathyroid hormone (iPTH) levels is also one of the most important diagnostic studies in this disorder. The aim of the current study was to assess the relation between MIBI imaging and iPTH levels. The authors retrospectively reviewed the records of patients with hyperparathyroidism who were referred to their department for Tc-99m MIBI scintigraphy. Sixty-five patients (24 primary and 41 secondary hyperparathyroidism) were included. The iPTH levels ranged from 66.06 to 2,836 pg/ml (normal, 10 to 55 pg/ml). Forty-two patients were MIBI positive and 23 were negative. The iPTH level in the MIBI-positive group was significantly greater than in the negative group in the primary (548 +/- 478 versus 124 +/- 45; = 0.002), secondary (1,155 +/- 692 versus 501 +/- 352; < 0.001), and overall (909 +/- 678 versus 386 +/- 341; < 0.001) groups. For the primary hyperparathyroidism group, 17 of the 24 patients were MIBI positive (71%). When iPTH levels exceeded 200 pg/ml (100%), the diagnostic sensitivity reached 100%. For the secondary hyperparathyroidism group, 25 of 41 patients (61%) were MIBI positive; 24 of 38 patients (63%) had an iPTH level greater than 200 pg/ml, 21 of 27 patients (78%) had an iPTH level greater than 500 pg/ml, and 11 of 12 patients (92%) had an iPTH value greater than 1,000 pg/ml. Tc-99m MIBI parathyroid scintigraphy showed a good correlation with iPTH level for both primary and secondary hyperparathyroidism. Visualization of hyperfunctioning parathyroid glands on Tc-99m MIBI parathyroid scintigraphy was more likely with a higher serum iPTH level in a dose-dependent manner.

Adult↗
PubMed1975

Demonstration of a diurnal variation in serum parathyroid hormone in primary and secondary hyperparathyroidism.

It had been reported previously that there is a diurnal variation in serum parathyroid hormone (PTH) in normal subjects but not in patients with primary hyperparathyroidism. Studies were performed to determine whether there is a diurnal variation in serum PTH in primary or secondary hyperparathyroidism and whether the nocturnal increase in serum PTH, if present, could be prevented by induced hypercalcemia. Serum PTH and calcium were measured in five normal subjects, two patients with pseudohypoparathyroidism, and fourteen patients with primary hyperparathyroidism, twelve of whom were subsequently found to have parathyroid adenomas. In the normals, there was a mean decline in serum PTH of 0.07 ng/ml before noon and a mean increase of 0.04 ng/ml after 8 PM. In primary hyperparathyroidism there was a mean decline in serum PTH before noon of 0.11 ng/ml and a mean increase of 0.11 ng/ml after 8 PM. In both groups, the lowest mean serum calcium values were noted between midnight and 6:00 AM. Patients with pseudohypoparathyroidism showed a nocturnal increase in serum PTH. In each of two normal subjects, two patients with primary hyperparathyroidism, and two patients with pseudohypoparathyroidism, calcium, 4 mg/kg body weight per hour for 4 hours (8:00 PM to 12 midnight), produced hypercalcemia and prevented the nocturnal increase in serum PTH. We have concluded that a diurnal variation in serum PTH often occurs in both normal subjects and in patients with primary or secondary hyperparathyroidism and that nocturnal increases in serum PTH can be prevented by induced hypercalcemia.

Adult↗
PubMed1987

Clodronate in the medical management of hyperparathyroidism.

The skeletal manifestations of hyperparathyroidism are due to the stimulation of osteoclast-mediated bone resorption by high circulating concentrations of parathyroid hormone (PTH). Since diphosphonates inhibit PTH-mediated bone resorption, we assessed the effects of clodronate in 42 patients with hypercalcaemia and increased bone resorption due to primary hyperparathyroidism (20 patients), secondary hyperparathyroidism in chronic renal failure (12 patients on haemodialysis replacement therapy) and tertiary hyperparathyroidism following successful renal transplantation (10 patients). Clodronate (0.8-1.6 g daily by mouth or 300 mg given as an intravenous infusion following five consecutive dialysis treatments) significantly decreased serum calcium and biochemical indices of bone resorption in the three groups studied. In primary and tertiary hyperparathyroidism, serum calcium values remained above the upper limit of the reference range despite suppression of bone resorption due to the unopposed effect of PTH on renal tubular reabsorption of calcium. Prolonged treatment (3 months) was associated with a partial recurrence of hypercalcaemia in 8 of 12 patients with primary hyperparathyroidism despite continued effects on bone resorption, possibly due to a secondary decrease in bone formation. These studies indicate that clodronate is capable of suppressing PTH-mediated bone resorption in disorders of parathyroid secretion and may prove to be a useful adjunct in their medical management.

Administration, Oral↗
PubMed1994

Pancreatic pseudocyst resolution after parathyroidectomy for hyperparathyroidism.

Hyperparathyroidism is a rare cause of pancreatic inflammatory disease. Appropriate treatment of coexistent hyperparathyroidism and pancreatitis, especially when complicated by pseudocyst formation, is unsettled. We describe two patients with primary hyperparathyroidism who developed pancreatitis associated with multiple pseudocysts. The largest cyst in each patient was 9 and 5 cm, respectively. After correction of hyperparathyroidism and normalization of serum calcium levels by removal of a parathyroid adenoma, the pseudocysts resolved in both patients, as documented with computed tomography. We conclude that uncomplicated pancreatic pseudocysts in patients with primary hyperparathyroidism can be treated expectantly. Surgical correction of hyperparathyroidism and normalization of serum calcium levels should precede pancreatic intervention when possible, since pseudocyst resolution is likely and the risks of postoperative hypercalcemia are avoided.

Acute Disease↗
PubMed1996

Reoperation for persistent or recurrent primary hyperparathyroidism.

OBJECTIVE: To analyze the causes and outcomes of reoperation for persistent or recurrent primary hyperparathyroidism. DATA SOURCES: Medical records of 102 patients with persistent or recurrent primary hyperparathyroidism who underwent reoperation by 1 surgeon between 1985 and 1995. STUDY SELECTION: Only patients with persistent or recurrent primary hyperparathyroidism were selected; patients with secondary hyperparathyroidism, parathyroid cancer, familial hyperparathyroidism, and previous thyroid operations were omitted. DATA EXTRACTION: Performed by a single unblinded researcher. DATA SYNTHESIS: Reasons for failed parathyroid operations included tumor in ectopic position (53%), incomplete resection of multiple abnormal glands (37%), adenoma in normal position missed during previous surgery (7%), and regrowth of previously resected tumor (3%). Of the ectopic glands, 28% were paraesophageal, 26% in the mediastinum (nonthymic), 24% intrathymic, 11% intrathyroidal, 9% in the carotid sheath, and 2% in a high cervical position. Eighty-three percent of ectopic glands were accessible via cervical incision. The success rate of reoperations was 95%. One patient (1%) became permanently hypocalcemic after reoperation; 1 patient (1%) suffered permanent unilateral vocal cord paralysis. The sensitivities of preoperative localization studies were as follows: technetium Tc 99m sestamibi scan, 77%; magnetic resonance imaging, 77%; selective venous catheterization for intact parathyroid hormone, 77%; thallium-technetium scan, 68%; ultrasonography, 57%; and computed tomography, 42%. CONCLUSIONS: Repeated parathyroidectomy can be avoided in more than 95% of patients if an experienced surgeon performs bilateral cervical exploration during the initial parathyroid operation. For patients with persistent or recurrent primary hyperparathyroidism, preoperative localization studies and a focused surgical approach can result in a 95% success rate with minimum complications.

Adult↗