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PubMed1976

[Primary hyperparathyroidism. An analysis of 152 patients with special references to acute life threatening complications (acute hyperparathyroidism)].

Tthe findings of 150 patients with proven primary hyperparathyroidism are reported. The purpose of the analysis was to find differences between the various clinical manifestations of the disease. Furthermore the occurrence of acute hyperparathyroid crisis in our series as well as in the literature are described. 65.8% of the patients were females, 34.2% were males. The leading symptom in 98 patients (group I) were kidney stones and in 23 patients (group II) cystic bone disease. Both manifestations of the disease occurred in only 7 patients (group III) and no symptoms related to the kidneys or to the bones occurred in 24 patients (group IV). Because of the difference of the clinical manifestations the additional data were analyzed for each group separately and compared with each other. There was no difference in the mean serum calcium levels for all four groups, however, patients of group I were on the average younger, the duration of the disease was longer and the weight of the parathyroid adenoma was lower compared to the other three groups. Data are presented regarding calcium excretion, phosphate clearance and tubular reabsorption of phosphate for each group. At operation single or multiple adenoma formation was present in 133 patients, whereas diffuse hyperplasia was found in 17 and carcinoma in 2 other patients. 46 of the adenomas were found in atypical anatomical localisation. This observation is responsible for the many unsuccessful or second explorations of the neck. The weight of the adenomas varied between 0.1 and 23.5 g. The most difficult diagnosis was that of diffuse hyperplasia. The success of the surgical intervention was usually established in over 80% of the cases within 24 to 48 hours after the operation with a significant fall of serum calcium. There is still no definite explanation for the variability of the clinical manifestations of primary hyperparathyroidism. Parathyroid hormone determinations on larger numbers of patients are not yet published. The assumption, that different hormones or peptide fragments are responsible for the different action on bone and kidney is discussed. In our series of 152 patients acute hyperparathyroid crisis occurred eight times. Our findings are compared to the other well documented cases in the literature. Main symptoms were nausea, vomiting abdominal pain and different states of cerebral dysfunction. Most of the patients had calcium levels over 16 mg/100 ml. Partial renal insufficiency with elevated blood urea and phosphate retention was found in ov er 50% of the cases. Overall mortality of all cases with acute parathyroid crisis is 52.5%. The pathogenesis of acute hyperparathyroidism and the implications of high calcium levels are discussed. According to our own experience hypercalcemia can be controlled with an intensive therapeutic program and emergency operation for acute parathyroid crisis is no longer necessary.

Acute Disease↗

PubMed1992

[Hypercalciuria and primary hyperparathyroidism in patients with kidney calculi. II. Primary hyperparathyroidism].

Among 1819 patients with renal stone disease 44 cases with primary hyperparathyroidism (p.h.p.) were diagnosed. In all cases the diagnosis of php was confirmed by histomorphological examination. In 34 patients with php solitary adenoma was found, in 5 patients an adenoma with concomitant hyperplasia of the parathyroid glands, in 2 patients hyperplasia and in 3 patients carcinoma of the parathyroid glands. Hypercalcemia was found in 86% of patients, while elevated plasma levels of PTH in 90% of patients with php. Not in all patients PTH secretion was entirely autonomous. No significant correlation was found between plasma levels of PTH and kind of pathology of the parathyroid glands as well as clinical feature of php respectively.

Adult↗

PubMed1979

Renal function in primary hyperparathyroidism and in non-hyperparathyroid hypercalcemia.

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Adult↗

PubMed1978

Primary hyperparathyroidism with multiple parathyroid gland enlargement: review of 53 cases.

Of 53 patients who had hyperparathyroidism assocated with multiple parathyroid gland enlargement, 39 (74%) had primary hyperparathyroidism without clinical or laboratory evidence of associated endocrine gland dysfunction, 2 had documented familial primary hyperparathyroidism, and 12 had hyperparathyroidism as part of the multiple endocrine neoplasia syndrome. When last studied, 31 of the 39 patients with nonfamilial hyperparathyroidism had normal serum calcium levels, 3 had permanent hypoparathyroidism, 2 had recurrent hyperparathyroidism, and 3 were lost to follow-up. The two patients with familial hyperparathyroidism were treated by removal only of enlarged parathyroid glands, and in each, hyperparathyroidism recurred. Five patients with multiple endocrine neoplasia, type 1, were treated by removal only of enlarged parathyroid glands, and hyperparathyroidism recurred in four. Four patients with multiple endocrine neoplasia, type 1, were treated by removal of three or more parathyroid glands, and there were no instances of recurrent hyperparathyroidism. In one patient, permanent hypoparathyroidism developed. Three patients with multiple endocrine neoplasia syndrome, type 2, had total parathyroidectomies as a part of thyroidectomy for medullary thyroid carcinoma. In each patient, permanent hypoparathyroidism developed. When primary hyperparathyroidism occurs in the absence of a definite history of polyendocrine or familial disease, only the glands that are definitely enlarged should be removed, and normal-appearing glands should be tagged rather than risk the possibility of permanent hypoparathyroidism that may attend routine subtotal parathyroid gland excision.

Adolescent↗

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↗

PubMed1991

Stimulation and suppression of intact parathyroid hormone (PTH1-84) in normal subjects and hyperparathyroid patients.

OBJECTIVE: Because of an overlap between serum PTH values in healthy controls and hyperparathyroid patients we sought to evaluate a short stimulation and suppression test for differentiating the two groups. SUBJECTS: Subjects were 34 patients with primary hyperparathyroidism (PHPT) and 25 healthy controls. DESIGN: After stimulation with intravenous EDTA (10 mg/kg body weight in 5 minutes) blood samples were obtained for up to 15 minutes. After an oral calcium dose of 1 g, blood samples were obtained at 1 and 2 hours. After an intravenous calcium dose (2.5 mg/kg body weight in 30 seconds), blood samples were obtained serially for 20 minutes. MEASUREMENT: Serum PTH(1-84) was measured by a double antibody technique. RESULTS: The intravenous EDTA test resulted in an average 2.6-fold increase of serum PTH(1-84) in hyperparathyroid patients, whereas it increased 10.5-fold in controls. A response was absent in three of 23 patients. There was an overlap in results between patients with mild hyperparathyroidism and controls. The oral calcium dose decreased serum PTH(1-84) in patients to 0.73 and in controls to 0.55 of the basal value, but six of 15 patients and two of 12 controls did not respond. The intravenous calcium test resulted in a drop of serum PTH(1-84) in hyperparathyroid patients to 0.51 and in control subjects to 0.40 of the basal value, and non-responders were not observed. There was a strong correlation between the responses to the EDTA and the calcium infusion tests in the patients (r = 0.97, P less than 0.01). Fasting serum calcium and serum PTH(1-84) showed a positive correlation in PHPT patients (r = 0.75, P less than 0.001) and a negative correlation in control subjects (r = -0.41, P less than 0.05). Based on these relationships, hyperparathyroid patients and controls could be completely separated. CONCLUSION: The wide range of responses to stimulation and suppression tests and the correlation between these responses in hyperparathyroid patients indicate various degrees of autonomy. As the response to these tests is less marked in patients than in controls and both groups still overlap, these tests are not useful for the diagnosis of primary hyperparathyroidism.

Adolescent↗

PubMed1978

[Hyperparathyroidism].

The overproduction of parathyroid hormone as caused by a simple hyperplasia or an adenoma leads to pathological changes in various organs which are termed primary hyperparathyroidism. The blood phosphates increase in case of long-standing disturbances of the metabolism, e.g. chronic renal insufficiency. In this way and due to other causes, the production of parathyroid hormone is increased. The resultant clinical picture is termed secondary hyperparathyroidism. Both forms are associated with osseous changes also in the maxillofacial skeleton. Tertiary hyperparathyroidism may develop from secondary hyperparathyroidism if the metabolic disorder in the renal form cannot be eliminated by kidney transplantation and if the process in the parathyroid becomes independent (autonomous hyperparathyroidism). Besides these three forms, there are two others, quaternary hyperparathyroidism and quinary hyperparathyroidism, which are described.

Bone Diseases↗

PubMed1991

Immunoassays for parathyroid hormone 1-84 in the diagnosis of hyperparathyroidism.

The two most frequent causes for hypercalcemia are primary hyperparathyroidism and hypercalcemia associated with malignancy. Elevated or inappropriately high PTH serum levels are the hallmark of hyperparathyroidism. Sensitive immunometric assays for the secreted, biologically active, intact parathyroid hormone molecule, PTH-(1-84), employ two populations of region-specific antibodies, take advantage of saturation kinetics rather than competitive binding, and have many technical advantages over conventional radioimmunoassay. Approximately 90% of patients with primary hyperparathyroidism have elevated serum levels of PTH-(1-84) by immunometric assay; the remainder have inappropriately elevated values of PTH for the serum calcium concentration. Clinical correlation studies comparing measurements of PTH using antisera that recognize the carboxyl, midregion, or amino terminus of PTH with PTH levels determined by immunometric assays demonstrate elevated values in equivalent numbers of hyperparathyroid individuals. Immunometric assays for PTH-(1-84) have their greatest value in separating patients with hyperparathyroidism from those with hypercalcemia of malignancy. In earlier studies using region-specific antisera, there was virtually always an overlap of serum PTH levels in hyperparathyroidism and hypercalcemia associated with malignancy. In contrast, analysis of results using PTH-(1-84) immunometric assays in several hundred reported patients shows a complete separation of PTH values. Clinical judgment, combined with measurement of PTH in the setting of hypercalcemia, can lead to the diagnosis of hyperparathyroidism with confidence in essentially all patients.

Antibodies↗

PubMed1991

Longitudinal changes in forearm bone mineral content in primary hyperparathyroidism.

Forearm bone mineral content was measured in 28 patients with primary hyperparathyroidism before and 1 year after successful parathyroidectomy. The forearm bone mineral content rose from a mean value of 1.068 to 1.092 g/cm (P less than 0.05, paired t-test). Those patients with the lower initial values had the largest rise. In an additional study, the forearm bone mineral content was measured in 10 women over the age of 40 years (mean age 58.6 +/- 7.9SD years) with hyperparathyroidism before and for 2 years after successful parathyroidectomy and compared with the forearm bone mineral content measured over 2 years in 12 women (mean age 56.3 +/- 5.5SD years) with continuing hyperparathyroidism and with the forearm bone mineral content of 12 eucalcemic control women (mean age 58.8 +/- 8.2SD years), also measured over 2 years. The parathyroidectomized group gained bone, whereas the ongoing hyperparathyroid group and the eucalcemic control group lost bone. The difference between the parathyroidectomized group and the ongoing hyperparathyroid group was significant after 2 years (P less than 0.05). The percentage loss of forearm bone mineral in the eucalcemic control subjects was not significantly different from the percentage loss of forearm bone mineral in the ongoing hyperparathyroid group, although the initial mean bone mineral content in the eucalcemic group was significantly higher than in the ongoing hyperparathyroid group, suggesting that a possible determinant of bone mineral loss in women in this age group is the initial bone mineral content.

Adult↗

PubMed1991

Diagnosis and management of asymptomatic hyperparathyroidism: safety, efficacy, and deficiencies in our knowledge.

Several recent articles question whether patients with asymptomatic hyperparathyroidism and minimal hypercalcemia should be treated by parathyroidectomy. We therefore reviewed our experience in 103 consecutive patients with primary hyperparathyroidism who were treated by parathyroidectomy to determine, first, how many of these patients had asymptomatic or symptomatic hyperparathyroidism, and second, did these patients benefit from parathyroidectomy? We also analyzed the safety of parathyroidectomy in 426 consecutive patients, including 79 who required reoperation for hyperparathyroidism, specifically looking for complications and the outcome of these procedures. Our study documents the following: (1) only 2 of 103 (2%) patients referred for parathyroidectomy had "true" asymptomatic hyperparathyroidism; (2) only symptoms of fatigue, bone pain, and weight loss correlated with the degree of hypercalcemia, whereas muscular weakness, psychiatric symptoms, nocturia, polyuria, recent memory loss, constipation, and nephrolithiasis did not; (3) only 1 of 15 patients who were referred as asymptomatic were truly asymptomatic after more thorough questioning, and all 14 improved following parathyroidectomy; (4) 81% of the patients who were referred with symptoms improved following parathyroidectomy; and (5) permanent complications occurred in only 4 patients. All but 1 had reoperations for persistent or recurrent hyperparathyroidism (3 vocal cord paralyses and 1 hypoparathyroidism requiring autotransplantation of cryopreserved parathyroid tissue). There was 1 death of an 84-year-old woman with hypercalcemic crisis. Thus, most patients with hyperparathyroidism are symptomatic and benefit symptomatically and metabolically from parathyroidectomy, which is a safe operation.

Female↗

PubMed1978

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.

Animals↗

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↗

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↗

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.

Calcium↗

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↗

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↗