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PubMed1977

Metabolic effects of diphosphonate in primary hyperparathyroidism.

Six patients with primary hyperparathyroidism (PHPT) and one with squamous cell carcinoma of the esophagus with parathyroid hormone excess received disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP) at a daily dose of 20 mg/kg orally. During treatment, the decrease in urinary calcium, total urinary hydroxyproline, and fasting urinary calcium suggested an inhibition of bone resorption. Serum calcium intestinal absorption of calcium and urinary cyclic adenosine monophosphate (cAMP) did not change significantly. This preliminary study indicates a possible role of diphosphonates in the management of inoperable cases of primary hyperparathyroidism or pseudohyperparathyroidism.

Adult↗

PubMed1978

Primary hyperparathyroidism and peptic ulcer disease.

To determine whether primary hyperparathyroidism is related to peptic ulcer disease, we evaluated 46 cases of concomitant primary hyperparathyroidism and peptic ulcer disease. Among these patients, there was no sex preponderance. The pathologic findings at parathyroid surgery, as well as the features of peptic ulcer disease, were the same as in patients with primary hyperparathyroidism or with peptic ulcer disease alone. The ulcer symptoms of 58% of the patients with adequate follow up improved after parathyroidectomy. Sixty-six percent of the patients who had active peptic ulcer disease at surgery improved as compared with only 44% of the patients who had complicated peptic ulcer disease. None of the factors studied (age, sex, serum calcium and serum parathyroid hormone levels, location, and duration of ulcer) had any effect on the peptic ulcer symptoms after parathyroidectomy. Our results and a critical review of the experimental and clinical literature suggest that the association between primary hyperparathyroidism and peptic ulcer disease is no more than coincidental.

Follow-Up Studies↗

PubMed1977

[A case of primary hyperparathyroidism sustained by parathyroid adenocarcinomatosis].

Primary hyperparathyroidism may at times be associated with carcinoma of the parathyroids. A personal case of primary hyperparathyroidism was operated on by total thyro-parathyroidectomy. The histological picture presented atypical cell patterns and infiltrations of the thyroid capsule, together with adenomatuous parathyroid formations suggesting the possibility of a malignant transformation of initially benign process. Given the benign clinical course, it is possible that when subjected to radical, timely measures, even atypical parathyroid processes may be cured completely.

Adenocarcinoma↗

PubMed2026

10-year cardiovascular disease risk and its contributing factors in primary hyperparathyroidism.

OBJECTIVE: Surgery indications for primary hyperparathyroidism (PHPT) mostly concern kidney and bone outcome, but not cardiovascular disease (CVD). Age less than 50 and eGFR less than 60 ml/min/1.73m2 are two surgery indications. This study aims to evaluate factors influencing the 10-year CVD risk in PHPT patients. METHOD: 159 PHPT patients diagnosed between January 2024 - March 2025 were enrolled. The relationships between biochemical and echocardiographic parameters with 10-year CVD risk score calculated by PREVENT™ were analyzed. Univariate, multivariate, logistic regression and receive operation curve (ROC) analysis were employed. RESULTS: 10-year CVD risk score was positively corelated with age (R2adjusted = 0.604, β = 0.541), systolic blood pressure (R2adjusted =0.149, β = 0.185), eGFR (R2adjusted =0.452, β=-0.252), triglyceride (R2adjusted =0.134, β = 3.629) with P < 0.001.These parameters together with smoking, diabetes and left ventricular end-diastolic diameter were responsible for 10-year CVD risk (R2adjusted =0.849, P < 0.001). Age and eGFR were the two strongest factors to discriminate moderate-to-high risk and low risk, with area under the curve 0.935 (95%CI 0.896–0.974) and 0.827 (95%CI 0.763–0.891), respectively. The optimal cutoffs to identify moderate-to-high CVD risk were age at 56.5 and eGFR at 98.5 ml/min/1.73m2, PHPT patients older or lower than these two thresholds had significantly higher CVD risk than their counterparts (P < 0.001). CONCLUSION: Age and eGFR were significant contributors to CVD risk in PHPT. Patients should be closely monitored and managed for dysregulated gluco-lipid metabolism. Less restrictive surgery indication for PHPT, such as age < 56, irrespective of renal function might be considered.

Humans↗

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↗

PubMed1977

Primary hyperparathyroidism and benign monoclonal gammopathy.

Three patients had primary hyperparathyroidism and monoclonal serum immunoglobulins. Although multiple myeloma was suspected in each case, subsequent evaluation was consistent with a "benign monoclonal gammopathy". Parathyroid adenomas were removed from two patients. The three patients are presented and compared to the four other cases that have been reported previously. The association between primary hyperparathyroidism and benign monoclonal gammopathy is discussed in terms of possible pathogenetic mechanisms. Primary hyperparathyroidism should be suspected in patients with hypercalcemia and benigh monoclonal gammopathy, as well as in other conditions, like multiple myeloma, that are known to be associated with hypercalcemia.

Adenoma↗

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↗

PubMed1977

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

Calcium↗

PubMed1979

Value of selective parathormone radioimmunoassay in primary hyperparathyroidism.

Nine cases of primary hyperparathyroidism (PHP) in patients with urinary calculi are reported and discussed. Selective venous catheterization and parathormone (PTH) radioimmunoassay confirmed the diagnosis in all cases, preoperatively discriminated between adenoma and diffuse parathyroid hyperplasia, and permitted exact preoperative localization of 5 of 7 adenomas. The interest of the urologist in PHP and the usefulness of selective PTH radioimmunoassay are discussed and emphasized.

Adenoma↗

PubMed1977

Primary hyperparathyroidism exacerbated by pregnancy.

Primary hyperparathyroidism may remain subclinical as long as there is adequate calcium in the diet. If the demand for calcium increases, as in pregnancy, the symptoms become evident. Any giant cell growths should alert the oral surgeon to the possibility of hyperparathyroidism. Untreated, hyperparathyroidism ultimately leads to fractures, irreversible kidney damage, and death by renal failure. Tetany must be guarded against after parathyroid surgery. Finally, the brown tumors of hyperparathyroidism need not be removed surgically since bone will regenerate if the disease is correctly treated by removal of the parathyroid adenoma.

Adenoma↗

PubMed1977

[Correlation of parathormone determination and bone biopsy in primary hyperparathyroidism].

Eleven patients with primary hyperparathyroidism confirmed by histologic examination were subjected to a comparative study of the results of quantitative determination of parathormone and of quantitative bone biopsy. Quantitative radioimmunologic determination of parathormone was carried out with the aid of an N-terminal specific anti serum, while the histologic features studied were the periosteocytic and osteoclastic absorption surfaces. On the basis of a combination of the results of these two techniques, the diagnosis could be made in all the cases studied. A statistically significant correlation was observed between the results of quantitative determination of parathormone and those of histologic examination of the surfaces of periosteocytic lacunae (r = 0.63; p = 0.05).

Bone and Bones↗

PubMed1979

Calcitonin secretion in primary hyperparathyroidism.

Plasma calcitonin (CT) was studied by RIA in 55 patients with surgically proven primary hyperparathyroidism. Basal hormone measurements were performed in all patients and provocative tests of CT secretion were performed in 7. Biochemical measurements were also made before and after parathyroidectomy in 34 patients. Plasma CT was significantly increased above normal in the male but not the female group of patients with primary hyperparathyroidism. A similar sex difference in plasma CT was also seen during provocative testing. In contrast to normal subjects, plasma CT was also significantly correlated to serum calcium concentration in the males but not the females. Hormone concentrations returned to normal after parathyroidectomy in the males and did not significantly change in the females. These studies demonstrate that some patients with primary hyperparathyroidism, especially males, may have an increase, perhaps compensatory, in plasma CT. As with normal females, females with primary hyperparathyroidism seem to have decreased CT reserve.

Adenoma↗

PubMed1978

Primary hyperparathyroidism and stone formation in medullary sponge kidneys.

The etiological role of primary hyperparathyroidism in stone formation in medullary sponge kidney was studied. The necessity of carrying out special biochemical tests for primary hyperparathyroidism has been shown. The combination of two diseases in cases of stones and nephrocalcinosis is explained by the genetic nature of sponge kidney and primary hyperparathyroidism. 4 patients have been under observation; all underwent successful parathyroidectomy.

Adult↗

PubMed1979

[Peptic ulcer disease and primary hyperparathyroidism (author's transl)].

The causal relationship of primary hyperparathyroidism and ulcer disease is reviewed. In contrast to earlier ideas careful clinical and clinico-chemical investigations have shown that in patients with manifest primary hyperparathyroidism neither is the incidence of ulcer disease raised nor are deviations from the normal behavior of acid secretion or the serum gastrin level to be observed in comparison with the average population.

Calcium↗

PubMed1977

Serum lipids before and after parathyroidectomy in patients with primary hyperparathyroidism.

Eight males and 36 females with hypercalcaemia were operated upon for primary hyperparathyroidism and parathyroid adenomata were revealed in every case. The serum levels of cholesterol and triglycerides were determined before the operations and 6,12 and 18 months after them. Furthermore, the serum lipids of the patients were compared with those of a normacalcaemic sex- and age-matched control group. The serum cholesterol concentration in primary hyperparathyroidism was about 8-10% lower in both females and males compared with the correspondeing control cases and the levels of serum trigycerides were about 22% and 60% lower. After operation the serum cholesterol concentration returned to a normal level and the triglycerides nomalized. The results are discussed in the light of present knowledge about dietary calcium intake, primary hyperparathyroidism and lipid metabolism.

Adenoma↗

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↗

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↗

PubMed1975

Back pain and vertebral crush fractures: an unemphasized mode of presentation for primary hyperparathyroidism.

During a 3-year period, 14 of 319 patients (4.4%) with surgically proved primary hyperparathyroidism had spinal rarefaction with vertebral crush fractures but no unequivocal roentgenographic evidence of osteitis fibrosa generalisata. All complained of back pain, and this was the presenting complaint in 9 of the 14 patients. This incidence was significantly higher (P less than 0.001 for women; P less than than 0.01 for men) than the incidence of similar roentgenographic findings among patients of the same age undergoing operation for protruded intervertebral disks during this same time period. Although tradition equates roentgenographically evident bone disease in primary hyperparathyroidism with the classis findings of osteitis fibrosa generalisata, our observations emphasize that patients with primary hyperparathyroidism occasionally may present in a manner that is indistinguishable symptomatically and roentgenographically from that of postmenopausal or senile osteoporosis.

Age Factors↗