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PubMed2006

Current pharmacological options for the management of primary hyperparathyroidism.

Drugs for treating primary hyperparathyroidism can be divided into two main groups: (i) antiresorptive drugs that inhibit the increased bone turnover, which can be divided into estrogen-like compounds (estrogen, oral contraceptives and selective estrogen receptor modulators [SERMs]), bisphosphonates and calcitonin; and (ii) drugs that interfere with parathyroid hormone (PTH) secretion (currently only cinacalcet is available). No drugs that interfere with PTH action are currently available. Available studies suggest that all classes of drugs are able to lower serum calcium levels. However, calcitonin does so only temporarily. Estrogen-containing compounds (hormone replacement therapy) may be less attractive because of the potential risk of breast cancer, cardiovascular disease and deep vein thromboembolism. Oral contraceptives have not been shown to be able to prevent fractures in the general population, and no data are available on their effect in women with primary hyperparathyroidism. The only SERM marketed for hyperparathyroidism is raloxifene and this has not been associated with an increased risk of breast cancer and cardiovascular diseases, and has been shown to be able to prevent vertebral fractures in postmenopausal women with osteoporosis. Two small trials suggest that raloxifene may increase bone mineral density (BMD) and decrease serum calcium levels in patients with primary hyperparathyroidism. Bisphosphonates have been shown to decrease serum calcium and increase BMD in patients with primary hyperparathyroidism, but PTH levels may increase. Cinacalcet effectively induces a sustained decrease in serum calcium and PTH for up to 1 year. However, BMD does not seem to increase. No data on hard endpoints such as fractures, kidney stones, cardiovascular disease etc. are available for any of the drugs available for the treatment of primary hyperparathyroidism.

Bone Density↗
PubMed2005

[Surgical treatment of primary hyperparathyroidism in pregnancy].

Primary hyperparathyroidism during pregnancy is a pathological entity with an unknown incidence that presents certain physiological, therapeutic and prognostic characteristics leading to greater difficulty in diagnosis and a high risk of complications. We present the case of a 16-week pregnant woman who presented with asymptomatic hypercalcemia secondary to a solitary parathyroid adenoma. Since conservative measures produced no improvement, surgery was performed in the second trimester of pregnancy, with satisfactory pre- and postnatal results. Surgery in the second trimester constitutes a safe alternative to conservative treatment.

Adult↗
PubMed2006

Biochemical markers of endothelial activation in primary hyperparathyroidism.

Patients with primary hyperparathyroidism (PHPT) have impaired vasodilation both dependent and independent of endothelium. The aims of our study were to measure three different biochemical markers of endothelial activation, i. e., plasma thrombomodulin, soluble(s) E-selectin, and von Willebrand factor, in PHPT patients before and one year after successful parathyroidectomy, and to distinguish the potential effect of hypercalcemia and/or high parathyroid hormone from that of major cardiovascular risk factors (diabetes mellitus, hyperlipidemia, hypertension, obesity, smoking habit) on endothelial function. Twenty consecutive patients with PHPT subdivided into two groups according to the absence (n = 8) or presence (n = 12) of one or more risk factors, and fifteen healthy normocalcemic subjects were studied. Baseline thrombomodulin levels were similar in the groups with and without risk factors, and in controls. In contrast, sE-selectin and von Willebrand factor were higher in PHPT patients with risk factors than in those without risk factors (p < 0.05 and p < 0.01, respectively) and controls (p < 0.01). Neither thrombomodulin nor sE-selectin changed after parathyroidectomy in either PHPT group. Plasma von Willebrand factor decreased (p < 0.01) in patients without risk factors, while persisting at high levels in patients with risk factors. In conclusion, in spite of a limitation due to the small number of patients, our study suggests that classic cardiovascular risk factors seem to be the main determinants for the high plasma levels of sE-selectin and vWF in PHPT. Together with unaltered thrombomodulin and sE-selectin levels, a plasma vWF decrease after parathyroidectomy might reflect a specific mechanism of its endothelial calcium- and/or PTH-stimulated secretion in some PHPT patients without risk factors. Whether a vWF reduction after parathyroidectomy may be used as a biochemical index for improved endothelial function in PHPT patients without risk factors has yet to be demonstrated in larger studies.

Biomarkers↗
PubMed2006

The usefulness of bone metabolic indices for the prediction of changes in bone mineral density after parathyroidectomy in patients with primary hyperparathyroidism.

Patients with primary hyperparathyroidism (pHPT) have reduced bone mineral density (BMD). Although pHPT causes high bone turnover, the exact metabolic bone markers useful for predicting changes in BMD after parathyroidectomy (PTX) remain elusive. The present study was performed to examine the relationship between bone metabolic indices and BMD changes after PTX in 29 pHPT Japanese patients, which received PTX successfully. BMD values were measured by dual-energy X-ray absorptiometry in the lumbar spine and distal one third of radius. As for bone metabolic indices, serum bone-type alkaline phosphates (BAP), serum osteocalcin (OCN), urinary deoxypiridinoline (Dpd), and urinary type I collagen cross-linked N-telopeptides (NTX) were measured. The study included 10 male and 19 female patients (17 postmenopausal). Urinary Dpd, but not NTX was significantly correlated with serum BAP and OCN. Either bone formation or bone resorption indices were significantly and highly correlated with Z-score of BMD in the radius, but not at lumbar spine. Urinary Dpd was significantly correlated with BMD changes at both lumbar spine and radius and at all time points over the two years after PTX. These correlations were most potent among bone metabolic indices in this study. The measurement of urinary Dpd would be useful for predicting long-term changes in BMD at radial and lumbar spine after PTX than other bone metabolic indices.

Bone Density↗
PubMed2005

[Peri-operative management of the primary hyperparathyroidism].

Surgery for primary hyperparathyroidism has become one of the least invasive and safe procedures with the recent advances in the diagnosis and surgical technique. However, it is still difficult to prospect detailed post-operative conditions of the patient from the data of pre-operative examination. Because many factors related each other to make the preoperative conditions complicated. Thus, integrated interpretation of the patient is necessary before surgery, including general condition, coincidental disease, renal function, bone mineral density and its turnover, size and location of the lesion. Prevention and proper management of postoperative complications, such as hemorrhage, hypocalcemia, hoarseness and bone disease, is important for successful treatment of the disease.

Humans↗
PubMed2005

[Hypercalcemic crisis associated with primary hyperparathyroidism during pregnancy].

Primary hyperparathyroidism is a rare occurrence in pregnancy with significant risks to the mother and the foetus, witch is related to the level of serum calcium. A 41-year-old women, gravida 2, para 1, presented at 22 weeks gestation with nausea, vomiting and mild cognitive dysfunction associated with hypercalcemic crisis. The hypercalcemia was observed to be related to parathyroid hyperplasia that was surgically removed. Complete resolution of her symptomatology and hypercalcemia occurred postoperatively. The pregnancy was complicated with transient hypertension. A small for gestational age healthy male infant was delivered at term with no neonatal complications related with this pathology.

Adenoma↗
PubMed1998

Osteomalacia secondary to celiac disease, primary hyperparathyroidism, and Graves' disease.

Primary hyperparathyroidism is seldom associated with other autoimmune disorders. The presence of normocalcemia in primary hyperparathyroidism should prompt the physician to look for vitamin D deficiency. This observation concerns a 34-year-old vegetarian woman with combined primary hyperparathyroidism, Graves' disease, and celiac disease. The patient presented with severe bone deformities; she was unable to walk, and had severe muscular weakness and weight loss. Biochemical findings revealed severe hyperparathyroidism with normocalcemia, hypophosphatemia, very low urinary calcium, and low 25-hydroxy vitamin D level. Thyroid tests showed hyperthyroidism with positive thyroid receptor antibodies, confirming the presence of Graves' disease. Positive antigliadin and antireticulin antibodies and complete villous atrophy on duodenal biopsy established the presence of celiac disease. The patient underwent a near-total thyroidectomy, with the removal of a parathyroid adenoma. To our knowledge, this observation is the first finding of an association between celiac disease, Graves' disease, and primary hyperparathyroidism. It emphasizes the need to rule out intestinal malabsorption in the case of normocalcemic hyperparathyroidism.

Adenoma↗
PubMed1982

Primary hyperparathyroidism in children.

Primary hyperparathyroidism is rare in children. This report describes a 15-year-old boy who had an intrathymic chief cell adenoma. The literature related to this condition in neonates and children is reviewed. Neonatal hyperparathyroidism differs from hyperparathyroidism in children. The severity of symptoms and osseous lesions, genetic inheritance in many, pathological changes in the parathyroid glands and the need for more extensive treatment in neonates and infants indicate that primary hyperparathyroidism in these patients should be considered as a different entity from that occurring in older children.

Adenoma↗
PubMed1990

Intact parathyroid hormone in primary hyperparathyroidism.

In 49 patients with primary hyperparathyroidism, intact parathyroid hormone (PTH) was measured with a recently developed immunoradiometric assay, and midregional PTH fragments (sequence 44-68) were measured with an established radioimmunoassay technique. In 47 normal subjects, the concentration of intact PTH ranged from 2.0 to 6.8 pmol/l, and in 49 patients with primary hyperparathyroidism it ranged from 6.4 to 80.0 pmol/l. In contrast, midregional PTH fragments were normal in seven of 49 patients with primary hyperparathyroidism. In five healthy controls and in 12 patients with surgically confirmed primary hyperparathyroidism and serum calcium levels below 3.0 mmol/l, a rapid calcium loading test was performed. In healthy controls, intact PTH was in the low normal to subnormal range within 2.5-5.0 min, and had recovered within 15 min of calcium infusion. In patients with primary hyperparathyroidism, the calcium infusion also led to a 30-50 per cent decrease in intact PTH levels within 5.0-7.5 min after injection, with a slow recovery after 10-15 min. In six of the patients with only slightly elevated basal intact PTH, a suppression to the normal range was observed. In 24 patients (16 patients with a solitary adenoma and eight patients with four-gland hyperplasia) the intact PTH levels were followed intraoperatively during parathyroidectomy, revealing a significantly different rate of decline for single adenomas compared with hyperplasia during the first 15 min after removal of the primary enlarged gland. Intact PTH values remained constantly elevated in one patient with primary hyperparathyroidism and an unsuccessful neck exploration. These results confirm that (a) the measurement of intact PTH in patients with primary hyperparathyroidism is superior to the measurement of midregional fragments; (b) PTH secretion in primary hyperparathyroidism is not totally autonomous; and (c) intraoperative monitoring of intact PTH values could be used to monitor the success of surgery.

Adenoma↗
PubMed2004

Primary hyperparathyroidism in pregnancy.

Primary hyperparathyroidism during pregnancy carries significant risks to both mother and fetus. Parathyroidectomy remains the only definitive treatment for the condition. The timing of surgery remains controversial, with ongoing debate regarding the safety of surgery during the third trimester. A case of symptomatic primary hyperparathyroidism treated by parathyroidectomy in the third trimester is described. The clinical features, investigations and treatment options are discussed.

Adult↗
PubMed1994

Familial isolated primary hyperparathyroidism.

UNLABELLED: Familial primary hyperparathyroidism (PHPT) is usually encountered in the context of multiple endocrine neoplasia (MEN) syndromes. Few families have been reported in the literature where PHPT was the only abnormality. However, in these families no long-term follow-up data were reported and no genetic linkage studies were performed. OBJECTIVE: We investigated a large family with a familial primary hyperparathyroidism for biochemical and genetic markers of multiple endocrine neoplasia syndromes. DESIGN: A family screening study. PATIENTS: Thirty-seven family members participated in this study including 7 patients who had been previously operated upon for PHPT. MEASUREMENTS: Serum calcium (albumin adjusted), was measured in all family members. Hypercalcaemic subjects and patients who had been operated upon for PHPT were assessed for biochemical markers of MEN syndromes (serum gastrin, prolactin, calcitonin, fasting plasma glucose and 24-hours urinary excretion of adrenaline, noradrenaline and vanillylmandelic acid (VMA)). Genetic linkage analysis was performed using DNA markers linked to chromosome 11q13, the presumed MEN type 1 (MEN-1) locus. RESULTS: Four new patients with PHPT and two with probable PHPT were discovered. No clinical or biochemical evidence of MEN syndromes could be detected. DNA marker pMS51(D11S97) was informative, maximum two-point lodscore of 2.12 at a recombination fraction of 0.05 confirming linkage to chromosome 11q13. CONCLUSIONS: Familial PHPT can exist as a separate clinical entity. Isolated familial PHPT is caused by mutation in a gene located in the MEN-1 region on chromosome 11q13, possibly the MEN-1 locus.

Adult↗
PubMed1984

Primary hyperparathyroidism during pregnancy.

Primary hyperparathyroidism during pregnancy is associated with significant risk of fetal loss and neonatal and maternal morbidity. Neonatal hypocalcemia probably results from transient hypoparathyroidism consequent to abnormal suppression by fetal hypercalcemia. Loss of the protective effect provided by the placental calcium transport mechanism produces significant maternal risk for development of acute hypercalcemia and possible crisis immediately postpartum. Management of maternal primary hyperparathyroidism diagnosed during pregnancy should be based on the patient's symptoms, severity of the disease, and gestational age of the fetus. Patients without symptoms and those with mild hypercalcemia may be managed effectively and safely for a short time with oral phosphate therapy, postponing operation until after delivery. More severe disease characterized by progressive symptoms and inadequately controlled hypercalcemia should be treated surgically after control of hypercalcemia has been achieved with diuretic and/or other medical therapy. Maternal operative morbidity is low and risk to the fetus is slight once organogenesis has been completed. Maternal parathyroidectomy should be performed preferably after the first trimester and should not be deferred unless delivery is imminent.

Adult↗
PubMed1993

Prospective comparison of technetium-99m-sestamibi/iodine-123 radionuclide scan versus high-resolution ultrasonography for the preoperative localization of abnormal parathyroid glands in patients with previously unoperated primary hyperparathyroidism.

Surgery for primary hyperparathyroidism is successful in 95% of patients, but ectopic glands and anatomic variations in location are causes of surgical failure. The radionuclide imaging agent, technetium (Tc)-99m-sestamibi, in conjunction with subtraction iodine-123 scanning, is a new method of preoperative localization of abnormal parathyroid glands. In a study approved by the Institutional Review Board, 22 patients with primary hyperparathyroidism underwent preoperative evaluation with high-resolution ultrasonography and Tc-99m-sestamibi/I-123 radionuclide scanning for attempted localization of abnormal parathyroid glands. Results of Tc-99m-sestamibi scanning and ultrasound were correlated with surgical and pathologic findings. Of 22 patients, 16 had a solitary parathyroid adenoma, 1 had a double adenoma, and 5 had diffuse parathyroid hyperplasia. The Tc-99m-sestamibi/I-123 radionuclide scan preoperatively identified a solitary adenoma in 14 of 16 patients (sensitivity: 88%). However, when the data were analyzed retrospectively along with surgical and pathologic findings, the Tc-99m-sestamibi scan correctly localized all parathyroid adenomas for a sensitivity of 100%. The one patient with a double adenoma had a localization image consistent with two enlarged glands. All patients with diffuse parathyroid hyperplasia had Tc-99m-sestamibi imaging consistent with diffuse hyperplasia, although delineation of individual enlarged glands was not possible. High-resolution ultrasound identified 11 of 16 parathyroid adenomas (sensitivity: 69%). The patient with a double adenoma had a negative ultrasound. Ultrasound was less accurate in five patients with diffuse hyperplasia: one scan was completely negative, two scans revealed only one enlarged gland, and two scans revealed two enlarged glands. The Tc-99m-sestamibi/I-123 subtraction radionuclide scan is more sensitive than high-resolution ultrasonography for the preoperative localization of abnormal parathyroid glands. Tc-99m-sestamibi/I-123 radionuclide scanning may be more useful than ultrasonography to the surgeon in the preoperative localization of abnormal parathyroid glands.

Adenoma↗
PubMed2001

Primary hyperparathyroidism.

Treatment of primary hyperparathyroidism depends on a clear diagnosis based on biochemical confirmation. Most patients have an elevated serum total or ionized calcium level in association with an elevated or inappropriate serum intact parathyroid hormone level. The serum calcium level can be lowered by hydration and by a variety of pharmacologic agents. However, none of these agents is effective in the long-term management of primary hyperparathyroidism. The extraordinarily high success rate of surgery, combined with its low morbidity and the ever-increasing acceptance of minimally invasive techniques, makes surgical resection the recommended treatment for virtually all patients.

Adenocarcinoma↗
PubMed1997

[Association between Paget's disease and primary hyperparathyroidism].

Association between primary hyperparathyroidism and Paget's disease of bone is extremely uncommon, despite the relatively high incidence of both entities. The mechanism of this association remains unknown. Dramatic changes in parathyroid function are found in patients with Paget's disease and, on the other hand, the evolution of Paget's disease is influenced by parathyroid functional disorders. We reviewed 175 patients with Paget's disease and 60 with primary hyperparathyroidism, followed during 10 years. We only found 5 cases with the association of the two diseases. Approximately equal number were male and female (ratio: 1.5/1) patients and the average age was 63.60 +/- 2.65 years. Hypercalcemia in Paget's patients, and in increase in alkaline phosphatase in post parathyroid adenoma surgery patients were the clues that suggested the presence of the second disease. Surgical treatment was indicated in 3 patients, and the others were treated with antiresorptive drugs. We also reviewed the cases published since 1934, comparing their diagnostic, clinical, treatment and evolution features with our own cases.

Aged↗
PubMed1993

Alterations of calcium and phosphate metabolism in primary hyperparathyroidism during pregnancy.

Primary hyperparathyroidism (PHP) is rare during pregnancy and has been claimed to be associated with significant increase of neonatal morbidity and mortality. Whether the well recognized changes in calcium (Ca) and phosphate (Pi) homeostasis occurring in pregnancy might influence the biochemical expression of PHP is unclear. We evaluated biochemical parameters of calcium and phosphate metabolism in two cases of PHP in pregnancy diagnosed in the third trimester (patient 1) and in the second trimester (patient 2). Both patients displayed increase in protein-adjusted plasma Ca, bone resorption evaluated by the fasting urinary Ca-to-creatinine ratio, renal tubular reabsorption of Ca, urinary cAMP excretion and decrease in renal tubular reabsorption of Pi. These alterations were identical to those found in 12 non-pregnant women with PHP. The biochemical expression of PHP did not change after delivery in patient 1. This patient underwent the excision of a 1 g parathyroid adenoma on the 13th day after delivery, which led to normalization of all biochemical parameters. The lowest plasma Ca of the newborn of patient 1 was 2.02 mM 72 hours after birth. Thus, the results indicate that these two pregnant women with PHP displayed biochemical alterations of calcium and phosphate metabolism similar to those observed in non-pregnant women with primary hyperparathyroidism.

Adult↗
PubMed1991

Hypercalcemia with low-normal serum intact PTH: a novel presentation of primary hyperparathyroidism.

The diagnosis of primary hyperparathyroidism has rested on the finding of hypercalcemia coupled with an elevated serum parathyroid hormone (PTH) level. Over 300 consecutive patients with primary hyperparathyroidism have had elevated or high-normal serum PTH levels using a specific immunoradiometric assay. Here we present a patient who proved to have surgically documented primary hyperparathyroidism in whom PTH levels were completely normal in all assays used. In the immunoradiometric assay, his normal result was unprecedentedly low (17 to 28 pg/mL; normal, 10 to 60 pg/mL) for this condition, and in a range consistent with non-PTH-dependent hypercalcemia or familial hypocalciuric hypercalcemia. This rare biochemical presentation of primary hyperparathyroidism should be considered in the differential diagnosis of hypercalcemia.

Humans↗
PubMedDate not supplied

[Recurrent brown tumors as initial manifestation of primary hyperparathyroidism. An unusual presentation].

Primary hyperparathyroidism is a rather frequent pathology characterised by hypersecretion of parathormone (PTH) which is caused by adenomas in 85% of all cases. At clinical onset, the most common symptoms are hypercalcemia-related (pain due to kidney stones, polyuria, gastrointestinal and neurological disorders) while rarer symptoms are due to brown tumors, expansive lesions often found in fibro-cystic osteitis. A case in which the patient showed recurrent mandibular brown tumors as initial clinical symptoms of primary hyperparathyroidism is described. This patient was examined for hypercalcemia, and a tumor mass at the left inferior mandibular branch was found. The patient had undergone surgical removal of a tumor in the left mandibular some years before, which was diagnosed as osteoclastoma. Primary hyperparathyroidism was diagnosed during recovery, and surgical removal of the parathyroid adenoma and mandibular tumor was performed. A histological diagnosis of large cell brown tumor was made. A microscopic observation of brown tumors which are made up of large multinuclear osteoclastic cells can often be confused with other large cell tumors during diagnosis. It is therefore necessary to exclude the presence of hyperparathyroidism with ionised calcium and, in cases of high values, intact PTH (iPTH), before performing a histological diagnosis of a large cell bone tumor. Throughout the course of primary hyperparathyroidism, brown tumors might appear in the absence of other specific symptoms and localize at the level of a single bone segment.

Adenoma↗