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PubMed2003

Abnormal bone scintigraphy and acute-onset severe primary hyperparathyroidism.

Acute-onset primary hyperparathyroidism in a previously asymptomatic individual is uncommon. We herein report the case of a 61-yr old woman who underwent bone scintigraphy for severe, rapidly worsening, diffuse bone pain, associated with weight loss, anxiety and confusion. The patient was asymptomatic until a few days before presentation. A marked redistribution of the tracer was observed, with poor bone uptake and relevant accumulation in liver, kidneys, lungs and spleen. Blood chemistry unequivocally allowed the diagnosis of primary hyperparathyroidism due to multiple parathyroid adenomas, as suggested by parathyroid scan. Unfortunately, the patient critically worsened and surgery was made impossible. She died despite intensive critical care. Autopsy confirmed both massive intraparenchymal calcium deposition in the kidneys, lungs, liver and spleen, as well as multiple parathyroid adenomas. One may speculate that some adaptation of the organism to progressively increasing blood calcium levels and to slowly increasing intraparenchymal calcium salt deposition occurred, until critically high concentrations were attained.

Adenoma↗

PubMed1997

[Personal experience with treatment of primary hyperparathyroidism].

The primary hyperparathyreosis needs the interdisciplinary approach. The ideal term for surgical intervention is the period of the latent HPT, that means the time, when the signs of irreversibly damaged organs are not yet present. In the Czech Republic they are approximately 100-300 such cases per year with the primary diagnosed HPT. These patients should be sent to the departments, specialized for this type of surgery.

Female↗

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↗

PubMed1991

Surgical therapy of patients with primary hyperparathyroidism: long-term benefits.

Primary hyperparathyroidism was thought 30 years ago to be a rare disease, and the diagnosis was most often made in patients presenting with either bone disease or kidney stones. Today the minority of patients with hyperparathyroidism present with such symptoms, a fact accounted for by the introduction into general medical practice three decades ago of laboratory technology for efficiently determining the serum concentrations of various blood minerals, including calcium. Hypercalcemia was detected more frequently, and it was realized that most patients with hyperparathyroidism either had minor symptoms, such as constipation, polyuria, tiredness, and muscle weakness, or they were "asymptomatic" and indistinguishable from normal subjects. It was thought that primary hyperparathyroidism was a progressive disease and that sooner or later all patients would become symptomatic and require parathyroidectomy. Since this operation was curative in a high percentage of cases, it was recommended for virtually all patients once the diagnosis was established. In this contribution the long-term benefits of parathyroidectomy in patients with and without symptoms from primary hyperparathyroidism are reviewed. It is concluded that a multicenter prospective randomized trial is needed to resolve the indications for operative and nonoperative management of patients with this disease.

Bone Density↗

PubMed1986

Absence of effect of 24,25-dihydroxyvitamin D3 in primary hyperparathyroidism.

Nineteen patients with primary hyperparathyroidism were treated with 25 micrograms 24,25-dihydroxyvitamin D3 or placebo daily for 3 months according to double-blind cross-over protocol. Serum immunoreactive PTH, total and ionized calcium, urinary calcium excretion, tubular reabsorption of phosphate/glomerular filtrate, and urinary hydroxyproline excretion did not change significantly. Serum 24,25-dihydroxyvitamin D3 levels increased significantly from 1.4 +/- 2.2 (SD) nmol/liter to 38 +/- 11 nmol/liter during the treatment period. Serum 25-hydroxyvitamin D3 and 1,25-dihydroxyvitamin D3 levels did not change. We conclude that pharmacological doses of 24,25-dihydroxyvitamin D3 have no suppressive effect on parathyroid function in primary hyperparathyroidism.

24,25-Dihydroxyvitamin D 3↗

PubMed1984

Long term follow up of untreated primary hyperparathyroidism.

Fourteen patients with primary hyperparathyroidism and whose initial serum calcium concentrations were 2.75 mmol/l (11.0 mg/100 ml) or more were followed up for five to 23 years without operative treatment. One had osteitis fibrosa when seen and died with a fibrosarcoma 22 years later. The remaining 13 patients, who were followed up for a mean of 10 years, came to little obvious harm from not being operated on. Their serum calcium concentrations did not rise and there was no evidence of progressive renal impairment. In four patients who presented originally with renal calculi there were three further episodes of renal colic in 54 patient years of follow up. Conservative management of primary hyperparathyroidism is not an unreasonable option, and patients who do not have symptoms need not necessarily be pressed to accept surgery.

Aged↗

PubMed1992

Renal handling of urate in two patients with hyperuricemia and primary hyperparathyroidism.

Two patients with primary hyperparathyroidism had hyperuricemia due to the decrease in urate clearance. In analysis by 4-component model system, the tubular secretion of urate commonly decreased without changes in either filtered urate or presecretory reabsorption of urate. Both patients had a reduction of urea clearance, and both parathyroidectomy in the former case and intravenous infusion of saline in the latter case could reduce the serum urate level associated with the increase in the ratio of urate clearance to creatinine clearance. It is of interest that the former case with a higher serum urate level had a relatively higher postsecretory reabsorption, even with the decrease in tubular secretion of urate. However, the latter patient with a lower serum urate level had a decrease in postsecretory reabsorption of urate in proportion to the decrease in tubular secretion. These results suggest that in hyperuricemia patients with primary hyperparathyroidism, the reduction of tubular urate secretion via hypoperfusion of the capillary network is typically present, however, the severity of the hyperuricemia might be dependent on the dysfunction of the postsecretory reabsorption of urate.

Aged↗

PubMed1990

Renal tubular reabsorption of calcium and sodium in primary hyperparathyroidism.

Nine patients with primary hyperparathyroidism were studied to investigate the renal tubular reabsorption of calcium and sodium. Fasting serum and urine samples were analysed, and the glomerular filtration rate and the renal plasma clearance of lithium were determined simultaneously. Comparison was made with 9 age- and sex-matched normocalcemic controls. In the proximal tubule, there was a significantly higher absolute reabsorption of calcium in patients than in controls, whereas the fractional reabsorption rate of calcium did not differ between the two groups. In the distal tubule, the absolute calcium reabsorption rate was significantly higher in the patients, whereas the fractional reabsorption rate of calcium was significantly lower than in controls. In the patient group there was a significantly positive linear correlation between the increased tubular capacity for calcium reabsorption and the absolute proximal calcium reabsorption rate, but not between the increased capacity and the absolute distal calcium reabsorption rate. No significant differences were found in the renal tubular handling of sodium between patients and controls. Our results suggest that the increased capacity for tubular calcium reabsorption in primary hyperparathyroidism mainly is localized in the proximal tubule, and that the renal tubular handling of calcium and sodium in this disease differs from that in familial hypocalciuric hypercalcemia.

Adult↗

PubMed1980

The importance of circulating 1,25-dihydroxyvitamin D in the pathogenesis of hypercalciuria and renal-stone formation in primary hyperparathyroidism.

Fifty patients with primary hyperparathyroidism were studied with an oral calcium-tolerance test, measurements of plasma levels of vitamin D metabolites, and determination of calcium excretion on both a low-normal (400 mg) and high-normal (1000 mg) calcium intake. There were strong positive correlations between plasma levels of 1,25-dihydroxyvitamin D (1,25(OH)2D) and both the calciuric response to the calcium-tolerance test (r = +0.75, P less than 0.001) and calcium excretion on the 1000-mg calcium diet (r = +0.65, P less than 0.001). The patients were classified into two subpopulations: 30 patients showed hyperabsorption with the calcium-tolerance test, striking hypercalciuria, marked elevations in plasma 1,25(OH)2D, and a high incidence (19 of 30 patients) of renal stones; 20 patients had a normal response to the tolerance test, normocalciuria, normal or high-normal plasma 1,25(OH)2D, and a low incidence of stones (three of 20 patients). The findings emphasize the importance of circulating 1,25(OH)2D in the pathogenesis of hypercalciuria and stone formation in primary hyperparathyroidism.

Calcium↗

PubMedDate not supplied

[Primary hyperparathyroidism: the recent findings].

Primary hyperparathyroidism is a quite frequent disease, the incidence of which has been found to increase over the past two decades. At the same time there has been a remarkable change in its clinical presentation; therefore this endocrine disorder earlier considered rare but almost always associated with complications, now appears a quite common and uncomplicated disease. In our series of 150 patients diagnosed between 1966 and 1989 the female/male ratio was found to be 1.77. The ratio has significantly increased (2.09), beginning from 1983; this was mainly due to the availability of a bone densitometer at our Mineral Metabolism Service with consequent greater demand of serum calcium determination as a part of routine metabolic screening for prevention of postmenopausal osteoporosis. Whilst the percentage of patients with renal manifestations of the disease has not significantly changed during these years, the amount of asymptomatic patients (yrs 1966-1983 = 3.7% vs yrs 1984-1989 = 39.7%) has progressively increased to the detriment of patients with skeletal symptoms. Serum intact parathyroid hormone determination by immunoradiometric assay (and possibly by immunochemiluminometric assay) seems to have overcome some of the methodological problems inherent in conventional radioimmunoassay. Surgical treatment of primary hyperparathyroidism is safe and highly effective in experienced hands. Recurrence has been observed only in three cases after resection of parathyroid adenoma, thus indirectly supporting a monoclonal origin of the tumor. Medical behavior (conservative or surgical management) in respect to patients with the mild or asymptomatic form of the disease, especially when diagnosed in old age, is uncertain at this point in time. Future prospective studies carried out on a large number of patients are needed to better clarify this issue.

Humans↗

PubMed1989

Clinical aspects of surgery in primary hyperparathyroidism.

60 patients suffering from primary hyperparathyroidism were operated during the period from 1980 till september 1988. The operation was successful in 55 cases. Most patients had single adenomas of the parathyroid glands. There was only one case with a four-gland-hyperplasia and one case with a parathyroid carcinoma. Rare observations were: one woman with a truly recurrent primary hyperparathyroidism, two patients with a papillary carcinoma of the thyroid gland in addition to the hyperparathyroidism and one patient with a large cystic parathyroid adenoma. Most of the patients had severe clinical symptoms of the primary hyperparathyroidism, mainly renal stones, in some cases bone changes. Only three patients were asymptomatic.

Adenoma↗

PubMedDate not supplied

Postural shortening due to primary hyperparathyroidism caused by parathyroid adenoma.

Osteoporosis can be primary or secondary. Secondary osteoporosis is the result of an underlying disease such as an endocrine abnormality, and an example of such is primary hyperparathyroidism. The most common cause of primary hyperparathyroidism is parathyroid gland adenoma. The diagnosis of primary hyperparathyroidism is based on the following biochemical examinations: parathyroid hormone, serum calcium, creatinine clearance, 24 hour urinary calcium, and another examination such as parathyroid gland scan. This is a rare case of an adult man who presented with a chief complaint of decreasing body height, back pain, difficulty in taking deep breaths and difficulty in his activities. The patient was diagnosed with primary hyperparathyroidism caused by parathyroid gland adenoma. His complaint was reduced after parathyroidectomy. His new complaint was that his tooth can be pulled out easily. We found high levels of parathyroid hormone and low levels of serum calcium caused by secondary hyperparathyroidism.

Adenoma↗

PubMed1998

Re-operative surgery for recurrent or persistent primary hyperparathyroidism.

BACKGROUND: While initial surgery for primary hyperparathyroidism, in experienced hands, will result in a cure in 98% of cases, re-operative surgery remains a significant challenge. Because attitudes as to who should perform initial exploration for hyperparathyroidism are significantly different around the world, the approach to re-operative surgery may also vary. The aim of the present study was to examine a local experience of re-operative surgery for recurrent or persistent primary hyperparathyroidism. METHODS: Information on indications for surgery, the procedure performed, pathology and complications of all re-operative procedures for primary hyperparathyroidism in the period January 1962 to December 1996 were obtained from a prospective database. RESULTS: Sixteen patients with persistent (n = 12) or recurrent (n = 4) primary hyperparathyroidism were treated in the unit over the study period. Eight patients had their initial operation within the unit at Royal North Shore Hospital and eight were referred from elsewhere for re-operation. Nine of the 12 patients with persistent hyperparathyroidism were cured by re-operation with failures due to spillage at first operation (n = 1) or failure to find any additional pathology (n = 2). All four patients with recurrent hyperparathyroidism were cured. All the failures occurred early in the learning phase of the unit, with a 100% cure rate for re-operative procedures performed in the last 15 years. The most common finding in patients referred from elsewhere with a failed initial operation was a missed inferior adenoma in association with the thymus. Localization studies had a variable sensitivity, with sestamibi scintigraphy, selective venous sampling and ultrasonography providing the most reliable information. CONCLUSIONS: Re-operative surgery for persistent or recurrent hyperparathyroidism is an uncommon procedure in Australia when compared to major centres in the USA. Successful surgery depends upon experience and an accurate knowledge of the embryology and anatomy of the parathyroid glands.

Adenoma↗

PubMed1993

Cervical exploration for primary hyperparathyroidism.

The classical presentation of primary hyperparathyroidism, "moans, bones, groans," is no longer commonly seen since the diagnosis of hypercalcemia is now made much earlier with the routine use of the SMA 12. In the past 8 1/2 years, 85 patients underwent cervical exploration in our institution for primary hyperparathyroidism. There were 34 male and 51 female patients, ranging in age from 18-84 years. The specific symptoms included hypertension in 40 patients, generalized weakness in 25, renal stones in 14, psychiatric problems in 2, and bone changes on X-ray in 4. Forty-one patients were totally asymptomatic. The diagnosis was made mainly on the basis of history, serum calcium and phosphorous levels, parathormone assay, and 24-hour urinary calcium studies. Preoperative localization studies were performed in 38 patients. Thallium technetium subtraction scans, when positive, were very helpful. The surgical approach involved stepwise exploration of both sides of the neck with identification of all four parathyroid glands. In patients with uniglandular pathology (87%), the adenoma was removed with biopsy of at least one normal gland. In multiglandular disease, the abnormal glands were removed. Frozen section was routinely performed to confirm the presence of parathyroid tissue and no attempt was made to pathologically distinguish adenoma from hyperplasia. Two patients had parathyroid carcinoma. In three patients, serum calcium levels did not fall, resulting in an operative success rate of 96%. One patient treated by subtotal parathyroidectomy developed permanent hypoparathyroidism and one other patient developed temporary hypocalcemia. Only a single patient developed vocal cord palsy. Early exploration in patients with primary hyperparathyroidism is indicated. The basic diagnostic workup is sufficient for initial exploration. It is important to distinguish uniglandular from multiglandular pathology after careful bilateral exploration and identification of all four parathyroid glands.

Adenoma↗

PubMed2004

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

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

Body Weight↗

PubMed1992

Non-autonomy of parathyroid hormone secretion in acute primary hyperparathyroidism.

A patient with acute primary hyperparathyroidism treated with mithramycin preoperatively, underwent neck exploration and two enlarged parathyroid glands were excised: one huge adenoma (6g) and another smaller gland. Mithramycin was administered preoperatively to lower life-threatening hypercalcaemia, and parathyroid slices from the huge adenoma removed at surgery were submitted in vitro to various calcium concentrations in the media to determine the influence of calcium on parathyroid adenoma secretory pattern in acute primary hyperparathyroidism. Mithramycin induced a significant decline in calcium levels and significant elevations of calciotrophic hormones (intact PTH, mid-region specific PTH, calcitonin and calcitriol). Significant suppression in PTH output in vitro was achieved by increasing calcium levels in the media. These results exclude autonomous PTH secretion (non-calcium dependent) as a possible aetiology of acute primary hyperparathyroidism. We suggest that a sudden increase in the set-point of the diseased parathyroid cells in the presence of a huge cell mass accounts, in large part, for both the marked hypercalcaemia and elevated PTH levels in this patient.

Acute Disease↗

PubMed1997

Early localization and reoperation for persistent primary hyperparathyroidism.

BACKGROUND: Reoperation for persistent primary hyperparathyroidism is often performed after a delay of 4-6 months. Success can be expected in over 90 per cent of cases but exploration is technically difficult and there is the possibility of creating permanent hypoparathyroidism and vocal cord paralysis. This is a study of early localization and reoperation. METHODS: In a consecutive series of 273 patients who had surgery for primary hyperparathyroidism, three remained hypercalcaemic and in three the abnormal parathyroid was not found at initial exploration. They underwent early (6-48 h) single-tracer 99mTc Sestamibi scintigraphy with factor analysis of dynamic structures (FADS) and single photon emission computed tomography (SPECT) followed by reoperation within 24-72 h. RESULTS: Scintigraphy with FADS and SPECT was helpful in all six patients, who were cured by reoperation with no morbidity or symptomatic hypocalcaemia. CONCLUSION: Reoperation for persistent primary hyperparathyroidism is possible and may be easier within days of an initially unsuccessful procedure. With the intact 1-84 parathyroid hormone measurement, the diagnosis is accurate. Single-tracer 99mTc Sestamibi scintigraphy with FADS and SPECT is non-invasive, easily and rapidly performed, and was accurate in these six patients.

Chronic Disease↗

PubMed1990

Bone disease in primary hyperparathyroidism.

The classic bone disease of primary hyperparathyroidism, osteitis fibrosa cystica, was characterized by subperiosteal bone resorption, osteopenia, and "brown tumors." Since the description of this skeletal disorder, the clinical profile of primary hyperparathyroidism has evolved markedly. The disease today is often characterized by no more than asymptomatic hypercalcemia, and severe bone disease is a distinct rarity. However, as we have endeavored to show in this article, newer and more sensitive techniques show significant evidence of the effect of excess parathyroid hormone on the skeleton. Bone density as measured by photon absorptiometry and bone histomorphometry show a deficit of cortical bone and a preservation or increase in cancellous bone elements in mild primary hyperparathyroidism with no clinical evidence of skeletal disease. Important questions exist as to the therapeutic implications of these data. Does the presence of parathyroid hormone effect on sophisticated testing portend the development of clinical bone disease? Should these data be used as a rationale for surgical intervention in patients who might otherwise be followed conservatively with mild primary hyperparathyroidism? The answers to these questions must await further data collection and study.

Bone Diseases↗