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PubMedDate not supplied

Efficacy of preoperative dual-phase sestamibi scanning in hyperparathyroidism.

PURPOSE: The objective of this article is to evaluate our experience with sestamibi scanning in patients with primary and secondary hyperparathyroidism. PATIENTS AND METHODS: A retrospective review of patients referred to the radiology department at the University of Kansas Medical Center for parathyroid studies between January 1, 1993, and August 1, 1998, was done. Patients included in the study were those who underwent both dual-phase technetium (Tc-99m) sestamibi scanning and subsequent parathyroidectomy at our institution (n = 34). Twenty-six patients had primary hyperparathyroidism and 8 patients had secondary hyperparathyroidism. Fifteen had previous history of neck exploration. RESULTS: Sensitivity of sestamibi scans in detection of all abnormal pathology in cases of primary hyperparathyroidism was 60% overall. Among the subset of adenoma cases, sensitivity was 82% (14/17). Among cases of primary parathyroid hyperplasia, no scan correctly localized all abnormal glands; however 60% (3/5) showed localization of at least one hyperplastic gland. Of the 2 patients with parathyroid carcinoma, in only one case was there evidence of sestamibi retention in the correct thyroid lobe. In patients with secondary hyperparathyroidism, sestamibi scanning was successful in identifying all hyperplastic tissue in only one case (sensitivity 13%). In 7 of the 8 cases of secondary hyperparathyroidism, the scan localized at least one hyperplastic gland. CONCLUSION: Sestamibi scanning is useful in the localization of abnormal pathology in cases of primary hyperparathyroidism, especially adenomas. In cases of hyperplasia, whether attributable to primary or secondary hyperparathyroidism, sestamibi imaging is less successful.

Adult↗
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↗
PubMed1997

Comparative analysis of clonality and pathology in primary and secondary hyperparathyroidism.

Parathyroid adenoma and hyperplasia are the most common causes for hyperparathyroidism, and distinction between them is controversial based on the current criteria for pathological diagnosis. We studied the clonality of hyperparathyroidism and its correlation with the pathological features, analysing 39 female patients with hyperparathyroidism. Clonality was successfully detected in 12 heterozygous cases by PCR amplification of PGK-1 gene. The 12 cases yielded 14 hypercellular glands, 8 affected by primary and 6 by secondary hyperparathyroidism. The results revealed that 7 of the 8 glands with primary hyperparathyroidism showed monoclonal proliferation. Only 1 gland pathologically diagnosed as adenoma showed a polyclonal pattern. In the 4 cases with secondary hyperparathyroidism, at least one monoclonal tumour was detected in each case. Our data indicate that monoclonal tumours are more common than expected in both primary and secondary hyperparathyroidism. Monoclonal tumours and polyclonal hyperplasia can co-exist in the same patient. Comparative study of the clonality and the pathological features showed that the clonality was consistent with the diagnosis of parathyroid adenoma, whereas it was in conflict with the diagnosis of hyperplasia with multigland involvement. One of the reasons for this is that we are ignorant of the true natures of hyperparathyroidism with multigland involvement.

Cell Line↗
PubMed1987

Hyperparathyroidism presenting as the first lesion in multiple endocrine neoplasia type 1.

In a study of 16 different families, 55 persons were considered to be affected by the syndrome of multiple endocrine neoplasia type 1 (MEN-1). Serum calcium measurements were available for all but six patients, long deceased, and hypercalcemia was invariably present. All but four of these patients have been subjected to surgery, and hyperparathyroidism was verified in each case. In all the patients studied, hyperparathyroidism was apparently the first manifestation of the MEN-1 syndrome. Pituitary tumors were detected in 23 patients, and there was evidence of pancreatic lesions in 32. Although either the pituitary or pancreatic manifestations dominated clinically in some patients, hyperparathyroidism was invariably present when sought. Measurement of serum calcium in asymptomatic relatives at risk for MEN-1 disclosed no case of hyperparathyroidism in children below the age of 18, whereas half of all screened persons between the ages of 18 and 30 were found to have hyperparathyroidism. In some, the serum calcium values were only marginally or even intermittently elevated. It is concluded that since hyperparathyroidism is apparently the first lesion in MEN-1, screening for this syndrome should primarily be directed toward the diagnosis of hyperparathyroidism. The temporal relationships suggest that hyperparathyroidism could be a prerequisite for the other types of endocrine neoplasms in the MEN-1 syndrome.

Adolescent↗
PubMed2005

Laboratory screening for hyperparathyroidism.

INTRODUCTION: The clinical syndrome produced by excess parathyroid hormone (PTH) is referred to as hyperparathyroidism (HPT). Autonomous growth of PTH producing cells is defined as primary hyperparathyroidism (pHPT). In its classic form pHPT is characterized by painful bones, kidney stones, abdominal groans, psychic moans, fatigue overtones and hypercalcemia. Chronic stimulation of the parathyroid glands secondary to low circulating calcium level results in secondary hyperparathyroidism (sHPT). Tertiary hyperparathyroidism (tHPT) results from prolonged secondary hyperparathyroidism when the glands take on an autonomous function manifested by hypercalcemia and high PTH levels despite resolution of the original stimulus. REVIEW: The paper reviews the physiologic regulation of PTH secretion and types and forms of HPT. Calcium homeostasis is discussed, emphasizing interactions of PTH, PO4 and vitamin D that can lead to HPT. In addition, the paper reviews the contribution of serum calcium, chloride, phosphorus and PTH levels to the diagnosis of HPT, the role of urinary calcium in the diagnosis of familial benign hypocalciuric hypercalcemia (FBHH), and the role of alkaline phosphatase and bone mass measurements as markers of severity of hyperparathyroid bone disease. CONCLUSIONS: It is concluded that the diagnosis of hyperparathyroidism can be made with a very high confidence rate by documenting an increased serum PTH level with an increased ionized or total calcium level in pHPT, increased serum PTH level with low or normal calcium level and an underlying renal failure or vitamin D deficiency in sHPT. Early management of HPT is important because many of the nonspecific complains, or classic symptoms, or metabolic conditions often improve after proper control of hyperparathyroidism.

Calcitonin↗
PubMed2004

Hypothesis: the case for quaternary hyperparathyroidism.

We report the case of a young woman with hyperparathyroidism due to a large parathyroid adenoma associated with severe vitamin D deficiency. The case is noteworthy for the size of the parathyroid adenoma and for the young age at presentation, and is more typical of the presentation of hyperparathyroidism seen in developing countries where the prevalence of vitamin D deficiency is high. Vitamin D is known to have a suppressive effect on parathyroid cell proliferation and parathyroid hormone synthesis. Vitamin D deficiency may result in a compensatory increase in the secretion of parathyroid hormone (secondary hyperparathyroidism) which involves hyperplasia of all four parathyroid glands. Secondary hyperparathyroidism can become autonomous and this has been termed tertiary hyperparathyroidism, the underlying pathology of which has been variably described in the literature as adenoma formation or four gland hyperplasia. The pathogenesis of parathyroid adenoma formation in vitamin D deficiency remains unclear. It is possible that a proportion of cases represent the coincidence of primary hyperparathyroidism in patients with vitamin D deficiency. Alternatively, we hypothesise that autonomous four gland hyperplasia or tertiary hyperparathyroidism may progress to adenoma formation and that this should be termed 'quaternary hyperparathyroidism'.

Adenoma↗
PubMed2000

Hyperparathyroidism after thyroid surgery and autotransplantation of histologically normal parathyroid glands.

BACKGROUND: Parathyroid autotransplantation is a well-established method to prevent hypoparathyroidism during parathyroid and thyroid operations. The reported success rate of parathyroid autotransplantation ranges from 75% to 100%. Recurrent hyperparathyroidism may develop after parathyroid autotransplantation, especially after the transplantation of hyperplastic or adenomatous parathyroid tissue. Hyperparathyroidism recurs most frequently after subtotal parathyroidectomy or total parathyroidectomy and autotransplantation, in patients with renal failure and secondary hyperparathyroidism, and in patients with familial primary hyperparathyroidism or MEN I or MEN II syndrome. We report three patients who experienced primary hyperparathyroidism after autotransplantation of normal parathyroid tissue during thyroid operations (two patients) or after a long period of hypoparathyroidism. STUDY DESIGN: We reviewed our records from 1983 to May 1998 and identified three patients in whom hyperparathyroidism developed after thyroid operations. RESULTS: One patient had a thyroidectomy with left modified radical neck dissection for papillary thyroid cancer, followed by radioiodine ablative therapy. Two patients had thyroid operations for benign thyroid disease. One of these patients had a history of radiation exposure for acne, and in the other one secondary hyperparathyroidism arose 6 years after a thyroidectomy for hyperthyroidism. CONCLUSIONS: Our study documents that hyperparathyroidism may develop after autotransplantation of histologically normal parathyroid tissue and after a period of hypoparathyroidism after thyroid operations. For this reason, it is important to mark the site of the parathyroid transplantation.

Adult↗
PubMed1999

Diabetes mellitus with hyperparathyroidism: another indication for parathyroidectomy?

BACKGROUND: Patients with hyperparathyroidism have alterations in carbohydrate metabolism characterized by insulin resistance, hyperinsulinemia, and glucose intolerance. The clinical significance of these findings in the management of patients with diabetes mellitus (DM) after parathyroidectomy for hyperparathyroidism has been controversial. METHODS: A retrospective review identified 87 patients with DM and hyperparathyroidism who underwent parathyroidectomy. The follow-up documentation of 70 patients who underwent diabetic management was then evaluated to assess the benefit of parathyroidectomy on glucose management. RESULTS: Thirteen patients had type 1 DM, and 74 patients had type 2 DM. Primary hyperparathyroidism was present in 93% of patients with type 2 DM; 64% of patients with type 1 DM had secondary hyperparathyroidism. At follow-up, glucose control was stable in 40% of patients, had improved in 37% of patients, and had deteriorated in 23% of patients (P = .003). Improved glucose control was not dependent on age, duration of DM, duration of hyperparathyroidism, length of follow-up, or calcium levels. The patients with decreased requirements had a significantly lower parathyroid hormone level (P = .05). Improved glucose control was most significant in patients whose condition was managed with oral hypoglycemics (P = .05) or insulin (P = .03). CONCLUSIONS: The clinical and laboratory investigations on the influence of hyperparathyroidism on DM support the benefit of parathyroidectomy in patients with DM. Patients with type 1 and type 2 DM show improvement in glucose control after parathyroidectomy. The presence of DM and hyperparathyroidism is an indication for parathyroidectomy because it results in either stabilization or improved glucose control in 77% of patients.

Adult↗
PubMed1998

Assessment of ultrasound guided percutaneous ethanol injection and parathyroidectomy in patients with tertiary hyperparathyroidism.

BACKGROUND: Tertiary hyperparathyroidism continues to cause significant morbidity in patients with chronic renal failure. This is frequently resistant to medical management and may ultimately require a surgical parathyroidectomy. Recent studies have reported upon the technique of percutaneous ethanol ablation for both primary and tertiary hyperparathyroidism. In this study we report on a 5 year experience using ethanol injection and compare the results with surgical parathyroidectomy. METHODS: A prospective study in 39 patients with tertiary hyperparathyroidism, 25 were dialysis dependent and 14 had a functioning renal allograft. Twenty-two patients underwent percutaneous fine needle ethanol injection (PFNEI) and 17 underwent surgical parathyroidectomy. RESULTS: A > 30% reduction in intact parathyroid hormone (iPTH) was achieved in 11 of 22 patients undergoing PFNEI after a mean of 1.8 +/- 1.4 injections per gland. In four patients, symptomatic hyperparathyroidism recurred and they required further PFNEI or surgical parathyroidectomy at 17, 28, 46, and 48 months later. There was no significant reduction in iPTH in 11 patients following PFNEI after a mean of 2.5 +/- 1.3 injections per gland. They all required a subsequent surgical parathyroidectomy for symptomatic hyperparathyroidism. Four patients developed a laryngeal nerve palsy following PFNEI, two of which were permanent. Seventeen patients underwent successful surgical parathyroidectomy as a primary procedure. CONCLUSION: Whilst PFNEI is successful in primary hyperparathyroidism, when typically only one adenoma is present, the effectiveness of PFNEI is unpredictable and the long term results are poor compared with those of surgical parathyroidectomy in tertiary hyperparathyroidism. The procedure is not without complications and makes subsequent surgery more difficult. Therefore it can only be recommended for patients with a known single parathyroid gland such as patients in whom hyperparathyroidism has recurred following a previous surgical subtotal parathyroidectomy and who are unsuitable for further surgery.

Administration, Cutaneous↗
PubMed1989

Aldosterone and pressor responses to angiotensin II in primary hyperparathyroidism.

The aim of this study was to assess the effect of hypercalcaemia due to primary hyperparathyroidism on the pressor and aldosterone responses to angiotensin II (Ang II) infusion. Five patients with hyperparathyroidism were studied, before and after parathyroidectomy, and were compared with five normal subjects. After 30 min of equilibration, Asp1-Val5 Ang II was infused in all subjects at stepwise increasing dose rates of 2 and 4 ng/kg per min for 30 min each. In the hyperparathyroid patients the baseline levels of plasma parathyroid hormone and calcium were significantly higher than in the controls, and returned to normal after the parathyroidectomy; plasma aldosterone and renin activity were normal both before and after the parathyroidectomy. Two hyperparathyroid patients had high blood pressure levels, which were normalized after surgery. The increase in the aldosterone response from baseline at each time point of the Ang II infusion was greater in the hyperparathyroid patients before than after the operation (P less than 0.05), and greater than in the normals (P less than 0.05). No difference in the increased response of systolic or diastolic blood pressure was observed between the hyperparathyroid patients, either before or after the parathyroidectomy, and the normal subjects. High levels of extracellular calcium or parathyroid hormone, or both, might play a primary role in the aldosterone hyper-responsiveness to Ang II in the hyperparathyroid patients. The similar pressor response to Ang II in hyperparathyroid patients and the normal subjects suggests that hypercalcaemia does not potentiate the vasoconstrictive action of Ang II.

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↗
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↗
PubMed2001

Secondary hyperparathyroidism and bone turnover in elderly blacks and whites.

This study was undertaken to describe the prevalence of secondary hyperparathyroidism in African-American and Caucasian participants in the Boston Low-Income Elderly Osteoporosis Study and to examine and compare associations of hyperparathyroidism with biochemical markers of bone turnover and bone density in the two racial groups. Serum osteocalcin and serum cross-linked N-telopeptides of type I collagen, and calcaneal bone mineral density were measured in February or March in 255 men and women, 64 yr of age and older. Subjects were categorized as normal or as having hyperparathyroidism, based on a serum PTH concentration below or above the top of the normal range (6.9 pmol/liter), respectively. The prevalence of hyperparathyroidism was 38% in the 144 black subjects and 20% in the 111 white subjects. Serum osteocalcin and cross-linked N-telopeptides of type I collagen were significantly higher in both black and white hyperparathyroid subjects (P < 0.05), and the hyperparathyroid-related difference in osteocalcin was greater among black than white subjects. Hyperparathyroidism was significantly associated with reduced heel bone mineral density in blacks (P = 0.008) but not in whites. This study provides evidence that secondary hyperparathyroidism is prevalent in elderly adults, both black and white, and that it should not be viewed as a benign condition in either group. Recent public health efforts to promote higher calcium and vitamin D intakes, targeted predominantly to older Caucasians, should also be directed to older African-Americans.

Black or African American↗
PubMed1982

[Suppressibility of parathyroid function in primary hyperparathyroidism as estimated by nephrogenous cyclic AMP (author's transl)].

The effects of calcium injection (3 mg/Kg/10 min) or oral calcium administration (calcium lactate 7.7 g) on plasma iPTH and Nephrogenous cyclic AMP (NcAMP) were studied in 6 normal controls and 13 patients with primary hyperparathyroidism. In the control subjects, plasma iPTH determined by a predominantly carboxyl-terminal antiserum was less than 0.3 ng/ml before and after both calcium loads, whereas 41 approximately 98% (mean 67%) of NcAMP was rapidly and uniformly suppressed to a level lower than the normal value. In 2 patients with primary hyperparathyroidism, iPTH was clearly reduced from 8.0 to 4.6 ng/ml and 1.6 to 0.96 ng/ml, respectively, by the calcium load. However, in the other 7 patients with primary hyperparathyroidism who showed only a slight elevation of iPTH: less than 0.3 approximately 0.9 ng/ml, the reductions in iPTH were not detected after the calcium load: less than 0.3 approximately 0.7 ng/ml. In contrast, 30 approximately 54% (1.02 approximately 3.85 nmol/dl GF) of NcAMP, which was greater than the diurnal variation, was suppressed after calcium injection in 5 patients with primary hyperparathyroidism (2 of 4 patients with urological, and 3 of 5 patients with chemical hyperparathyroidism). But NcAMP was not suppressed in all 4 patients with skeletal hyperparathyroidism including one with proximal renal tubular dysfunction whose basal iPTH was elevated markedly but reduced clearly by the calcium load. In general, suppression of NcAMP was followed by a decrease of phosphate excretion. On the other hand, even in a patient with primary hyperparathyroidism whose NcAMP was not suppressed at all after the calcium injection, calcium infusion (15 mg/Kg/3h) resulted in some (23%) decrease in NcAMP. Oral calcium administration resulted in responses which were almost the same as those produced by calcium injection. These results suggest that NcAMP provides a useful index in the parathyroid suppression test in patients with primary hyperparathyroidism, especially those who display a rather mild elevation of iPTH. This is not the case, however, in a few patients who show a marked elevation of iPTH and/or proximal renal tubular dysfunction.

Adult↗
PubMed2005

Relationship between parathyroid calcium-sensing receptor expression and potency of the calcimimetic, cinacalcet, in suppressing parathyroid hormone secretion in an in vivo murine model of primary hyperparathyroidism.

Cinacalcet HCl, an allosteric modulator of the calcium-sensing receptor (CaR), has recently been approved for the treatment of secondary hyperparathyroidism in patients with chronic kidney disease on dialysis, due to its suppressive effect on parathyroid hormone (PTH) secretion. Although cinacalcet's effects in patients with primary and secondary hyperparathyroidism have been reported, the crucial relationship between the effect of calcimimetics and CaR expression on the parathyroid glands requires better understanding. To investigate its suppressive effect on PTH secretion in primary hyperparathyroidism, in which hypercalcemia may already have stimulated considerable CaR activity, we investigated the effect of cinacalcet HCl on PTH-cyclin D1 transgenic mice (PC2 mice), a model of primary hyperparathyroidism with hypo-expression of CaR on their parathyroid glands. A single administration of 30 mg/kg body weight (BW) of cinacalcet HCl significantly suppressed serum calcium (Ca) levels 2 h after administration in 65- to 85-week-old PC2 mice with chronic biochemical hyperparathyroidism. The percentage reduction in serum PTH was significantly correlated with CaR hypo-expression in the parathyroid glands. In older PC2 mice (93-99 weeks old) with advanced hyperparathyroidism, serum Ca and PTH levels were not suppressed by 30 mg cinacalcet HCl/kg. However, serum Ca and PTH levels were significantly suppressed by 100 mg/kg of cinacalcet HCl, suggesting that higher doses of this compound could overcome severe hyperparathyroidism. To conclude, cinacalcet HCl demonstrated potency in a murine model of primary hyperparathyroidism in spite of any presumed endogenous CaR activation by hypercalcemia and hypo-expression of CaR in the parathyroid glands.

Aging↗
PubMed2005

Pretreatment clinical and laboratory findings in dogs with primary hyperparathyroidism: 210 cases (1987-2004).

OBJECTIVE: To evaluate pretreatment clinical and laboratory findings in dogs with naturally occurring primary hyperparathyroidism. DESIGN: Retrospective study. ANIMALS: 210 dogs with primary hyperparathyroidism and 200 randomly selected, age-matched control dogs that did not have primary hyperparathyroidism. PROCEDURE: Medical records for dogs with primary hyperparathyroidism were reviewed for signalment; clinical features; and results of clinicopathologic testing, serum parathyroid hormone assays, and diagnostic imaging. RESULTS: Mean age of the dogs with primary hyperparathyroidism was 11.2 years (range, 6 to 17 years). The most common clinical signs were attributable to urolithiasis or urinary tract infection (ie, straining to urinate, increased frequency of urination, and hematuria). Most dogs (149 [71%]) did not have any observable abnormalities on physical examination. All dogs had hypercalcemia, and most (136 [65%]) had hypophosphatemia. Overall, 200 of the 210 (95%) dogs had BUN and serum creatinine concentrations within or less than the reference range, and serum parathyroid hormone concentration was within reference limits in 135 of 185 (73%) dogs in which it was measured. Urolithiasis was identified in 65 (31 %) dogs, and urinary tract infection was diagnosed in 61 (29%). Mean serum total calcium concentration for the control dogs-was significantly lower than mean concentration for the dogs with primary hyperparathyroidism, but mean BUN and serum creatinine concentrations for the control dogs were both significantly higher than concentrations for the dogs with primary hyperparathyroidism. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that urolithiasis and urinary tract infection may be associated with hypercalcemia in dogs-with primary hyperparathyroidism, but that development of renal insufficiency is uncommon.

Animals↗
PubMed1997

The rise and fall of primary hyperparathyroidism: a population-based study in Rochester, Minnesota, 1965-1992.

BACKGROUND: The introduction of routine measurement of serum calcium levels led to a sharp increase in the incidence of primary hyperparathyroidism in the early 1970s. OBJECTIVE: To evaluate the trends in the incidence of primary hyperparathyroidism since the mid-1970s. SETTING: Rochester and Olmsted County, Minnesota. DESIGN: Population-based descriptive study. PATIENTS: All residents of Rochester, Minnesota, who received an initial diagnosis of primary hyperparathyroidism between 1965 and 1992 were identified through the medical records linkage system of the Rochester Epidemiology Project. Included as persons having definite cases (92% of the total) were patients with pathologically confirmed hyperparathyroidism, hypercalcemia with inappropriately elevated parathyroid hormone levels, or hypercalcemia that had lasted for more than a year and had no cause other than primary hyperparathyroidism. MEASUREMENTS: Incidence rates were calculated and directly standardized to the population structure of white persons in the United States in 1990. RESULTS: From 1965 to June 1974 (the prescreening era), the age- and sex-adjusted incidence of primary hyperparathyroidism in Rochester was 15 cases per 100,000 person-years. After measurement of calcium levels was added to the automated serum chemistry panel in July 1974, the incidence increased to 112 per 100,000 person-years in 1975 and then decreased somewhat, reflecting a sweeping effect. Despite improved case ascertainment, however, the incidence rate has continued to decrease; in 1992, the incidence was 4 per 100,000 person-years. A few patients had complications that might have been caused by hyperparathyroidism (22% between 1965 and June 1974 and 6% thereafter), and survival was not impaired in either period. The maximum serum calcium levels did not change (P = 0.15). CONCLUSIONS: The progressive decrease in the incidence of primary hyperparathyroidism is unexpected and suggests a significant change in the epidemiology of this disease.

Adult↗
PubMed2001

[Results and complications of parathyroidectomy in secondary hyperparathyroidism].

Retrospective study was performed to measure the results of parathyroidectomy in patients with secondary hyperparathyroidism. From 1987 to 2000, 48 patients underwent surgery for secondary hyperparathyroidism. There were 30 of 48 patients on haemodialysis treatment, and 11 patients were in pre-dialysis stage. Parathyroidectomy was performed after successful kidney transplantation in 4 cases. Indication of the surgery was extremely elevated serum level of parathyroid hormone (at least 10 fold elevation), which was resistant for the conservative medical therapy. Subtotal parathyroidectomy (3 1/2) was performed in 30 patients. Five patients underwent total parathyroidectomy and autotransplantation. Only 2 or 3 parathyroid glands have been removed in 13 patients. Haematoma occurred in 3 cases after parathyroidectomy. Recurrent nerve injury or septic complication did not occur. Two patients died in the early postoperative period due to cardiac failure. Tetania was noted in 2 patients after surgery. Permanent postoperative hypocalcaemia (over 6 months) occurred in 3 cases. Persistent hyperparathyroidism was diagnosed in 5 patients. In these patients 2 parathyroid glands were removed during the primary operation. Recurrent hyperparathyroidism was detected in 2 patients. Subtotal parathyroidectomy was carried out in these cases previously. At the reoperation for persistent and recurrent hyperparathyroidism, total parathyroidectomy and autotransplantation was performed. Serum alkaline phosphatase level and serum parathyroid hormone value decreased after surgery, except those patients with persistent hyperparathyroidism. Bone pain decreased in 96% of the cases and pruritus decreased in 92% of the patients after parathyroidectomy. Soft tissue calcification showed improvement in 45% of cases. In conclusion, the subtotal parathyroidectomy or total parathyroidectomy with autotransplantation cause a rapid decrease of PTH level and the improvement of the clinical symptoms in patients with medical treatment resistant secondary hyperparathyroidism. Persistent hyperparathyroidism occurs in those cases when inadequate parathyroidectomy was performed.

Adolescent↗