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PubMed1993

[Diabetes mellitus and carbohydrate metabolism in primary hyperparathyroidism].

It is generally known that patients with primary hyperparathyroidism (pHPT) feature disturbances in carbohydrate metabolism and hypertension. The incidence and prevalence of frank diabetes mellitus is significantly increased in these patients. The etiology and pathogenesis of the vascular and metabolic aberrations in this condition are still unclear. Glucose intolerance in pHPT is characterized by severe insulin resistance associated with pancreatic beta cell hypersecretion of insulin. Hypercalcemia is thought to be mainly responsible for the impaired glucose metabolism. However, several studies demonstrated that hypophosphatemia can also induce insulin hypersecretion and impair peripheral glucose uptake. Hypertension in primary hyperparathyroidism is mainly attributed to hypercalcemia. However, high peripheral insulin levels are also proposed to contribute to the development of essential hypertension and hyperinsulinemia per se is regarded as an important independent cardiovascular risk factor. After parathyroidectomy and decrease of the calcium levels to within the normal range, the blood pressure levels of the patients with pHPT normalised very quickly, whereas normalization of the high peripheral insulin levels was only found in a subgroup of patients. Thus, hypercalcemia seems to be mainly responsible for hypertension in primary hyperparathyroidism. Another important, yet unresolved issue is the question as to whether or to which extent the disturbances in glucose homeostasis are reversible after surgical correction of pHPT. At an early stage of the disease, insulin resistance and insulin hypersecretion are fully reversible after parathyroidectomy, whereas in patients with long-standing primary hyperparathyroidism and severely impaired glucose tolerance the metabolic disturbances will only partially improve. These results argue for improved screening to identify asymptomatic patients with primary hyperparathyroidism and for early surgical intervention in this disease.

Blood Glucose↗

PubMed1990

[Plasma and tumor gastrin in patients with primary hyperparathyroidism].

It is well known that primary hyperparathyroidism is often associated with peptic ulcer. The purpose of this study is to confirm the relationship between the gastrin-levels before and after parathyroidectomy in fourteen patients with primary hyperparathyroidism, and to determine the localization of gastrin in the surgically resected parathyroid tumor. The results obtained were as follows: 1) Three patients had peptic ulcer (gastric ulcer and duodenal ulcer), the incidence being 21%. 2) The basal serum gastrin levels were 123.0% +/- 68.1 pg/ml before operation and decreased to 90.2 +/- 44.5 pg/ml after operation. In the 3 patients with slightly elevated gastrin levels, the mean level before operation was 209.1 +/- 61.2 pg/ml. The gastrin level decreased to 116.4 +/- 62.0 pg/ml after operation. 3) Gastrin immunoreactivity was detected in 10 out of 14 tumors and its localization was at the periphery of tumor cells. From these results, we conclude that extragastric gastrin secretion from parathyroid tumors may be one of the cause of peptic ulcer in patients with primary hyperparathyroidism.

Calcium↗

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↗

PubMed1994

[Primary hyperparathyroidism. Clinical, epidemiological and histological aspects].

Primary hyperparathyroidism is most frequently caused by a single parathyroid adenoma and is more frequent in females than in males. Its frequency increases with age. Its annual incidence has been estimated at 41 per 100,000 in Rochester, and its prevalence at 4.3 per 1000 in Stockholm. Since the introduction of automated serum calcium measurements, the recognition of primary hyperparathyroidism has increased and the clinical presentation of the disease has changed. Classical osseous and renal features of the disease have become rare, due to the increased proportion of asymptomatic forms and to earlier diagnosis. Primary hyperparathyroidism is nowadays usually recognized because serum calcium is measured either systematically or in the clinical setting of mild manifestations, such as arthenia, anxiety, hypertension... Bone histology gives evidences of an accelerated bone turn-over, without major unbalance between formation and resorption. Bone densitometry has shown only minor decrease of mineral content of the lumbar spine in several modern series, so that the deleterious effect of mild or asymptomatic hyperparathyroidism on cancelous bone is presently questioned by several authors.

Adult↗

PubMed2000

Primary hyperparathyroidism: pathophysiology and impact on bone.

Primary hyperparathyroidism has been associated with bone loss, especially at cortical skeletal sites. Results from studies evaluating the mineral density of cancellous bone have been more difficult to interpret. Most densitometry studies support the concept that the parathyroid hormone appears to be catabolic at cortical sites and may have anabolic effects at cancellous bone sites. Studies completed to date, however, have been limited by design, definitions of fracture and inadequate control groups. Primary hyperparathyroidism is now increasingly being detected during the asymptomatic phase. The need for parathyroidectomy has been questioned in such patients because there may be no disease progression in the absence of surgery. Medical management of primary hyperparathyroidism has to date been limited to estrogen replacement therapy in postmenopausal women. Identification of the calcium receptor has improved our understanding of calcium homeostasis, and significant reductions in calcium receptor levels have been detected in parathyroid adenomas. Thus, a new class of therapeutics may include the calcimimetic agents. Bisphosphonates are also currently being evaluated with regard to their impact on fracture prevention and their beneficial effects on bone mineral density.

Bone Density↗

PubMed1995

Parathyroid adenoma weight and the risk of death after treatment for primary hyperparathyroidism.

BACKGROUND: Patients operated on for primary hyperparathyroidism run an increased risk of death, as was found in a previous long-term follow-up of 896 patients. METHODS: In the present study the adenoma weight was determined in 713 patients with single parathyroid gland disease operated on between 1956 and 1982 and followed up in 1986. The adenoma weight was investigated for its usefulness as a prognostic factor. RESULTS: The analysis showed that the adenoma weight was significantly related to the risk of death (p < 0.001). Also a relationship was noted between glandular weight and preoperative serum calcium level (p < 0.001), although the serum calcium level had no predictive value in relation to the risk of death beyond that of the adenoma weight. The risk increase was also estimated as a function of adenoma weight. A moderate adenoma weight increase in a patient with primary hyperparathyroidism was found to imply an increased risk of death, corresponding to the increased risk of smokers as compared with nonsmokers. CONCLUSIONS: The results of this study support surgical treatment at an early stage of primary hyperparathyroidism.

Adenoma↗

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↗

PubMed1994

[Chronic pancreatitis and primary hyperparathyroidism].

The frequency of acute or chronic pancreatitis in primary hyperparathyroidism has decreased from the former 5-10% to 1-2% thanks to earlier diagnosis and operative treatment. Chronic pancreatitis, which occurs only in prolonged primary hyperparathyroidism, should therefore virtually disappear. We investigated this topic in a prospective long term study of chronic pancreatitis (1963-1992). Over the last three decades 336 patients with chronic pancreatitis have been studied at regular intervals. 245 suffered from alcohol-induced (84% with calcifications) and 91 from non-alcohol-induced chronic pancreatitis (77% with calcifications). The average period of observation in the group with non-alcohol-induced chronic pancreatitis was 10.6 years. Primary hyperparathyroidism was found in 6 patients (4 male, 2 female), i.e. 6.6% of non-alcohol-induced chronic pancreatitis (100% with calcifications). They were evenly distributed over the 30 years' study period. 3 patients had acute attacks of pancreatitis prior to the diagnosis of chronic calcific pancreatitis (2 months, 3 + 8 years). In 3 patients with primary painless chronic calcific pancreatitis the condition was diagnosed twice incidentally and once because of diabetes mellitus. Chronic pancreatitis was diagnosed 3 times before primary hyperparathyroidism (8.3 +/- 2.1 years), once simultaneously and twice afterwards (2 + 14 years). In three patients chronic pancreatitis was initially misinterpreted as alcohol-induced. Severe exocrine pancreatic insufficiency was present in 4 of 5 patients (no data in one), and diabetes mellitus in 3 of 6 patients. At the time of diagnosis of primary hyperparathyroidism, mean serum calcium was 3.08 +/- 0.43 mmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcoholism↗

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↗

PubMed2005

Primary hyperparathyroidism in pediatric patients.

OBJECTIVE: Primary hyperparathyroidism (HPT) is unusual in children. We reviewed our experience with HPT to better characterize these children. METHODS: The retrospective review of patients <19 years old who underwent parathyroid resection for primary HPT from 1970 to 2000 was performed at a single institution.. RESULTS: Fifty-two patients were identified. Median age was 16.8 years (range: 4-18.9) with a female-to-male ratio of 3:2. Eighty-five percent had an elevated parathyroid hormone (PTH) level, and 15% had an inappropriately normal PTH level during hypercalcemia. Serum calcium was elevated in all patients except for 2 with multiple endocrine neoplasma (MEN)-IIA and 1 with familial non-MEN HPT, but both had elevated PTH levels. Alkaline phosphatase levels were significantly higher in children with documented bone involvement. At presentation 41 patients (79%) were symptomatic and end-organ damage (nephrocalcinosis, nephrolithiasis, acute pancreatitis, or bone involvement) occurred in 23 patients (44%). Thirty-four patients (65%) had a single adenoma; hyperplasia was identified in 16 patients (27%), and of these cases, 57% occurred in patients diagnosed with MEN-I. Short-term complications included transient hypocalcemia in 29 patients (56%) and transient vocal cord paralysis in 2 patients (4%). Long-term complications were significant for permanent hypocalcemia in 2 patients (4%) and no recurrent laryngeal nerve injuries. No parathyroid abnormalities were identified during exploration in 4 (8%) children. Long-term follow-up was achieved in 98% of patients for a mean and median of 13 years. Resolution of hypercalcemia was achieved in 94% of cases. CONCLUSION: The diagnosis of primary HPT in pediatric patients is frequently delayed, is commonly symptomatic, and has significant morbidity. For children in whom HPT is suspected, evaluation of serum calcium and PTH levels is diagnostic in 100% of children. Parathyroid resection is effective at restoring normal serum calcium, has few complications, and is the treatment of choice for children with primary hyperparathyroidism.

Adenoma↗

PubMed2005

Brown tumour: presenting symptom of primary hyperparathyroidism.

The skeletal lesions of primary hyperparathyroidism, including brown tumour, are rare nowadays, with the practice of checking serum calcium levels leading to an earlier diagnosis of hyperparathyroidism. Clinical, laboratory, radiographic and histological investigations can lead to a correct diagnosis. Treatment of brown tumour focuses on the hyperparathyroidism, and is usually followed by a regression of the brown tumour. The diagnosis of hyperparathyroidism and brown tumour should be considered in patients with hypercalcaemia and an osteolytic expansive bone lesion. We present a patient where a brown tumour of the mandible was the presenting symptom of primary hyperparathyroidism.

Adenoma↗

PubMed2002

Primary hyperparathyroidism in pregnancy: evidence-based management.

UNLABELLED: Primary hyperparathyroidism during pregnancy poses significant risks to the mother and the fetus. Fortunately, prompt diagnosis and effective management can improve outcomes for both. There is controversy regarding appropriate management of these patients, especially late in gestation. The objective of this article, therefore, is to review the literature and to propose an evidence-based approach to managing these patients. The prevalence of primary hyperparathyroidism in the general population is 0.15%. This condition is more common in women and 25% of cases appear in women during the childbearing years. The true incidence during pregnancy, however, is not known. Because up to 80% of gravid patients with primary hyperparathyroidism are asymptomatic, diagnosing this condition is more difficult. Complications associated with primary hyperparathyroidism in pregnancy have been reported to occur in up to 67% of mothers and 80% of fetuses. In addition to many constitutional symptoms, maternal complications include nephrolithiasis, bone disease, pancreatitis, hyperemesis, muscle weakness, mental status changes, and hypercalcemic crisis. Reported fetal complications include intrauterine growth retardation, low birth weight, preterm delivery, intrauterine fetal demise, postpartum neonatal tetany, and permanent hypoparathyroidism. A four-fold decrease in perinatal complications may be achieved with appropriate therapy. Conservative intervention may be appropriate under certain circumstances, but excision of a parathyroid adenoma remains the only definitive treatment. Debate continues regarding the safety of surgery in the third trimester. However, several cases of successful surgery have been reported. TARGET AUDIENCE: Obstetricians & Gynecologists, Family Physicians. LEARNING OBJECTIVES: After completion of this article, the reader will be able to describe the typical presentation of a patient with hyperparathyroidism, summarize the work up and management of a patient with hyperparathyroidism, and list the treatment options for a pregnant patient with hyperparathyroidism.

Adenoma↗

PubMed1991

Characterization and evaluation of asymptomatic primary hyperparathyroidism.

Data are presented on 97 patients with primary hyperparathyroidism who constitute a representative cohort of the disease seen today. The average calcium (11.1 +/- 0.1 mg/dl; normal 8.7-10.7), phosphorus (2.8 +/- 0.1 mg/dl; normal 2.5-4.5), and parathyroid hormone level by immunoradiometric assay (119 +/- 7 pg/ml; normal 10-65) are typical of the modern presentation of primary hyperparathyroidism. Most patients were asymptomatic in that there was evidence for nephrolithiasis in only 18% and for radiologically evident bone disease in only 1% of patients. Nevertheless, when patients were evaluated with bone densitometry and with histomorphometric analysis of the bone biopsy specimen, evidence for the hyperparathyroid process could be shown in the majority of patients. Selective reduction of cortical bone and preservation of cancellous bone were apparent. Among patients with nephrolithiasis, no particular feature distinguished them from patients without nephrolithiasis. All biochemical data were similar between both stone and non-stone formers. The selective reduction in cortical bone was seen to the same extent among those with stones as among those without stones. The average 1,25-dihydroxyvitamin D level was not increased among those with stones. When the population was divided into groups with elevated or normal 1,25-dihydroxyvitamin D levels, the incidence of nephrolithiasis was unchanged. The results indicate that bone involvement can be demonstrated among most patients with asymptomatic primary hyperparathyroidism and that no pathophysiologic mechanisms are yet apparent to account for nephrolithiasis in primary hyperparathyroidism.

Adult↗

PubMed1999

Localization of parathyroid tumors using endoscopic ultrasonography in primary hyperparathyroidism.

Parathyroid adenomas responsible for primary hyperparathyroidism may be difficult to detect preoperatively. Furthermore parathyroid adenomas may arise behind the (nodular) thyroid gland, in a deep cervical location, and plans should be plane. The purpose of the present prospective study was to evaluate echoendoscopy, and to compare its accuracy to that of non invasive tests. Fourteen consecutive patients with primary hyperparathyroidism were prospectively studied. All patients underwent echoendoscopy, ultrasonography (US), CT scanning or magnetic resonance imaging (MRI) and Tc 99m sestamibi scanning before undergoing initial neck exploration. The parathyroid pathology was a solitary adenoma in 13 patients and a 4 glands hyperplasia in one. All tests were corroborating in 5 cases. Four adenomas were localized to the correc tside (33%), and no test accurately localized all hyperplastic glands. EUS, sestamibi and CT scanning or MRI correctly identified 10 parathyroid tumors in 14 cases (71%). US correctly localized only 5 adenomas (sensitivity 36%). The sensitivity of EUS to detect parathyroid adenomas is superior to US (p<0.05) and comparable to that of other non invasive tests. We conclude that EUS may be an useful tool to localize parathyroid lesions. This method may replace US prior to initial neck exploration with further miniaturization of probes, or find an intermediate place among invasive and noninvasive preoperative localization procedures in patients with persistent or recurrent PHPT.

Adenoma↗

PubMedDate not supplied

The role of intraoperative quick PTH measurements in primary hyperparathyroidism.

BACKGROUND: In patients with primary hyperparathyroidism (PHPT), circulating concentrations of intact parathyroid hormone (PTH), decline dramatically within minutes following surgical excision of hyperfunctioning parathyroid tissue. The magnitude of this decay correlates with the completeness of resection of hyperfunctioning parathyroid tissue and can be monitored during the operation. METHOD: Intraoperative Quick PTH (QPTH) monitoring and pitfalls of more than 350 patients, who were operated because of primary hyperparathyroidism are analyzed. Special attention is given to correct baseline values and interpretation of QPTH values. RESULTS: QPTH monitoring is able to distinguish reliably between single and multiple gland disease and is an indispensable prerequisite for any form of limited parathyroid exploration. Experience with QPTH monitoring is necessary to achieve the excellent results known from bilateral neck exploration. CONCLUSION: Applying correct baseline values and cautious interpretation of QPTH values results in excellent results. Nevertheless more data must be collected to allow reliable interpretation of QPTH monitoring in all patients with PHPT.

Humans↗

PubMed1994

Effect of bisphosphonate therapy and parathyroidectomy on the urinary excretion of galactosylhydroxylysine in primary hyperparathyroidism.

BACKGROUND: In patients with mild or asymptomatic primary hyperparathyroidism a reliable index of bone resorption might be useful for appropriate management. Hydroxyproline is the most commonly used marker of bone resorption but its low specificity and sensitivity are known. Galactosylhydroxylysine, an amino acid mainly represented in bone collagen, has been proposed as a more suitable index of bone resorption. In this study we evaluated the sensitivity of galactosylhydroxylysine and hydroxyproline assays in following the changes of their urinary levels in 12 patients with mild primary hyperparathyroidism before and after treatment with bisphosphonate and surgery. METHODS: Serum and fasting urine specimens were obtained from 12 women with mild primary hyperparathyroidism before and after bisphosphonate treatment (2.5 mg daily for 5 days, intravenously) and after a further 25 days; in 7 patients biochemical tests were also performed 1 and 6 days after parathyroidectomy. Galactosylhydroxylysine was assayed by an HPLC method and hydroxyproline by a RIA commercial kit. RESULTS: Baseline galactosylhydroxylysine urinary levels were far above the normal range in all the patients whilst in 8 of them baseline hydroxyproline levels were normal. Bisphosphonate treatment significantly decreased bone turnover as shown by a significant fall in serum calcium (from 2.9 to 2.6 mmol/l; P < 0.001) and in galactosylhydroxylysine and hydroxyproline (-55 and -31% respectively). Twenty-five days after the end of treatment, resorption increased again and serum calcium and galactosylhydroxylysine, but not hydroxyproline, rose significantly towards basal levels. One day after parathyroidectomy serum calcium, galactosylhydroxylysine and PTH showed reduction below normal ranges. PTH and galactosylhydroxylysine returned to normal values at day 6 after parathyroidectomy. No changes in hydroxyproline levels were seen. Galactosylhydroxylysine, but not hydroxyproline, correlated significantly with serum calcium and PTH. CONCLUSION: Galactosylhydroxylysine appears to be a sensitive index of bone resorption, useful in the clinical assessment of bone involvement and in the management of patients with mild primary hyperparathyroidism.

Aged↗