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PubMed1996

Accelerated bone loss in post-menopausal women with mild primary hyperparathyroidism.

OBJECTIVES: Osteopenia is regarded as an indication for parathyroidectomy in primary hyperparathyroidism. However, uncertainty exists as to the extent and degree of the skeletal effects in those with mild disease. We sought to determine whether mild primary hyperparathyroidism affects the rate of bone loss in postmenopausal women. DESIGN: Prospective 2-year comparison of rates of bone loss throughout the skeleton in 17 post-menopausal women with untreated mild asymptomatic primary hyperparathyroidism, and 48 age-matched, eucalcaemic controls. RESULTS: The women with primary hyperparathyroidism had a greater annual rate of loss of bone mineral density (BMD) of the total body (mean +/- SE, primary hyperparathyroidism -1.15 +/- 0.31%, controls -0.39 +/- 0.10%; P = 0.04) and its spine subregion (primary hyperparathyroidism -2.08 +/- 0.88%, controls 0.04 +/- 0.35%; P = 0.02). Lumbar spine BMD tended to decline in the primary hyperparathyroidism group (-0.35 +/- 0.33%) in contrast to the control group (+0.28 +/- 0.22%) (P = 0.10). There were no significant differences between the groups in rates of changes of BMD in the legs or the proximal femur. In the primary hyperparathyroidism group, the rate of total body bone loss in the eight women known at study entry to have had long-standing (> 5 years) primary hyperparathyroidism was -1.52 +/- 0.61%/year, similar to that of the whole group. CONCLUSION: Primary hyperparathyroidism is associated with an increased rate of loss of total body bone mineral density in post-menopausal women. Prolonged disease duration is therefore likely to be associated with an increasing risk of osteopenia, such that skeletal surveillance and interventions designed to reduce bone loss should be considered.

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PubMed1999

[Early diagnosis and reoperation in persistent primary hyperparathyroidism].

INTRODUCTION: The persistence rate of primary hyperparathyroidism after cervical exploration was estimated and early diagnosis and reoperation were evaluated in a prospective study. METHODS: Between 1 August 1987 and 31 October 1998, 370 patients underwent surgery. The postoperative course is known in 94.6 % of these patients (follow-up 1 month-10 years, median 24 months). RESULTS: Cervical exploration was successful in 97.5 % (n = 353) of the 361 patients with the first manifestation of primary hyperparathyroidism and in all patients with recurrence or persistence of the disease after initial operation elsewhere. In persistent primary hyperparathyroidism serum calcium levels remained elevated 4 days after surgery (n = 9, 2.5 %). Localization studies, preferably with (99m)Tc-MIBI-scintigraphy were attempted during the first postoperative week and could be performed in 4 patients. Four patients wished the procedure to be performed later. CONCLUSION: Within one week after the initial intervention the diagnosis of persistent primary hyperparathyroidism can be established and localization studies as well as cervical reexploration can be carried out. An interval of 3 months from the initial operation to reexploration of the parathyroid area is recommended if the reexploration is impossible within one week. Mediastinal reoperations or surgical interventions in the neck sparing the perithyroid area may be carried out without consideration of specific intervals.

Adenoma↗

PubMed1988

Hormone, calcium and blood pressure relationships in primary hyperparathyroidism.

The cause of hypertension in primary hyperparathyroidism and its response to corrective surgery remains a matter of controversy. We therefore studied blood pressure, vasoactive hormones and plasma calcium responses to parathyroidectomy in six hypertensive and two normotensive patients with primary hyperparathyroidism. Twenty-four-hour intra-arterial pressure recordings, together with hourly blood sampling for plasma renin activity (PRA), aldosterone, cortisol, catecholamines and calcium levels, were undertaken in each patient before surgery and were repeated under identical conditions 3-6 months after parathyroidectomy. Mean plasma calcium was 3.03 +/- 0.1 before, and 2.35 +/- 0.02 mmol/l after, parathyroidectomy. Changes in arterial pressure were small and variable in individual patients. Group mean arterial pressures before and after surgery were identical. Plasma cortisol and PRA were significantly higher in the hypercalcaemic state (P less than 0.01 and P less than 0.05, respectively) but there was no significant difference in plasma aldosterone or catecholamine levels. No correlations between changes in plasma calcium or parathyroid hormone levels and concomitant changes in plasma concentration of other hormones were observed. Our findings show that correction of primary hyperparathyroidism has no systematic effect on arterial pressure in a heterogeneous group, including some patients with probable background essential hypertension, when evaluated 3-6 months after surgery. Compared with values after corrective surgery, mean levels of PRA and cortisol-but not aldosterone or catecholamines--are elevated in patients with primary hyperparathyroidism. These findings are consistent with an inhibitory effect of raised ionic calcium concentration on the response of the adrenal glomerulosa to angiotensin and adrenocorticotrophic hormone.

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PubMed2007

Psychiatric and cognitive aspects of primary hyperparathyroidism.

PURPOSE OF REVIEW: Clinical guidelines for the treatment of primary hyperparathyroidism have been established by the 2002 NIH workshop on asymptomatic primary hyperparathyroidism. The panel called for further study of the ill-defined psychiatric and cognitive changes often seen in patients with primary hyperparathyroidism. The present paper provides a rigorous, updated review of the most recent advances and studies that have measured health-related quality of life, neurocognitive and psychiatric changes, as well as neurophysiologic imaging in patients with primary hyperparathyroidism undergoing parathyroidectomy. RECENT FINDINGS: In studies conducted pre and postparathyroidectomy, six recent articles have described improvements in health-related quality of life. Five studies included evaluations with validated psychiatric and cognitive tests in prospective case-control trials, and showed varied improvements in depression, memory and concentration after parathyroidectomy. Two studies evaluated in a preliminary fashion the brains of patients with primary hyperparathyroidism with functional imaging studies, showing regional cerebral blood flow changes and prefrontal cortical activation with sleep improvement in postsurgical patients. SUMMARY: The studies described in this paper underline the benefits of surgical treatment on nontraditional symptoms in patients with primary hyperparathyroidism, and open the door to the continued study of the endocrine effects of primary hyperparathyroidism on brain function.

Cognition Disorders↗

PubMed2000

New insights on the pathogenesis of hypercalcemia in primary hyperparathyroidism.

The pathogenesis of hypercalcemia in primary hyperparathyroidism is attributed to increased calcium release from bone, increased calcium reabsorption in renal distal tubules, and increased intestinal calcium absorption. However, it remains unclear which factor is the main process. We encountered a 56-year-old woman with myasthenia gravis, in whom hypercalcemia and elevated serum parathyroid hormone (PTH) level were observed. Diagnosis of primary hyperparathyroidism was made. Treatment with methylprednisolone for myasthenia gravis was associated with a marked decrease in both biochemical markers of bone formation and resorption without any changes in endogenous cAMP and serum levels of calcium, PTH, and 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3]. These findings suggest that the possible pathogenesis of hypercalcemia in primary hyperparathyroidism may be attributed to the increased calcium reabsorption in the kidney and the increased intestinal calcium absorption as a result of stimulated production of 1,25-(OH)2D3 in the kidney. It thus follows that the renal tubular effect rather than the skeletal effect of the PTH excess may play a pivotal role in the development of hypercalcemia in primary hyperparathyroidism.

Bone Resorption↗

PubMedDate not supplied

Coincident diabetes mellitus and primary hyperparathyroidism.

The prevalence of diabetes mellitus in primary hyperparathyroidism is approximately 8% and that of primary hyperparathyroidism in diabetic patients is approximately 1%. Both values are about three-fold higher than the respective expected prevalences in general populations. Patients with both disorders are over 40 years of age and 80% are female; 22% have type 1 and 78% type 2 diabetes. Primary hyperparathyroidism presents first in approximately 20% of patients, and diabetes mellitus in 40%; both disorders present together, or within 1 year, in 40%. Approximately 40% of patients with primary hyperparathyroidism have impaired glucose tolerance. Insulin resistance is present in hyperparathyroidism and probably arises from a raised intracellular free calcium concentration which, by decreasing normal insulin-stimulated glucose transport, increases the requirement for insulin: if this insulin resistance progresses, impaired glucose tolerance and diabetes mellitus would result. Parathyroidectomy has been followed by regression of diabetes and of impaired glucose tolerance in some but not all patients. Early diagnosis of the second disorder is clinically desirable when one disorder is present. Hyperparathyroid patients should therefore be screened for impaired glucose tolerance and diabetes annually, and pre-operatively. Diabetic patients should be checked for hypercalcaemia at appropriate intervals; although only 1% of them may have hyperparathyroidism, this disorder if untreated is associated with hypertension, to which diabetic patients are already prone.

Animals↗

PubMed2004

Major depression due to primary hyperparathyroidism: a frequent and correctable disorder.

While primary hyperparathyroidism (primary HPT) is recognized as a correctable cause of nephrolithiasis and osteoporosis, its role as an organic cause of major depression is less clear. The rate of major depression in primary HPT, response of symptoms to parathyroidectomy, and potential cost benefits were reviewed. From August 1994 to September 2002, 360 patients underwent parathyroidectomy for primary HPT. Thirty-five patients met Diagnostic and Statistical Manual of Mental Disorders IV-Text Revision (DSM IV-TR) criteria for major depression. Postoperatively, a modified form of the Outcomes Institutes Health Status Questionnaire 2.0 was used to evaluate patient mood and continued need for antidepressant medication (ADM). Cost analysis of ADM use was performed. Thirty-five of 360 patients (10%) with primary HPT met criteria for major depression. Thirteen of 35 (37%) required ADM preoperatively. Postoperatively, 29/35 (83%) patients responded to a phone survey: 90 per cent stated depression no longer impacted their ability to work or activities of daily living; 52 per cent reported an improved quality of life; 27 per cent discontinued preoperative ADM; and 27 per cent reduced their ADM dose. Reduction in ADM resulted in a savings of dollars 700 to dollars 3000 per patient per year. Major depression occurs in 10 per cent of patients undergoing parathyroidectomy for primary HPT. Parathyroidectomy reduces symptoms of major depression, improves quality of life, and can eliminate or reduce the need for antidepressant medication in up to 54 per cent of patients.

Antidepressive Agents↗

PubMedDate not supplied

West Germany: still an underdeveloped country in the diagnosis and early treatment of primary hyperparathyroidism?

Early diagnosis of asymptomatic patients with primary hyperparathyroidism (primary HPT) has been achieved in Scandinavia, the United States of America, and the United Kingdom during the last 20 years. Comparable results have been reported from some medical centers from West Germany; however, clinical manifestations were pronounced and patient symptoms were high in our population with primary HPT (N = 128) operated on at the University of Düsseldorf from April, 1986 to July, 1989. Only 19 patients (14.8%) were asymptomatic while the others suffered from nephrolithiasis (39%), osteopathy (32%), gastrointestinal disturbances (28.9%), and depression (11.7%). In 46 (35.9%) of our patients, the duration of these clinical symptoms exceeded 10 years, in 27 patients (21%) 15 years, and in 12 patients (9.3%) even 25 years. We, therefore, conclude that primary HPT is still a grossly underdiagnosed illness in parts of West Germany, presently, with patients suffering from severe clinical symptoms for more than 1-2 decades before definitive treatment.

Adult↗

PubMed1996

Effect of hormone replacement therapy on bone mineral density in postmenopausal women with mild primary hyperparathyroidism. A randomized, controlled trial.

BACKGROUND: Most patients with primary hyperparathyroidism are postmenopausal women. The presence of osteopenia in persons with mild primary hyperparathyroidism is considered an indication for parathyroidectomy. No prospective, controlled trials have assessed medical therapies for osteopenia in primary hyperparathyroidism. OBJECTIVE: To examine the effects of estrogen-progestin therapy (hormone replacement therapy) on bone mineral density and biochemical indices in postmenopausal women with mild primary hyperparathyroidism. DESIGN: Double-blind, randomized, placebo-controlled trial. SETTING: University teaching hospital. PATIENTS: 42 postmenopausal women with mild primary hyperparathyroidism. INTERVENTION: Patients were randomly assigned to receive either conjugated estrogens, 0.625 mg/d, and medroxyprogesterone, 5 mg/d, or placebo. MEASUREMENTS: Bone mineral densities of the total body, lumbar spine, proximal femur (femoral neck, Ward triangle, trochanter), and proximal forearm were measured every 6 months using dual-energy x-ray absorptiometry. Biochemical indices of bone turnover and calcium metabolism were measured at baseline, 6 months, and 2 years. RESULTS: In the placebo group, bone mineral densities of the total body and the proximal forearm decreased significantly from baseline (mean +/- SE, -2.3% +/- 0.7% [p = 0.005] and -3.5% +/- 1.2% [p = 0.01], respectively). At the other sites, bone mineral density also tended to decline. In the hormone replacement therapy group, bone mineral density increased from baseline in the total body (1.3% +/- 0.4%; P = 0.004), lumbar spine (5.2% +/- 1.4%; p = 0.002), and femoral neck (3.4% +/- 1.5%; p = 0.05). The between-group differences in bone mineral density at the end of the study ranged from 3.6% to 6.6% and were significant at all sites (P > 0.001 and P < 0.05) except for the Ward triangle (p = 0.06). In the hormone replacement therapy group, serum alkaline phosphatase levels decreased by 22% (p = 0.0004 compared with baseline), urinary hydroxyproline excretion decreased by 42% (p = 0.0004), urinary N-telopeptide excretion decreased by 54% (p = 0.001), and urinary calcium excretion decreased by 45% (p = 0.007). Hormone replacement therapy did not change levels of serum ionized calcium or intact parathyroid hormone. CONCLUSIONS: Although hormone replacement therapy has little effect on serum calcium levels, it suppresses bone turnover, reduces urinary calcium excretion, and increase bone mineral density throughout the skeleton in postmenopausal women with mild primary hyperparathyroidism. This therapy is thus an important management option for these patients.

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PubMed1993

Expression of parathyroid hypertensive factor in hypertensive primary hyperparathyroid patients.

Hypertension is frequently associated with primary hyperparathyroidism, yet the mechanism of such hypertension is unknown. Parathyroid hypertensive factor (PHF) is a circulating hypertensive factor found in a proportion of human essential hypertensive patients as well as in spontaneously hypertensive rats (SHR). In the latter case, PHF has been shown to be secreted by the parathyroid gland. The purpose of this study was to determine if PHF expression might be responsible for the hypertension seen in primary hyperparathyroidism. Ten hypertensive and 10 normotensive primary hyperparathyroid patients underwent measurement of blood pressure and PHF pre- and post-parathyroidectomy. Cases reported are those of parathyroid adenomas. There were no significant differences between the hypertensive and normotensive groups preoperatively except that 9 out of 10 of the hypertensive group had significant PHF levels (mean 11 +/- 2 mm Hg vs 0.6 +/- 2 mm Hg, respectively, p = 0.003). Post-operative change in mean arterial pressure could be predicted by pre-operative PHF level, with all PHF-positive patients showing a fall in blood pressure (r = -0.73, p < 0.01). Post-operatively, PHF was undetectable in PHF-positive patients. These results suggest that the parathyroid gland can express PHF in humans and that such expression may be responsible for a proportion of the high reported incidence of hypertension in primary hyperparathyroidism.

Analysis of Variance↗

PubMed1997

Primary hyperparathyroidism with cardiac abnormalities: a case report.

Primary hyperparathyroidism, characterized by hypersecretion of parathyroid hormone (PTH) leading to hypercalcemia and relative hypophosphatemia, is quite common in the elderly. Most patients with primary hyperparathyroidism have only mild hypercalcemia and are symptomless. But others experience various other organ diseases. Primary hyperparathyroidism is also associated with cardiovascular abnormalities, including QT interval shortening, heart block, cardiac arrhythmias, hypertension, myocardial hypertrophy, myocardial calcification and, though rarely, with valvular heart disease. We described a case of primary hyperparathyroidism associated with cardiac abnormalities. An 82-year-old male presented with the complaints of chest discomfort, fatigue, general weakness, nausea and vomiting over a period of months and was admitted in July 1996. Physical examination with heart auscultation showed a pansystolic murmur over the right sternal border and apex region, and a blowing diastolic murmur over the left sternal border. Biochemistry profiles revealed elevations of serum calcium (14.3 mg/dl) and chloride/phosphate ratio (> 33). Endocrinological studies showed elevations of serum PTH-C (4.8 ng/ml) and PTH-intact (705 pg/ml) concentrations. Kidney ultrasonography revealed a left renal stone. A spine X-ray revealed spondylosis and a compression fracture of the lumbar-spine with osteoporotic change. Thyroid ultrasonography and Thallium (Tl201)-technetium (Tc99m) subtraction scan showed parathyroid adenoma in the low pole of the right thyroid bed. Parathyroid aspiration cytology revealed few and discrete cells. Echocardiogram revealed moderate to severe aortic valvular calcification as well as stenosis with moderate aortic regurgitation, mitral regurgitation and myocardial calcification. The patient received parathyroidectomy one month later. During his postoperative days, he suffered from muscle twitching with positive Trousseau's sign and Chvostek's sign. The patient received calcium carbonate and vitamin D for hypocalcemia, diltiazem and capoten for his heart problems. A repeated echocardiogram two months after surgery showed no improvement of valvular calcification.

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PubMed1993

Bilateral neck exploration for primary hyperparathyroidism.

Controversy about the operative approach for primary hyperparathyroidism has prompted a review of our operative experience since 1980. We treated 73 patients with primary hyperparathyroidism during this 10-year period, all of whom underwent bilateral neck exploration in which the surgeons attempted to locate all parathyroid tissue. Thirty-eight patients (52%) were found to have a solitary adenoma, while 35 (48%) patients had multiple gland pathology. There were two cases of persistent hypercalcemia because of a synchronous parathyroid hormone-secreting malignancy in one patient and aberrant fifth gland adenoma in the other patient. Without bilateral neck exploration, about one-half of the patients in our series would not have been cured of primary hyperparathyroidism. Because of the high incidence of multiple parathyroid gland involvement, we conclude that thorough bilateral neck exploration must be considered the goal for surgical treatment of primary hyperparathyroidism.

Adenoma↗

PubMed1989

Primary hyperparathyroidism. A surgical perspective.

Primary hyperparathyroidism is a common disorder and one that can usually (approximately 95%) be successfully treated by parathyroidectomy. PTH assays have become quite accurate for confirming the diagnosis. In patients with malignancy-associated hypercalcemia, parathyroid-like protein levels are usually increased, and radioimmunoassays being developed to quantitate serum levels of this protein will make the diagnosis easier. Treatment for a parathyroid adenoma is removal of the tumor and identification of the normal parathyroid glands. Treatment for primary or secondary hyperplasia is usually subtotal parathyroidectomy. Recurrent hyperparathyroidism is uncommon, except in patients with familial hyperparathyroidism, MEN-1 parathyroid carcinoma, or renal failure and secondary hyperparathyroidism. Persistent hyperparathyroidism is more common and is usually due to surgeon inexperience, but it is also caused by ectopically situated parathyroid glands, multiple abnormal parathyroid glands, or supranumerary parathyroid glands. Preoperative localization studies using ultrasound, thallium-technetium scanning, MRI, or CT scanning are reliable in patients with solitary parathyroid adenomas, but often fail to detect all of the abnormal parathyroid tissue in patients with multiple abnormal parathyroid glands. Intraoperative use of urinary cyclic AMP assays and rapid PTH assays have recently been used experimentally during parathyroid explorations to determine whether all hyperfunctioning parathyroid tissue has been removed, but these methods are not yet reliable or fast enough to be generally accepted. Most patients with primary hyperparathyroidism who are successfully treated by parathyroidectomy experience psychological, clinical, and metabolic benefits.

Calcium↗

PubMed1994

Diagnosis and management of primary hyperparathyroidism.

Since the introduction of biochemical autoanalyzers primary hyperparathyroidism is no longer an uncommon diagnosis. The diagnosis is established by clinical evaluation and persistently elevated serum calcium and parathyroid hormone levels. Management of symptomatic primary hyperparathyroidism is relatively straightforward and the disease can be effectively treated with surgery. Most surgeons agree patients without previous neck operations need not undergo preoperative localization studies; in addition, they feel that bilateral neck exploration should be the rule. However, the management of primary hyperparathyroidism in the asymptomatic patient is controversial. In this paper the natural history, diagnosis, and management of primary hyperparathyroidism is reviewed.

Combined Modality Therapy↗

PubMed2001

Familial isolated primary hyperparathyroidism--a multiple endocrine neoplasia type 1 variant?

OBJECTIVE: Familial isolated primary hyperparathyroidism (FIHP) is defined as hereditary primary hyperparathyroidism without the association of other diseases or tumors. Linkage analyses suggest that different genotypes can lead to the same phenotype of primary hyperparathyroidism. Hereditary syndromes associated with primary hyperparathyroidism are multiple endocrine neoplasia type 1 and type 2 (MEN 1 and MEN 2). In MEN 1, multiple parathyroid adenomas occur in more than 90% of the patients. Therefore, it has been suggested that FIHP could represent a variant or partial expression of MEN 1. DESIGN: We report on a large FIHP kindred with a MEN1 gene mutation. Nineteen family members (aged 10 to 87 years) were screened. Furthermore, statistical comparison by Fisher's exact tests of FIHP families with MEN1 gene mutations and MEN 1 families with two or more endocrinopathies was carried out to investigate genotype-phenotype correlations. METHODS: Mutational analysis of leucocyte DNA was carried out by direct sequencing of the complete coding region of the MEN1 gene. Screening of MEN 1 manifestations was carried out by determination of serum calcium, phosphate, parathyroid hormone, prolactin, ACTH, cortisol, IGF-I, gastrin, glucose, insulin, glucagon, serum potassium, aldosterone, plasma renin and urinary hydroxyindoleacetic acid. RESULTS: We detected an in-frame deletion mutation in exon 8 of the MEN1 gene resulting in the deletion of one glutamine acid residue at position 363. It was found in eight individuals. Two of these family members (aged 42 and 60 years) were operated for primary hyperparathyroidism, and three (aged 13 to 40 years) showed mild hypercalcemia and parathyroid hormone levels within the upper normal range or slightly elevated, without any clinical symptoms. Two individuals (aged 12 and 19 years) were normocalcemic. One could not be tested. None of them had clinical evidence of other MEN 1 manifestations. Statistical comparison of the mutation types in families with FIHP and families with two or more MEN 1-associated endocrinopathies reported in other studies reveals a significant difference. In families with FIHP, missense/in-frame mutations have been found in 87.5% of cases whereas in families with tumors in various endocrine glands these mutation types occur much less frequently (21-34%, P<0.05). CONCLUSIONS: These studies indicate that FIHP can represent a partial MEN 1 variant and is often caused by missense/in-frame mutations.

Adolescent↗

PubMed2006

[Cinacalcet--a new drug for the treatment of secondary hyperparathyroidism in patients with uraemia, parathyroid cancer or primary hyperparathyroidism].

Cinacalcet is a new drug with antiparathyroid effects that belongs to the class of calcimimetics. It increases the sensitivity of the calcium-sensing receptor (CaSR) to calcium, thus inducing a decrease in plasma parathyroid (PTH) levels. In patients with uncontrolled secondary hyperparathyroidism due to uremia, cinacalcet has been shown to decrease the levels of PTH even in those optimally treated with calcium and 1-ahydroxylated vitamin D. Cinacalcet decreases plasma calcium and plasma PTH levels in patients with primary hyperparathyroidism or parathyroid cancer.

Calcium↗

PubMed1998

Clinical profile of primary hyperparathyroidism in adolescents and young adults.

OBJECTIVE: Primary hyperparathyroidism (PHPT) is an uncommonly diagnosed condition among adolescents and young adults. We review the clinical characteristics of these patients based on our institutional experience. SUBJECTS: Patients aged 12-28 years treated for PHPT at our institution from 1990 to 1996 were evaluated by a review of medical records and current follow-up data. This consisted of 22 patients (8M:14F), constituting approximately 3% of all patients operated for PHPT during this period. MEASUREMENTS: Serum and urinary calcium concentrations, renal function, and serum intact parathyroid hormone (IPTH) levels were measured in all patients. After biochemical confirmation of diagnosis, the patients completed a questionnaire to evaluate the presence of symptoms and/or conditions associated with PHPT. All the patients underwent parathyroidectomy and their tumour characteristics were evaluated. Surgical outcome was determined by measurements of serum calcium and IPTH levels postoperatively and during long-term follow-up. RESULTS: A third of the patients were diagnosed by routine serum chemistry whereas two-thirds presented with symptoms or conditions associated with hypercalcaemia. Non-specific complaints such as fatigue or exhaustion, and weakness or lethargy constitute the most common findings on questionnaire review. A family history of PHPT was present in only 2 patients. The preoperative peak serum calcium levels ranged from 2.67 to 4.19 mmol/l (norm: 2.10-2.54 mmol/l), with a median of 3.07 mmol/l. Surgical pathologies revealed 59% solitary adenoma, 27% hyperplasia, 9% multiple adenomas and 5% carcinoma. Comparison between the adolescents (aged 12-18 years) and young adults (aged 19-28 years) revealed no differences in the clinical, pathological or laboratory profiles, except for a male predominance in adolescent patients. Fifteen patients had resection of one or more adenomas while 7 underwent subtotal parathyroidectomy. Six patients (27%) were reoperated cases, all received primary treatment elsewhere. All patients with benign PHPT were cured surgically, with a median follow-up of 47 months (range 3-77 months). One reoperated patient developed permanent hypocalcaemia. One patient with carcinoma underwent several operations for recurrence; he is now eucalcaemic despite persistent disease at 80 months from diagnosis. CONCLUSIONS: We found a high incidence of multiglandular disease and relatively non-specific symptomatology in our adolescent and young adult patients with primary hyperparathyroidism. In view of the heterogeneous clinical expression noted in young patients, one should consider primary hyperparathyroidism in the differential diagnosis of unexplained non-specific complaints, and perform serum calcium estimations more readily in these subjects. Our experience suggests that primary hyperparathyroidism can be a serious disease with significant morbidity if left untreated, whereas parathyroidectomy provides successful results.

Adolescent↗

PubMed1986

Trabecular bone remodeling and balance in primary hyperparathyroidism.

The total remodeling sequences in 19 primary hyperparathyroid patients and 16 approximately age-matched and sex-matched controls were reconstructed from histomorphometric analyses of bone specimens obtained after intravital tetracycline double labeling. In the primary hyperparathyroid group the total amount of work performed by resorptive cells was reduced, as indicated by the significantly lower three-dimensional mononuclear and preosteoblast-like cell resorption depths (35.8 microns vs 44.5 microns in normals, P less than 0.01 and 45.3 microns vs 56.6 microns in normals, P less than 0.01, respectively). The active resorption period (i.e., the function period for osteoclasts and mononuclear cells) was reduced to 19 days compared to 29 days in normals (P less than 0.05), but no difference with respect to bone resorption rates could be demonstrated between the two groups. The median bone formation period (Sigmaf) in primary hyperparathyroid patients was not different from the value obtained in normals (172 days vs 134 days, respectively), and the matrix appositional rate (Ama), as well as the mineralization lag time (tm), were also unchanged. The initial mineralization rate (Ami(i)) was not significantly different from the value obtained in normals, but averaged over the total bone formation period, a reduced mineralization rate could be demonstrated (0.32 micron3/micron2 per day vs 0.46 micron3/micron2 per day in normals, P less than 0.01). The measured final three-dimensional thickness of bone formed during Sigmaf (mcwTm) was reduced in the primary hyperparathyroid group (51.1 microns vs 55.9 microns in normals, P less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗