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Coeliac disease and primary hyperparathyroidism: an association?

Primary hyperparathyroidism may present with non-specific symptoms, and this may be one reason why patients with coeliac disease fail to improve despite compliance with a gluten-free diet. Seven case reports of primary hyperparathyroidism due to sporadic adenoma occurring in a series of 310 patients with coeliac disease are presented, highlighting the importance of looking for this condition in this population group. A prevalence of primary hyperparathyroidism of 2.3% in this series suggests a significant association between hyperparathyroidism and coeliac disease; most studies have indicated a prevalence of 3 in 1000 in the general population, although one study found that it may be as high as 21 in 1000 in women aged 55-75 years. The average age of patients in our series was 59 years and all but one were women. Further studies are needed to establish a possible association between primary hyperparathyroidism and coeliac disease.

Adenoma↗

Immunoheterogeneity of parathyroid hormone pre- and postoperatively in primary hyperparathyroidism.

In primary hyperparathyroidism (pHPT), a preferential release of intact PTH (i-PTH) versus carboxylterminal PTH fragments is known to occur. We studied whether the release of amino-terminal PTH fragments (N-PTH) is also changed. Serum levels of i-PTH and N-PTH were determined under basal conditions and following oral intake of calcium in six patients with pHPT before and immediately after surgery and in seven healthy subjects. In the patients, baseline levels of both i-PTH and N-PTH were increased preoperatively. The increase was larger in i-PTH compared to N-PTH. Therefore, the N/i ratio was reduced compared to healthy subjects (P < 0.05). On the first postoperative day, serum i-PTH decreased to a larger extent than N-PTH, which increased the N/i ratio above that in healthy subjects (P < 0.05). On the 5th postoperative day, the N/i ratio was normalized. Preoperatively, the suppressibility of i-PTH calcium was impaired in the patients (P < 0.05), whereas the suppressibility of N-PTH was normal, resulting in unchanged N/i ratio during the oral calcium load. In contrast, the N/i ratio increased normally during the calcium load at day 5 postoperatively (P < 0.05). We therefore conclude that: (1) in pHPT, circulating PTH immunoheterogeneity is altered with a preferential release of intact PTH compared to N-terminal PTH fragments and this alteration is normalized after surgery, (2) the secretion of intact PTH and N-terminal PTH shows different sensitivity to inhibition by calcium.

Adenoma↗

Maintained normalization of cardiovascular dysfunction 5 years after parathyroidectomy in primary hyperparathyroidism.

BACKGROUND: Primary hyperparathyroidism (pHPT) has been associated with premature death in cardiovascular diseases. Short-term prospects for normalization of cardiovascular derangements have been described after parathyroidectomy. This study explores long-term effects of parathyroidectomy on cardiovascular functions in pHPT. METHODS: Thirty consecutive patients with pHPT were reexamined 1 and 5 years after parathyroidectomy, together with 30 matched controls, with echocardiography and a bicycle exercise test. RESULTS: Serum calcium was normal in all patients and control subjects at follow-up. The maximal blood pressure during the exercise was higher before parathyroidectomy (median 223 [range, 200-268] mm Hg vs 202 [165-277] mm Hg, P < .05) but not 5 years after (230 [155-270] mm Hg vs 219 [165-252] mm Hg. The ST-segment depression diminished from -1.4 (-8.3-0) to -0.8 (-3.3-0) mm 1 year after parathyroidectomy and further to -0.1 (-3.3-0.0) mm after 5 years but was unchanged in the control group. The number of ventricular extrasystolic beats at exercise testing in the pHPT group before parathyroidectomy was higher than in the control group (1 [0-340] vs 0 [0-3]). The isovolemic relaxation time at rest was prolonged before parathyroidectomy (mean 100 +/- 17 ms [SD] vs 89 +/- 14 ms, P < .05). CONCLUSION: Parathyroidectomy can induce long-lasting improvement in regulation of blood pressure, left ventricular diastolic function, cardiac irritability (ventricular extrasystolic beats), and other signs of myocardial ischemia, with potential implications for the postoperative life expectancy of patients with pHPT who have undergone parathyroidectomy.

Adult↗

Pre- and postoperative bone metabolism of primary hyperparathyroidism.

UNLABELLED: Primary hyperparathyroidism (PHPT) is a well-known indicator of severe bone loss. However, the recovery process of bone mineral density after surgery in PHPT patients is not sufficiently clear. We examined postoperative bone metabolism in 24 PHPT patients. PATIENTS AND METHODS: Subjects were 24 patients with PHPT upon whom we performed parathyroidectomy in the Department of Surgery II, Fukushima Medical University. Mean age was 54.2 years and the male-to-female ratio was 10:14; mean time of follow-up was 27.3 months. Patients were divided histopathologically into 16 adenomas and eight hyperplasias, and classified by heredity into seven familial (six, MEN 1; one, MEN 2) and 17 sporadic types. Bone mineral density was measured by dual energy X-ray absorptometry (DXA) and digital image processing (DIP). Age-matched values of these parameters were obtained. Serum bone metabolic parameters; ionized calcium (CaF), phosphorus, intact PTH (iPTH), c-PTH, ALP, osteocalcin (OC) and PTHrP were measured. RESULTS: PHPT patient preoperative bone mineral densities were significantly lower than those of healthy controls. Those by DIP method were lower than those by DXA. High CaF, iPTH, OC and ALP levels were indicated before surgery, but all parameters immediately became normal. Longitudinal bone mineral density changes of asymptomatic cases increased more than those of patients with renal stone and/or ostitis fibrosa. In adenoma cases, tumor weights were significantly inversely, which correlated with preoperative DIP bone density measurements. CONCLUSION: Preoperative PHPT patients showed decreased bone density; bone loss in symptomatic cases was especially prominent compared to asymptomatic cases. Most PHPT patients had not completed the BMD recovery after surgery, so even asymptomatic and mild PHPT patients should undergo parathyroidectomy to minimize irreversible bone loss.

Absorptiometry, Photon↗

Association of polymorphic alleles of the calcium-sensing receptor gene with the clinical severity of primary hyperparathyroidism.

OBJECTIVE: Primary hyperparathyroidism (pHPT) is a heterogeneous disease in its clinical course and severity. Previous studies have suggested an association between the clinical severity of pHPT and the genotypes of vitamin D receptor, oestrogen receptors and PTH molecules. The Ca-sensing receptor (CaR) is activated by an extracellular calcium ion and controls PTH secretion, and thus polymorphisms of CaR might be associated with the magnitude of PTH secretion and the clinical severity of pHPT. In this study, we examined the relationship between CaR polymorphisms and biochemical markers in pHPT patients. METHODS: We analysed 105 Japanese pHPT patients (85 females and 20 males; mean age 55.6 +/- 14.0 years). We determined the CaR genotypes of G990R and intron 5 polymorphisms with genomic DNA extracted from peripheral lymphocytes. The intron 5 polymorphism was defined as T/T, T/C and C/C. RESULTS: In the G990R polymorphism, serum levels of both intact PTH and alkaline phosphatase (ALP) were significantly higher and the serum level of phosphorus was significantly lower in the RR group than in the GG group. In the intron 5 polymorphism, the T/T group showed significantly lower serum levels of intact PTH and Ca. Furthermore, patients with both the codon 990 RR and the intron 5 C allele (the RRC(+) group) had significantly higher serum levels of intact PTH and ALP than did the other patients. CONCLUSIONS: The present study is the first to show that CaR polymorphisms of G990R and intron 5 were closely associated with the magnitude of PTH secretion and/or PTH degradation as well as the clinical severity in pHPT patients.

Adolescent↗

Coincidence of multiple endocrine neoplasia types 1 and 2: mutations in the RET protooncogene and MEN1 tumor suppressor gene in a family presenting with recurrent primary hyperparathyroidism.

CONTEXT: Primary hyperparathyroidism (HPT) presents as a part of inherited syndromes such as multiple endocrine neoplasia (MEN) types 1 and 2. In patients with MEN1, parathyroid hyperplasia or multiple adenomas occur in approximately 90-95%. MEN2A-related HPT is characterized by a mild hypercalcemia, which is mostly asymptomatic. OBJECTIVE: Here we present a family with coexistence of MEN1 gene mutation and RET mutation. RESULTS: Six family members carrying MEN1 gene mutation IVS5 + 1G>A only, one family member with RET mutation Y791F, and three family members with both MEN1 gene and RET mutation were studied. The key to diagnosis was recurrent HPT in a young male carrying RET mutation Y791F, a mutation not likely to give rise to recurrent HPT. CONCLUSION: MEN1 gene mutation and RET codon 791 mutation in the same patient did not affect the typical phenotype of MEN1 or MEN2, and also the course of diseases seems to be unchanged. The reason may be that both mutations, although contributing to tumor pathogenesis, do not interact and induce a worsening of the cancer syndromes.

Adult↗

Exclusive underexpression of vitamin D receptor exon 1f transcripts in tumors of primary hyperparathyroidism.

OBJECTIVE: Primary hyperparathyroidism (pHPT) is characterized by excessive production of parathyroid hormone (PTH) due to parathyroid adenomas while uremic secondary HPT (sHPT) is caused by parathyroid hyperplasia in response to renal failure. Active vitamin D, 1,25-dihydroxyvitamin D(3) (1,25-(OH)(2)D(3)), with the vitamin D receptor (VDR) is involved in regulation of the calcium homeostasis together with PTH. In a feedback loop, 1,25-(OH)(2)D(3) has a direct action on the parathyroid gland to regulate PTH transcription, PTH secretion and cell proliferation. We have previously demonstrated reduced VDR mRNA expression in parathyroid adenomas and hyperplasia of sHPT using a probe detecting all 14 variant VDR transcripts expressed in parathyroid cells. Here we have assessed which of the 5'-terminal exon 1a, 1d and 1f variant VDR transcripts are reduced in pathological parathyroid glands. METHODS: The relative VDR/glyceraldehyde-3-phosphate dehydrogenase mRNA levels for each VDR exon were determined by real-time quantitative RT-PCR in five normal parathyroid glands, seventeen parathyroid adenomas and ten hyperplastic glands of sHPT. RESULTS: The results demonstrated exclusive underexpression of VDR exon 1f transcripts in parathyroid adenoma, while all measured VDR transcripts were reduced in secondary hyperplasia. CONCLUSIONS: We suggest that exclusive underexpression of VDR exon 1f transcripts in adenomas of pHPT, which derive from a distal promoter active in tIssues involved in calcium regulation by 1,25-(OH)(2)D(3), may either reflect a defective cell type-specific transcription factor or other physiologically important pathway(s) for tIssue-specific VDR gene expression.

Adenoma↗

Non-classical target organs in primary hyperparathyroidism.

Classical primary hyperparathyroidism (PHPT) was a multisystem disorder with clear neurologic, psychiatric, gastrointestinal, and cardiovascular consequences. The nature and extent of involvement of these target organs in the modern presentation of the disease are controversial. Although hypertension has been associated with PHPT, it is not cured after parathyroidectomy, nor is it easier to control. Despite significant data on European patients, information on the incidence of cardiovascular abnormalities in American patients with mild disease are limited. Investigation is turning to more subtle abnormalities, such as vascular reactivity and endothelial function, where data are conflicting. Many patients complain of nonspecific neuropsychiatric symptoms. This has been a difficult area to study quantitatively. Classical neuromuscular disease is rare in mild PHPT, although weakness and easy fatigability remain common complaints. These nonspecific symptoms may or may not improve with surgery. While no clear causal association exists between sporadic PHPT and peptic ulcer disease, this is not the case in patients with multiple endocrine neoplasia type 1 (MEN1). Gastrinoma is more severe in those with coexisting PHPT, and Zollinger-Ellison Syndrome improves with treatment of PHPT. Further efforts are necessary to characterize the cardiovascular and neuropsychological profiles of mild PHPT and to determine the longitudinal course of such alterations. With available data suggesting that many asymptomatic patients with PHPT can be safely followed without parathyroidectomy, this information will be of key importance in the management of such individuals.

Behavioral Symptoms↗

Focused, minimally invasive radio-guided parathyroidectomy: a feasible and safe option for elderly patients with primary hyperparathyroidism.

BACKGROUND: Primary hyperparathyroidism in elderly patients is usually associated with additional co-morbidity that increases operative risk, and thus many geriatric patients are denied the benefit of surgery for a single parathyroid adenoma. OBJECTIVES: To evaluate the safety and efficacy of accurate single photon emission computed tomography sestamibi scintigraphy, enabling precise localization of a single adenoma, in the geriatric population. METHODS: Twenty-two patients aged 70 years and over with biochemically proven PHPT and with a single parathyroid adenoma identified by localization studies (sestamibi SPECT scan and ultrasonography) underwent 23 operations over 29 months (out of a total of 140 patients operated upon during the same period). Immediate preoperative sestamibi scintigraphy and marking of focal adenoma uptake followed by intraoperative hand-held gamma probe were used for the removal of the parathyroid adenoma by unilateral minimal access surgery. Associated major co-morbid conditions and pre- and postoperative calcium, phosphorus and parathormone levels were recorded. Indications for surgery were listed and operative and postoperative complications were noted. The patients were followed for a mean period of 17.7 months using the same parameters. RESULTS: The 22 patients with PHPT had a mean age of 76.3 +/- 5.9 years (range 70-88 years) and a female to male ratio of 13:9. Associated co-morbidity included ischemic heart disease (n = 15), hypertension (n = 22), non-insulin-dependent diabetes mellitus (n = 9), chronic obstructive pulmonary disease (n = 3), and previous neck surgery (n = 3). Mean preoperative serum calcium, phosphorous and PTH were 11.7 +/- 1.3 mg/dl, 2.5 +/- 0.5 mg/dl and 160.9 +/- 75.4 pg/ml respectively. In 20 of the 22 patients, surgery was successful in curing PHPT (91%). One patient had persistent hypercalcemia due to a missed adenoma, and repeat operation (by focused minimal accesss surgery) was successfully performed 2 weeks later. There were no complications and no morbidity postoperatively. Mean postoperative serum calcium, phosphorous and PTH were 9.6 +/- 1.2 mg/dl, 3.0 +/- 0.5 mg/dl and 35.2 +/- 24 pg/ml respectively. In all patients, serum calcium levels remained normal (9.7 +/- 1.3 mg/ml) after long-term follow-up (mean 17.7 +/- 9.6 months). CONCLUSIONS: Minimally invasive, radio-guided focused parathyroidectomy for a single adenoma is a safe and effective method to cure hyperparathyroidism in the elderly. Success of surgery is directly related to the surgeon's experience and to the precise localization marking provided by sestamibi scintigraphic SPECT localization and concurrent sonographic findings.

Adenoma↗

[Diagnosis of primary hyperparathyroidism].

The primary hyperparathyroidism (pHPT) is one of the most frequent endocrine diseases and is characterized of various forms of manifestations. In 50 patients there was made a screening test to verify a pHPT in patients with recurrent calcium urolithiasis. In 4 patients a strong suspicion existed on pHPT, in 9 patients occured a normalcalcemic pHPT. Since the parathyroid hormone concentrations were measured by predominantly amino-terminal-directed antiserum the results must be considered critically.

Calcium↗

[Bone histomorphometric analysis in primary hyperparathyroidism].

In primary hyperparathyroidism, bone remodeling is increased due to an enhanced activation frequency which is caused by excessive PTH. In mild cases, eroded, osteoid and labeled surfaces are increased. But as bone balance per remodeling cycle in cancellous bone is zero or even slightly positive, bone volume and structure are relatively maintained. In advanced cases, bone resorption is predominant in the endosteal surface of cortical bone, resulting in progressive thinning and increased porosity, cancellisation. As far cancellous bone resorption depth is deepened to occur trabecular perforation associated with fibrous tissue replacement, osteitis fibrosa.

Bone Remodeling↗

Parathyroid hormone secretion after operation for primary hyperparathyroidism.

BACKGROUND: Primary hyperparathyroidism (pHPT) is associated with a defective regulation of the secretion of parathyroid hormone (PTH). Thus in pHPT, higher than normal calcium concentrations are required to inhibit PTH release. However, it is not known if this defective regulation is normalized by removal of the parathyroid adenoma (i.e., whether the regulation of PTH secretion is normal in the remaining glands). In this study we therefore investigated the PTH secretion in patients operated on for parathyroid adenoma 1 year after operation. METHODS: Na2 ethylenediamine tetraacetic acid and CaCI2 were infused at constant rates in six patients operated on for parathyroid adenoma and six healthy individuals. Serum levels of intact PTH and ionized calcium were determined during the infusions. RESULTS: No significant differences between the two groups were found in baseline levels of serum ionized calcium and PTH. Furthermore, no significant differences between patients and control subjects were found in the maximum serum PTH levels during the hypocalcemic infusion of ethylenediamine tetraacetic acid or in the minimum serum PTH levels during the calcium infusion. In contrast, the set point (the calcium concentration required for half-maximal inhibition of PTH secretion) was significantly lower in the patients (1.20 +/- 0.01 mmol/L) compared with control subjects (1.22 +/- 0.01 mmol/L; p < 0.05). CONCLUSIONS: We conclude that the elevation of set point in patients with parathyroid adenoma is corrected by successful operation. This suggests a monoclonal origin of parathyroid adenomas.

Adenoma↗

Management of primary hyperparathyroidism in children.

Primary hyperparathyroidism is unusual in children. It is most commonly due to a solitary sporadic parathyroid adenoma, though parathyroid hyperplasia and related familial syndromes should be considered. In the case presented here, an 11-year-old boy with primary hyperparathyroidism had preoperative imaging studies that localized to the inferior aspect of the left side of the neck anteriorly, and a parathyroid adenoma was successfully resected. Screening for familial syndromes involving hyperparathyroidism should be individually considered in children with primary hyperparathyroidism. Preoperative localizing studies and the role of unilateral surgery are controversial issues in adults with primary hyperparathyroidism. Although such issues have not been addressed in children, localization and unilateral surgery proved successful in this case.

Adenoma↗

Pregnancy complicated by concurrent primary hyperparathyroidism and arrhythmia.

Primary hyperparathyroidism during pregnancy results in a high rate of fetal complications and maternal morbidity. Maternal hypercalcemia in pregnancy results in fetal hypercalcemia, which leads to suppression of fetal parathyroid function. Spontaneous abortion and stillbirth can occur, and the loss of maternal calcium after birth leads to neonatal hypocalcemia. It is essential to detect primary hyperparathyroidism during pregnancy because early diagnosis and management can decrease the rate of fetal and maternal complications. We present the case of a 27-year-old gravida 1, para 0 woman whose pregnancy was complicated by hyperparathyroidism and arrhythmia. The patient complained of dyspnea and palpitations in the seventh and 15th weeks of gestation. Electrocardiography showed ventricular premature contraction bigeminy and trigeminy in association with hypercalcemia (3.3 mmol/L). A parathyroidectomy in the second trimester revealed parathyroid adenoma. Hypercalcemia and arrhythmia resolved completely and the patient delivered a term baby without any maternal or fetal complications. The simultaneous occurrence of arrhythmia with ventricular premature contractions and hyperparathyroidism in pregnancy is rarely reported. Palpitations and dyspnea due to arrhythmia may be associated with primary hyperparathyroidism in pregnancy and should be considered in the differential diagnosis. In the management of symptomatic primary hyperparathyroidism during pregnancy, surgical intervention is preferable in the second trimester when organogenesis is completed and the risk of spontaneous abortion is low.

Adult↗

Primary hyperparathyroidism in infancy.

Primary hyperparathyroidism in the neonate is a rare and often fatal disorder. These infants typically display severe hypercalcemia, respiratory distress, muscular hypotonia, and skeletal demineralization. They are usually diagnosed within the first three months of life and have hyperplasia of the four parathyroid glands. Twenty-nine infants with primary hyperparathyroidism are reported in the literature. Mortality is 87.5% in medically managed patients and 24% in surgically managed patients. Surgical management has not been satisfactory, in that recurrent hypercalcemia has been encountered in most patients undergoing subtotal parathyroidectomy, and total parathyroidectomy has resulted in the need for lifelong calcium and vitamin D supplementation. We have recently cared for a term newborn female in whom the diagnosis of primary hyperparathyroidism was made clinically on the second day of life, and later was confirmed biochemically. The baby underwent neck exploration on the 11th day of life and was successfully treated with total parathyroidectomy and parathyroid autotransplantation. Although initially rendered eucalcemic, the infant subsequently developed recurrent hypercalcemia requiring the removal of some of the autograft. Currently, the child is more than 2 years following surgery, growing well, and off all medication. The world literature is reviewed in this report of one of the first and the youngest infants, to our knowledge, to undergo parathyroid autotransplantation. In view of its success in avoiding the complication of repeated neck exploration for recurrent hyperparathyroidism or the creation of permanent hypoparathyroidism, we recommend this surgical approach for the rare neonate with primary hyperparathyroidism.

Biopsy↗

[Primary hyperparathyroidism in children].

Primary hyperparathyroidism in children is an extremely rare condition. Slightly more than a hundred cases have been published in children or adolescents aged under 16. Forms with a neonatal presentation, the most rare, should be viewed apart since they rapidly become life-threatening. They involve hyperplasia of the chief cells of the parathyroid glands. Treatment is always surgical and should be rapid, consisting of total parathyroidectomy with autotransplantation. Primary hyperparathyroidism in older children more closely resembles that seen in adults. Sporadic forms are most often due to an adenoma and familial forms, which may occur alone or within the context of a polyendocrine syndrome, are most often due to hyperplasia. Treatment consists of parathyroidectomy, the extent of which depends upon the familial context, visual investigative findings and results of frozen section histology at the time of exploratory cervicotomy. Regardless of the age of the child, family investigation is always required to detect primary hyperparathyroidism occurring in the context of a hereditary disorder.

Adolescent↗

Vitamin D status in primary hyperparathyroidism in India.

OBJECTIVES: Primary hyperparathyroidism is a syndrome with variable clinical expression, presenting as asymptomatic hypercalcaemia in Western countries and with predominant bone disease in developing countries. Vitamin D deficiency has been implicated as the cause of bone disease. There is a paucity of information on the vitamin D (25-OHD3) status of patients with primary hyperparathyroidism presenting with bone disease. The present study aims to evaluate the vitamin D status in patients with primary hyperparathyroidism and to correlate it with the bone disease. DESIGN: Twenty consecutive patients with primary hyperparathyroidism admitted to the endocrinology and metabolism wards of the All India Institute of Medical Sciences were analysed to assess their clinical, radiological and biochemical features, as well as parathyroid hormone (mid-molecular, PTH-MM) and 25-OHD3 levels. MEASUREMENTS: PTH-MM levels and 25-OHD3 levels were measured using RIA kits. RESULTS: Bone disease (osteitis fibrosa cystica) was the mode of presentation in 90%. Radiologically, sub-periosteal resorption was present in 90% of the total group of patients, brown tumours in 60%, and pathological fractures in 40%. Renal stones and/or nephrocalcinosis was present in 50% of patients. Mean serum calcium, phosphate and alkaline phosphatase concentrations (mean of 3 days values) were 2.72 +/- 0.24 mmol/l; 1.01 +/- 0.28 mmol/l and 425 +/- 249 IU/l respectively. The 24-hour (mean of 3 days values) urine calcium and phosphate excretions were 8.0 +/- 4.2 mmol and 19.0 +/- 13 mmol. Only 50% of the patients had hypercalcaemia ( > 2.7 mmol/l). However, 90% of the whole group of patients had hypercalciuria. The mean serum creatinine concentration of patients with hypercalcaemia was 108 +/- 38 mumol/l and of those with normocalcaemia 89 +/- 33 mumol/l. The mean serum PTH-MM was 438 +/- 350 pmol/l (the detection limit for the kit was 34 pmol/l). Ultrasound examination detected adenomas in 72% of the cases and computerized tomography of the neck localized adenomas in 71% of the cases. The median weight of the adenoma was 4.6 g (range 0.125-25 g). Two patients had coexistent hyperplasia of the other parathyroid glands and two had recurrent adenomas. 25-OHD3 levels were assessed in all 20 patients under fasting conditions. The mean value of 25-OHD3 observed (8.4 +/- 5.1 micrograms/l) was comparable to the mean value measured in 14 healthy age and sex matched controls (8.3 +/- 2.5 micrograms/l). CONCLUSION: Patients with primary hyperparathyroidism in India presented with bone and renal diseases; half were normocalcaemic. All the patients had hypercalciuria despite the bone disease. The PTH-MM levels were increased and 25-OHD3 levels were low. The predominant bone disease is probably due to prolonged primary hyperparathyroidism coexisting with low calcium intake and/or 25-OHD3 deficiency. The mean weight of the adenoma was higher than that reported for patients in the Western literature.

Adenoma↗

Surgical contribution to the management of primary hyperparathyroidism.

Surgical management of primary hyperparathyroidism is a very effective method. The target is to cure primary hyperparathyroidism and to reach normal calcium levels. This results in an improvement of health condition and resolution or at least moderation of symptoms. Complications are infrequent and mortality is very low. Surgical management is definite, safe and effective. Authors of this article address the diagnosis of primary hyperparathyroidism, clarify bone, metabolic and biochemical syndromes and present series of 151 patients that have been operated on at the 3rd Department of Surgery of the Motol University Hospital, Prague, with the diagnosis of primary hyperparathyroidism. The survey is focused on the primary hyperparathyroidism concomitant diseases and on the possible sequelae in the postoperative period.

Adolescent↗