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PubMedDate not supplied

Surgical treatment of renal hyperparathyroidism.

Advanced secondary (renal) hyperparathyroidism induced by chronic renal disturbance is one of the most serious complications for long-term hemodialysis patients. Parathyroidectomy is indicated in patients with severely advanced renal hyperparathyroidism refractory to medical treatment (including calcitriol pulse therapy) and the clinical effect of parathyroidectomy is striking. However, skeletal deformity, vessel calcification, and remarkable reduction of bone content is irreversible, and it is important to perform parathyroidectomy at right time. Based on histopathological and pathophysiological investigations, nodular hyperplasia is monoclonal neoplasia with abnormal parathyroid hormone (PTH) response to extracellular calcium and vitamin D. When parathyroid hyperplasia progresses to nodular hyperplasia, parathyroidectomy should be required. Total parathyroidectomy with forearm autograft is the preferable procedure for renal hyperparathyroidism, especially for patients who need to continue hemodialysis treatment after parathyroidectomy. Removal of all parathyroid glands, including supernumerary glands, at the initial operation, and proper choice of adequate parathyroid tissue for autograft, are important to prevent persistent and recurrent hyperparathyroidism. Preoperative image diagnosis is useful for localization, and routine resection of thymic tissue is necessary to remove supernumerary glands. In our series of 548 patients, graft-dependent recurrent hyperparathyroidism was not negligible and the incidence was about 20% at the 5th year postoperatively. Enlarged autografts of parathyroid tissue could be removed from forearm under local anesthesia with fewer invasions. The function of autografted parathyroid tissue is nearly satisfactory and no re-transplantation of cryopreserved parathyroid tissue was necessary. To avoid adynamic bone disease, relatively high PTH level is required-over-suppression of PTH by excess of vitamin D and calcium salts should be avoided. In our experience, total parathyroidectomy with forearm autograft is very effective and adequate treatment for advanced renal hyperparathyroidism, and parathyroid function can be controlled after parathyroidectomy.

Adult↗
PubMed1988

Pancreatitis and hyperparathyroidism.

Hypercalcaemia is considered to be a rare cause of pancreatitis but the true cause-and-effect relationship between hyperparathyroidism and pancreatic inflammatory disease remains controversial. Over 100 patients have been reported in whom both processes have occurred concurrently, but doubts have been expressed as to whether or not this association is due to chance. We report 10 new cases of hypercalcaemic hyperparathyroidism associated with different types of pancreatitis. Seven patients had primary hyperparathyroidism and three had hyperparathyroidism after renal transplantation. Two experienced acute pancreatitis after parathyroidectomy. Of the remaining eight patients, five had hypercalcaemia equal to or above 120 mg/l. The prevalence of pancreatitis in our series of 86 cases of primary hyperparathyroidism is 8 per cent. Acute and chronic calcifying types of pancreatitis were observed. Three patients died of the disease, two of them after renal transplantation. It is suggested that pancreatitis may complicate the clinical course of hyperparathyroidism, particularly when hypercalcaemia is moderate to severe and/or there are other risk factors such as treatment with steroids and azathioprine after renal transplantation.

Adult↗
PubMedDate not supplied

Management of hyperparathyroid patients with grave hypercalcemia.

During recent years the total number of patients undergoing surgery for hyperparathyroidism has markedly increased, but the annual number of cases with substantial hypercalcemia has remained unchanged. Parathyroid carcinoma and water clear cell hyperplasia cause more severe hypercalcemia than other kinds of hyperparathyroidism. Grave hypercalcemia due to hyperparathyroidism is more common among the elderly, but can occur during pregnancy and also among children. Occasionally, a patient with hyperparathyroidism can also have another cause of the hypercalcemia and does not become normocalcemic until adequately treated for both. The suspicion of grave hypercalcemia should arise due to its clinical features. Determination of serum calcium and intact parathyroid hormone concentrations establishes the diagnosis. The basic treatment of grave hypercalcemia is to rehydrate the patient and to restore the sodium losses. To further lower the serum calcium value we have found bisphosphonates to be very effective. The definitive treatment of grave hypercalcemia due to hyperparathyroidism is surgery. As a last resort, frail patients with grave hyperparathyroidism can undergo surgery under local anesthesia. Repeat operations can improve the prognosis of patients with metastatic parathyroid carcinoma. Selective venous catheterization with blood sampling for determination of intact parathyroid hormone can be helpful in localizing recurrent disease.

Acute Disease↗
PubMed1987

Adrenal responses to subtotal parathyroidectomy for primary hyperparathyroidism.

Although it is well known that hypertension is often associated with primary hyperparathyroidism and that parathyroidectomy reverses or reduces this abnormality, the etiology of elevated blood pressure in hyperparathyroidism is still conjectural. We have analyzed serum calcium, blood pressure, and metabolites of adrenal cortical hormones before and after surgical therapy for hyperparathyroidism in 10 normotensive and six hypertensive patients with primary hyperparathyroidism. Successful parathyroidectomy lowered serum calcium (P less than 0.01) and diastolic blood pressure (P less than 0.05) in all subjects. Mean urinary aldosterone and Porter-Silber chromagens were within normal limits preoperatively in normotensive as well as hypertensive subjects. After parathyroidectomy, aldosterone levels as well as Porter-Silber chromagens decreased significantly in all patients (P less than 0.01). However, when normotensive and hypertensive subjects were analyzed separately, the decrease in aldosterone levels was significant only in the normotensive group (P less than 0.05) whereas the decrease in Porter-Silber chromagens reached significancy only in the hypertensive group (P less than 0.01). The results indicate that surgical therapy for hyperparathyroidism lowers serum calcium and blood pressure and is associated with a decrease in the excretion of adrenal steroid metabolites. It is suggested that the temporal relationship which exists between ionized calcium and steroidogenesis in hyperparathyroid patients contributes at least in part to the generalized decrease in blood pressure observed after successful parathyroidectomy.

17-Hydroxycorticosteroids↗
PubMed2001

Increased prevalence of primary hyperparathyroidism in treated breast cancer.

UNLABELLED: Hypercalcemia occurring in patients with advanced breast cancer (BC) is generally due to osteolytic metastases or to the activity of circulating tumor-derived products. In these conditions, the production of endogenous PTH is reduced. The frequency of hypercalcemia due to primary hyperparathyroidism in breast cancer is unknown. We examined the occurrence of primary hyperparathyroidism in a large group of women with treated BC. A total of 100 consecutive women aged 28-80 years with treated breast cancer were enrolled. One hundred and two healthy age-matched women and 60 age-matched female patients with differentiated thyroid carcinoma examined before thyroidectomy were used as controls. Intact serum PTH and serum calcium were measured in all patients and controls. Hypercalcemia associated with elevated serum PTH concentration indicating primary hyperparathyroidism was found in 7 BC patients (7%) and in none of healthy women or patients with thyroid cancer. The pre-operative staging of BC patients with primary hyperparathyroidism was I in six and II in one of them, and no patient had evidence of distant metastases. A parathyroid adenoma was found in all 6 BC patients submitted to neck exploration, one patient refused surgery. Serum calcium and PTH concentrations returned to normal levels after surgery. Two BC patients had increased serum PTH and normal calcium concentrations. One of them had low serum 25-hydroxyvitamin D [25(OH)D]. One patient with spread bone metastases had neoplastic hypercalcemia with undetectable serum PTH concentration. All remaining 90 BC patients had serum calcium and PTH concentrations within normal limits, but their mean (+/-SD) values (9.6+/-0.5 mg/dl for serum calcium, 38.0+/-16.4 mg/dl for serum PTH ) were slightly but significantly greater than in normal controls (9.3+/-0.5 mg/dl, p=0.003 and 27.9+/-10.6 pg/ml, p=0.0001, respectively) and in patients with thyroid cancer (9.2+/-0.6 mg/dl, p=0.001 and 26.2+/-11.0 pg/ml, p=0.001), with no relationship with clinical staging or anti-tumor therapy. IN CONCLUSION: 1) an increased frequency of parathyroid adenoma was found in BC patients with mildly aggressive neoplastic disease; 2) in BC patients with no evidence of primary hyperparathyroidism mean serum PTH and calcium concentrations were significantly greater than in healthy controls and in patients with thyroid carcinoma; and 3) this finding was unrelated to clinical staging or anti-tumor therapy. Thus, primary hyperparathyroidism should be considered as a possible cause of hypercalcemia in patients with non-aggressive breast cancer. We suggest that serum PTH should be determined in all BC patients with increased serum calcium concentration, especially in those with no evidence of metastatic disease.

Adenoma↗
PubMed1994

Primary hyperparathyroidism and hypertension: persistently abnormal pressor sensitivity in normotensive patients after surgical cure.

To examine the effects of primary hyperparathyroidism separately from those of hypertension per se on blood pressure regulation in patients with primary hyperparathyroidism, we studied the pressor response to infused angiotensin II (AII) and to norepinephrine (NE) in 7 normotensive patients with primary hyperparathyroidism before and after surgical cure, and compared it to that observed in 10 subjects with idiopathic hypertension and 10 normal controls. While the subjects were on an ad libitum diet, we measured urinary and plasma electrolytes, creatinine, and plasma renin activity. Except for calcium, these values were not significantly different among the three groups. The blood pressure was measured basally and in response to graded doses of AII or of NE until a 20-mmHg increase in the diastolic blood pressure was reached ("pressor dose"). The pressor doses of AII and of NE were lower in the normotensive patients with primary hyperparathyroidism than in normal controls [4.6 +/- 2.0 vs. 7.3 +/- 3.5 ng/kg/min (p < 0.05) and 164 +/- 114 vs. 302 +/- 176 ng/kg/min (p < 0.05) respectively] and not significantly different from those found in idiopathic hypertension (3.1 +/- 1.2 and 137 +/- 95 ng/kg/min). When the patients with primary hyperparathyroidism were studied again between 2-6 months after surgical cure, their pressor doses of AII and of NE remained unchanged from their preoperative values (5.4 +/- 2.9 and 137 +/- 80 mg/kg/min). We conclude that the hyperparathyroid condition can disrupt the normal responsiveness to pressor agents even if the blood pressure remains within normal limits, and that this abnormality may persist after surgical cure.

Adult↗
PubMed1998

Late outcome of 304 consecutive patients with multiple gland enlargement in primary hyperparathyroidism treated by conservative surgery.

The aim of this study was to assess the late outcome of patients with primary hyperparathyroidism and multiple gland enlargement (MGE) treated by conservative surgery. MGE in primary hyperparathyroidism is the presence of two or more enlarged glands weighing more than 50 mg. Conservative surgery consists in resecting the grossly enlarged glands without biopsying the normal glands. Some authors have suggested that this approach overlooks minute hyperplasia, leading to late recurrences of hyperparathyroidism; conversely, it may result in the unnecessary resection of grossly enlarged, but not hyperfunctioning, glands. Altogether 1231 patients were operated on for primary hyperparathyroidism between 1966 and 1995. Of these patients, 304 (24.9%) had MGE, including 42 cases of multiple endocrine neoplasia (MEN), 12 familial cases, and 250 seemingly sporadic cases. Two, three, or four glands (or more) were involved in 61.8%, 21.4%, and 16.4% of cases, respectively. During the early postoperative period one patient died and ten were reoperated for persistent hypercalcemia. The pathologic diagnoses were double adenomas (13.5%), hyperplasia (35.8%), association of the two (39.8%), and a normal second gland (10.8%) on light microscopy findings. None of the 30 deaths that occurred during follow-up was related to hyperparathyroidism. Altogether 190 patients (79%) were available for follow-up (average 89.3 months): 90% were normocalcemic, 4.7% hypocalcemic, and 5.2% hypercalcemic. A late iPTH assay was done in 147. PTH was appropriate to the serum calcium level in 84.3% and appropriate to normal calcemia in 91.6% of 132 cases. Conservative surgery is thus an acceptable treatment for MGE in patients with hyperparathyroidism. Few late recurrences occur, for which there are no individual predictive criteria.

Adenoma↗
PubMed2002

Total parathyroidectomy without autotransplantation as a standard procedure in the treatment of secondary hyperparathyroidism.

BACKGROUND: Total parathyroidectomy with autografting of parathyroid tissue and subtotal resection of the parathyroid glands are currently considered as standard surgical procedures for the treatment of severe secondary hyperparathyroidism. However, a considerable recurrence rate following these procedures ranges from 5% to 80%. We present a retrospective analysis of the results of parathyroidectomy with autotransplantation to the forearm versus parathyroidectomy alone. PATIENTS AND METHODS: We analyzed the clinical course of 11 consecutive patients who had undergone parathyroidectomy between 1995 and 1999, and who were not simultaneously autografted. Controls were 11 patients in whom autotransplantation of parathyroid tissue into the forearm had been routinely performed between 1993 and 1996 at our institution. Clinical symptoms and recurrence of hyperparathyroidism were assessed for comparison of the alternative treatment modalities. Recurrence of disease was defined by elevated parathormone (PTH) levels (>7.6 pmol/l) with clinical symptoms and/or need for reoperation. RESULTS: No recurrence of hyperparathyroidism was observed in patients without autotransplantation after a mean follow-up of 23 months (range 1-49). Measurement of intact serum PTH revealed residual PTH secretion even after removal of four glands (mean 2.02 pmol/l). Clinical symptoms improved substantially after surgery. In the historical control group 3 of the 11 autotransplanted patients (27%) required resection of transplanted tissue. Additionally, two patients (18%) presented with increased PTH secretion and clinical symptoms of recurrent hyperparathyroidism during follow-up. Thus, a total of five patients (45%) experienced relapsing hyperparathyroidism caused by the implanted tissue. CONCLUSIONS: Total parathyroidectomy without autotransplantation is a safe procedure with a low rate of recurrent hyperparathyroidism when compared to parathyroidectomy with autotransplantation to the forearm in a historical control. These preliminary results mandates further investigations including a randomized trial.

Adult↗
PubMed2004

Mucolipidosis II presenting as severe neonatal hyperparathyroidism.

UNLABELLED: Mucolipidosis II (ML II or I-cell disease ) (OMIM 252500) is an autosomal recessive lysosomal enzyme targeting disorder that usually presents between 6 and 12 months of age with a clinical phenotype resembling Hurler syndrome and a radiological picture of dysostosis multiplex. When ML II is severe enough to be detected in the newborn period, the radiological changes have been described as similar to hyperparathyroidism or rickets. The biological basis of these findings has not been explored and few biochemical measurements have been recorded. We describe three unrelated infants with ML II who had radiological features of intrauterine hyperparathyroidism and biochemical findings consistent with severe secondary neonatal hyperparathyroidism (marked elevation of serum parathyroid hormone and alkaline phosphatase levels). The vitamin D metabolites were not substantially different from normal and repeatedly normal calcium concentrations excluded vitamin D deficiency rickets and neonatal severe hyperparathyroidism secondary to calcium-sensing receptor gene mutations (OMIM 239200). The pathogenesis of severe hyperparathyroidism in the fetus and newborn with ML II is unexplained. We hypothesize that the enzyme targeting defect of ML II interferes with transplacental calcium transport leading to a calcium starved fetus and activation of the parathyroid response to maintain extracellular calcium concentrations within the normal range. CONCLUSION: Newborns with mucolipidosis II can present with radiological and biochemical signs of hyperparathyroidism. Awareness of this phenomenon may help in avoiding diagnostic pitfalls and establishing a proper diagnosis and therapy.

Bone Diseases, Metabolic↗
PubMed1987

Acute primary hyperparathyroidism.

Acute primary hyperparathyroidism is an unusual form of primary hyperparathyroidism characterized by life-threatening hypercalcemia. Forty-three cases reported in the literature since 1974 are reviewed, along with five new cases. The average age of the patients was 55 (27 to 82), with an even distribution between men and women. Marked hypercalcemia (17.5 +/- 2.1 mg/dl) was accompanied by parathyroid hormone levels 20 times normal. Virtually all patients had symptoms. Hyperparathyroid bone disease occurred in 53 percent of patients; even more (69 percent) had nephrolithiasis or nephrocalcinosis. Combined renal and skeletal involvement was seen in 50 percent. Only three deaths were recorded. The pathophysiology of the acute hyperparathyroid state is unknown but appears to consist of uncontrolled parathyroid hormone secretion followed by cycles of hypercalcemia, polyuria, dehydration, reduced renal function, and worsening hypercalcemia. These features of acute primary hyperparathyroidism are compared with the features reported in the literature antedating multichannel screening, and with the features of the common form of primary hyperparathyroidism. Clinical guidelines by which the diagnosis may be suspected are also reviewed.

Acute Disease↗
PubMed1993

Primary hyperparathyroidism: incidence of cardiac abnormalities and partial reversibility after successful parathyroidectomy.

PURPOSE: This prospective study was designed to assess the effect of primary hyperparathyroidism on heart muscle, valves, and myocardial function. Echocardiography was used to evaluate changes in mechanical performance, the thickness of the left ventricular wall, myocardial calcific deposits, and valvular calcifications in patients with primary hyperparathyroidism. METHODS: Echocardiography was performed in 54 patients with hyperparathyroidism prior to surgery and 12 +/- 2 months after successful parathyroidectomy. A matched control group was followed for comparison. RESULTS: In a blinded fashion, aortic and mitral valve calcifications were detected in 63% and 49% of patients with primary hyperparathyroidism (controls: 12% and 15%, respectively). Calcific deposits in the myocardium were found in 69% of patients with hyperparathyroidism and 17% of the control subjects. After parathyroidectomy and 12 months of normocalcemia, a significant regression of left ventricular hypertrophy (p < 0.001) was observed. CONCLUSIONS: The present data show a high incidence of left ventricular hypertrophy, calcific deposits in the myocardium, and/or aortic and mitral valve calcification in patients with primary hyperparathyroidism. A 1-year follow-up after parathyroidectomy (and restoration of normocalcemia) discloses regression of hypertrophy, while calcifications persist without evidence of progression.

Adult↗
PubMed1977

Hyperparathyroidism in thyrotoxicosis.

The frequency of hypercalcemia in 295 patients treated for thyrotoxicosis was 2 per cent. The combination of thyrotoxicosis and hyperparathyroidism is rare and only twenty-seven well documented cases could be found in the literature. Among ninety-two patients operated on for hyperparathyroidism, ten of them had thyrotoxicosis. In the present study, data on thirty-seven patients are reported. Hypercalcemia was found in all the patients and four of them had acute hyperparathyroidism. Hypophosphatemia was recorded in 60 per cent and hypercalcuria in 75 per cent of the patients. In ten patients there were renal concretions. Skeletal roentgenograms showed abnormalities in 65 per cent of the patients. In no instance had hyperparathyroidism commenced before thyrotoxicosis. Other recent reports on the etiology of hyperparathyroidism are discussed and it is concluded that hyperparathyroidism in thyrotoxicosis is a secondary disease. If a thyrotoxic patient with hypercalcemia still has elevated calcium values when becoming euthyroid after thyrostatic treatment, an operation should be performed. Because of a high recurrence rate in such patients with adequate follow-up, "near total parathyroidectomy" is recommended.

Adult↗
PubMed2006

[Results of systematic subtotal parathyroidectomy with thymectomy for tertiary hyperparathyroidism after renal transplantation - 70 patients].

BACKGROUND: Due to the relatively small number of patients involved, there is currently no consensus on what operation should be performed in patients with tertiary hyperparathyroidism after renal transplantation. METHOD: Retrospective analysis of the 70 patients with tertiary hyperparathyroidism who all underwent subtotal parathyroidectomy with transcervical thymectomy in the same institution between 1978 and 2003. RESULTS: The delay between transplantation and parathyroidectomy was 4,1+/-4,3 years. Follow up was available for all patients. Mean follow-up was 5,6+/-5 years. Glomerular filtration rate (GFR) was 53+/-21 ml/min at parathyroidectomy and 42+/-29 ml/min at follow-up [<30 ml/min in 26 patients (37%), 30 - 60 ml/min in 25 patients (36%) et>60 ml/min in 19 patients (27%)]. One patient was successfully reoperated for persistent tertiary hyperparathyroidism during follow-up. No patient was hypercalcemic at follow-up. Four patients with a GFR<30 ml/min had a PTH level>fourfold normal values (6%) without signs or symptoms of hyperparathyroidism. One patient was hypocalcemic (1,5%) and two patients were normocalcemic with undetectable or infranormal PTH level (3%) under oral vitamin D and calcium medication. CONCLUSION: This approach permits not only to cure the majority of patients with tertiary hyperparathyroidism but also to avoid recurrence when the renal function declines. When medical management has failed, we recommend systematic subtotal parathyroidectomy with thymectomy for patients with tertiary hyperparathyroidism and this should usually be performed during the second year after transplantation.

Adult↗
PubMed2004

Normocalcemic hyperparathyroidism presented with mandibular brown tumor: report of a case.

Brown tumor is a rare clinical entity complicating hyperparathyroidism. It may occur in the head and neck, with the mandible being the most frequent site. Hyperparathyroidism is usually associated with hypercalcemia. We report a case of madibular Brown tumor secondary to primary hyperparathyroidism. In this case in spite of hyperparathyroidism and the bony lesion the serum calcium level was within normal range. The case managed by surgical excision of the mandibular tumor with an en-bloc hemithyroidectomy with inclusion of the diseased parathyroid gland. This case demonstrates that in osteolytic bony lesions a hyperparathyroid complication can be expected even with normal serum calcium level. The presence of normocalcemia in primary hyperparathyroidism should prompt the physician to look for vitamin D deficiency.

Biopsy, Needle↗
PubMed2006

Primary hyperparathyroidism and the cardiovascular system.

The role of primary hyperparathyroidism (PHPT) in heart disease is still somewhat uncertain in many respects. Patients with PHPT seem to have an increase in mortality and this seems mainly due to an overrepresentation of cardiovascular death. PHPT is reported to be associated with hypertension, disturbances in the renin-angiotensin-aldosterone system, cardiac arrhythmias as well as structural and functional alterations in the vascular wall. There is an increased prevalence of cardiac structural abnormalities such as LVH and functional properties of the heart may be affected by the hyperparathyroid condition as well. We report the case of a 65-year-old woman with no cardiac risk factors apart from her age and type 2 diabetes who presented in cardiogenic shock. Extensive evaluation for the aetiology of the cardiomyopathy revealed solely a diagnosis of primary hyperparathyroidism. Cardiac manifestations of primary hyperparathyroidism have been reported before but to our knowledge this is the first description of severe left ventricular function secondary to PHPT. We believe that this atypical presentation of primary hyperparathyroidism causing left ventricular cardiomyopathy warrants further attention, and that a diagnosis of primary hyperparathyroidism should always be considered in patients with systolic as well as diastolic left ventricular dysfunction, and no other obvious cause.

Female↗
PubMed2005

25-hydroxyvitamin D deficiency is a risk factor for symptoms of postoperative hypocalcemia and secondary hyperparathyroidism after minimally invasive parathyroidectomy.

BACKGROUND: Patients with primary hyperparathyroidism who undergo minimally invasive parathyroidectomy (MIP) may have postoperative symptoms of hypocalcemia or secondary hyperparathyroidism. This study sought to identify factors predictive of these events. METHODS: Between 1998 and 2004, 190 patients with primary hyperparathyroidism underwent MIP with excision of a single adenoma. Age, gender, race, prior head and neck surgery, use of preoperative thyroid hormone or calcium-channel blockers, preoperative levels of calcium, 25-hydroxyvitamin D (25[OH]D) and intact parathyroid hormone (iPTH), the presence of osteopenia or osteoporosis, intraoperative iPTH levels, and adenoma weight were evaluated by univariate analysis as predictors of postoperative symptoms of hypocalcemia and secondary hyperparathyroidism. RESULTS: None of the following were predictors of postoperative symptoms of hypocalcemia: age, gender, race, prior head and neck surgery, preoperative medications, preoperative calcium and iPTH levels, osteopenia or osteoporosis, intraoperative iPTH levels, or adenoma weight. However, patients with postoperative symptoms of hypocalcemia had significantly lower preoperative 25[OH]D levels (P = .01). Further, higher preoperative iPTH levels (P < .01) and lower preoperative 25[OH]D levels (P = .05) were associated with secondary hyperparathyroidism postoperatively. CONCLUSIONS: A low preoperative 25[OH]D level is associated with postoperative symptoms of hypocalcemia and secondary hyperparathyroidism in patients undergoing MIP. One might consider instituting empiric calcium supplementation postoperatively in patients with low 25[OH]D levels.

Adenoma↗
PubMed1989

Neuromuscular involvement in mild, asymptomatic primary hyperparathyroidism.

PURPOSE: The classic neuromuscular abnormalities of primary hyperparathyroidism are based on observations from an earlier time when the disease presented commonly with signs and symptoms. The purpose of the present study was to test for neuromuscular abnormalities among patients currently seen with primary hyperparathyroidism, in whom the vast majority are asymptomatic. PATIENTS, METHODS, AND RESULTS: Forty-two patients (30 women, 12 men) were studied. Serum calcium level was 11.1 +/- 0.1 mg/dL (normal, 8.7 to 10.7 mg/dL); phosphorus level was 2.8 +/- 0.1 mg/dL (normal, 2.5 to 4.5 mg/dL). Parathyroid hormone levels by radioimmunoassay for N-terminal and for mid-molecule regions were 32.6 +/- 2.4 pg/mL (normal, 8 to 24 pg/mL) and 831 +/- 127 pg/mL (normal, 50 to 330 pg/mL), respectively. Although generalized weakness and easy fatigability were common complaints, they were not seen on neurologic examination. No patient showed typical neuromuscular findings such as muscle weakness or atrophy, hyperreflexia, abnormal gait, tongue fasciculations, or objective changes in mental status. On the other hand, paresthesias and muscle cramps were reported by 22 patients (52%). Neurologic examination in 12 patients (29%) demonstrated findings consisting of either stocking-glove loss of pain sensation or loss of vibratory sensation with diminished reflexes. Creatine phosphokinase levels were normal in all patients. Electromyography and nerve conduction studies were performed in nine patients. None showed myopathy or signs of motor unit denervation. Isolated nerve abnormalities (n = 6) and nonspecific sensory neuropathy (n = 2) were observed. CONCLUSION: We conclude that the classic neuromuscular syndrome of primary hyperparathyroidism is rarely seen among a typical modern-day group of patients with primary hyperparathyroidism. The results suggest that the neurologic component of primary hyperparathyroidism should be included among those features of the disease that have changed along with other aspects of the clinical profile of primary hyperparathyroidism.

Aged↗
PubMed1999

The effects of vitamin D insufficiency in patients with primary hyperparathyroidism.

PURPOSE: Differences in the prevalence of vitamin D deficiency may explain why the frequency of symptoms in patients with primary hyperparathyroidism varies geographically. This study was performed to determine the prevalence in the United States of low 25-hydroxyvitamin D levels among patients with mild primary hyperparathyroidism, and the effect of 25-hydroxyvitamin D status on disease severity. METHODS: We studied 124 patients with mild primary hyperparathyroidism. Biochemical, bone mineral density, and bone histomorphometric indices were compared among patients whose serurm 25-hydroxyvitamin D levels were in the lowest and highest tertiles. RESULTS: Serum 25-hydroxyvitamin D levels (mean +/- SD) were in the low range of normal (21 +/- 11 ng/mL, normal 9 to 52 ng/mL). Levels were below normal in 9 (7%) patients, and below the level suggested for vitamin D "sufficiency" (20 ng/mL) in 66 (53%) patients. Those with lowest 25-hydroxyvitamin D levels had the highest parathyroid hormone levels (low tertile 158 + 66 pg/mL versus high tertile 103 +/- 2 pg/mL, P <0.0001). Other evidence of more active hyperparathyroidism in those with low 25-hydroxyvitamin D levels included higher serum alkaline phosphatase activity (114 +/- 48 U/L versus 91 +/-35 U/L, P <0.03), lower serum phosphorus levels (2.7 +/- 0.4 mg/dL, versus 3.0 +/- 0.4 mg/dL, P <0.01), and greater bone mineral density at the lumbar spine (0.94 +/- 0.03 g/cm2 versus 0.83 +/- 0.03 g/cm2, P <0.05) reflecting the protective effects of parathyroid hormone on cancellous bone. They also had enhanced bone turnover on bone biopsy. Despite the expected differences in vitamin D metabolism in African-Americans, results did not differ by race. CONCLUSION: Vitamin D insufficiency or deficiency is common among patients with mild primary hyperparathyroidism. In these patients, the effects of primary hyperparathyroidism on biochemical, densitometric, and histomorphometric indices are more pronounced.

Adult↗