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At least 19 recordsLinked to original sources
PubMed1984

A case of primary hyperparathyroidism, primary hyperaldosteronism and Cushing's disease.

The rare association of parathyroid adenoma with primary hyperaldosteronism, occurring in each of 2 patients, was recently reported from this unit. The present communication records the subsequent development, in one of these patients, of Cushing's syndrome with an anterior pituitary adenoma. Screening for other endocrine abnormalities was negative. A literature search failed to produce any other cases of the association of these three conditions in one patient.

Adenoma↗
PubMed1976

Geriatric primary hyperparathyroidism.

Primary hyperparathyroidism occurs in a significant number of patients over 60 years of age; about one-third of the 182 patients we studied were in this age group. Primary hyperparathyroidism has been recognized with greater frequency in recent years, particularly in patients without manifestations of renal lithiasis or osteitis fibrosa cystica and in older patients. Age alone is not critical in the occurrence of serious complications from hypercalcemia, the presence of other life-endangering disease, or the development of major postoperative complications in the management of primary hyperparathyroidism. A liberal but selective policy is advocated in advising operation for primary hyperparathyroidism in the elderly. Different clinical patterns of primary hyperparathyroidism are recognized in all age groups. The operative procedure for primary hyperparathyroidism is determined primarily by the surgeons at the time of operation, on the basis of gross characteristics of the parathyroid glands. A precise correlation is not found between microscopic changes, gross changes, and clinical features of primary hyperparathyroidism.

Aged↗
PubMed2006

[Primary hyperparathyroidism].

Primary hyperparathyroidism is the most frequent cause of hypercalcemia in ambulatory patients. Elevated serum parathyroid hormone in the presence of persistent hypercalcemia is the diagnostic sine qua non for primary hyperthyroidism. Since examination of serum calcium became a routine diagnostic test, most patients with primary hyperparathyroidism are asymptomatic at the time of diagnosis. Primary hyperparathyroidism in most of patients is caused by parathyroid adenoma, and parathyroid hyperplasia and cancer are rare causes of the disorder. Parathyroidectomy is the primary treatment of choice for primary hyperparathyroidism by any cause. Parathyroidectomy should be performed in most of patients with primary hyperparathyroidism, but asymptomatic or only mildly hypercalcemic patients are treated according to the guidelines for surgical treatment established by the NIH Consensus Development Conference in 2002. For patients with osteoporosis who are not indicated for or decline surgical procedures can be treated with bisphosphonates.

Humans↗
PubMed1991

Etiologies of parathyroid gland dysfunction in primary hyperparathyroidism.

Primary hyperparathyroidism is caused by defects in the parathyroid gland. Investigations have implicated three interesting genes whose mutation can cause primary hyperparathyroidism. Familial hypocalciuric hypercalcemia is believed to be an atypical form of primary hyperparathyroidism with an inherited defect in calcium recognition expressed not only in all parathyroid chief cells (thus a polyclonal defect) but in some renal tubular cells as well. In typical primary hyperparathyroidism a monoclonal parathyroid tumor is usually the central cause. Either of two apparently different genes on the long arm of chromosome 11 has been implicated in development of a parathyroid tumor clone. One gene (D11S287) was shown to have undergone a rearrangement with the parathyroid hormone gene on the short arm of the same chromosome (pericentromeric inversion) in a small fraction of tumors; the D11S287 locus may encode a growth stimulator. Another gene, the locus for familial multiple endocrine neoplasia type 1 (FEMEN1), is likely to encode a growth inhibitor. Inactivation of this gene or another nearby gene by somatic mutation has been indirectly implicated in one-quarter of sporadic parathyroid adenomas and in more than half of parathyroid tumors in FMEN1. In conclusion, studies have suggested three different mechanisms for parathyroid gland dysfunction in primary hyperparathyroidism: (1) a defect in calcium recognition, (2) a monoclonal tumor from overexpression of a growth stimulator, or (3) a monoclonal tumor from inactivation of a growth inhibitor.

Adenoma↗
PubMed1992

[Diagnosis and treatment of primary hyperparathyroidism].

Primary hyperparathyroidism is nowadays not uncommon in Japan. The incidence is considered to be one in every 2,500 to 5,000 persons. Many advances have occurred in diagnosis, localization study, and treatment of the disease. Surgery remains the treatment of choice for patients with primary hyperparathyroidism. Notwithstanding, there are still controversies concerning the management of primary hyperparathyroidism. One of the current disputable points is whether the use of localization study in patients who are undergoing and initial operation is justified or not. Another is whether unilateral exploration is justified or not. The basic reasons for these persistent controversies is the lack of consensus about incidence of multiglandular hyperplasia or double adenomas. Our observation implies that the incidence of hyperplasia or double adenomas among all the patients with primary hyperparathyroidism in Japan is lower than that in western countries. Since diagnostic accuracy of noninvasive localization studies has recently improved, it seems reasonable to adopt unilateral neck exploration in our country. It is also characteristic in Japan that the incidence of parathyroid carcinoma is relatively high (6%) compared with that reported in many other countries.

Adenoma↗
PubMed1982

The medical management of primary hyperparathyroidism.

Primary hyperparathyroidism has become a relatively common endocrine disorder. Greater recognition of this disease has led to earlier detection. Consequently, primary hyperparathyroidism is now characterized frequently by asymptomatic mild hypercalcemia rather than by the more classical presentation with bone or renal involvement. Patients who have hypercalcemia and signs or symptoms should undergo neck surgery and removal of the abnormal parathyroid tissue. For the growing population of asymptomatic patients, however, indications for surgery are not as clear. The natural history of primary hyperparathyroidism is variable, and predicting who will develop complications of this disorder is not possible. Alternatives to surgery are careful and regular observation combined with various general and specific approaches currently receiving attention. Available information on the medical management of asymptomatic, mild primary hyperparathyroidism is summarized.

Calcitonin↗
PubMed2004

Genetics of primary hyperparathyroidism.

Primary hyperparathyroidism, a genetically heterogeneous disease, usually occurs as a sporadic disorder due to the presence of parathyroid adenoma/s, hyperplasia or, rarely, carcinoma. In the last decades familial forms of primary hyperparathyroidism have been described. Recognizing such forms is essential for a correct clinical management of affected individual subjects and families. In fact, primary hyperparathyroidism may be the typical feature of familial syndrome or alternatively only an associated disorder within the context of a more complex syndromic picture. Several responsible genes have been so far identified, making their mutational analysis possible, which provides not only early identification of asymptomatic gene carriers, but could also add new important knowledge of the molecular mechanisms underlying parathyroid tumorigenesis. Such mechanisms could, in the near future, become an ideal target for new therapeutic strategies of primary hyperparathyroidism.

DNA Mutational Analysis↗
PubMed2006

Asymptomatic primary hyperparathyroidism.

Primary hyperparathyroidism is a common disorder of mineral metabolism characterized by incompletely regulated, excessive secretion of parathyroid hormone from one or more of the parathyroid glands. In adults with the disease, a single, benign adenoma is seen approximately 80 percent of the time, with multiple gland involvement comprising most of the remaining patients. Very rarely, a parathyroid cancer is responsible but it is seen in less than 0.5 percent of patients with primary hyperparathyroidism. In this article, we will review important clinical and diagnostic features of asymptomatic primary hyperparathyroidism as well as considerations for surgical or medical management of the disease.

Biomarkers↗
PubMed2002

[Descriptive analysis and surgical outcome of primary hyperparathyroidism].

Primary hyperparathyroidism (PHPT) was a rare but serious disease with massive biochemical, renal and skeletal signs at the time of diagnosis. In the last decades it has become a more common disorder often diagnosed by chance. The disease usually shows minimal symptoms. These clinical changes are due to advances in biochemical screening procedures, which have led to a remarkable increase in the incidence of PHPT. The aim of this study is to describe the clinical profiles, biochemical data, operative findings and postoperative results. Seventy one consecutive patients were prospectively enrolled and underwent surgical examination. Most of them showed symptoms: 6 patients were asymptomatic and 11 had a normocalcemic hyperparathyroidism. After surgery 5 patients showed persistent primary hyperparathyroidism. Parathyroid hormone concentration returned to normal levels in 95.77% of the patients studied. Parathyroidectomy is a safe and effective approach to the treatment of primary hyperparathyroidism.

Adolescent↗
PubMed2006

Bisphosphonate pretreatment attenuates hungry bone syndrome postoperatively in subjects with primary hyperparathyroidism.

Primary hyperparathyroidism is characterized by hypercalcemia with loss of bone mass. After parathyroidectomy, hypocalcemia may develop in some patients due to unregulated bone mineralization. Preoperative administration of bisphosphonates, potent inhibitors of osteoclast activity, may prevent postoperative hypocalcemia after parathyroidectomy. We retrospectively reviewed medical records to investigate the effect of bisphosphonate pretreatment on serum calcium level changes after parathyroidectomy. Twenty-three patients with a diagnosis of primary hyperparathyroidism underwent parathyroidectomy between April 1997 and August 2002. Clinical and laboratory data were collected before and after the operation. These patients were divided into two groups; those showing hungry bone syndrome (n = 9) and those not (n = 14). None of the 9 patients with hungry bone syndrome had received bisphosphonate pretreatment. Of the 14 patients without hungry bone syndrome, 6 had received bisphosphonate pretreatment (P < 0.05). Furthermore, preoperative calcium concentration was not related to the occurrence of hypo-calcemia in those without bisphosphonate pretreatment. In conclusion, administration of bisphosphonates in primary hyperparathyroidism can prevent the occurrence of hungry bone syndrome after parathyroidectomy.

Adult↗
PubMedDate not supplied

Primary hyperparathyroidism.

Primary hyperparathyroidism is the most common cause of hypercalcemia seen in the outpatient setting (Bilezikian, 1992). Skeletal involvement is evident in most patients, even in the vast majority who show no symptoms. Bone histomorphometric studies reveal that the greatest bone diminution occurs in the radial shaft, the femoral neck is intermediate, and the spine is less affected (Parisien et al., 1990). An understanding of this condition is vital for the professional nurse so that effective nursing care can be provided to those who are at risk of developing rapid bone loss and other complications of primary hyperparathyroidism. This article reviews the medical diagnosis and nursing management of primary hyperparathyroidism.

Female↗
PubMedDate not supplied

[Primary hyperparathyroidism].

Primary hyperparathyroidism (PHPT) is characterized by excessive PTH secretion in respect to calcium homeostasis needs, due to parathyroid adenoma (80% of cases), hyperplasia (15-20%), or carcinoma (1-2%). In familial forms of PHPT, several mutations have an established role: menin gene for MEN type 1, RET for MEN type 2a, calcium-sensing receptor gene for familial hypocalciuric hypercalcemia, parafibromin gene for PHPT-jaw tumour and carcinoma. Etiology of sporadic adenomas (80% of PHPT cases) is less defined, being most commonly found a mutation of menin gene or activation of PRAD1 oncogene. In recent years, the classical features of the disease became less common. Typically, bone involvement is now represented by a reduced bone mass at skeletal sites more rich in cortical tissue. Prominently trabecular skeletal sites are relatively spared, because of the anabolic effects of a slight PTH excess on trabecular tissue. PHPT patients may have increased fracture risk, though it is not clear why bone damage is more severe in a subgroup of patients. Clinical features of hypercalcemia may be fatigue, anorexia, thirst, and polyuria. Vague neurological and psychiatric symptoms, such as weakness, anxiety, depression, paresthesias, and muscular cramps may ameliorate after parathyroidectomy. Recent reports indicate increased cardiovascular mortality in PHPT patients. Diagnosis is based on the detection of hypercalcemia, together with inappropriately high serum PTH levels. Preoperative localization of the diseased glands is mandatory in persistent or recurrent PHPT, as like as when minimally invasive surgery is planned. High resolution ultrasonography and SPECT double-phase 99m Tc-sestamibi scintigraphy are the most commonly employed techniques. Intraoperatory PTH assay may confirm successful surgery when serum concentrations decrease more than 50%. Surgical therapy is indicated in patients with renal or skeletal complications, such as in those with previous parathyrotoxic crisis. Many surgeons in recent years adopted minimally invasive parathyroidectomy. Medical treatment is an option for patients unwilling or unfitted for surgery because of severe concomitant diseases. Employed therapy includes estrogens, SERMs, bisphosphonates and calcimimetics.

Adult↗
PubMed1995

The diagnosis and management of primary hyperparathyroidism.

Primary hyperparathyroidism is being diagnosed with increasing frequency in recent years due to more widespread availability and reliability of the various appropriate diagnostic tests. Except in unusual circumstances patients with documented primary hyperparathyroidism are probably best served by early operation performed by an experienced parathyroid surgeon. Under such circumstances cure rate should approximate 95 percent, with less than a one percent incidence of recurrent laryngeal nerve injury or permanent hypoparathyroidism. The cure rate in the currently reported series of cases was 98 percent with no instances of recurrent laryngeal nerve injury or permanent hypoparathyroidism.

Adenoma↗
PubMed1998

[Primary hyperparathyroidism].

Primary hyperparathyroidism was initially regarded as a rare and severe disease. In recent years, introduction of routine screening of serum calcium has contributed to a dramatic increased rate of detection of primary hyperparathyroidism in the population, and asymptomatic forms of this disease are now the rule. Surgery remains the only curative treatment. However a medical follow-up may be justified in asymptomatic patients whose serum calcium levels are only midly elevated and whose renal and bone status are close to normal. The medical follow-up is considered to be safe only with conscientious long-term monitoring. Surgery becomes mandatory if the follow-up shows worsening hypercalcemia, bone deterioration, renal impairment, calcium stone, or increased hypercalciuria.

Female↗
PubMed2000

[Non-specific symptoms and primary hyperparathyroidism].

Primary hyperparathyroidism is diagnosed with increasing incidence. Many patients are misinterpreted as being asymptomatic, but they do indeed suffer from a broad variety of non-specific symptoms. Investigations show that patients with primary hyperparathyroidism may be lethargic, apathic, demented and depressed. Many suffer from bone and joint pain. Surgical treatment can be done with few complications and a high cure rate, resulting in reversal of symptoms. Since symptoms do not correlate with S-Ca++ or S-parathyroid hormone and since the symptoms can be attributed to many other causes, we need more research to find those patients, who will benefit from surgical treatment.

Diagnosis, Differential↗
PubMed2003

Brown jaw tumors: today's unusual presentation of primary hyperparathyroidism.

Primary hyperparathyroidism (pHPT) has changed its clinical features in the last decade becoming a mild biochemical disease, in which the classical fibrous cystic osteitis is a rare complication. The more frequent bone involvement in primary hyperparathyroidism is observed at the distal 1/3 of the radius, where the cortical bone is primarily represented. However, lumbar and femoral osteopenia or osteoporosis prevalently affect hyperparathyroid post-menopausal women. We report two, otherwise healthy, young male patients, who presented a painful jaw swelling. In both patients standard radiographic imaging revealed a low-density well-defined lesion, which caused jaw bone destruction. High levels of serum calcium (14.1-16.6 mg/dl, n.v. 8.1-10.4) and PTH (1172-1928 pg/ml, n.v. 10-65) indicated the presence of pHPT associated with hypertension, asymptomatic renal involvement and osteoporosis with normal serum 25-hydroxyvitamin D levels in both patients. A single huge parathyroid adenoma was successfully removed and within 2 months jaw lesions were almost completely re-mineralized without any other therapeutic intervention in both patients. In conclusion, although brown jaw tumors are a rare complication of the hyperparathyroidism, they should be considered and identified in young patients with severe pHPT. Moreover, such a complication seems to be independent from vitamin D deficiency, suggesting the involvement of other pathogenetic factors.

Adult↗
PubMed1994

Nonadenomatous thymic unencapsulated parathyroid tissue as a cause of persistent primary hyperparathyroidism.

Primary hyperparathyroidism may be caused by ectopic intrathymic parathyroid adenomas or hyperplastic parathyroid glands. The association of the ectopic inferior parathyroid glands and the thymus is due to their common embryologic origin from the third pharyngeal pouch. We report a case of primary hyperparathyroidism due to an unusual pathologic parathyroid gland formation: nonadenomatous thymic unencapsulated parathyroid tissue. Two unsuccessful neck exploration revealed only two normal parathyroid glands within the cervical area. Radiologic imaging studies failed to localize an ectopic parathyroid adenoma. Mediastinal exploration and thymectomy showed one small focus of unencapsulated hypercellular parathyroid tissue expanding peripherally along the septa of thymic adipose tissue. The hyperparathyroidism resolved with the surgical procedure.

Adipose Tissue↗