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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Records of 46 patients who were treated for primary hyperparathyroidism at King Khalid University Hospital, Riyadh Saudi Arabia from 1st July 2000 to 30th June 2006 were reviewed. Mean age at diagnosis was 44 years (range 13-70 years) and average duration of symptoms was 39 months (1 month to 11 years). There were 35 females and 11 males with a ratio of 3.2:1. Bone pains were the major symptoms at presentation in 45.7% followed by no symptom in 23.9%, renal stones in 15.2%, polyuria in 6.5%, while 4.3% each presented with depression, and constipation. Males had significantly more severe disease with higher serum calcium, higher urinary calcium excretion, and higher serum creatinine. Ninety six percent of patients had successful surgery and 4% (two patients) each had recurrence and hungry bone syndrome. It is concluded that PHPT in Saudi Arabia continues to be a symptomatic disorder with skeletal and renal manifestations occurring at a younger age and males having more severe disease. Further prospective studies are needed to verify our findings.
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PMID:Primary hyperparathyroidism in Saudi Arabia: a review of 46 cases. 1855 29

Hypercalcaemic crisis is a rare endocrine emergency. Often, an acute renal failure develops due to hypercalcaemia-induced polyuria. The molecular causes comprise stimulation of the calcium-sensing receptor in the ascending Henle loop and a reduced aquaporin expression in the collecting ducts. We report on a 54-year-old woman who was admitted for hypercalcaemic crisis and acute renal failure. Immediate rehydratation, bisphosphonate administration, and slow-extended daily dialysis (SLEDD) were initiated leading to a marked reduction of serum calcium. Endocrine work-up revealed primary hyperparathyroidism due to a parathyroid adenoma, which was treated by emergency surgery. Haemodialysis was continued in the first post-operative weeks for prolonged acute renal failure.
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PMID:[Hypercalcaemic crisis and acute renal failure due to primary hyperparathyroidism]. 1918 Apr 12

Primary hyperparathyroidism is a fairly frequent pathologic diagnosis characterized by hypersecretion of parathyroid hormone, which results from adenomas in 80% to 85% of all cases. At clinical onset, the most common symptoms are hypercalcemia-related and some of them are pain due to kidney stones, polyuria, gastrointestinal, and neurologic disorders, whereas rarer symptoms are due to brown tumors and expansive lesions often found in fibrocystic osteitis. Brown tumors represent the terminal stage of the remodeling processes caused by an increased osteoclastic activity and fibroblastic proliferation during primary or secondary, albeit more seldom, hyperparathyroidism. The manifestation of primary hyperparathyroidism as skeletal disease has nearly disappeared in the last 2 decades. Cases are now most often diagnosed by the coincidental finding of asymptomatic hypercalcemia. Advanced screening techniques have made clinical evidence of bone disease rare. This article contains a case of brown tumor on the maxilla, palate, and mandible in addition to nephrectomy and proximal femur fracture, which are probably associated with primary hyperparathyroidism although less common nowadays. The diagnosis was suggested by the clinical history and confirmed by biochemical, radiologic, and histopathologic evidence. Excision of a parathyroid adenoma normalization of the metabolic status was then realized.
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PMID:Primary hyperparathyroidism presenting as a palatal and mandibular brown tumor. 1988 50

Patients with calcium concentrations above 3 mmol/L typically start to develop symptoms of hypercalcaemia, which can include nausea, vomiting, thirst and polyuria, malaise, confusion, lowered pain threshold and coma. Milder hypercalcaemia (calcium concentrations <3 mmol/L) is often asymptomatic, and the problem is therefore usually discovered as an incidental finding on routine biochemical screening. Primary hyperparathyroidism is a common cause of hypercalcaemia. Here, we consider the recognition and further management of patients presenting with asymptomatic primary hyperparathyroidism in primary care.
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PMID:Managing primary hyperparathyroidism in primary care. 2020 Jan 46

A 13-year-old spayed Labrador Retriever cross dog presented for polyuria and polydipsia. Serum total calcium, free calcium, and intact parathyroid hormone concentrations were elevated. Surgical exploration of the ventral neck revealed a grossly enlarged right external parathyroid gland. The histopathological diagnosis for the excised right parathyroid gland was an incompletely resected parathyroid carcinoma. Parathyroid carcinoma in the dog is an infrequent cause of hypercalcemia and primary hyperparathyroidism.
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PMID:Diagnosing the etiology of hypercalcemia in a dog: a case of primary hyperparathyroidism. 2047 10

The kidney is one of the classical target organs of PTH action. Symptomatic primary hyperparathyroidism (PHPT) is nowadays less frequent but mostly occurs with renal symptoms, in particular kidney stones. Nephrocalcinosis and polyuria, the latter closely related to the severity of hypercalcemia, are uncommon. Parathyroidectomy leads to a marked and long-lasting improvement of nephrolithiasis, whereas it has a limited effect on nephrocalcinosis. Kidney failure is one of the long-term complications of PHPT and is associated with a more severe clinical expression of the disease and a higher risk of morbidity and mortality. Current guidelines on the management of asymptomatic PHPT, the most common presentation of PHPT today, recommend surgical treatment if renal function is decreased. However, in this particular clinical setting it is unclear whether PHPT is really associated with a more rapid decline of renal function or whether successful parathyroidectomy could protect renal function.
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PMID:[Renal function in primary hyperparathyroidism]. 2092 3

Background. Primary hyperparathyroidism in childhood is a very rare entity, often being diagnosed late after the onset of its presenting symptoms. It most commonly affects patients in their fourth decade of life and beyond. The inclusion of primary hyperparathyroidism in the differential diagnosis is necessary when evaluating patients presenting with nonspecific symptoms such as polyuria, fatigue, weight loss, abdominal pain, nausea, and vomiting. Methods. We report the case of an eleven-year-old girl presenting with three years history of headaches, visual disturbance, along with episodes of emotional lability. Neuroimaging confirmed a large posterior fossa arachnoid cyst. It was decided to manage this lesion conservatively with surveillance. Only after further hospital admissions with recurrent loss of consciousness, dizziness, and nausea to add to her already existing symptoms, a full biochemical and endocrine assessment was performed to look for more specific causes for her presentation. These pointed to a diagnosis of primary hyperparathyroidism. Conclusions. The inclusion of primary hyperparathyroidism in the differential diagnosis should be considered when evaluating paediatric patients presenting with nonspecific (neurological, gastrointestinal, and renal) symptoms in order to establish a prompt diagnosis of the disorder and to avoid severe complications of prolonged hypercalcaemia and end-organ damage.
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PMID:Posterior fossa arachnoid cyst masking a delayed diagnosis of hyperparathyroidism in a child. 2322 72

We present a 27-year-old male with multiple organ dysfunction caused by parathyroid adenoma-induced primary hyperparathyroidism (PHPT). Initially, the patient experienced a sudden onset of gastrointestinal symptoms, polyuria, polydipsia, bone pain, renal dysfunction, nephrolithiasis, and acute pancreatitis, symptoms associated with hypercalcemia. Biochemical findings suggested PHPT. Renal biopsy showed an acute tubular injury and massive calcium deposits in the tubular epithelial cells and tubular lumina. Moreover, neck ultrasonography suggested the possibility of a parathyroid tumor. We excised his right parathyroid gland. Histopathological analysis revealed features of a parathyroid adenoma. Post-operatively this patient had normal serum calcium concentration, but was renally insufficient. A recent repeat biopsy showed chronic renal tubular injury. Our findings illustrate the complications of various systems that can occur in patients with PHPT caused by a parathyroid adenoma.
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PMID:Multiple organ dysfunction caused by parathyroid adenoma-induced primary hyperparathyroidism. 2432 22

Primary hyperparathyroidism results from the excessive secretion of PTH and typically produces frank hypercalcaemia. With the advent of multiphasic screening of serum chemistries, it has been recognized that primary hyperparathyroidism is not an uncommon disorder. Here, a 32 years old lady with burning to colicky recurrent upper abdominal pain, polyuria, polydipsia associated with anorexia, dyspepsia, generalized body ache, joint pain, constipation and weight loss has been described. An initial abdominal ultrasound was performed at hospital and revealed features of cholelithiasis and bilateral nephrocalcinosis. Serum biochemistries revealed that her serum calcium was 12.60mg/dl, serum PTH was 222.80ng/dl, serum creatinine was 0.90mg/dl, 99 Tc-sestamibi scanning for parathyroid evaluation revealed features suggestive of parathyroid adenoma adjoining the lower pole of right lobe of thyroid gland. Bone densitometry of femur and spine by DEXA showed osteoporosis with T score value <-3.5 SD. Right hemithyroidectomy with parathyroid adenoma excision was performed. Patient was closely monitored. Serum calcium and parathyroid hormone levels were markedly reduced near to the normal range within two weeks of surgery. Following five months after surgery, serum PTH was 29.59ng/dl, six months after surgery serum calcium was 9.2mg/dl. Patient is now in good physical condition and under regular follow up.
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PMID:Primary hyperparathyroidism: a case report. 2485 70

Lithium-associated hyperparathyroidism is the leading cause of hypercalcemia in lithium-treated patients. Lithium may lead to exacerbation of pre-existing primary hyperparathyroidism or cause an increased set-point of calcium for parathyroid hormone suppression, leading to parathyroid hyperplasia. Lithium may cause renal tubular concentration defects directly by the development of nephrogenic diabetes insipidus or indirectly by the effects of hypercalcemia. In this study, we present a female patient on long-term lithium treatment who was evaluated for hypercalcemia. Preoperative imaging studies indicated parathyroid adenoma and multinodular goiter. Parathyroidectomy and thyroidectomy were planned. During the postoperative course, prolonged intubation was necessary because of agitation and delirium. During this period, polyuria, severe dehydration, and hypernatremia developed, which responded to controlled hypotonic fluid infusions and was unresponsive to parenteral desmopressin. A diagnosis of nephrogenic diabetes insipidus was apparent. A parathyroid adenoma and multifocal papillary thyroid cancer were detected on histopathological examination. It was thought that nephrogenic diabetes insipidus was masked by hypercalcemia preoperatively. A patient on lithium treatment should be carefully followed up during or after surgery to prevent life-threatening complications of previously unrecognized nephrogenic diabetes insipidus, and the possibility of renal concentrating defects on long-term lithium use should be sought, particularly in patients with impaired consciousness.
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PMID:Lithium-associated primary hyperparathyroidism complicated by nephrogenic diabetes insipidus. 2650 22


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