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

In pregnant women with symptomatic hyperparathyroidism, parathyroidectomy should be undertaken during the second trimester. We feel that the woman who is initially diagnosed well into the third trimester should be treated medically unless the hypercalcemia worsens or other complications occur. Since the treatment of asymptomatic hyperparathyroidism itself is controversial, it is even more difficult to define the treatment plan for an asymptomatic pregnant patient who has primary hyperparathyroidism. However, a recent consensus panel recommended that young patients with asymptomatic hyperparathyroidism be treated surgically. Accordingly, we believe that the asymptomatic pregnant patient should also be treated surgically, preferably in the second trimester. Whether a patient is treated medically or surgically in these situations, the pregnancy should be considered high-risk. The neonate should be monitored carefully for signs of hypocalcemia or impending tetany. If the mother is treated medically to term (or if spontaneous or elective abortion occurs), the mother should be monitored for hyperparathyroid crisis postpartum. Sudden worsening of hypercalcemia can result from the loss of the placenta (active placental calcium transport may be somewhat protective) and dehydration. Finally, every effort should be made to make the definitive diagnosis early in pregnancy in order to initiate optimal management. The diagnosis should be suspected during pregnancy if the following conditions exist: appropriate clinical signs or symptoms (especially nephrolithiasis or pancreatitis), hyperemesis beyond the first trimester, history of recurrent spontaneous abortions/stillbirths or neonatal deaths, neonatal hypocalcemia or tetany, or a total serum calcium concentration greater than 10.1 mg/dL (2.52 mmol/L) or 8.8 mg/dL (2.2 mmol/L) during the second or third trimester, respectively.
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PMID:Hyperparathyroidism and pregnancy: case report and review. 150 54

The establishment of an abnormal calcemia first requires confirmation by a second measurement that should then be interpretated in relation to albuminemia. Should the abnormality be confirmed, measurement of intact parathormone in serum can help distinguishing between a parathyroid or nonparathyroid source of origin. In presence of a plasma calcium level lower than or equal to 2.9 mmol/l regular monitoring should be investigated and aggravating factors such as thiazide diuretics, dehydration or high calcium intake avoided. If plasma calcium is greater than 3 mmol/l the patient should first be rehydrated. In case of primary hyperparathyroidism, parathyroidectomy is the only effective treatment. In neoplastic hypercalcemia, bisphosphonates are the first-choice treatment when antitumoral therapy turns out to be insufficient. Hypocalcemia can be effectively corrected by calcium and by vitamin-D derivatives.
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PMID:[Hyper- and hypocalcemia--diagnosis and therapy]. 158 71

The establishment of an abnormal calcemia first requires confirmation by a second measurement that should then be interpreted in relation to albuminemia. Should the abnormality be confirmed, measurement of intact parathormone in serum can help distinguishing between a parathyroid or non parathyroid source of origin. In presence of plasma calcium level lower than or equal to 2.9 mmol/L regular monitoring should be provided and aggravating factors such as thiazide diuretics, dehydration or high calcium intake, avoided. If plasma calcium is greater than 3 mmol/L the patient should first be rehydrated. In case of primary hyperparathyroidism, parathyroidectomy is the only effective treatment. In neoplastic hypercalcemia bisphosphonates are the first choice treatment when antitumoral therapy turns out to be insufficient. Hypocalcemia can be effectively corrected by calcium and vitamin D derivatives.
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PMID:[Hyper- and hypocalcemia: diagnosis and treatment]. 159 69

Of 118 consecutive white patients referred for asymptomatic primary hyperparathyroidism, the diagnosis was clinically confirmed in 100, of whom 85 adults had a serum calcium less than 3.0 mM (12 mg/dl) and no skeletal, rheumatic, or significant neuropsychiatric symptoms, azotemia, or other significant illnesses. Among these 85, 68 had both asymptomatic and medically uncomplicated hyperparathyroidism, whereas 17 had historical, radiographic, or ultrasonic evidence of renal stone disease. The 20% with past or present renal calculi concentrated their urine significantly better than the 68 others (p = 0.05), but these two groups were otherwise not distinguished by the tests we performed, so all 85 patients were analyzed together. Systolic and diastolic blood pressures were normal, but premature osteopenia and/or impaired renal function were present in 29-36% of the patients. Micrometer measurements of metacarpal radiographs and 125I photon absorptiometry at the shaft of the radius revealed cortical osteopenia. Osteopenia was equally significant in the distal radius (cortical plus trabecular bone). These quantitative measurements were superior to routine bone radiography, and ROC analysis showed that 125I absorptiometry at either site was superior (p less than 0.01) to metacarpal cortex measurements for detecting premature osteopenia, which was present in more than a third of these patients. Creatinine clearances (24 h) and maximum urine concentrating capacity (overnight dehydration plus the synthetic vasopressin analog DDAVP) were each significantly reduced, despite all patients' normal BUN and serum creatinine levels. Sequential performance of a 24 h creatinine clearance and a urine concentration test revealed abnormalities in the renal function of 27 of 74 patients (36%), with a specificity of 95% and a higher sensitivity than either test alone (27-29%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Asymptomatic primary hyperparathyroidism. 176 60

Based on the author's experience with more than 20 cases of immobilization hypercalcemia following spinal cord injury, current concepts of this condition are presented. Symptoms may be mild or severe: laboratory findings are essential for differential diagnosis in older individuals, in whom preinjury Paget's disease and mild primary hyperparathyroidism must be ruled out. Most cases of immobilization hypercalcemia are seen in adolescent boys following recent spinal cord injury. Besides sex (male), risk factors include age (less than 21 years), complete neurologic injuries, high cervical levels of spinal cord injury, dehydration, and a prolonged period of immobilization. A preinjury history of large ingestion of milk and/or extreme exposure to sunshine may also be contributory factors. Therapy includes vigorous hydration, saline infusions and diuretics, calcitonin, and steroids. The clinical course, without treatment, may be prolonged to 14 months, but the condition is always self-limiting.
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PMID:Immobilization hypercalcemia following spinal cord injury. 293 20

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.
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PMID:Acute primary hyperparathyroidism. 381 20

After confirming hypercalcemia by 3 successive measurements of the total plasma calcium corrected for a plasma protein concentration of 72 g/l, which excludes spurious hypercalcemia due to dehydration, the physician orientates the aetiological diagnosis bearing in mind that primary hyperparathyroidism PHPT is the cause of 85 p. 100 of all asymptomatic forms of hypercalcaemia whilst overt or occult malignancy is the main cause (60 p. 100) of symptomatic forms of hypercalcaemia with PHPT responsible for 20 p. 100 of cases. Other causes, including drug toxicity with Vit D, calcium, Vit A, lithium, thiazide and aluminium hydroxide, sarcoidosis, hyperthyroidism, Addison's disease, pheochromocytoma and familial endocrine disorders are much rarer. Nevertheless, these rarer causes must be excluded on the clinical history and examination followed by radiological (chest X ray, plain abdomen X ray, bone X rays) and simple biological tests. The latter and/or scans tests should also help in a rapid diagnosis of metastatic carcinoma and multiple myeloma, so that the major diagnostic problem is to distinguish primary HPT from occult malignancy. This problem is greatly facilitated by reliable assays of C terminal or medium PTH rather than renal CAMP which is increased in 80 p. 100 of occult malignancies. When PTH assays is unavailable or unreliable Dent's hydrocortisone suppression test may be useful as a fall in'serum calcium is associated with occult malignancy in 70 p. 100 of cases and non-suppression is associated with PHPT in 91 p. 100 of cases. Discriminant analysis of the usual biochemical parameters may be helpful in this differential diagnosis and is accurate in about 90 p. 100 of cases. However, the association of PHPT and malignancy is also possible and not fortuitous.
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PMID:[Stages of the etiological diagnosis of hypercalcemia]. 389 Jun 61

Hypercalcaemia can be caused by many disorders, but is most commonly due to primary hyperparathyroidism in outpatients, and to malignant disease in hospital inpatients. When mild (less than 3 mmol/L) it does not cause symptoms, but can have long term effects such as renal calculi. It is important that the aetiology of the hypercalcaemia be established, as it can reflect serious disease. In most patients the correct diagnosis can be suspected from clinical history and examination, and confirmed by laboratory tests and x-rays. The most difficult diagnostic problem is the patient with negative clinical findings, mild hypercalcaemia and mild renal impairment, when the parathyroid hormone level is normal or slightly elevated. When hypercalcaemia is severe (greater than 3.5 mmol/L), it can cause vomiting, polyuria, dehydration and renal impairment, and is then an important therapeutic problem. Therapy includes treatment of the cause, such as radiotherapy for malignant disease or surgery for primary hyperparathyroidism. In addition, it is usually necessary to treat the hypercalcaemia itself, and the initial step is always rehydration. If the plasma calcium concentration remains high, drug treatment must be added, the most effective and reliable agent being intravenous mithramycin. Aminohydroxypropylidene diphosphonate (APD), though less studied, may be equally useful in this situation. Glucocorticoids are not always effective, and phosphate may cause renal damage, particularly when given intravenously. For long term treatment of malignant hypercalcaemia, oral glucocorticoids and phosphate are often effective, and can be given in combination. When primary hyperparathyroidism cannot be corrected surgically, the hypercalcaemia (and hypercalciuria) are probably best treated with a low calcium diet and cellulose phosphate, a regimen also effective for the hypercalcaemia of sarcoidosis.
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PMID:Hypercalcaemia. What does it signify? 394 Aug 49

207 hypercalcaemic patients, discovered in an urban area of 1 million people over a period of 5 months, were examined to determine the current incidence and mode of presentation of primary hyperparathyroidism. Primary hyperparathyroidism was diagnosed in 111 patients and those most at risk were women over the age of 70 (55% of all patients). In 57% of all patients the initial indication of primary hyperparathyroidism was hypercalcaemia found unexpectedly on biochemical screening of the serum. The next most common mode of presentation was an acute hypercalcaemic syndrome in elderly patients, characterised by confusion and dehydration (14% of all patients). Modern diagnostic methods and routine estimations of serum calcium can be expected to yield at least 250 new cases of primary hyperparathyroidism per million population per year.
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PMID:Primary hyperparathyroidism: changes in the pattern of clinical presentation. 610 28

Impairment of urine-concentrating ability is common in persons with chronic hypercalcemia. We assessed urine-concentrating ability in 40 patients with typical primary hyperparathyroidism and 10 patients with familial hypocalciuric hypercalcemia, a disorder resembling typical primary hyperparathyroidism but lacking some of its clinical complications. Urine-concentrating ability was determined during a dehydration test of 18-22 h. The two patient groups were comparable with respect to serum calcium concentration and creatinine clearance. In the group with familial hypocalciuric hypercalcemia, the duration of hypercalcemia was probably greater, because it commences during infancy; the urinary excretion rate for calcium was lower [6.6 +/- 5.4 (mean +/- 1 SD) vs. 14.8 +/- 7.5 meq/day; P less than 0.005]. Patients with familial hypocalciuric hypercalcemia showed higher maximal urinary osmolality (800 +/- 150 vs. 664 +/- 130 mosmol/kg; P less than 0.0005). Among the patients with typical primary hyperparathyroidism, there was a negative association between maximal urinary osmolality and urinary cAMP (r = -0.40; P less than 0.05), but there was no significant relation between maximal urinary osmolality and the urinary excretion rate for calcium. Among 18 patients retested within 1 month after surgical correction of typical primary hyperparathyroidism, urine-concentrating ability did not improve. In patients with typical primary hyperparathyroidism, impairment in urine-concentrating ability reflects features of the chronic disease state, as it is not rapidly reversible by correction of that state. However, in patients with familial hypocalciuric hypercalcemia, longstanding hypercalcemia is not associated with obvious impairment of urine-concentrating ability. Complete or partial freedom from impairment of urine-concentrating ability and from calcareous renal disease are expressions of the generally mild course in familial hypocalciuric hypercalcemia.
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PMID:Maximal urine-concentrating ability: familial hypocalciuric hypercalcemia versus typical primary hyperparathyroidism. 625 92


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