Hypercalcemia with low-normal serum intact PTH: a novel presentation of primary hyperparathyroidism
Article Abstract:
Parathyroid hormone (PTH), which is secreted by a gland located close to the thyroid gland, is an important regulator of calcium absorption and excretion. Primary hyperparathyroidism, in which an excess of PTH is produced and the cause is not due to some other disorder, is marked chiefly by hypercalcemia (high blood calcium levels) and high blood PTH levels. Recent technical developments have improved the sensitivity and specificity of the detection of PTH, which enhances the ability to distinguish hypercalcemia caused by PTH from non-PTH-related disorders. A case is described of a 50-year-old man with primary hyperparathyroidism with hypercalcemia, but with normal-to-low PTH levels. The patient had hypercalcemia over a two-year period, but the cause was unclear. Older types of laboratory tests had found normal blood PTH levels. His family and medical history had been extensively studied, hormonal and metabolic status had been evaluated, and factors such as the use of vitamins or lithium were examined. A new examination, including an immunoradiometric assay (a sensitive test using antibodies against PTH), showed that PTH was inappropriately low. PTH responses to infusion of calcium were tested. In normal patients, the PTH level decreases in response to infused calcium, but this patient's PTH levels were suppressed only partially and did not decrease when steroids were given. Surgery showed that one of the four parathyroid glands was enlarged and contained a mass. After the mass was removed, PTH blood levels dropped six-fold and calcium levels normalized. The cause of the low PTH level in this case of hyperparathyroid hormone remains unclear. This type of phenomenon should be considered when diagnosing some cases of hypercalcemia. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1991
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Neuromuscular involvement in mild, asymptomatic primary hyperparathyroidism
Article Abstract:
Hyperparathyroidism is an abnormal increase in the activity of the parathyroid glands located on either side of the thyroid gland in the front of the neck. The classic symptoms are excessive fatigue, muscle weakness and atrophy, overactive reflexes, tongue fasciculations (growth of nerve bundles), kidney stones and gait abnormalities. Recently, there has been an increase in a mild form of hyperparathyroidism, in which the patient is usually asymptomatic (without symptoms). The authors sought to determine whether patients with mild disease exhibited any of the neuromuscular abnormalities of the classic hyperparathyroidism. Of 42 patients studied, 20 (42 percent) had no neuromuscular symptoms; 22 patients (52 percent) had neuromuscular symptoms in the form of either cramps (45 percent) or paresthesias (pins and needles; 45 percent). Eighteen percent of these patient experienced both cramps and paresthesias. Of the 22 patients who had neuromuscular symptoms, 10 had normal neuromuscular examinations. Twelve had abnormal signs such as loss of pain sensation or diminished vibratory sensation. Of the entire group, 71 percent had normal neuromuscular examinations and no patient had the classic symptoms of hyperparathyroidism. The authors question the possibility that some of the symptoms observed may have been caused by conditions other than primary hyperparathyroidism. It is concluded that the clinical profile of primary hyperparathyroidism has changed and the classic symptom complex associated with the disease in the past is rarely seen today. Modern cases are characterized by more subtle symptoms.
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1989
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Nephrolithiasis and bone involvement in primary hyperparathyroidism
Article Abstract:
Parathyroid hormone (PTH) removes calcium from bones to maintain blood levels of calcium, and also acts on calcium metabolism at several other sites. Hyperparathyroidism consequently results in elevated blood calcium levels, and symptomatic patients have decreased bone density and kidney stones. However, many patients are asymptomatic and the extent to which skeletal changes and kidney stones occur in these patients has been unclear. These parameters were studied in 62 patients (48 female) with hyperparathyroidism. Eleven of the patients had kidney stones, but did not differ from other patients in levels of calcium, PTH, phosphorus, or vitamin D. Urinary excretion of calcium was similar in the two groups as well. However, patients with stones did excrete higher levels of hydroxyproline, indicating higher levels of calcium removal from the skeleton (bone resorption). Bone density was less than 80 percent of normal in 61 percent of all patients, but no differences between patients with or without kidney stones were apparent. Bone density was negatively correlated with urinary calcium excretion, and urinary calcium levels thus reflect bone resorption as well as vitamin D status. The study found no apparent distinguishing characteristics in disease process between hyperparathyroid patients with kidney stones and those without kidney stones. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1990
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