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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two patients with coexistent Graves' disease and primary hyperparathyroidism were studied during medical treatment of their hyperthyroidism. Serum free calcium level was initially quite elevated (1.61 and 1.71 mM, normal 1.12 to 1.28 mM), but immunoreactive parathyroid hormone values were only slightly increased. The immunoreactive parathyroid hormone values of 153 and 173 nleq/ml (normal less than 150 nleq/ml) were far lower than expected in hyperparathyroid patients with a similar degree of hypercalcemia. As the patients became euthyroid during thionamide treatment, calcium values decreased to 1.39 and 1.61 mM, respectively, and parathyroid hormone increased to values clearly suggestive of hyperparathyroidism (454 and 229 nleq/ml, respectively). Parathyroidectomy and subtotal thyroidectomy cured both the hyperparathyroidism and the thyrotoxicosis in each case. These observations suggest that thyroid hormone had potentiated the osteoclastic effects of parathyroid hormone and that the resulting exacerbation of hypercalcemia had produced a relative suppression of hormone secretion by the abnormal parathyroid tissue.
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PMID:Concomitant Graves' disease and primary hyperparathyroidism. Influence of hyperthyroidism on serum calcium and parathyroid hormone. 375 85

This 55-year-old woman presented with primary adrenal insufficiency that led to multiple endocrine gland dysfunctions. Despite symptoms suggestive of hypothyroidism, she had mildly elevated serum thyroid hormone levels associated with elevated thyrotropin levels, hyperprolactinemia, and mild hypercalcemia. These abnormalities corrected with corticosteroid replacement but could be reproduced, in part, when the corticosteroids were temporarily withdrawn. The findings in this patient suggest that physiologic concentrations of glucocorticoids modulate prolactin secretion and the pituitary-thyroid axis. Adrenal insufficiency should be considered in the differential diagnosis of hyperprolactinemia and hyperthyrotropinemia with or without associated hyperthyroxinemia.
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PMID:Reversible hyperthyrotropinemia, hyperthyroxinemia, and hyperprolactinemia due to adrenal insufficiency. 402 80

The parameters of calcium metabolism were determined in 22 patients with untreated hyperthyroidism (5 males and 17 females) and 5 control subjects. Hypercalcemia was found in the patients with hyperthyroidism in comparison with the control subjects (serum Ca: 10.0 +/- 0.56 vs. 9.0 +/- 0.18, p less than 0.001 and Ca++: 5.1 +/- 0.28 vs. 4.6 +/- 0.15 mg/dl, p less than 0.001, mean +/- SD). Although the urinary excretion of calcium was decreased in many patients, abnormalities of phosphate metabolism were not found in this study. The parameters of bone resorption, urinary hydroxyproline, serum alkaline phosphatase and acid phosphatase, were increased in all patients with hyperthyroidism. Serum immunoreactive PTH was decreased (0.23 +/- 0.05 vs. 0.29 +/- 0.05 ngEq/ml, p less than 0.05). In vitamin D metabolites, 25-OH-D did not differ from the control (16.9 +/- 7.76 vs. 17.9 +/- 5.52 ng/ml), 1,25-(OH)2D showed a tendency to decrease (32.6 +/- 19.53 vs. 37.2 +/- 13.75 pg/ml) and 24,25-(OH)2D was obviously increased (5.57 +/- 3.582 vs. 1.73 +/- 0.619 ng/ml, p less than 0.001) in the hyperthyroid patients. Thus, the parathyroid function was suppressed in the patients with hyperthyroidism, and hypercalcemia in hyperthyroidism was suggested to be due to the direct action of thyroid hormone upon the bone.
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PMID:[The parathyroid function in patients with hyperthyroidism]. 650 Jan 1

Hypothyroidism is known to affect calcium homeostasis by decreasing bone turnover and serum calcium level, and by increasing parathyroid hormone and 1,25-dihydroxyvitamin D concentrations. A 52-year-old hypothyroid woman is described who had hypercalcemia associated with elevated parathyroid hormone and 1,25-dihydroxyvitamin D levels, but decreased 24-hour urinary calcium excretion and ratio of calcium to creatinine clearance. These parameters normalized following thyroid hormone replacement therapy. Hypercalcemia appeared to result from a combination of reduced renal calcium excretion and a change in the "set point" for calcium feedback inhibition of the parathyroid glands. These data suggest that thyroid hormone has a direct effect on the parathyroid glands, regulating parathyroid hormone secretion, and on the kidney's ability to excrete calcium. It is recommended that parathyroid hormone, 1,25-dihydroxyvitamin D, and urinary calcium excretion values be interpreted in light of thyroid hormone status.
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PMID:Reversible hypocalciuric hypercalcemia associated with hypothyroidism. 654 73

Lipoadenoma is the accepted diagnosis of a single enlarged parathyroid gland that contains large quantities of mature fat cells and focal myxoid stroma, all widely separating small parenchymal cell nests in patients with hyperparathyroidism. Here we are reporting, for the first time, on five cases of hyperparathyroidism in which all four parathyroid glands are enlarged and each gland is noted to have an admixture of fat and parenchymal cells. We will introduce the descriptive diagnosis of lipohyperplasia to name this condition and keep it in perspective with other forms of parathyroid disease. All five patients were women between the ages of 36 and 62 years who underwent neck exploration, at which time four enlarged light-tan parathyroid glands were observed. Three and one half gland resections were performed, and all patients returned to a normocalcemic state except one who had borderline serum hypercalcemia after operation. Most of the resected parathyroid glands weighed in the range of 100 to 200 mg. The largest measured gland weighed 820 mg. Parathyroid histology showed an admixture of mature fat cells with parathyroid parenchymal cells often in a 1:1 ratio. One patient who had renal failure exhibited a lower ratio of fat cells. Two patients had chronic lymphocytic thyroiditis that was severe enough to require synthetic thyroid hormone therapy. Two patients had a history of urinary tract infections. Three patients had hypertensive cardiovascular disease, and several patients had arteriosclerotic cardiovascular disease. One patient had diabetes mellitus, one had a history of pituitary adenoma, and one had polydipsia. All of these patients were first seen with parathyroid glands measuring an average of five times normal size, yet they showed the usual 50% fat/50% parenchyma pattern of normal mature parathyroid glands. This means that the enlarged glands contain a 500% increase in parathyroid tissue, justifying the diagnostic term "lipohyperplasia." This easily represents enough parathyroid tissue to generate excessive parathyroid hormone production. At this time, there is no explanation of the pathogenesis of lipohyperplasia or how it varies from other previously described forms of parathyroid hyperplasia.
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PMID:Five cases of parathyroid lipohyperplasia. 664 2

Serum total reverse triiodothyronine (rT3) levels are normal in patients with renal diseases with and without renal insufficiency but elevated in nonrenal nonthyroidal illnesses. To evaluate the role of secondary hyperparathyroidism of renal diseases in this difference, serum thyroid hormone levels were studied in 27 patients with primary hyperparathyroidism (PHP) and normal renal function. In PHP, total T3 levels were reduced (118 +/- 6 ng/dL, normal: 147 +/- 3 ng/dL) and correlated with PTH levels. Serum rT3 levels were also decreased (27 +/- 3 ng/dL, normal: 34 +/- 2 ng/dL). Values for serum total thyroxine (T4), T3 uptake ratio, free T4 index, and thyrotrophin were not altered. Serum rT3 levels were increased (63 +/- 13 ng/dL) in patients with hypercalcemia due to malignant neoplasms who had low T3 levels, undetectable PTH and normal renal function. Thus, PTH excess may be the factor responsible for the failure of rT3 levels to increase in PHP and secondary hyperparathyroidism.
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PMID:Serum thyroid hormone indexes in patients with primary hyperparathyroidism. 669 68

Symptomatic osteopenia accompanied by subclinical hyperthyroidism developed in three women who were receiving excess thyroid hormone medication. Excessive thyroid replacement therapy resulted in mild hypercalcemia, hyperphosphatemia, and hyperphosphatasemia associated with diffuse skeletal demineralization and multiple fractures. Nondecalcified sections of double tetracycline-labeled iliac crest bone showed an accelerated rate of bone turnover with marked osteoclastosis and resorption of the cortical as well as the trabecular bone, typical of endogenous hyperthyroidism. Since thyroid hormones are among the most frequently prescribed medications, bone loss caused by exogenous hyperthyroidism may be more common than previously recognized.
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PMID:Exogenous hyperthyroidism with osteoporosis. 683 Mar 80

Normal calcium regulation depends on the complex interactions of several systems. The specific calcium regulating hormones, parathyroid hormone, calcitriol and calcitonin, affect calcium and phosphorus concentration and supply by acting on bone, kidney and intestine. The changing concentration and supply of ions not only regulate these hormones, but may also influence the function of the target organs, particularly bone, directly. Systemic hormones such as growth hormone and somatomedins, glucocorticoids, sex hormones and thyroid hormone are essential for skeletal growth and development and interact with calcium regulators. Prostaglandins and osteoclast activating factor may be important in local regulation of bone. Disorders of calcium regulation are common, particularly hypercalcemia; however, measurements of parathyroid hormone are not yet ideal and the factors which produce hypercalcemia in malignancy have not been identified. The role of calcium regulating hormones in the pathogenesis and treatment of osteoporosis is controversial. Solution to these problems may be dependent on the identification of additional factors which influence mineral metabolism.
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PMID:Calcium regulation. 703 24

Hyperthyroidism is often associated with hypercalcemia which is provoked by osteoclastic activity of the thyroid hormones. These data show that hypercalcemia develops with increasing age and in the presence of a special type of hyperthyroid goiter. Total serum calcium, total protein, and albumin as well as different parameters of thyroid function, namely T3 RIA1, T4 test, ETR and TRH test were determined in a group of 147 patients. The ionized calcium level was estimated from total calcium and albumin. 211 measurements were performed. Hyperthyroidism existed in 92 cases. Total calcium was not significantly elevated in hyperthyroidism. Hyperthyroid patients under 61 years of age showed elevated ionized calcium levels in only 2.3% and patients over 60 years of age in 18.8% of cases. Elevated ionized serum calcium levels were observed in 43.8% of hyperthyroid patients with multinodular goiters. The linear correlation between ionized calcium levels and different parameters of thyroid function is much more pronounced in the older group and it was found to be highly significant. 7 of 9 hyperthyroid patients with elevated ionized calcium levels showed multinodular goiters, though no autonomous adenoma. In the hyperthyroid group of patients of over 60 years of age with multinodular goiters the incidence of hypercalcemia was 43.8%. Direct action of thyroid hormone on calcium turnover as well as increasing age and special goiter type seem to be responsible for disturbances in calcium metabolism. A possible calcitonin deficiency in the above mentioned conditions is discussed.
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PMID:Hypercalcemia in hyperthyroidism. Role of age and goiter type. 723 Jul 26

We describe a young woman with lymphocytic hypophysitis presenting in the early post-partum period. She had selective corticotroph failure causing secondary adrenal insufficiency. At the time of presentation she had transient hyperthyroidism due to thyroiditis, and hypercalcaemia. This is the third case to be described of hypercalcaemia occurring in association with lymphocytic hypophysitis. Hypercalcaemia is not a recognized complication of other forms of pituitary failure. The two previously described cases also had selective corticotroph failure and hyperthyroidism due to thyroiditis. This pattern of presentation supports the concept that thyroid hormone action in the presence of glucocorticoid deficiency is responsible for the increased calcium efflux from bone into the circulation. Reduced renal excretion of calcium due to a reduction in calcium delivery to the glomerulus and increased proximal tubular reabsorption are also implicated in the aetiology of hypercalcaemia associated with adrenal failure.
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PMID:Secondary hypoadrenalism presenting with hypercalcaemia. 788 23


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