Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A radioreceptor assay for serum 1,25-dihydroxyvitamin D (calcitriol) was used to screen patients with hypercalcemia of malignancy. Three patients with non-Hodgkin's lymphoma and hypercalcemia (serum Ca, 12.0, 13.4, and 13.0 mg/dL, respectively) had increased serum calcitriol levels (56, 72, and 77 pg/mL, respectively; normal, less than 50 pg/mL). Elevated levels of calcitriol, an active vitamin D metabolite, occurred in the presence of significant renal impairment (creatinine clearance, 8 to 19 mL/min) and relative parathyroid suppression (serum immunoreactive parathyroid hormone, 17 to 39 microL-eq/mL; mean value in end-stage renal disease, 182 +/- 39 microL-eq/mL). Hypercalcemia and excessive serum calcitriol levels responded to glucocorticosteroid therapy. In two patients, the hypercalcemia and increased serum calcitriol level were related to a tumor, but not to the serum immunoreactive parathyroid hormone level. Fractional intestinal 47Ca absorption, measured in one patient, was increased (0.94; normal, less than 0.61) and varied directly with the serum calcitriol level. No patient had evidence of sarcoidosis. Hypercalcemia associated with certain lymphomas may be caused by the increased synthesis of calcitriol by lymphoma cells.
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PMID:Hypercalcemia associated with increased serum calcitriol levels in three patients with lymphoma. 654 27

In an effort to identify new trends in the presentation and treatment of primary hyperparathyroidism, 66 patients treated since 1975 were compared with 100 patients diagnosed and treated from 1948 to 1970. Despite widespread use of multichannel analyzers, the late patients had an insignificant increase in diagnosis while asymptomatic (18 percent versus 9 percent in the early group). Hypertension was the most common presenting complaint in patients seen since 1975, compared with renal disease in patients seen before 1970. Findings of diffuse hyperplasia were more common in the late patients (17 percent versus 3 percent in the early patients). There were no differences in rates of operative complications or persistent postoperative hypercalcemia. In the late series of patients persistent hypercalcemia after surgery for hyperplasia was due to inadequate resection of parathyroid tissue. In the adenoma patients, failure to locate the abnormal parathyroid gland was the cause of operative failure.
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PMID:Primary hyperparathyroidism in the seventies. A decade of change? 661 28

A number of advances which took place during the last decade have increased our understanding of the physiology and pathophysiology of urinary concentrating defects. The development of a highly sensitive radioimmunoassay for plasma vasopressin concentration has shed new light on vasopressin control mechanisms. The cellular action of vasopressin in biological membranes has been studied by various techniques. The role of adenylate cyclase, cyclic adenosine monophosphate (cAMP), microtubules, and microfilaments, in the response of vasopressin-sensitive membranes is now partially understood. New models of countercurrent multiplication systems, in which urea plays a prominent role, offer a better explanation of certain experimental facts. Such advances had permitted a better understanding of clinical conditions characterized by concentrating defects, including hyperkalemia, hypercalcemia, parenchymal renal disease, obstructive renal disease, and polyuria induced by certain drugs.
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PMID:Pathophysiology of renal concentrating defects. 679 72

Paraproteinemias can be subdivided in 1. obligatory paraproteinemias (myeloma, macroglobulinemia, heavy chain diseases); 2. accompanying paraproteinemias (Non-Hodgkin's lymphomas, myeloproliferative diseases, immune deficiency diseases, autoimmune diseases, transitory paraproteinemias after infection, paraproteinemias in association with nonlymphatic neoplasms); 3. benign paraproteinemias: a) with symptoms (primary amyloidosis, chronic cold agglutinin disease, paraproteinemias with further autoantibody function, monoclonal cryoglobulinemia); b) asymptomatic forms. Myeloma is the most common type of obligatory paraproteinemias. Characteristic findings are: Paraproteinemia and/or paraproteinuria in 98%, increase of plasma cells in the bone marrow in 84%, alterations in the roentgenograms of the skeleton in 79%. Clinical staging is of importance for the prognosis (amount of paraproteins, Hb level, renal disease, hypercalcemia, lytic lesions of bone). Neurologic complications, hemostasis dysfunction, cryopathies may be other symptoms. The terminal phase of the disease is determined by plasma cell proliferation, immune deficiency and renal disease or myelomonocytic leukemia. As to Non-Hodgkin's lymphomas the accompanying paraproteinemia is to be found in immunocytomas and in CLL. At last it has to be mentioned that B-cell disorders will influence the T-cell populations and vice versa.
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PMID:[Clinical aspects of monoclonal gammopathies in diseases of the lympho-plasmacytic cell system]. 681 57

A patient with hypertension and chronic renal disease was evaluated for hypercalcemia and hypophosphatemia. Serum parathyroid hormone and urine nephrogenous cyclic adenosine monophosphate levels were both elevated. Absolute and fractional urine excretion of calcium was low, thereby raising the suspicion of hypocalciuric hypercalcemia. Surgical removal of a parathyroid adenoma led to normalization of the serum calcium, and phosphate values associated with the complete absence of calcium from the 24-hour urine collection returned to normal.
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PMID:Hypocalciuric hyperparathyroidism with chronic renal failure. 687 85

The long-term effects of vitamin D analogues and metabolites on renal function were assessed in 24 patients with and without chronic renal failure. Treatment for periods of 5-45 months did not adversely affect renal function in 10 of 11 patients with stable renal function, although transient hypercalcaemia did cause transient rises in plasma creatinine. Of 13 patients with progressive renal failure before treatment, vitamin D-like compounds or the vehicle used for their administration may have accelerated renal failure in 3 patients independently of changes in plasma calcium or phosphate. Particular difficulties in assessing the effects of vitamin D-like compounds in progressive renal disease are discussed.
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PMID:Effects of vitamin D metabolites and analogues on renal function. 689 66

It is generally agreed that the kidneys are the only site of 1-hydroxylation of vitamin D and that the abnormal calcium metabolism in sarcoidosis is caused by increased production of 1,25-dihydroxyvitamin D (1,25-[OH]2D). We describe a patient with sarcoidosis with hypercalcemic nephropathy and end-stage renal disease undergoing long-term maintenance hemodialysis who was initially seen with hypercalcemia and elevated serum levels of 1,25-(OH)2D. Prednisone administration resulted in decreased serum calcium and 1,25-(OH)2D levels. These results confirm the recent evidence for extrarenal production of 1,25-(OH)2D in sarcoidosis and illustrate the importance of altered vitamin D metabolism in the development of hypercalcemia in sarcoidosis.
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PMID:Elevated 1,25-dihydroxyvitamin D levels: occurrence with sarcoidosis with end-stage renal disease. 689 30

Thirty-seven cases of canine hypoadrenocorticism were compared with 39 previously reported cases. The 2 series were compared because it was believed that a study of 37 consecutive cases diagnosed at 1 institution (Michigan State University) and compiled by 1 group of veterinarians would yield data that were more representative of the disease than multiple cases from various institutions. Age, sex, and breed data were similar in both series. The frequency of anorexia, vomiting, depression, and the mean values for the clinicopathologic data were similar for both series except for blood glucose concentration (P less than 0.025). The Michigan State University series was different in that it had a lower frequency of eunatremia, increased plasma total solids, and hypoglycemia but a higher frequency of lymphocytosis, lymphopenia, hyponatremia, hyperglycemia, and hypercalcemia. Further, 3 dogs in the Michigan State University series had azotemia plus near isosthenuric urine, suggesting renal disease, but they seemingly responded to therapy for hypoadrenocorticism. Only 1 such case was identified in the literature. Finally, we detected fewer instances of P waves not being evident in lead II of an electrocardiogram.
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PMID:Canine hypoadrenocorticism: report of 37 cases and review of 39 previously reported cases. 703 23

Persistent hyperparathyroidism and its attendant hypercalcemia have been implicates as possible etiologic factors in posttransplant hypertension. To better define the role of parathyroid hormone (PTH) and calcium in posttransplant blood pressure homeostasis, we measured the acute response of blood pressure, ionized calcium (Ca++), plasma renin activity (PRA), and parathyroid hormone (PTH) to a 4-hr infusion of calcium (15 mg/kg) and an isoproterenol injection (0.15 mg SC) in seven normal subjects and 13 renal transplant (Tx) recipients with stable graft function and persistent hyperparathyroidism. Transient hypercalcemia produced a significant (p less than 0.01) increase in the systolic blood pressure (delta SBP) and suppression of PTH (p less than 0.001) in the posttransplant subjects. There was a significant (p less than 0.02) inverse correlation between changes (delta) in PTH and delta SBP in these subjects. There was no correlation between the delta SBP and either the change in Ca++ (delta Ca++) or the change in PRA (delta PRA) observed in the Tx recipients administered calcium. Following isoproterenol administration, SBP increased (p less than 0.01), PTH fell (p less than 0.05) and Ca++ was only minimally increased in the Tx recipients. A virtually identical, significant (p less than 0.05) inverse correlation existed between the delta PTH and delta SBP observed in the transplant subjects. Greater suppression of PTH was associated with a larger increase in systolic blood pressure. Transient hypercalcemia of comparable degree in normal subjects caused an insignificant increase in their blood pressure. The fact that PTH suppression in the normals was substantially (0.01) less (delta PTH -13 microliter/Eq/ml versus -65 microliter/Eq/ml in the transplant group) with a similar increase in serum calcium suggests that the blood pressure response to transient hypercalcemia is more dependent on PTH suppression than the level of ionized calcium. Plasma renin activity was unchanged during the blood pressure fluctuations induced by either the calcium or the isoproterenol administration to the normal subjects. Under the conditions of this study, endogenous parathyroid hormone has the characteristics of a vasodepressor hormone and may have a role in blood pressure regulation in transplant recipients with hyperparathyroidism. Since the vasodepressor effect can be dissociated from delta Ca+ and delta PRA, such a conclusion seems warranted. The implications of these findings for all subjects with renal disease requires further investigation.
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PMID:Parathyroid hormone: a determinant of posttransplant blood pressure regulation. 703 14

Patients with hyperparathyroidism of renal failure fall into two categories: those with hypocalcemia and those with hypercalcemia. If medical management fails and operative indications are present--bone pain or fracture, metastatic calcification, progressive hypercalcemia or uncontrolled pruritus--parathyroid exploration should be done. Total parathyroidectomy and autotransplantation is the procedure of choice when hypocalcemia is present and more than one gland (usually all) is enlarged (which is the case in most patients). Parathyroid adenomectomy is the procedure of choice where autonomy of parathyroid function is established or a single gland is enlarged and all others are small; hypercalcemia is present in these patients. In other instances of hypercalcemia associated with advanced renal disease, total parathyroidectomy and autotransplantation should be performed; that is, in patients in whom more than one gland is enlarged or irregular or in whom all glands are not identified. Continued follow-up is necessary to confirm this rationale of therapy.
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PMID:Management of hyperparathyroidism in patients with renal failure. 725 4


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