UMLS:C0020437 - FACTA Search

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

Measurement of parathyroid hormone-related peptide (PTHrP) associated with that of parathyroid hormone, allows to establish, in most cases, diagnosis of hypercalcemia of malignancy and more exactly of patients with Malignancy Humoral Hypercalcemia (MHH). Because of the variety of molecular forms of PTHrP, linked to its catabolism, its immunoassay remains difficult. After a study evaluating the methodological reliability, we measured the contribution of PTHrP to the hypercalcemia by 2 assays: a N-terminal RIA and a 1-72 IRMA in samples from 47 control subjects, 10 patients with chronic renal failure (IRC), 13 patients with primary hyperparathyroidism (HPT), and 48 patients with solid tumors classified by their level of calcemia: 48 normocalcemia and 23 hypercalcemia. We noted a strong correlation (r = 0.92) between the two assays. They do not show increases in renal insufficiency; they have a good diagnostic discrimination between HPT, normal subjects and patients with MHH. Elevated levels of PTHrP are similar in both assays. However, IRMA appears to be more sensitive and more practical than RIA. Moreover, it shows the best correlation between serum calcium and phosphorus in patients with MHH.
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PMID:[Performances of two kits for parathyroid hormone-related peptide (PTHrP) assay in the additional study of malignant hypercalcemias]. 874 2

Feeding problems, anorexia and vomiting are common in infants and children with chronic renal failure (CRF), and play a major role in the growth failure often found in this condition. However, the gastroenterological and nutritional aspects of CRF in children have received little attention, hence therapeutic interventions are usually empirical and often ineffective. Gastritis, duodenitis and peptic ulcer are often found in adults with CRF on regular haemodialysis and following renal transplantation. Despite persistent hypergastrinaemia, gastric acid secretion is decreased rather than increased in most of these patients, and active peptic disease appears to be promoted by the removal of the acid output inhibition (neutralisation of gastric acid by ammonia) that follows active treatment. Helicobacter pylori, on the other hand, does not seem to play a significant role in the pathogenesis of peptic disease in CRF. Gastro-oesophageal reflux has been found in about 70% of infants and children with CRF suffering from vomiting and feeding problems, and thus appears to be a major problem in these patients. In a number of symptomatic patients with CRF, gastric dysrhythmias and delayed gastric emptying have also been found; hence there appears to be a complex disorder of gastrointestinal motility in CRF. Serum levels of several polypeptide hormones involved in the modulation of gastrointestinal motility [e.g. gastrin, cholecystokinin (CCK), neurotensin] and the regulation of hunger and satiety (e.g. glucagon, CCK) are significantly raised as a consequence of renal insufficiency, and can be reverted to normal by renal transplantation. Furthermore, several other humoral abnormalities (e.g. hypercalcaemia, hypokalaemia, acidosis, etc.) are not uncommon in CRF. By directly affecting the smooth muscle of the gut or stimulating particular areas within the central nervous system, all these humoral alterations may well play a major role in the gastrointestinal dysmotility, anorexia, nausea and vomiting in patients with CRF. Specific pharmacological and nutritional interventions should thus be considered for the treatment of vomiting and feeding problems in CRF.
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PMID:Gastrointestinal function in chronic renal failure. 874 22

A case of humoral hypercalcemia of malignancy in cutaneous squamous cell carcinoma is reported. An 82-year-old male underwent surgery for cutaneous squamous cell carcinoma (SCC) of the left hand in 1992. He subsequently developed clouding of consciousness with remarkable hypercalcemia, a high parathyroid hormone related protein (PTHrP) level, and elevated plasma cytokine levels [tumor necrosis factor alpha (TNF alpha), interleukin-6 (IL-6)]. Diagnosis of humoral hypercalcemia of malignancy (HHM) was made on the basis of these findings. He died of renal insufficiency due to this hypercalcemia in spite of several replacement therapies and chemotherapies. The PTHrP might have derived from the SCC and have been responsible for the HHM in conjunction with IL-6 and TNF alpha.
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PMID:Humoral hypercalcemia of malignancy with elevated plasma PTHrP, TNF alpha and IL-6 in cutaneous squamous cell carcinoma. 877 24

Increased calcitonin (CT) levels have been reported in chronic renal failure, even before the uraemic phase and in the absence of hypercalcaemia. Furthermore, a sigmoidal CT-calcium relationship was recently observed in rats and haemodialysed patients. We carried out the present investigation in order to assess: (a) whether the sigmoidal CT-calcium relationship is also evident in renal patients with a variable degree of renal failure and in normal subjects; (b) whether the four secretory parameters already described for the PTH-calcium relation curve might be described for CT too; (c) whether any change in some, if any, of these secretory parameters could be found at a variable degree of renal insufficiency. We studied 33 renal patients (RP), with a variable degree of renal failure (creatinine clearance ranging from 16 to 164 ml/min), and 10 normal subjects (C). All RP and C were submitted to a basal evaluation including the assessment of (1) basal concentrations of 1,25(OH)2 vitamin D, 25(OH) vitamin D, monomeric CT, intact PTH; (2) GFR by Cr51EDTA clearance. On the 2 subsequent days, a hypocalcaemic test (Na2-EDTA about 37 mg/kg of body-weight/2 h) and a hypercalcaemic test (Ca gluconate giving 8 mg/kg body-weight/2 h of Ca element) were carried out for the assessment of both CT and PTH secretory parameters. According to GFR values, the RP were divided into three groups: group RP1 (GFR > 70 ml/min per 1.73 m2; n = 10), group RP2 (GFR between 30 and 70 ml/min per 1.73 m2; n = 15), group RP3 (GFR < 30 ml/min per 1.73 m2; n = 8). In most, but not all, RP and C a sigmoidal CT-calcium relationship was evident, opposite in direction to the PTH-calcium relation curve. In these RP and C the four secretory parameters, characteristic for the PTH-calcium secretion curve, were calculated for CT too. When pooled RP and C were considered, both minimal (9.0 +/- 6.4 pg/ml) and maximal CT levels (71.8 +/- 56.2 pg/ml) significantly differed from basal levels (24.3 +/- 18 pg/ml; P < 0.001). The CT set point (CT SP) and sensitivity (CT SENS) values were significantly higher and lower than the corresponding PTH secretory parameters (CT SP 1.39 +/- 0.08 mmol/l, PTH SP 1.23 +/- 0.05 mmol/l, P < 0.001) (CT SENS 243 +/- 67%/mmol, PTH SENS 598 +/- 329%, P < 0.001). However, the CT SP values were strictly correlated with PTH SP values (r = 0.78, P < 0.001). When CT secretory parameters were considered separately in the RP groups, increased levels of basal (36.1 +/- 28.6 pg/ml), minimal (17.9 +/- 10.4), and maximal (139.9 +/- 39.7) CT levels were found in the RP3 group, when compared with both the other RP groups and C. No significant difference was found as regards the CT SP and CT SENS values between RP and CT. These results suggest that (1) CT secretion is homeostatically controlled by calcium changes in the same range of the PTH-calcium system; (2) a sigmoidal CT-calcium relationship is demonstrable in most (but not all) RP and C; in these subjects it is possible to calculate the CT secretory parameters as for PTH; (3) the increase in CT levels in the course of chronic renal failure is quite similar to the already known increase of PTH, and is characterized by the increase of basal, minimal and maximal CT values, suggesting that an increased secretion of CT by the thyroid C-cells (rather than CT retention due to a decrease in renal function), is responsible for these findings.
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PMID:The calcitonin-calcium relation curve and calcitonin secretory parameters in renal patients with variable degrees of renal function. 880 22

MGUS is characterized by a serum M-protein concentration of less than 30 milligrams (3 g/dl), fewer than 10% plasma cells in the bone marrow, no or only small amounts of M-protein (Bence Jones protein) in the urine, the absence of lytic lesions, anaemia, hypercalcaemia and renal insufficiency, and most importantly, stability of the M-protein and failure of the development of additional abnormalities. Electrophoresis on agarose, followed by immunoelectrophoresis or immunofixation for the identification of the type of M-protein, is recommended. In 1994, 971 patients at the Mayo Clinic were found with a serum M-protein. The most frequent diagnosis was MGUS, which occurred in 52% of patients. MGUS is found in approximately 3% of people older than 70 years and in at least 1% of those aged over 50. The incidence of monoclonal gammopathies increases with advancing age and is higher in African-Americans than in Caucasians. Two hundred and forty-one patients from the Mayo Clinic with a monoclonal gammopathy but no evidence of MM, macroglobulinaemia, amyloidosis, lymphoma or related disorders were followed for 24-38 years. In 62 patients (26%), multiple myeloma, macroglobulinaemia, amyloidosis or a malignant lymphoproliferative disorder developed (the actuarial rate of development of serious disease at 10 years was 16%; at 20 years, 33%; and at 25 years, 40%). Thirty patients (12%) were alive and had a stable M-protein value. In 23 patients (10%), the serum M-protein level increased to 30 milligrams (3 g/dl) or more, but they did not require therapy for myeloma or related disorders. Fifty-two per cent of patients (126) died of unrelated diseases without the development of a malignant plasma cell lymphoproliferative disorder. The actual rate of development of serious disease was the same for those with IgG, IgA and IgM M-proteins. Differentiation of MGUS from myeloma or macroglobulinaemia is difficult. The M-protein value must be measured periodically and clinical evaluation carried out to determine whether or not serious disease has developed.
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PMID:Monoclonal gammopathy of undetermined significance (MGUS). 884 71

MGUS is characterized by the presence of a serum M-protein less than 3 g/dL; fewer than 10% plasma cells in the bone marrow; no, or only small amounts of, M-protein in the urine; absence of lytic lesions, anemia, hypercalcemia, and renal insufficiency; and, most importantly, stability of the M-protein and failure of development of other abnormalities, MGUS is found in approximately 3% of persons older than 70 years and in 1% of those 50 years or older. During long-term follow-up, approximately one fourth of patients develop multiple myeloma (MM), amyloidosis, macroglobulinemia, or a similar malignant lymphoproliferative disorder. Actuarial rate of development of serious disease was 16% at 10 years, 33% at 20 years, and 40% at 25 years in our experience. The interval from recognition of the M-protein to the diagnosis of MM ranged from 2 to 29 years (median, 10 years). The size of the M-protein, hemoglobin value, percentage of bone marrow plasma cells, amount of light-chain excretion, presence of hypercalcemia or renal insufficiency, and presence of lytic bone lesions are often helpful in differentiating MGUS from MM and macroglobulinemia. The plasma cell labeling index and the presence of circulating plasma cells in the peripheral blood are indicators of active disease; however, there are no findings at the diagnosis of MGUS that reliably distinguish patients who will remain stable from those in whom a malignant condition will develop. Thus, a physician must perform serial measurements of the M-protein in the serum and periodic evaluation of the pertinent clinical and laboratory features to determine whether MM, macroglobulinemia, systemic amyloidosis, or related disorders have developed. Solitary plasmacytoma is characterized by the presence of a tumor consisting of monoclonal plasma cells identical to those in MM. In addition, skeletal roentgenograms must show no lytic lesions, a bone marrow aspirate must contain no evidence of MM, and immunoelectrophoresis or immunofixation of the serum and concentrated urine should show no M-protein. Exceptions to the presence of an M-protein occur, but therapy of the solitary lesion often results in disappearance of the M-protein. Tumoricidal irradiation (4000 to 5000 cGy) for approximately 4 weeks is the treatment of choice. Overt MM occurs in approximately 50% of patients with solitary plasmacytoma. Progression occurs in most patients within 3 years. The three patterns of failure are (1) development of MM, (2) local recurrence, and (3) development of new bone lesions in the absence of MM.
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PMID:Monoclonal gammopathy of undetermined significance and solitary plasmacytoma. Implications for progression to overt multiple myeloma. 908 Dec 5

During recent decades, primary hyperparathyroidism (pHPT) has appeared as one of the more common endocrine disorders. Previously, the disease was the obvious cause of severe, symptomatic bone disease, recurrent renal stones, and sometimes devastating muscular weakness. The condition often progressed rapidly and ultimately ended in renal insufficiency. Today, pHPT is frequently recognized in patients with less obvious symptoms and markedly slower disease progression. However, if thoroughly examined, many of these patients will also present typical symptoms and complications of the disease. Surgery in pHPT has also developed as a highly efficient procedure with low failure rate and few complications. Further, successful operation is likely to decrease the risk of developing long-term disturbances of calcium metabolism and recently recognized cardiovascular complications of the disease. However, in a group of generally elderly patients with especially mild hypercalcemia and no obvious symptoms, disease progression may be slow, and it is possible that some of these patients can be followed safely without surgery. These patients also constitute a majority of cases detected in population surveys. Pathophysiological studies of pHPT have revealed more or less disturbed secretory regulation as a characteristic feature of pathological parathyroid glands, and this accounts principally for the patients' hypercalcemia. This abnormality has been related to decreased expression or capacity of parathyroid cell surface receptors executing a crucial calcium-sensing function. Recent progress has also led to the identification of causes of a growth regulatory disturbance in pathological parathyroid glands. Exploration of molecular mechanisms behind these abnormalities are likely to further unveil disease characteristics and help explain differences in clinical symptoms and disease progression among the patients with pHPT.
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PMID:Non-familial primary hyperparathyroidism. 908 66

Multiple myeloma typically presents with monoclonal proteinemia, marrow plasmacytosis, anemia, bony involvement, hypercalcemia and renal insufficiency. Less frequent presentations include hepatic and splenic enlargement (5% of cases), lymphadenopathy (4%) and biclonal gammopathy (1%). Chemotherapy may produce remissions in 50% of cases, but relapses are the rule and mean survival is approximately 2.5 years. To improve survival, marrow transplantation is being explored as a therapeutic modality in younger patients. In this report we describe a unique case of multiple myeloma presenting clinically as lymphoma. The patient presented with fever, widespread lymphadenopathy and pleuropulmonary involvement and responded promptly to multiagent doxorubicin-based chemotherapy. This was followed by high-dose chemotherapy and allogeneic bone marrow transplantation and the patient remains in remission more than 36 months post transplant. This case report suggests that myeloma simulating lymphoma may be a chemosensitive and potentially curable myeloma variant.
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PMID:Multiple myeloma presenting clinically as lymphoma. 949 20

The Ca(2+)-sensing receptor (CaR) is a member of the seven-transmembrane domain, G protein-coupled receptor super-family. In the parathyroid gland, it mediates the inhibitory effects of extracellular Ca2+ on the secretion of parathyroid hormone. In the kidney, activation of the CaR causes decreased reabsorption of Ca2+ from the tubular lumen. Mutations in the CaR gene produce abnormalities of Ca2+ homeostasis. Heterozygous loss-of-function mutations cause familial hypocalciuric hypercalcemia. Homozygous loss-of-function mutations cause neonatal severe hyperparathyroidism. In contrast, gain-of-function CaR mutations result in autosomal dominant and sporadic hypoparathyroidism. The resulting hypoparathyroidism and hypocalcemia can range from asymptomatic to life-threatening. Patients with hypocalcemia due to CaR mutations also show disproportionate hypercalciuria that may increase the risk of nephrocalcinosis, nephrolithiasis, and renal insufficiency.
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PMID:Molecular biology and clinical importance of the Ca(2+)-sensing receptor. 975 71

Retinoids are commonly used for the treatment of nonmalignant skin disorders and occasionally for the treatment of various neoplasms including epidemic Kaposi sarcoma (KS). Dry skin and mucus membranes, muscle and joint aches, alopecia, headaches, and liver and lipid abnormalities are the most frequent medication-related side effects. Very rarely, this class of drugs is associated with the development of hypercalcemia. The authors report the case of a man with acquired immunodeficiency syndrome (AIDS)-associated KS who, while participating in a phase II clinical trial of LGD 1057 (9-cis-retinoic acid) for treatment of epidemic KS, developed hypercalcemia, mental status changes, and renal insufficiency. The etiologic factors of retinoid-induced hypercalcemia are imperfectly understood, but with drug withdrawal his serum calcium, mental acuity, and renal function quickly normalized. Hypercalcemia occurs infrequently in the setting of AIDS and when present, is usually mediated by opportunistic infections. Clinicians should be alert to this potentially life-threatening iatrogenic complication that responds favorably to drug withdrawal.
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PMID:Retinoid-induced hypercalcemia in a patient with kaposi sarcoma associated with acquired immunodeficiency syndrome. 978 12

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