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)

Although uremia is well known as the most common cause of pruritus, the mechanisms of pruritus in chronic hemodialysis patients remain unclear. The purpose was to characterize uremic pruritus in more detail and to investigate whether severe pruritus is a marker for poor prognosis. A total of 1773 adult hemodialysis patients were studied. A questionnaire was given to each patient to assess the intensity and frequency, as well as pruritus-related sleep disturbance. We analyzed the relationship between clinical and laboratory data and the severity of pruritus in hemodialysis patients and followed them for 24 months prospectively. In total, 453 patients had severe pruritus with a visual analogue scale (VAS) score more than or equal to 7.0. Among them, more than 70% complained of sleep disturbance, whereas the majority of patients with a VAS score of less than 7.0 had no sleep disturbance. Male gender, high levels of blood urea nitrogen, beta2-microglobulin (beta2MG), hypercalcemia, and hyperphosphatemia were identified as independent risk factors for the development of severe pruritus, whereas a low level of calcium and intact-parathyroid hormone were associated with reduced risk. During the follow-up, 171 (9.64%) patients died. The prognosis of patients with severe pruritus was significantly worse than the others. Moreover, severe pruritus was independently associated with death even after adjusting for other clinical factors including diabetes mellitus, age, beta2MG, and albumin. Severe uremic pruritus caused by multiple factors, not only affects the quality of life but may also be associated with poor outcome in chronic hemodialysis patients.
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PMID:Etiology and prognostic significance of severe uremic pruritus in chronic hemodialysis patients. 1667 24

The calcium-sensing receptor has a key role in calcium homeostasis, it is involved in the regulation of the serum calcium level within minutes via the secretion and action of parathyroid and the excretion of calcium in the kidney in a negative feedback manner. Mutations of the calcium sensing receptor gene leads to inactivating and activating mutations resulting in diseases with hypercalcaemia and hypocalcaemia. The loss of function mutations are associated with familial benign hypocalciuric hypercalcaemia (FHH), an autosomal dominant disease characterised by lifelong mild hypercalcaemia, low urinary calcium excretion, and inappropriate high parathyroid hormone levels, sometimes difficult to distinguish from mild asymptomatic primary hyperparathyroidism. Patients with FHH did not profit from parathyroidectomy, a calcium lowering therapy is not necessary. The gain of function mutations of the calcium-sensing receptor are associated with autosomal dominant hypocalcaemia (ADH), a disease characterised by a generally asymptomatic hypocalcaemia, inappropriately high urinary calcium excretion and normal PTH levels. A therapy to raise the serum calcium concentration has to be done carefully and is only indicated in symptomatic patients, because of enhancement of hypercalciuria with the risk of nephrocalcinosis and nephrolithiasis. Molecular genetic analysis of the calcium sensing receptor gene facilitates the sometimes difficult diagnosis. The development of compounds modulating the calcium sensing receptor function and thereby the section of PTH may become an important role in treatment of diseases of calcium metabolism.
Exp Clin Endocrinol Diabetes 2006 Sep
PMID:The role of the extracellular calcium-sensing receptor in health and disease. 1703 19

Calcitonin is an endogenous regulator of calcium homeostasis, which acts principally on bone. At present, the principal indications for the therapeutic use of calcitonin are disorders involving hypercalcemia Paget's disease, acute pancreatitis, high-bone-turnover osteoporosis, pain associated with osteoporosis or bone metastases, and Sudeck's atrophy. The aim of this study was to compare the analgesic effects on postoperative pain of salmon calcitonin versus opioids administered epidurally. Our prospective study included 53 ASA I-II patients who were scheduled for total hip arthoplasty under epidural anaesthesia and who did not fulfill 1 or more of the exclusion criteria: a history of pituitary gland dysfunction; diabetes mellitus; obesity; contraindications to performing an epidural block and/or an allergy to calcitonin. These patients were randomly allocated into 3 groups (A, B, and C), each of which received postoperatively a different analgesic epidural mixture of 10 mL to control postoperative pain. Group A was given bupivacaine 0.5% (5 mL) + fentanyl 100 (2 mL) + NaCl 0.9% (3 mL). Group B was given bupivacaine 0.5% (5 mL) + salmon calcitonin 100IU (1 mL) + NaCl 0.9% (4 mL). Group C was given salmon calcitonin 100IU (1 mL) + NaCl 0.9% (9 mL). Perioperatively, 4 blood samples were taken from each patient at the following specific times: 1. Before the induction of anesthesia; 2. At the end of the operation and before the epidural administration of the analgesic mixture; 3. At the end of the first postoperative hour (1 hour after the administration of the analgesic mixture); and 4. At the end of the second postoperative hour (2 hours after the administration of the mixture). In each blood sample, glucose, cortisol, growth hormone, and prolactin plasma levels were determined in order to investigate the changes of these parameters as a result of the endocrine reaction to stress, and to pain relief. The analgesic solution was administered immediately after the second blood sample was taken. At the same time as the 4 blood samples were taken, haemodynamic parameters and pain scores were recorded. Epidural salmon calcitonin in combination with local anaesthetic produces an analgesic effect similar to fentanyl and with stable hemodynamic results. It also eliminates postoperative hyperglycaemia. The cortisol plasma level does not increase during the first postoperative hour, but increases significantly during the second postoperative hour. Growth hormone and prolactin plasma levels were stable in all patients in all 3 groups. This study shows that calcitonin is a suitable alternative for the treatment of acute postoperative pain.
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PMID:Epidural calcitonin: does it provide better postoperative analgesia? An analysis of the haemodynamic, endocrine, and nociceptive responses of salmon calcitonin and opioids in epidural anesthesia for hip arthroplasty surgery. 1715 40

A 69-year-old man with a 10-year history of diabetes mellitus and 1-year history of steroid treatment for nonspecific interstitial pneumonia presented with a nightly fever of over 39 degrees C after surgery for a false abdominal aortic aneurysm. Hypercalcemia was detected, despite acute renal dysfunction. There was no laboratory evidence of collagen disease or infection including tuberculosis. Polymerase chain reaction (PCR)-based amplification of DNA from a bone marrow biopsy specimen revealed Mycobacterium tuberculosis. Antituberculous chemotherapy was initiated. Early bone marrow biopsy and the use of new techniques such as PCR can avoid delay in initiating the proper treatment for compromised patients.
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PMID:Miliary tuberculosis with hypercalcemia, and a false abdominal aortic aneurysm, but no pulmonary findings. 1717 May 4

Endocrine emergencies constitute only a small percentage of the emergency workload of general doctors, comprising about 1.5% of all hospital admission in England in 2004-5. Most of these are diabetes related with the remaining conditions totalling a few hundred cases at most. Hence any individual doctor might not have sufficient exposure to be confident in their management. This review discusses the management of diabetic ketoacidosis, hyperosmolar hyperglycaemic state, hypoglycaemia, hypercalcaemia, thyroid storm, myxoedema coma, acute adrenal insufficiency, phaeochromocytoma hypertensive crisis and pituitary apoplexy in the adult population.
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PMID:Diabetic and endocrine emergencies. 1730 9

Dietary reference intakes (DRIs) for Vitamin D (VitD) have been traditionally established based on plasma 25-OHD concentration sufficient to prevent rickets and osteomalacia. While nutritional rickets is still prevalent in developing countries, hypovitaminosis D is becoming widespread around the world regardless the latitude. Emerging evidence has unravelled the physiological roles of VitD beyond calcium homeostasis. Hypovitaminosis D has been linked to cancers, diabetes, CVD, periodontal diseases and influenza. Hypovitaminosis D is multifactorial and is related to VitD scarcity in foods, latitude, solar-irradiation, atmospheric-pollution, skin-pigmentation, clothing, sunscreen-use and indoor activities, etc. Plasma 25-OHD concentration range from 25-138 nmol/L. A higher plasma 25-OHD concentration is linked to higher bone-mass in adolescents, pre- and post-menopausal women. Plasma 25-OHD > or =75 nmol/L has been shown to enhance calcium absorption, suppress PTH elevation, reduce the risks of bone loss and fractures, and certain extra-skeletal diseases. VitD supplementation with 10 microg/d is insufficient to lower fracture risks. Combined VitD and calcium supplementation in higher doses has been found superior to VitD alone to increase bone-mass in adolescents and to reduce non-vertebral fractures in postmenopausal women. In future, DRIs for VitD are likely to be established beyond its skeletal roles to include multiple health outcomes. However, the desirable level of VitD has yet to be defined. Furthermore, redefining the upper-tolerable-level of VitD intake is necessary to prevent hypercalcemia and toxicity. There is also a urgent need to harmonize laboratory methods in VitD assay in different laboratories.
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PMID:The resurgence of the importance of vitamin D in bone health. 1829 22

Cinacalcet is a type II calcimimetic agent which is an allosteric modulator of the calcium-sensing receptor (CaR) located on the surface of the parathyroid cells. Cinacalcet increases the sensitivity of CaR via binding to the transmembrane region of CaR. Increasing sensitivity of CaR causes reduced secretion of parathyroid hormone (PTH) and suppression of serum calcium levels. Cinacalcet has recently been approved by Federal Drug Administration (FDA) for the treatment of patients with secondary hyperparathyroidism on maintenance dialysis and hypercalcemia in patients with parathyroid cancer. It is used also in Europe for both indications. Several controlled studies have shown that cinacalcet is effective in normalizing serum calcium levels also in primary hyperparathyroidism. Cinacalcet is metabolized primarily in the liver by N-dealkylation leading to carboxylic acid and oxidation of naphthalene ring to form dihydrodiols. The safety and optimal dosage of the drug in hypercalcemic patients with liver impairment remains unclear. We present a patient with Child-Pugh B class primary biliary cirrhosis who presented with moderate hypercalcemia and was diagnosed as primary hyperparathyroidism. As she refused having parathyroid surgery for her parathyroid adenoma at first, her hypercalcemia was treated successfully with 30 mg/day cinacalcet for 6 months. Cinacalcet was discontinued after 6 months. Her calcium level increased gradually. As she accepted surgery this time, her parathyroid adenoma was removed by minimally invasive parathyroidectomy. Parathyroid adenoma was confirmed pathologically. Her calcium levels maintained within the normal ranges after surgery.
Exp Clin Endocrinol Diabetes 2009 Mar
PMID:Hypercalcemia of primary hyperparathyroidism was treated by cinacalcet in a patient with liver cirrhosis. 1856 Oct 96

The aim of this paper is to report an atypical presentation of MEN2A, in a patient carrying the C634R mutation of the RET-protooncogene. A 41-year-old Tunisian woman was admitted to our department with newly diagnosed hyperglycemia. She had a history of bilateral urinary stone recurrence, managed successfully on two occasions. On physical examination a thyroid node of 1cm on the left side was found. Laboratory evaluation and imaging findings confirmed the diagnosis of primary hyperparathyroidism. During cervicotomy, the parathyroid adenoma was resected and the thyroid node was suspected to be a carcinoma. Total thyroidectomy, with appropriate neck nodal resection, was performed. Histological examination confirmed the diagnosis of parathyroid adenoma and revealed a multifocal and bilateral medullary carcinoma. These findings led to the diagnosis of multiple endocrine neoplasia. DNA-analysis demonstrated a germline Cys634Arg mutation in the RET-protooncogene. During the postoperative follow-up, blood pressure as well as the level of urinary methoxylated metabolites increased progressively. Imaging findings were compatible with the diagnosis of bilateral pheochromocytoma. In conclusion, this case report of MEN 2A linked to a 634 RET mutation was peculiar by its revelation mode (1) hyperparathyroidism moreover linked to an adenoma and (2) associated with diabetes, mechanisms of which are probably multifactorial (familial type 2 diabetes, hypercalcemia, catecholamines excess).
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PMID:Unusual presentation of multiple endocrine neoplasia type 2A in a patient with the C634R mutation of the RET-protooncogene. 1875 92

Antihypertensive pharmacologic treatment may be associated with diverse disturbances of electrolyte homeostasis. These drug-induced disorders are relatively common, typically including hyponatraemia, hypokalaemia, hyperkalaemia, hypomagnesaemia, hypophosphataemia and hypercalcaemia. Diuretics, beta-blockers, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are particularly likely to cause these complications. Recognised risk factors include high-dosage regimens (especially diuretics), old age, diabetes and impairment of renal function. Strategies to prevent these adverse drug reactions involve careful consideration of risk factors and clinical and laboratory evaluation in the course of treatment.
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PMID:Blood pressure drug therapy and electrolyte disturbances. 1882 27

Autoimmune hypercalcemia has been reported in only a few cases, and never in the context of autoimmune polyglandular syndrome. A patient with type 1, insulin-dependent diabetes mellitus, Graves' disease, and antiparietal cell antibodies presented with persistent hypercalcemia with inappropriate PTH secretion. Other causes of hypercalcemia were excluded. In this context of two associated organ-specific autoimmune diseases we searched for autoantibodies directed to parathyroid tissue and to calcium-sensing receptor. Anti-parathyroid autoantibodies were detected by indirect immunofluorescence on parathyroid adenomas, and autoantibody against a peptide of the extracellular domain of the calcium-sensing receptor were detected by immunoblotting. Autoimmune hypercalcemia may be another organ-specific feature of autoimmune polyglandular syndrome.
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PMID:Hyperparathyroidism in a patient with autoimmune polyglandular syndrome. 1898 36


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