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)

Fourteen trained male anabolic steroid-using bodybuilders (SBBs) (19-41 years) were recruited for the study. Three-day diet records were obtained from SBBs and analyzed. A resting venous blood sample was drawn, and serum/plasma was subsequently analyzed for various nutritionally related factors. Results showed that mean dietary energy (4,469 +/- 1,406 kcal), protein 252 +/- 109 g), and vitamin and mineral intakes of SBBs greatly exceeded U.S. Recommended Dietary Allowances. Dietary cholesterol intake was 2.8 times the recommended levels. Mean serum/plasma nutrient concentrations of SBBs were within normal range. However, individual SBBs had a number of serum/plasma values outside of the normal or recommended range, the most notable of which was hypercalcemia, which was present in 42% of SBBs. Serum/plasma lipids were such as to increase the risk of cardiovascular disease in these subjects.
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PMID:Nutritional status and lipid profiles of trained steroid-using bodybuilders. 887 44

Anesthesia for surgery of primary hyperparathyroidism (HPT) usually concerns asymptomatic elderly women with moderate hypercalcemia. Cardiovascular repercussions of the endocrine disorder are possible, but they are not frequent except for hypertension. Hyperparathyroid crisis is a life-threatening condition with severe hypercalcemia. Intravenous diphosphonates are very effective drugs to control hypercalcemia. The improvement is transient but allows curative parathyroidectomy to be performed with a minimal risk of cardiac arrhythmias. Anesthesia for surgery of secondary HPT concerns patients with chronic renal failure treated by hemodialysis. Cardiovascular disease is frequent and aggravated by the endocrine disorder. In patients with marked aortic stenosis or severe left ventricular dysfunction, parathyroidectomy should be performed by cervicotomy under local anesthesia. Hyperparathyroidism may persist after renal transplantation (tertiary HPT): in this case cardiovascular disease is minimal and the hypercalcemia is moderate. Parathyroidectomy is usually performed by cervicotomy under general anesthesia. Sternotomy is required in the case of an abnormal mediastinal location of a gland. An interaction between myorelaxants and hyperparathyroidism has been observed. Total blood calcium must be systematically assayed postoperatively because postoperative hypocalcemia is constant. Hypocalcemia is moderate in primary and tertiary HPT, due to transient functional hypoparathyroidism, with lowest observed the 2nd or 3rd postoperative day. Hypocalcemia should not be treated when asymptomatic because it resolutes on the 4th or 5th postoperative day. Intravenous calcium infusion may be necessary for 1 or 2 days, if serum calcium is below 1.9 mmol per liter with symptoms of tetany. Persistent hypocalcemia is due to an hungry bone syndrome or organic hypoparathyroidism that should be treated by oral vitamin D and calcium. In secondary HPT, hypocalcemia is early, marked and asymptomatic. Treatment must often be started on the 6th postoperative hour by intravenous calcium infusion, followed by oral vitamin D and calcium. The absence of postoperative hypocalcemia indicate incomplete removal of all abnormal parathyroid tissue. At the third postoperative day, a second cervicotomy may be performed to complete the neck exploration.
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PMID:[Anesthesia and postoperative recovery for parathyroid gland surgery]. 1008 69

The plasma soluble melanins (PSM) form spontaneously in vitro and in vivo and their formation involves oxidative polymerization and copolymerization of dopa, catecholamines, homogentisic acid, 3-hydroxyanthranilic acid, p-aminophenol, p-phenylenediamine, and other end(ex)ogenous ortho and para polyhydroxy-, (poly)hydroxy(poly)amino- and polyamino-phenyl compounds. The build up of PSM is visible within 2-3 h after the start of incubation at 37 degrees C with 1 mg/ml of plasma. PSM also form similarly in blood and these processes cause hemolysis. The mean quantity of PSM in normal human plasma is 1.61+/-0.1 (S.D.) mg/ml (n = 20) and in normal human urine is 1.1+/-1.2 g/24 h collection (n = 8). They contribute to the yellow color of plasma and urine. Antioxidants delay the formation of PSM. The deposited melanins also form from these precursors. Reactive oxygen side products (ROSP) are generated during and after melanogenesis. Melanins in vivo are generally associated with proteins or with proteins and lipids. The PSM-protein-lipid complexes are called plasma soluble lipofuscins (PSL), because they have histochemical and fluorescence properties similar to those of solid lipofuscins. The soluble and deposited melanins (SDM) and their intermediates have similar toxic chemical reactivities. The oxidizing quinoid (they can produce partially and completely substituted conjugates) and the semiquinoid free radical intermediates are also moieties in most human melanin structures. Soluble melanins formed from dopa, or dopamine, or norepinephrine in weak alkaline solution have been shown to be toxic to human CD4+ lymphoblastic cells (MT-2) at higher than 10 microg/ml concentrations. Alkaptonuria with high levels of homogentisic acid in the plasma is a potentially fatal disease, exhibiting the toxic effects of the homogentisic acid melanin (soluble and deposited), its intermediates and the ROSP. Patients with alkaptonuria develop arthritis and often suffer from other diseases too, including cardiovascular disease (frequent cause of death) and kidney disease. Pheochromocytoma, with high levels of catecholamines in the plasma is another potentially fatal disease. The catecholamine PSM of pheochromocytoma have very light yellow or practically no colors, due to the concentrations and chemical structures. Pheochromocytomas can cause hypertension, cardiovascular disease (frequent cause of death), kidney disease, stroke, cancer, amyloid formation and can mimic many other diseases, including acute pancreatitis, carcinoid, neuroblastoma, psychiatric illness, hypercalcemia, retinal vascular lesions, and diabetes mellitus. Pheochromocytoma is potentially fatal even in patients without hypertension. Following trauma and surgery, heavily pigmented eyes are apt to experience greater inflammation than lightly pigmented eyes. In Parkinson's disease those neurons are lost first in the substantia nigra and locus ceruleus which contain the greatest amounts of neuromelanins. The antihypertensive alphamethyldopa causes Parkinson's syndrome. It forms PSM in a short time in vitro. The side effects of L-dopa (immobility episodes alternate with normal or involuntary movements; psychotic abnormalities) suggest that the SDM, their intermediates and the ROSP present naturally in vivo are involved in the cause of Parkinson's disease and Alzheimer's disease. There is a large overlap between these two diseases. (ABSTRACT TRUNCATED)
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PMID:The probable involvement of soluble and deposited melanins, their intermediates and the reactive oxygen side-products in human diseases and aging. 1124 35

The mortality risk from cardiovascular disease is increased in patients with end-stage renal disease (ESRD). This is due to both traditional and dialysis-specific factors. Recently, a number of the dialysis-specific risk factors have been implicated in the pathogenesis of cardiovascular calcification. These include: hyperphosphatemia, high calcium-phosphate (Ca x P) product, elevated parathyroid hormone levels, duration of dialysis, and treatment with calcium-containing phosphate binders and vitamin D analogs. The recent availability of electron beam computed tomography (EBCT) has triggered increased awareness of the occurrence of cardiovascular calcification in ESRD patients. Given the development of transient hypercalcemia with calcium-containing binders, a link between calcium load from use of calcium-containing phosphate binders and development coronary calcification has been proposed. However, a causal relationship between use of these agents and cardiovascular calcification has not been established. Moreover, this phenomenon had been recognized over a century ago, long before these phosphate binders became available. Although its pathogenesis is likely to be multifactorial, available data strongly implicate elevated serum phosphorus as the primary culprit. Furthermore, the risk of calcification may be aggravated by vitamin D therapy, particularly in patients with severe secondary hyperparathyroidism. Therefore, achieving vigorous control of serum phosphorus, Ca x P product and parathyroid hormone level might decrease cardiovascular calcification and improve survival of patients on maintenance hemodialysis. Since calcium acetate is the most cost-effective phosphate binder available, we recommend that it should remain the first line treatment of hyperphosphatemia in patients with ESRD.
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PMID:Cardiovascular calcification in patients with end-stage renal disease: a century-old phenomenon. 1241 Aug 60

Abnormalities in calcium and phosphorus metabolism are common, and metabolic bone disease develops often in patients with chronic renal failure (CRF). Effective clinical management includes measures to control phosphorus retention and prevent hyperphosphataemia, to maintain serum calcium concentrations within the normal range and to prevent excess parathyroid hormone (PTH) secretion by the judicious use of vitamin D sterols. Certain of these interventions appear to increase the risk of soft tissue and vascular calcification in patients with end-stage renal disease (ESRD), changes that may contribute to the development of cardiovascular disease. Current therapeutic approaches are thus being re-evaluated in an effort to limit these risks. Despite the importance of controlling phosphorus retention and preventing hyperphosphataemia in patients with CRF, current management strategies often are inadequate, particularly in those ingesting diets containing adequate amounts of protein. Results from clinical trials using daily haemodialysis strongly suggest that thrice-weekly haemodialysis regimens are only marginally adequate for achieving weekly phosphorus balance in many patients with ESRD. The safety of large oral doses of calcium as a phosphate-binding agent in patients with ESRD has also been questioned because excess amounts of calcium that are absorbed from the gastrointestinal tract may lead to ongoing calcium retention in those with little or no residual renal function. Arterial calcification and cardiac valve calcification are two serious complications that adversely affect cardiovascular haemodynamics. The use of large, often supraphysiological, doses of calcitriol or other vitamin D sterols to treat secondary hyperparathyroidism may aggravate hypercalcaemia and hyperphosphataemia, further increasing the risk of soft tissue and vascular calcification. Phosphate-binding agents that do not contain calcium, new vitamin D analogues and calcimimetic compounds offer new therapeutic alternatives for managing renal osteodystrophy. The integration of these novel agents into existing treatment regimens may provide safer and more effective methods for controlling secondary hyperparathyroidism and renal bone disease, while limiting the risks of soft tissue and vascular calcification in patients with CRF.
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PMID:Medical management of secondary hyperparathyroidism in chronic renal failure. 1277 Dec 90

A 5-year-old boy with Williams syndrome received open reduction of fracture of the antebrachium twice. He had been diagnosed as having Williams syndrome with some characteristic symptoms, including elfin face, mental retardation and primary pulmonary hypertension. Williams syndrome has a tetrad of cardiovascular disease, elfin face, mental retardation and hypercalcemia. Operations were performed twice under general anesthesia. Airway management with mask technique was easily performed. Tracheal intubation was accomplished successfully. Anesthesia was induced with propofol, fentanyl, and vecuronium, and maintained with propofol, fentanyl and the inhalation of oxygen with nitrous oxide. Both anesthetic courses were uneventful and he was discharged without any complications. Special anesthetic considerations should be taken for difficulties of intubation, management of circulatory system, malignant hyperthermia, and hypercalcemia in this syndrome.
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PMID:[Two occasions of anesthetic management for a patient with Williams syndrome]. 1367 82

Mortality rates in ESRD are unacceptably high. Disorders of mineral metabolism (hyperphosphatemia, hypercalcemia, and secondary hyperparathyroidism) are potentially modifiable. For determining associations among disorders of mineral metabolism, mortality, and morbidity in hemodialysis patients, data on 40,538 hemodialysis patients with at least one determination of serum phosphorus and calcium during the last 3 mo of 1997 were analyzed. Unadjusted, case mix-adjusted, and multivariable-adjusted relative risks of death were calculated for categories of serum phosphorus, calcium, calcium x phosphorus product, and intact parathyroid hormone (PTH) using proportional hazards regression. Also determined was whether disorders of mineral metabolism were associated with all-cause, cardiovascular, infection-related, fracture-related, and vascular access-related hospitalization. After adjustment for case mix and laboratory variables, serum phosphorus concentrations >5.0 mg/dl were associated with an increased relative risk of death (1.07, 1.25, 1.43, 1.67, and 2.02 for serum phosphorus 5.0 to 6.0, 6.0 to 7.0, 7.0 to 8.0, 8.0 to 9.0, and >/=9.0 mg/dl). Higher adjusted serum calcium concentrations were also associated with an increased risk of death, even when examined within narrow ranges of serum phosphorus. Moderate to severe hyperparathyroidism (PTH concentrations >/=600 pg/ml) was associated with an increase in the relative risk of death, whereas more modest increases in PTH were not. When examined collectively, the population attributable risk percentage for disorders of mineral metabolism was 17.5%, owing largely to the high prevalence of hyperphosphatemia. Hyperphosphatemia and hyperparathyroidism were significantly associated with all-cause, cardiovascular, and fracture-related hospitalization. Disorders of mineral metabolism are independently associated with mortality and morbidity associated with cardiovascular disease and fracture in hemodialysis patients.
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PMID:Mineral metabolism, mortality, and morbidity in maintenance hemodialysis. 1528 7

Vascular calcifications are more frequent in dialysis patients than in the general population or in patients with cardiovascular disease and normal renal function. The reasons for this high incidence are multiple. They include traditional factors such as hypertension, diabetes, dyslipidaemia, and specific factors such as sodium overload, hyperomocysteinaemia, chronic inflammation, oxidative stress as well as disturbance of mineral metabolism. Specifically, hyperphosphataemia and the elevated calcium (Ca) x phosphate product have been associated with an increased risk for development of vascular calcification and death. Even though a causal relationship between the use of Ca- containing phosphate binders and the development of vascular calcifications has not been documented, treatment with Ca salts can induce hypercalcaemia, increased Ca x phosphate product, and Ca overload. A net intestinal Ca absorption of 180-500 mg has been documented in uraemic patients after a meal containing 1200 mg of Ca. Thus, treatment with Ca salts may induce Ca overload when a patient is dialyszed against a high dialysate Ca (> 1.5 mmol/L) solution, which is known to determine a positive dialysis balance. On the contrary, an overall negative Ca balance can result from the use of a low Ca dialysate (1.25 mmol/L) when the patients do not receive Ca supplements or vitamin D metabolites. Maintaining a normal Ca and phosphate balance remains one of the primary goals in the management of dialysis patients. Control of hyperphopshataemia should be obtained using either Ca and aluminium- free phosphate binders, such as sevelamer, or Ca salts, while avoiding a daily oral elemental Ca intake > 1.5 g.
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PMID:[Disturbances of mineral metabolism and vascular calcifications in dialysis patients (review)]. 1528 2

Vascular calcifications are more frequent in dialysis patients than in the general population or in patients with cardiovascular disease (CVD) and normal renal function. The reasons for this high incidence are multiple; they include traditional factors such as hypertension, diabetes, dyslipidemia, and specific factors such as sodium overload, hyperomocysteinemia, chronic inflammation and oxidative stress, as well as mineral metabolism disturbances. Specifically, hyperphosphatemia and the elevated calcium (Ca) x phosphate product have been associated with an increased risk for the development of vascular calcification and death. Treatment with Ca salts can induce hypercalcemia, increased Ca x phosphate product and Ca overload. Sevelamer substitution for Ca salts has been documented to attenuate the progression of coronary artery and aortic calcification. A possible mechanism explaining this observation could be ongoing Ca loading related to oral Ca ingestion. Treatment with Ca salts could induce Ca overload, particularly in patients dialyzed against a high dialysate Ca (>1.5 mmol/L) solution, which is known to determine a positive dialysis balance. Conversely, an overall negative Ca balance can result from low Ca dialysate use (1.25 mmol/L) when the patients do not receive Ca supplements or vitamin D metabolites. Maintaining normal Ca and phosphate balances remains a primary goal in the management of dialysis patients. Control of hyperphopshataemia should be achieved either using Ca and aluminum-free phosphate binders, such as sevelamer, or Ca salts, alone or in combination, provided that a daily oral elemental Ca intake of 1.5 g is not exceeded.
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PMID:[Control of calcium and phosphate metabolism and prevention of vascular calcifications in uremic patients]. 1578 2

Calcium and phosphate imbalances are important mutable risk factors for cardiovascular disease in chronic kidney disease (CKD). Nearly all dialysis patients require phosphate binders. These include traditional calcium-based compounds and, more recently, the calcium-free, metal-free, non-absorbed agent, sevelamer hydrochloride. Both binder types reduce serum phosphorus, but differ with respect to calcium load and metabolism. Absorption from calcium-based agents very likely promotes positive total calcium balance in many patients. Positive calcium balance is inappropriate in adults and may promote or accelerate soft-tissue and vascular calcification even in the absence of hypercalcemia. Calcium accumulation in heart and vascular tissues contributes to rapidly progressive cardiovascular calcification - a strong predictor of cardiovascular and all-cause mortality in stage 5 CKD. More than two-thirds of stage 5 CKD patients have calcification scores above the 75th percentile for matched controls -- scores associated with extremely high risk of cardiovascular events and death.
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PMID:Calcium loading, calcium accumulation, and associated cardiovascular risks in dialysis patients. 1583 18


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