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Diagnosis is generally based on a blood phosphate level exceeding 1.46 mmol/L (4.5 mg/dL). [1] Levels may appear falsely elevated with high blood lipid levels, high blood protein levels, or high blood bilirubin levels. [1] Treatment may include a phosphate low diet and antacids like calcium carbonate that bind phosphate. [1]
Elevated levels are also associated with diabetes, hypertension, and cardiovascular disease; it was found that elevated levels are associated with elevated serum C-reactive protein (CRP), which could reflect an inflammatory and atherogenic milieu, possibly an alternative cause for elevated serum alkaline phosphatase. [10] Chronic kidney disease ...
Primary hyperparathyroidism has high calcium, vitamin D, and PTH levels and a low phosphate level. [30] [31] Secondary hyperparathyroidism has low serum calcium and vitamin D levels, and high phosphate and PTH levels. [30] [31] Tertiary hyperparathyroidism has high serum calcium, phosphate, and PTH and low vitamin D levels.
In contrast, optimal (health) range or therapeutic target is a reference range or limit that is based on concentrations or levels that are associated with optimal health or minimal risk of related complications and diseases. For most substances presented, the optimal levels are the ones normally found in the population as well.
The enzyme alkaline phosphatase (ALP, alkaline phenyl phosphatase, also abbreviated PhoA) is a phosphatase with the physiological role of dephosphorylating compounds. The enzyme is found across a multitude of organisms, prokaryotes and eukaryotes alike, with the same general function, but in different structural forms suitable to the environment they function in. Alkaline phosphatase is found ...
High turnover of tumor cells leads to spill of potassium into the blood. Symptoms usually do not manifest until levels are high (> 6.5 mmol/L) [normal 3.5–5.0 mmol/L] and they include [8] palpitations, cardiac conduction abnormalities, and arrhythmias (can be fatal) muscle weakness or paralysis; Hyperphosphatemia.
Renal management of phosphate is impaired in secondary hyperparathyroidism which results in hyperphosphatemia. [4] [6] Primary hyperplasia of the parathyroid gland, results from both hypocalcaemia and increased phosphate levels by decreasing expression of calcium sensing receptors and vitamin D receptors at the parathyroid gland.
Phosphate binders are used to control the serum phosphate levels, which are usually elevated in advanced chronic kidney disease. Phosphodiesterase-5 inhibitors and zinc may improve sexual dysfunction in men. [42]