Phosphate serum

Check parathyroid hormone (PTH), vitamin D and precursors, magnesium, and phosphate levels ° Pharmacological causes of decreased ionized calcium may include excess infusions of citrate, EDTA, lactate, fluoride poisoning, foscarnet, cinacalcet, bisphosphates, or unrelated increase in serum phosphate or decrease in serum magnesium levels... 

More than 99% of total body calcium is found in bone the remaining less than 1% is in the ECF and ICE Calcium plays a critical role in the transmission of nerve impulses, skeletal muscle contraction, myocardial contractions, maintenance of normal cellular permeability, and the formation of bones and teeth. There is a reciprocal relationship between the serum calcium concentration (normally 8.6 to 10.2 mg/dL [2.15 to 2.55 mmol/L]) and the serum phosphate concentration that is regulated by a complex interaction between parathyroid hormone, vitamin D, and calcitonin. About one-half of the serum calcium is bound to plasma proteins the other half is free ionized calcium. Given that the serum calcium has significant protein binding, the serum calcium concentration must be corrected in patients who have low albumin concentrations (the major serum protein). The most commonly used formula adds 0.8 mg/dL (0.2 mmol/L) of calcium for each gram of albumin deficiency as follows ... 

ECF. Note that phosphorus is the major anion within the cells. Given this distribution, serum phosphate concentration does not accurately reflect total body phosphorus stores. Phosphorus is expressed in milligrams (mg) or millimoles (mmol), not as milliequivalents (mEq). Because phosphorus is the source of phosphate for adenosine triphosphate (ATP) and phospholipid synthesis, manifestations of phosphorus imbalance are variable. 

Elevated corrected serum calcium level greater than or equal to 10.5 g/dL (2.6 mmol/L), serum albumin, low to normal serum phosphate... 

Parathyroid hormone stimulates bone resorption by increasing the number and activity of osteoclasts. This demineralization process in the bone releases calcium and phosphate into the blood. Although the action of PTH on the bone appears to increase blood phosphate, its action on the kidney, which increases phosphate excretion in the urine, more than compensates for this increase and the net effect is a decrease in serum phosphate. 

Calcitonin is a polypeptide hormone that (along with PTH and the vitamin D derivative, 1,25-dihydroxycholecalciferol) plays a central role in regulating serum ionized calcium (Ca2+) and inorganic phosphate (Pi) levels. The adult human body contains up to 2 kg of calcium, of which 98 per cent is present in the skeleton (i.e. bone). Up to 85 per cent of the 1 kg of phosphorus present in the body is also found in the skeleton (the so-called mineral fraction of bone is largely composed of Ca3(P04)2, which acts as a body reservoir for both calcium and phosphorus). Calcium concentrations in human serum approximate to 0.1 mg ml-1 and are regulated very tightly (serum phosphate levels are more variable). 

PhosLo - For adult dialysis patients, the initial dose is 2 tablets/capsules/gelcaps with each meal. The dosage may be increased gradually to bring the serum phosphate value less than 6 mg/dL, as long as hypercalcemia does not develop. Most patients require 3 to 4 tablets with each meal. 

Parathyroid hormone is a single-chain polypeptide of 84 amino acids which is produced in the parathyroid glands. It increases serum calcium and decreases serum phosphate. In bone it promotes resorption of calcium. It indirectly increases osteoclastic activity by promoting the action of osteoblasts. It has been shown that in low doses PTH may even increase bone formation without stimulating bone resorption. In the kidney PTH increases resorption of calcium and it increases excretion of phosphate. An other important activity in the kidney is the enhanced synthesis of 1,25-dihydroxyvitamin D. An increased serum calcium level inhibits PTH secretion and increased serum phosphate decreases free serum calcium and thus stimulates PTH secretion. 

Osteomalacia is the condition in which bone becomes demineralised due to deficiency of vitamin D. In this condition parathyroid hormone (PTH) acts on the bone to maintain serum calcium, resulting in demineralisation. Serum calcium is usually normal or slightly low alkaline phosphatase levels are high, reflecting excessive osteoblast activity, and serum phosphate falls as an effect of PTH on the kidney. The same condition in children results in defects in long bone formation, and is termed rickets. 

A variety of adverse effects have been reported following the use of antacids. If sodium bicarbonate is absorbed, it can cause systemic alkalization and sodium overload. Calcium carbonate may induce hypercalcemia and a rebound increase in gastric secretion secondary to the elevation in circulating calcium levels. Magnesium hydroxide may produce osmotic diarrhea, and the excessive absorption of Mg++ in patients with renal failure may result in central nervous system toxicity. Aluminum hydroxide is associated with constipation serum phosphate levels also may become depressed because of phosphate binding within the gut. The use of antacids in general may interfere with the absorption of a number of antibiotics and other medications. 

Mechanism of Action An antacid that reduces gastric acid by binding with phosphate in the intestine, and then is excreted as aluminum carbonate in feces. Aluminum carbonate may increase the absorption of calcium due to decreased serum phosphate levels. The drug also has astringent and adsorbent properties. Therapeutic Effect Neutralizes or increases gastric pH reduces phosphates in urine, preventing formation of phosphate urinary stones reduces serum phosphate levels decreases fluidity of stools. 

Dietary supplement (RDA) PO 1200 mg/day. Maximum 2.5 g/day. Hyperphosphatemia PO (calcium acetate) 2 tablets 3 times a day with meals. May increase gradually to bring serum phosphate level to less than 6 m dl as long as hypercalcemia does not develop. 

D/C drug if hypercalcemia, hyperphosphatemia, or serum Ca X serum phosphate product >70, resume when parameters decreased, at a dose 2.5 meg or less... 

Net Serum calcium increased, serum Serum calcium and phosphate both increased Decreased serum phosphate... 

In the absence of PTH (idiopathic or surgical hypoparathyroidism) or an abnormal target tissue response to PTH (pseudohypoparathyroidism), serum calcium falls and serum phosphate rises. In such patients, l,25(OH)2D levels are... 

Mild asymptomatic hypercalcemia is common during treatment with parathyroid hormone (15). The hypercalcemia is persistent, and requires dosage reduction in 3% of patients using 20 micrograms/day and in 11% using 40 micrograms/day (16). Transient mild hypercalciuria and increased serum phosphate are common but do not usually limit therapy. 

Phosphate is critical to normal bone mineralization when phosphate stores are deficient, a clinical and pathologic picture resembling vitamin D-deficient rickets develops. However, such children fail to respond to the usual doses of vitamin D employed in the treatment of nutritional rickets. A defect in l,25(OH)2D production by the kidney has also been noted, because the serum l,25(OH)2D levels tend to be low relative to the degree of hypophosphatemia observed. This combination of low serum phosphate and low or low-normal serum l,25(OH)2D provides the rationale for treating such patients with oral phosphate (1-3 g daily) and calcitriol (0.25-2 Mg daily). Reports of such combination therapy are encouraging in this otherwise debilitating disease. 

No studies were located that specifically address white phosphorus metabolism in humans or animals after inhalation exposure. However, since orthophosphate is a stable end-product of the inorganic oxidation and hydrolysis of white phosphorus, it is appropriate to examine data on serum phosphate levels in humans and animals (these data are discussed further in Section 2.2). 

An epidemiology study (Hughes et al. 1962) compared the mean serum phosphate level of five occupationally-exposed phosphorus plant workers with the mean serum phosphate level of five healthy control men not exposed to phosphorus. The exposure duration ranged from 1 to 17 years in the exposed group. Although the route of exposure was not reported, it is assumed to be inhalation of airborne phosphorus. It is likely that oral exposure (ingestion of airborne phosphorus) also occurred. The serum phosphorus levels of phosphorus plant workers and controls were reported to be 2.85 and 2.9 mg/100 mL, respectively. Both values are below the normal range for adult humans of 3.0 1.5 mg/100 mL (Harper 1969). There was no statistical difference between the workers and controls serum phosphate levels (test and p value not reported). 

The serum phosphate level of a worker with phossy jaw was within the normal range of values for an adult human (Hughes et al. 1962). Excretion of phosphate via urinary and fecal routes was reported qualitatively to be approximately normal. The daily output of phosphorus in the feces was about 1/4 to 1/3 of the total output in both urine and feces. 

Serum phosphate was reported in three human cases of dermal white phosphorus bum following explosion of incendiary munitions. Serum phosphate ranged between 1.34 and 8.7 mg/100 mL. The normal range of adult human serum phosphate is 3.0-4.5 mg/100 mL (Harper 1969). No patterns with respect to bum intensity or time after exposure were evident. 

In a series of controlled studies using rats (Applebaum et al. 1975 Ben-Hur and Applebaum 1973 Ben-Hur et al. 1972) significant increases (p<0.01) in 72-hour serum phosphate ranging from 100% to 120% over controls were observed. Anesthetized animals were burned in inguinal incisions after application of 26-200 mg/kg white phosphoms. 

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