Phosphates in serum

H)2D helps to maintain calcium and phosphate in serum by its actions on intestine, bone, kidney, and the parathyroids. In the small intestine, l,25(OH)2D stimulates calcium absorption, primarily in the duodenum, and phosphate absorption by the jejunum and At... 

Daly JA, Ertingshausen G. Direct method for determining inorganic phosphate in serum with Centri-fichem. Clin Chem 1972 18 263-5. 

Wentz PW, Savory J, Cross RE. Improved method for measurement of inorganic phosphate in serum with a centrifugal analyzer. Clin Chem 1976 22 257-60. 

Exposure Levels in Humans. Methyl parathion has been detected in serum and tissue shortly after acute exposure (EPA 1978e Ware et al. 1975). It is rapidly metabolized and does not persist in serum and tissues for long (Braeckman et al. 1983). Two metabolites of methyl parathion, 4-nitrophenol and dimethyl phosphate, can be detected in urine and tissues for up to 2 days following exposure (Morgan et al. 1977). These compounds are specific for methyl parathion when there is a history of exposure. 

Figure 3. Addition, of the GOT coenzymes pyridoxal and pyridoxamine phosphates in concentrations up to 200 /tg/ml lias no effect on human serum GOT but activates bu 45% the pig heart GOT activity of VersatoUE, a commercial reference serum...

Babson proposed a-naphthyl phosphate as an essentially specific substrate for the activity of prostatic acid phosphatase in serum (104). However Marshall, Price, and Amador found that this substrate is not specific for the prostatic enzyme because urine of human females contain 50 times more acid a-naphthyl phosphatase than male serum and 50% as much activity as male urine. Platelets have significant activity and the serum activity can increase to abnormal values following clotting. These workers also observed elevated activities in females with skeletal metastases of the breast. In 50 hospitalized male patients who had no evidence of prostatic cancer and 25 hospitalized female patients, the incidence of false positive results was 12%, a magnitude sufficient to preclude meaningful clinical interpretation (105). 

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... 

Phosphate-Binding Agents When serum phosphorus levels cannot be controlled by restriction of dietary intake, phosphate-binding agents are used to bind dietary phosphate in the GI tract to form an insoluble complex that is excreted in the feces. Phosphorus absorption is decreased, thereby... 

Normally, the number of anions and cations in each fluid compartment are equal. Cell membranes play the critical role of maintaining distinct ICF and ECF spaces which are biochemically distinct. Serum electrolyte concentrations reflect the stores of ECF electrolytes rather than that of ICF electrolytes. Table 24-4 lists the chief cations and anions along with their normal concentrations in the ECF and ICF. The principal cations are sodium, potassium, calcium, and magnesium, while the key anions are chloride, bicarbonate, and phosphate. In the ECF, sodium is the most common cation and chloride is the most abundant anion while in the ICF, potassium is the primary cation and phosphate is the main anion. Normal serum electrolyte values are listed in Table 24—5. 

Phosphorus is provided as sodium or potassium phosphate in PN. Approximately 10 to 15 mmol of phosphate are needed per 1000 kilocalories to maintain normal serum phosphorus concentrations (provided the patient is well nourished and has normal renal function).15 Patients with renal insufficiency may require phosphorus restriction. 

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. 

Wakabayashi et al. [51] determined penicillamine in serum by HPLC. Serum (0.1 mL) was vortex-mixed for 30 s with 50 pL of 0.1% EDTA and 0.2 mL of 10% TCA. The solution was centrifuged at 1500 x g and filtered. A 5 pL portion was analyzed on a Shodex C18 column (15 cm x 4.6 mm i.d.), using a mobile phase of 19 1 methanolic 0.05 M phosphate buffer (pH 2.8) containing 1 mM sodium octylsulfate and 10 pM EDTA. Liver or kidney samples were similarly extracted, and the extracts were cleaned up on a Bond-Elut cartridge prior to HPLC analysis. Detection was effected with an Eicom WE-3G graphite electrode maintained at +0.9 V versus Ag/AgCl. The calibration graph was linear up to 500 ng, and the detection limits were 20 pg. For 1 pg of penicillamine added to serum, liver, or kidney, the respective relative standard deviations (n = 5) were 3.6, 5.1, and 4.4%. 

C for 1 h. A 100 pL portion of the solution was injected onto a column (15 cmx 3.2 mm) of LiChroscob RP-18 (7 pm) for HPLC at room temperature, using acetonitrile-0.033 M phosphate buffer of pH 8.2 (1 2) containing 0.05% of ethyle-nediamine as the mobile phase (eluted at 1 mL/min). Fluorimetric detection involved excitation at 338 nm and measurement at 540 nm (or with a 430 nm cutoff filter). For 50 300 ng of drug injected on to the column, the coefficient of variation was 7-8%. The method permits a simple determination of (z>)-penicilla-mine in serum at therapeutic levels. 

Feldman and co-workers117) described a procedure for determining as little as 10 ppb of chromium in serum. The normal level is 30 ppb. At least 2 ml of serum are digested or dry ashed and treated with not permanganate to oxidize chromium to chromium(VI). The chromium(VI) is extracted from 3M HC1 into 5 ml MIBK in the cold. This method has been used to measure chromium levels in studies relating this element to diabetes. Thousands of analyses have been performed. Devoto (198) dry ashed 10 ml of blood and extracted the chromium with 5 ml of 10 % tributyl phosphate in MIBK. Recently, Feldman 119) has determined... 

Chloride ion-selective electrodes The most important region of application is the determination of chlorides in waters, including sea water (for a review, see [167]), in serum [110,112,371] (review in [167]) and in soil [151,219,341], The determination of chloride ions in sweat made screening for cystic fibrosis possible in new-born babies (review, [45,55a, 262]). Br , I and S " interfere in the determination of chlorides in phosphate rocks [81]. Sulphite can be determined directly using an electrode with an Hgj CI2 - HgS membrane [398] on the basis of the reaction... 

Many of the adverse effects of lithium can be ascribed to the action of lithium on adenylate cyclase, the key enz)nne that links many hormones and neurotransmitters with their intracellular actions. Thus antidiuretic hormone and thyroid-stimulating-hormone-sensitive adenylate cyclases are inhibited by therapeutic concentrations of the drug, which frequently leads to enhanced diuresis, h)rpoth)n oidism and even goitre. Aldosterone synthesis is increased following chronic lithium treatment and is probably a secondary consequence of the enhanced diuresis caused by the inhibition of antidiuretic-hormone-sensitive adenylate cyclase in the kidney. There is also evidence that chronic lithium treatment causes an increase in serum parathyroid hormone levels and, with this, a rise in calcium and magnesium concentrations. A decrease in plasma phosphate and in bone mineralization can also be attributed to the effects of the drug on parathyroid activity. Whether these changes are of any clinical consequence is unclear. 

Brydon and Roberts- added hemolyzed blood to unhemolyzed plasma, analyzed the specimens for a variety of constituents and then compared the values with those in the unhemolyzed plasma (B28). The following procedures were considered unaffected by hemolysis (up to 1 g/100 ml hemoglobin) urea (diacetyl monoxime) carbon dioxide content (phe-nolphthalein complex) iron binding capacity cholesterol (ferric chloride) creatinine (alkaline picrate) uric acid (phosphotungstate reduction) alkaline phosphatase (4-nitrophenyl phosphate) 5 -nucleotidase (adenosine monophosphate-nickel) and tartrate-labile acid phosphatase (phenyl phosphate). In Table 2 are shown those assays where increases were observed. The hemolysis used in these studies was equivalent to that produced by the breakdown of about 15 X 10 erythrocytes. In the bromocresol green albumin method it has been reported that for every 100 mg of hemoglobin/100 ml serum, the apparent albumin concentration is increased by 100 mg/100 ml (D12). Hemolysis releases some amino acids, such as histidine, into the plasma (Alb). 

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. 

With the exception of the possible development of a hypervitaminosis associated with high-dose administration of vitamin D2 or D3, the compounds discussed in this chapter are relatively safe. Allergic reactions to the injection of calcitonin and PTH have occurred and chronic use of some bisphosphonates has been associated with the development of osteomalacia. The principal side effects of intravenous bisphosphonates are mild and include low-grade fever and transient increases in serum creatinine and phosphate levels. Oral bisphosphonates are poorly absorbed and can cause esophageal and gastric ulceration. They should be taken on an empty stomach the individual must remain upright for 30 minutes after ingestion. 

Capsel PAC C-18 UV228 nm MeOH/5 mM Phosphate Buffer, pH 2 (2/8) Benzoic acid, hippurate in Serum 40... 

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. 

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