Albumin, half-life

Estrogens - Ethinyl estradiol is rapidly absorbed with peak concentrations attained in 1 to 2 hours. It undergoes considerable first-pass elimination. Mestranol is demethylated to ethinyl estradiol. Ethinyl estradiol is approximately 97% to 98% bound to plasma albumin. Half-life varies from 6 to 20 hours. It is excreted in bile and urine as conjugates, and undergoes some enterohepatic recirculation. 

Noort and colleagues (2008) investigated the persistence of sulfur mustard adducts to albumin and hemoglobin in rats. The albumin adduct (S -2-hydroxyethylthioethyl)-Cys-Pro-Tyr was detectable up to 7 days after the exposure, while the adduct to the N-terminal valine in hemoglobin was still detected after 28 days. The decrease of adduct concentration corresponded with albumin half-life and the hfetime of the rat erythrocyte, respectively. 

Short-Term Monitors. These include labile pre-Hb Aj (several days), glycosylated serum transferrin, half-life of 8 days (K3, K4) and glycosylated serum albumin, half-life of 20 days (D23, J6). These estimations... 

Medroxyprog esteroneAcetate. Accurate pharmacokinetic and metaboHsm studies on MPA have been difficult because the radioimmunoassays employed caimot differentiate between MPA and its metaboHtes (346). Comparison of MPA plasma levels assayed by hplc and radioimmunoassay show that radioimmunoassay may overestimate intact MPA concentrations by about fivefold (347). However, values of the mean elimination half-life of MPA were similar, being 33.8 and 39.7 h when measured by hplc and radioimmunoassay, respectively (347). Approximately 94% of MPA in the blood is bound to albumin (348). When taken orally, MPA is rapidly absorbed with Htde or no first-pass metaboHsm (13). Peak semm levels ate reached after 3 h. Steady state occurs after three days of daily adininistration (349). The pharmacokinetics of MPA when adininistered in a depot formulation have been described (350). 

EoUowing po administration moricizine is completely absorbed from the GI tract. The dmg undergoes considerable first-pass hepatic metabolism so that only 30—40% of the dose is bioavailable. Moricizine is extensively (95%) bound to plasma protein, mainly albumin and a -acid glycoprotein. The time to peak plasma concentrations is 0.42—3.90 h. Therapeutic concentrations are 0.06—3.00 ]l/niL. Using radiolabeled moricizine, more than 30 metabolites have been noted but only 12 have been identified. Eight appear in urine. The sulfoxide metabolite is equipotent to the parent compound as an antiarrhythmic. Elimination half-life is 2—6 h for the unchanged dmg and known metabolites, and 84 h for total radioactivity of the labeled dmg (1,2). 

The absorption of metoprolol after po dosing is rapid and complete. The dmg undergoes extensive first-pass metabolism in the liver and only 50% of the po dose in bioavailable. About 12% of the plasma concentration is bound to albumin. The elimination half-life is 3—7 h and less than 5% of the po dose is excreted unchanged in the urine. The excretion of the dmg does not appear to be altered in patients having renal disease (98,99,108). 

Thyroxine (3, 5, 3,5-L-teraiodothyronine, T4) is a thyroid hormone, which is transformed in peripheral tissues by the enzyme 5 -monodeiodinase to triiodothyronine. T4 is 3-8 times less active than triiodothyronine. T4 circulates in plasma bound to plasma proteins (T4-binding globulin, T4-binding prealbumin and albumin). It is effective in its free non-protein-bound form, which accounts for less than 1%. Its half-life is about 190 h. 

When levels of conjugated bilirubin remain high in plasma, a fraction can bind covalently to albumin (delta bilirubin). Because it is bound covalently to albumin, this fraction has a longer half-life in plasma than does conventional conjugated bilirubin. Thus, it remains elevated during the recovery phase of obstructive jaundice after the remainder of the conjugated bilirubin has declined to normal levels this explains why some patients continue to appear jaundiced after conjugated bilirubin levels have returned to normal. 

Absorption kinetic studies on fasted rats dosed by lipid-emulsion gavage revealed rapid appearance of triehloroethylene in the blood (typieally peaking at 15 minutes post-exposure) followed by rapid disappearance (Templin et al. 1993). Rats similarly dosed with radiolabelled trichloroethylene showed rapid serum albumin adduction which peaked at 4-8 hours, then decayed with a half-life consistent with that of albumin itself (Stevens et al. 1992). However, some of the detected radioactivity may have been due to trichloroethylene metabolites rather than the parent compound. 

Haemoglobin, described in Section 5.3.1.3, is the most well known but it is just one of a number of carrier proteins present in blood. Albumin is quantitatively the most abundant protein in plasma. It is synthesized in the liver and circulates with a half life of about 3 weeks before being degraded or eliminated. Albumin has two very important functions to fulfil. First, it makes a significant contribution to the oncotic pressure of the blood and so influences the distribution of fluid between the intracellular and... 

There is substantial variability in the pharmacokinetics of vinblastine in patients. Evidence has been obtained that implicates altered liver function and dose-dependent elimination as contributing factors to the variable pharmacokinetics. When vinblastine was administered by a bolus injection, a mean terminal elimination half-life of 29.2 hr was estimated for a group of 24 patients, but the half-lives ranged from a low value of 16 hr to a high value of 65 hr (55). When vinblastine was administered by intravenous infusion, clearance of the drug appeared to decrease with time over a 4-month period decreases in serum albumin values were found to be correlated with decreases in the clearance of vinblastine. 

Serum alkaline phosphatase elevations have been reported following administration of salt-poor albumin (B5). Placenta is very rich in a heat-stable alkaline phosphatase, and albumin prepared from placental blood has a high activity of this enzyme. In one cirrhotic patient who received 1-6 units per day of albumin obtained from pooled human blood and/or human placenta, the alkaline phosphatase before infusion was 5 Bodansky units and by the thirteenth day of administration had reached a value of 160 units. The physician administering the albumin at first thought the patient was having a severe toxic liver reaction and stopped the therapy. The alkaline phosphatase then started to go down and within 10 days returned to normal levels. Analysis of the albumin indicated that it contained 470 units of alkaline phosphatase activity and was probably responsible for the observed elevations in the serum enzyme activity. Albumin prepared from venous blood did not cause an alkaline phosphatase elevation, but placenta-albumin caused elevations with a half-life of about 8 days (Ml). 

Pharmacokinetics It is well absorbed from the Gl tract after oral administration (40% to 70%) peak plasma levels occur in 1 to 3 hours. Most (80%) of the plasma penicillamine is protein bound, primarily to albumin. Penicillamine is rapidly excreted in the urine 50% is excreted in the feces. Metabolites may be detected in the urine for up to 3 months after stopping the drug. Half-life ranges are 1.7 to 3.2 hours. 

Pharmacokinetics Oral zafirlukast is rapidly absorbed. Peak plasma concentrations are achieved 3 hours after dosing. The mean terminal elimination half-life is about 10 hours. Zafirlukast is more than 99% bound to plasma proteins, predominantly albumin. 

The plasma protein binding of tacrolimus is approximately 99%. Tacrolimus is bound mainly to albumin and alpha-1-acid glycoprotein and has a high level of association with erythrocytes. It is extensively metabolized by the mixed-function oxidase system, primarily the cytochrome P450 system (CYP3A). The disposition of tacrolimus from whole blood was biphasic with a terminal elimination half-life of 11.7 hours in liver transplant patients. 

Phenprocoumon has a long plasma half-life of 5 days and thus a duration of action that can last 7-10 days. On the other hand acenocoumarol has a half-life of 10-24 hours and therefore a shorter duration of action. The half-life of warfarin ranges from 25-60 hours and its the duration of action is 2-5 days. Both warfarin and phenprocoumon are highly protein bound and interactions may occur with other drugs that bind to albumin. 

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