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In breast milk

Phenytoin s absorption is slow and variable yet almost complete absorption eventually occurs after po dosing. More than 90% of the dmg is bound to plasma protein. Peak plasma concentrations are achieved in 1.5—3 h. Therapeutic plasma concentrations are 10—20 lg/mL but using fixed po doses, steady-state levels are achieved in 7—10 days. Phenytoin is metabolized in the fiver to inactive metabolites. The plasma half-life is approximately 22 h. Phenytoin is excreted primarily in the urine as inactive metabolites and <5% as unchanged dmg. It is also eliminated in the feces and in breast milk (1,2). Prolonged po use of phenytoin may result in hirsutism, gingival hyperplasia, and hypersensitivity reactions evidenced by skin rashes, blood dyscrasias, etc... [Pg.113]

Mexifitene is well absorbed from the GI tract and less than 10% undergoes first-pass hepatic metabolism. In plasma, 60—70% of the dmg is protein bound and peak plasma concentrations are achieved in 2—3 h. Therapeutic plasma concentrations are 0.5—2.0 lg/mL. The plasma half-life of mexifitene is 10—12 h in patients having normal renal and hepatic function. Toxic effects are noted at plasma concentrations of 1.5—3.0 lg/mL, although side effects have been noted at therapeutic concentrations. The metabolite, /V-methy1mexi1itene, has some antiarrhythmic activity. About 85% of the dmg is metabolized to inactive metabolites. The kidneys excrete about 10% of the dmg unchanged, the rest as metabolites. Excretion can also occur in the bile and in breast milk (1,2). [Pg.113]

The GI absorption of the dmg after po adrninistration is slow and variable with estimates ranging from 20—55%. Once absorbed, 96% of the dmg is bound to plasma proteins and other tissues on the body. Whereas peak plasma concentrations may be achieved in 3—7 h, the onset of antiarrhythmic action may occur in 2—3 days or more. This may result, in part, from distribution to and concentration of the dmg in adipose tissue, Hver, spleen, and lungs. Therapeutic plasma concentrations are 1—2 p.g/mL, although there appears to be no correlation between plasma concentration and antiarrhythmic activity. The plasma half-life after discontinuation of the dmg varies from 13—103 days. The dmg is metabolized in the Hver and the principal metaboHte is desethylamiodarone. The primary route of elimination is through the bile. Less than 1% of the unchanged dmg is excreted in the urine. The dmg can also be eliminated in breast milk and through the skin (1,2). [Pg.121]

The GI stimulants are contraindicated in patients witii known hypersensitivity to the drug, GI obstruction, gastric perforation or hemorrhage, or epilepsy. These drugs are secreted in breast milk and should not be used during lactation. [Pg.472]

The available evidence suggests that excretion of methyl parathion metabolites in humans and animals following acute oral exposure is essentially the same and occurs rapidly. Excretion occurs primarily via the urine. Methyl parathion can also be excreted in breast milk, although it has been detected only in a limited number of samples from women of central Asia, for which exposure data were not available (Lederman 1996) (see also Section 3.4.2.2). A study in rats also reported excretion of methyl parathion in the milk (Golubchikov 1991 Goncharuk et al. 1990). [Pg.96]

Lederman SA. 1996. Environmental contaminants in breast milk from the central Asian republics. Reprod Toxicol 10(2) 93-104. [Pg.218]

No data were located concerning whether pharmacokinetics of endosulfan in children are different from adults. There are no adequate data to determine whether endosulfan or its metabolites can cross the placenta. Studies in animals addressing these issues would provide valuable information. Although endosulfan has been detected in human milk (Lutter et al. 1998), studies in animals showed very little accumulation of endosulfan residues in breast milk (Gorbach et al. 1968 Indraningsih et al. 1993), which is consistent with the rapid elimination of endosulfan from tissues and subsequent excretion via feces and urine. There are no PBPK models for endosulfan in either adults or children. There is no information to evaluate whether absorption, distribution, metabolism, or excretion of endosulfan in children is different than in adults. [Pg.200]

Of the 91 samples of breast milk analyzed, only 2 had detectable quantities of endosulfan (concentrations not specified). In another study, the transfer of endosulfan and its metabolites were studied in breast milk of lactafing goats (Indraningsih et al. 1993). Endosulfan residues in milk of goats administered a daily dose of 1 mg/kg for 28 days reached 0.02 mg/kg on day 1. However, by day 8, no residues or metabolites could be detected. Likewise, no endosulfan residues could be detected in the tissues of kids except for a-endosulfan in the liver at a concentration of 0.0011 mg/kg. Analysis of milk from cows... [Pg.238]

Infliximab is FDA category B and also appears to carry minimal risk in pregnant patients. Little is known about excretion of infliximab in breast milk, so benefit versus risk should be considered if it is used during nursing. [Pg.292]

Since no human data exist to determine its safe use in pregnant women, sibutramine is not recommended therefore, women of childbearing potential should use effective methods of contraception while taking sibutramine. Further, sibutramine is not recommended for lactating mothers because its excretion in breast milk is likewise unknown.29... [Pg.1534]

No adequate studies have been conducted using diethyl-propion in pregnant women therefore, the drug should be used only if the benefit outweighs potential fetal risk. Use with caution in nursing mothers because the drug is excreted in breast milk.40... [Pg.1537]

In the Angara River basin (Russia) in 1968, in the region where bodies of water were treated with mineral-oil DDT emulsions [A61], this formulation was observed in 90% of breast milk samples in women who had just given birth (the average was 180 mkg/l), and DDE in 60% (with an average of 110 mkg/l). Table 3.7 shows comparative data on DDT content in breast milk in different countries. [Pg.68]

Table 3.7. Average DDT content in breast milk samples from different countries (in mkg/l) [76]... Table 3.7. Average DDT content in breast milk samples from different countries (in mkg/l) [76]...
Table 3.8. DDT content (mkg/l) in breast milk in several countries [77]... Table 3.8. DDT content (mkg/l) in breast milk in several countries [77]...
Table 3.9. Average stable OCP content in breast milk in 1984, in several regions of the USSR [76]... Table 3.9. Average stable OCP content in breast milk in 1984, in several regions of the USSR [76]...
Gulson et al. (1998) used measured lead isotope ratios (207Pb/206Pb and 206Pb/204Pb) in mothers breast milk and in infants blood to establish that, for the first 60-90 days postpartum, the contribution from breast milk to blood lead in the infants varied from 36% to 80%. Maternal bone and diet appear to be the major sources of lead in breast milk. Mean lead concentration ( standard deviation) in breast milk for participants in the study was 0.73 0.70 pg/kg. [Pg.433]

Gulson BL, Jameson CW, Mahaffey KR, et al. 1998. Relationships of lead in breast milk to lead in blood, urine, and diet of the infant and mother. Environ Health Perspect 106(10) 667-674. [Pg.529]

Stemowsky HJ, Wessolowski R. 1985. Lead and cadmium in breast milk. Arch Toxicol 57 41-45. [Pg.578]

WolffMS. 1983. Occupationally derived chemicals in breast milk. AmJIndMed 4 259-281. [Pg.587]

The main rout of excretion of the drug and its metabolites is the kidney with a half-life of 9-18 h in human. In contrast to human, animal models have a lower elimination half-life ranging from 0.6-9 h [78]. The elimination half-life of valproic acid and some metabolites was found to be much longer in the neonates (40-50 h) than adult subjects (9-18 h) [78,81]. One study reported no difference between the elimination half-life between elderly and young subjects (15.4 and 13.0 h, respectively) while other found an increase in for older patients (14.9 versus 7.2 h for young patients) [78,90], Insignificant amounts of valproic acid are found in breast milk, approximately 3% of maternal drug levels [84]. [Pg.236]

Canfield LM, Guillado AR, Neilson EM, Yap HH, Graver FJ, Cui HA and Blashill BM. 1997. Carotene in breast milk and serum is increased after a single (3-carotene dose. Am J Chn Nutr 66 52-61. [Pg.212]

Antipsychotics appear in breast milk with milk-to-plasma ratios of 0.5 to 1, however, 1-week post-delivery, clozapine milk concentrations were found to be 279% of serum concentrations. Use of clozapine during breast-feeding is not recommended. [Pg.826]

Bingham, P.M., Sreven-Tuttle, D. Lavin, E., and Acree, T. (2003). Odorants in breast milk. Arch. Pediatr. Adolesc. Med. 157, 1031. [Pg.334]

Experiments in rats and mice have shown little effect of //-hexane exposure on the development of the fetus. It is probable that //-hexane and its breakdown products can cross the placenta and also be excreted in breast milk, but no accurate measurements have been made in people. [Pg.26]


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See also in sourсe #XX -- [ Pg.125 ]




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