Teratogenic human infant

There is no information on in utero developmental effects in humans exposed to HCB, but oral exposure of young children has caused small or atrophied hands, short stature, pinched facies, osteoporosis of the carpal, metacarpal, and phalangeal bones, and painless arthritic changes. HCB has been demonstrated to cross the placenta in humans and in rodents. HCB residues have been detected in human milk and adipose tissue and in the blood of the umbilical cord of newborn infants and their mothers. Teratogenic effects were not... 

Saquinavir is subject to extensive first-pass metabolism by CYP3A4 and functions as a CYP3A4 inhibitor as well as a substrate thus, there are many potential drug-drug interactions (Table 49-4). A decreased dose of saquinavir is recommended when -administered with nelfinavir. Increased saquinavir levels when -administered with omeprazole necessitate close monitoring for toxicities. Digoxin levels may increase if co administered with saquinavir and should therefore be monitored. Liver function tests should be monitored if saquinavir is -administered with delavirdine or rifampin. There is no evidence of human teratogenicity from saquinavir there is short-term safety data for both mother and infant. 

The teratogenic syndrome of in utero VPA exposure in humans includes neural, craniofacial, cardiovascular, and skeletal defects. A similar teratology is exhibited in rodents, rabbits, and nonhuman primates. The most dramatic of malformations associated with gestational VPA exposure is spina bifida, a neural tube defect that is estimated to occur in 1-2% of VPA exposed infants. Mice are the only known animal model to exhibit a comparable effect of VPA on neural tube development. 

BZDs should be avoided during the first trimester and at delivery. Malformation and CNS dysfunction have been described in infants born of mothers using BZDs during pregnancy. Both animal data and human epidemiological studies suggest that BZDs are teratogens. 

No studies have demonstrated that selenium or its compounds are teratogenic in humans. Robertson (1970) reported on the outcome of pregnancies in a laboratory in which workers handled sodium selenite. Of the five pregnancies, four ended in spontaneous abortion and one resulted in an infant with bilateral clubfoot. The urinary selenium levels in all subjects were similar to those in other individuals living in the same area. The limited number of cases, possible exposure to other toxic agents, and other confounding factors leave the relationship between sodium selenite and developmental effects inconclusive. 

There are no adequate studies of teratogenicity for gold sodium thiomalate in pregnant humans however, a potential risk to the fetus exists because gold was found in the serum and red blood cells of a nursing infant. 

There have been few studies on the fetal toxicity of Cd transported across the placenta, which acts as a barrier to Cd. Nevertheless, a small amount may reach the fetus. Cd is also transferred to neonates through lactation. Maternal hypertension and decrease in birth weight have been associated with elevated levels of Cd in the neonate [155]. A depletion of zinc with increasing number of births and a progressive increase in Cd in smokers negatively affect infant birth weight [156]. Moreover, Marlowe et al. [157] found an association between mental retardation and raised concentrations of Cd in hair in school age children. But overall, there is no substantial evidence that Cd has caused teratogenic effects in humans. 

Several reviews and studies have failed to identify any potential for deet to cause harm to the developing fetus or a breast-fed infant. The safety of 20% deet in the second and third trimester was established by a study involving 897 snbjects and only trace amounts of deet could be detected in 8% of the cord samples. Human data for the first trimester are lacking, but animal work does not indicate any teratogenic effect. ... 

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