Lead toxicity calcification

Although animal studies and small studies in humans have shown this strong association of vitamin K deficiency with vascular calcification, this has not been utilized as a standard therapy for vascular calcification. It is still unclear if vitamin K replenishment can affect the morbidity and mortality associated with vascular and valvular calcification in humans. Further studies are needed to determine the appropriate formulation of vitamin K (K1 vs. K2), dose, and duration of vitamin K therapy that would lead to beneficial effects in prevention of vascular calcification. Because of their very low toxicity and potentially beneficial effects on attenuation of arterial calcification, vitamin K supplementation can be considered in susceptible patients, such as patients with end-stage renal disease who are on hemodialysis. 

Placental transport of lead may be associated with placental transport of calcium. Barltrop (1969) observed that femur lead increased rapidly in the third trimester, corresponding to onset of ossification and deposition of calcium. There is a question whether the increased deposition of lead in the femur along with calcium is because of some commonality between lead and calcium metabolism. Figure 2 shows the close correlation between size of fetal brain and increase in lead content as the brain matures. Whether the movement of lead into the brain is a matter of simple diffusion or whether there is some relationship to brain calcium is not known. Calcium deficiency does enhance lead absorption and the pathological effects of lead (Mahaffey et al. 1973). The placenta also contains a calcium-binding protein identical to that present in the intestine (Van Dijk 1981). A comparison of placental transfer of toxic metals by Nakano and Kurosa from the Minamata Institute in Japan (unpublished observation) found that lead levels in the placenta were strongly correlated with calcium, suggesting that lead deposition is associated with calcium deposition or with areas of dystrophic calcification that are present in the mature placenta. 

TOXICITY. Normally, the small intestine acts as an effective control and prevents excess calcium from being absorbed. However, a breakdown of this control may raise the level of calcium in the blood and lead to pathological calcification of the kidneys and other internal organs. This may occur in infants who have been fed on artificial foods fortified with excessive amounts of vitamin D and calcium. 

Within the control limits, increased intakes of vitamin D lead to increased blood levels of 25-OHD but not of l,25-(OH)2D and homeostasis is maintained. However, at higher dietary levels of vitamin D, toxic manifestations of hypercalcaemia become increasingly evident with deformation of bone and even calcification of soft tissues. Thus vitamin D is toxic at dietary levels which overload the control processes. 

If fluorine is taken in excess during childhood, the diii spots on teeth are developed. It is toxic if taken more than 20 ppm. It increases bone density and calcification at the point of muscle insertion to bone. In advance stages, it leads to stiff joints mainly of spinal cord. 

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