Cibus DCP Oral Powder

Indications

• Hypophosphatemia
• Bone disorders (e.g., osteomalacia, rickets)
• Nutritional supplementation in deficiency states

Dosage

Children: Refer to BNF for Children for specific paediatric dosing guidance based on the condition being treated.

Adults: Refer to BNF for specific adult dosing guidance based on the condition being treated.

Mechanism of action

Phosphorus decreases the absorption of intercellular calcified cartilage matrix by osteoclasts in the metaphyseal region of growing bones, leading to increased bone density and thickness, observable as 'phosphorus bands' on radiographs. Additionally, exposure to white phosphorus damages the rough and smooth endoplasmic reticulum, impairing protein synthesis and lipid transport, particularly affecting the synthesis of very low-density lipoproteins (VLDL) and causing hepatic steatosis and fibrosis.

Pharmacodynamics

Phosphorus is involved in bone metabolism and energy transfer within cells. It contributes to the structural framework of bones and teeth, and its role in ATP formation is crucial for energy metabolism. The balance of phosphorus with calcium and vitamin D is essential for maintaining bone health and preventing disorders such as osteomalacia and rickets.

Pharmacokinetics

Phosphorus is absorbed in the gastrointestinal tract, with absorption rates affected by factors such as dietary composition and the presence of other minerals. It is distributed throughout body tissues, particularly in bones and teeth. Phosphorus is primarily excreted through the kidneys, and its serum levels are regulated by hormonal influences, including parathyroid hormone and calcitriol.

Pregnancy

Phosphorus is essential for fetal development; however, excessive intake should be avoided. Consult healthcare professionals for appropriate supplementation.

Breast-feeding

Phosphorus is secreted in breast milk; adequate maternal intake is important for infant health. Consult healthcare professionals for guidance.

Storage

Store in a cool, dry place, away from direct sunlight and moisture. Ensure it is kept out of reach of children.

Mechanism of action

Phosphorus apparently decreases the absorption of intercellular calcified cartilage matrix by osteoclasts, in the metaphyseal region of growing bones. Administration of phosphorus to growing animals or children produces "phosphorus bands" of increased bone density and thickness that are visible grossly or from radiograms. The "phosphorus bands" are observed in the metaphyseal region of growing bones, and represent areas of decreased absorption of the calcified cartilage matrix. Exposure to white phosphorus has been shown to damage the rough endoplasmic reticulum and cause a disaggregation of polyribosomes. This damage results in impairment of protein synthesis, in particular, a decrease in the synthesis of the apolipoprotein portion of very low density lipoproteins (VLDL), which are required for the transport of triglycerides. A significant decrease in protein synthesis has been detected as early as 3 hours after oral exposure. The smooth endoplasmic reticulum is also involved in the formation of the VLDLs, and damage to the smooth endoplasmic reticulum also impairs the formation of VLDLs. The net result of these ultrastructural changes is an accumulation of triglycerides in the liver. This results in steatosis and fibrosis, which is one of the mechanisms involved in the hepatotoxicity of white phosphorus. The mechanism behind the damage to the endoplasmic reticulum is not known; also, it is not known whether white phosphorus itself or a metabolite of white phosphorus is the damaging agent. In addition to these damages, white phosphorus or a metabolite causes damage to the mitochondria and nuclei in the livers of animals orally exposed to white phosphorus. The damage to the mitochondria may impair the cell's ability to produce ATP, thus resulting in necrosis of the cell. Fatty infiltration and/or cellular damage has also been observed in the kidney, brain, and heart. It is possible that white phosphorus (or a metabolite) also impairs the ability of cells in these organs to produce ATP. The mitochondrial damage may also inhibit fatty acid oxidation (also contributing to the decreased availability of ATP) which could result in an accumulation of fat in the organs.