Sunday 17 March 2013

Nutritional Secondary Hyperparathyroidism



In this post we'll take a look at the pathogenesis behind secondary nutritional hyperparathyroidism as well as the clinical signs of the disease and how it can be treated. 

This is a disease caused by the excess production and release of parathyroid hormone (PTH) into the blood in response to low calcium levels in the blood. 

Pathogenesis

Nutritional Secondary Hyperparathyroidism (NSH) is caused by several factors including:
  • diets with an absolute calcium deficiency, 
  • diets with low calcium bioavailablilty (due to the presence of phytate and oxalates), 
  • excess phosphorus intake, 
  • and low calcium to phosphorus ratios

Low calcium levels cause the release of PTH in order to increase the amount of calcium in the blood and maintain homeostasis. This results in increased calcium reabsorption from the kidneys and increased resorption from bone. In addition, there is increased conversion of vitamin D to Calcitriol which increases calcium reabsorption from the gut and resorption from bone. 

When calcium and phosphorus are mobilised from the bones, the mineral matrix is replaced with connective tissue. Excessive resorption of bone leads to osteodystrophia fibrosa. 

Clinical Signs

Young, growing bone is most susceptible to osteodystrophia fibrosa and may become brittle. Fractures may also be common and are unlikely to heal well. In addition, excessive fibrous deposition in the bones may leads to swelling and softening of the bone which is more severe in non-weight bearing bones (such as the head and jaw – this is why this NSH is sometimes called ‘big head disease’ in horses). The spine and long bones become affected in chronic cases. Lameness is also common. 

Interestingly, blood concentrations of affected patients do not reflect a dietary deficiency of calcium. This is because the PTH works to increase plasma calcium levels. Plasma inorganic phosphorus levels in the blood may also be higher than normal. Serum alkaline phosphatase is also increased. 

Treatment

Treatment involves correcting the ration to supply sufficient calcium, maintain the dietary Ca:P between 1:1 and 1:2, and reduce oxalates and phytates.

That's all for now, see you next time :)

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