Disorders of calcium metabolism

Parturient Hypocalcemia (or) Milk fever (Parturient paresis) in dairy cows and Puerperal tetany or eclampsia are the Disorders of calcium metabolism.

Parturient Hypocalcemia or Milk fever

Parturient hypocalcemia or Milk Fever is a metabolic disease of high producing dairy cows characterized by the development of severe hypocalcemia, hypophosphatemia and paresis near the time of parturi­tion.

Total and ionized calcium levels in plasma decrease progres­sively beginning several days before parturition. Serum magnesium may increase reciprocally as calcium declines.

The blood glucose concentration is often increased in response to hypocalcemia due to an interference with the secretion of insulin from b cells. An adequate amount of calcium ion in extracellular fluid is required for insulin secretion in response to glucose.

Parathyroid Hormone level is increased during this condition . In certain cows, especially those fed high calcium diets during prepartum show increased secretion of calcitonin which might result in the inability of PTH to mobilise calcium rapidly from bone reserve to maintain blood calcium levels during the critical period near parturition.

Immediately after parturition the target cells in bone become temporarily refractive to the action of elevated levels of PTH (Parathyroid Hormone).

Bone turnover, particularly resorption is low and only few osteoclasts are present on smooth inactive trabecular bone surfaces.

Urinary excretion of hydroxyproline does not in­crease significantly during late gestation which indicates poor breakdown of bone matrix.

Calcium homeostasis in pregnant cows fed a high Ca diet appears to be maintained principally by intestinal Ca absorp­tion.

Feeding balanced or relatively low Ca diets during pre­partum (last two weeks of gestation) prevents this disorder by mobilizing the required level of calcium from the bony matrix.

Puerperal tetany or Eclampsia

This condition is seen in small hyper excita­ble breeds of dogs.

The Female dog may develop severe hypocalcemia and often hypophosphatemia near the time of peak lactation (1‑3 weeks) postpartum which is the result of failure of calcium homeostasis.

This failure is due to low Ca²⁺inflow to the body and high outflow of Ca²⁺ in the milk.

There will be restlessness, panting, nervous­ness, trembling, muscular tetany and convulsive seizures in 8‑ 12hours.

Administration of intravenous Ca²⁺combined with temporary removal of pups to reduce lactational drain of Ca²⁺will correct this problem .

Chronic hypocalcemia from dietary Ca deficiency, vitamin D deficiency or from kidney diseases is more frequent in animals. This hypocalcemia leads to hyperparathyroidism that produces skeletal demineralisation or excess bone reabsorption– e.g. rubber jaw syndrome in dogs.

Vitamin D deficiency leads to poor intestinal absorption of Ca with poor mineralization of bone leading to rickets in young animals and children and osteomalacia is adults.