Jesse P. Goff, DVM, PhD.
Veterinary Medical Officer, Periparturient Diseases Unit, National Animal Disease Center, USDA-Agricultural Research Service, Ames, IA 50010
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Jesse P. Goff DVM, PhD. National Animal Disease Center USDA- Agricultural Research Service Ames, IA 50010
515-663-7547 515-663-7458 fax
1Adequate blood calcium (Ca) and phosphorus (P) concentrations are vital to normal function of animals. Mechanisms for maintaining blood Ca and P concentrations perform efficiently most of the time. Occasionally these homeostatic mechanisms fail and metabolic diseases such as milk fever occur. An understanding of how and why these mechanisms fail may arise from a thorough understanding of howthese mechanisms work under normal circumstances and then exploring the possible sites for breakdown of homeostasis. Ca Homeostasis Blood Ca in the adult cow is maintained around 8.5-10 mg / dl. This means there is about 3 g Ca in the entire plasma pool of a 600 kg cow. The entire extracellular pool will have only 8-9 g Ca. Many cows are producing colostrum and milk that contains 20 -30 g Ca eachday. In order to prevent blood Ca from decreasing, which has a variety of severe consequences to life processes beyond paresis, the cow must replace Ca lost to milk by withdrawing Ca from bone or by increasing the efficient absorbtion of dietary Ca (Figure 1). While this is potentially damaging to bones and can lead to osteoporosis the main objective - to maintain normocalcemia - can be achieved.Bone Ca mobilization is regulated by parthyroid hormone (PTH) which is produced whenever there is a decline in blood Ca. Renal tubular reabsorption of Ca is also enhanced by PTH, however the total amount of Ca that can be recovered is relatively small. A second hormone, 1,25-dihydroxyvitamin D, is required to stimulate the intestine to efficiently absorb dietary Ca. This hormone is made within thekidney from vitamin D in response to an increase in blood PTH. Put simply, hypocalcemia and milk fever occur when cattle do not remove enough Ca from their bones and the diet to replace Ca lost to milk. Why this might happen is explored below as each strategic point in Ca homeostasis is examined. I. Factors affecting PTH secretion A. Hypomagnesemia PTH secretion is normally increased greatly inresponse to even slight decreases in blood Ca concentration. However hypomagnesemia can blunt this response (56). This appears to be a factor in the development of some hypomagnesemic tetany syndromes of grazing beef and dairy cattle. Blood mineral profiles of lactating beef cows in one study demonstrated that plasma Mg concentrations declined slowly over several weeks after cows were placed on lowMg, high potassium pastures. Blood Mg concentrations declined to between 0.8 and 1.4 mg / dl. However in animals with clinical disease (tetany) blood Ca had also fallen below 5 mg/dl only occurred when plasma Ca concentrations also declined. Blood Ca concentration had remained within normal limits until the day the animals developed tetany. Plasma PTH concentrations did not increase as a result ofthe decline in blood Ca concentration and the authors concluded that hypomagnesemia had blocked PTH secretion preventing the cows from maintaining normal Ca homeostasis (42). B. Low Ca prepartal diets When cows are fed a diet that supplies less Ca than they require, the cows are in negative Ca balance. This causes a minor decline in blood Ca concentration which stimulates PTH secretion, which inturn stimulates osteoclastic bone resorption and renal production of 1,25dihydroxyvitamin D. This increases bone Ca efflux and the intestine is ready to absorb Ca efficiently should it become available. At parturition the lactational drain of Ca is more easily replaced since the cow’s bone osteoclasts are already active and in high numbers and, if supplied with Ca in the lactation ration, the...