Phosphorus metabolism in cattle with reference to calcinosis ("pasture disease")
Leibetseder, J.; Skalicky, M.; Kment, A.
Deutsche Tierärztliche Wochenschrift 78(22): 603-605
1971
ISSN/ISBN: 0341-6593 PMID: 4941933 Document Number: 41602
The disease, manifested by emaciation, declining performance and locomotor disturbances resulting from calcification of cardiac vessels, kidneys, lung and musculature, has been observed over the past 10 years in alpine areas of Germany and Austria heavily fertilized with phosphates [see V.B. 41, abst. 1410-1412]. Phosphorus balance studies and compartment analysis were conducted on four healthy, non-lactating cows, 5-11 years of age, and one 8-year-old cow with calcinosis (confirmed P.M.). After a dose of P-32, the specific plasma activity declined continuously and more steeply in the affected cow than the others, and, despite a high P intake and normal resorption coefficient, endogenous faecal P excretion was low, there was no excretion of P across the kidneys, while mobilization of skeletal P was scarcely detectable, indicating a continual loss of P from the central compartment and deposition in mineralized tissues. To investigate the possible role of the parathyroid gland (known to be scarcely functional in calcinosis) a dose of 1,000 Collip units of parathormone was given s/c on two successive days to another 8-year-old in a nutritional state similar to calcinosis. Subsequent compartment analysis indicated that a reduction of skeletal P deposition, raised excretion in the faeces and urine, a higher resoprtion quotient and slightly lower transfer rates took place after hormone administration. Although the aetiology of the condition is still unclear, it is suggested that the mechanism may be comparable to that for the action of vitamin D.