Nutritional Secondary Hyperparathyroidism in the Horse

Serum Phosphorus, Calcium, and Alkaline Phosphatase 75
relationship between serum calcium and phosphorus was still very
obvious.
In the analyses of the solubility of calcium and phosphorus in
blood serum the total values of these elements were used. MCLEAN and
URIST (1 961) commented upon this empirical product, introduced by
HOWLAND and KRAMER (1921), as follows: “Moreover, since the proportions
of Ca++ and HP04-- to the total Ca and total P are relatively
constant, HOWLAND and KRAMER’S empirical formulation, Ca x P, is
as reliable as the ion product itself, or as the product of the activities of
the ions.”
The product of total calcium and phosphorus in blood serum
showed that, in this respect, the changes in serum phosphorus were
more decisive than those in serum calcium. The regression lines of the
products were quite similar to those of serum phosphorus. The increase
in the product reached remarkable heights. At the highest levels
the products were 43, 57, and 38% higher in the three NSH horses,
respectively, than in the control horse. As the blood serum is normally
almost saturated [ALBRIGHT and REIFENSTEIN (1948), in man], at least
the highest values must indicate supersaturation in the sense of
MCLEAN et al. (1946). Even at the end of the experiment, when there
was a partial compensation for the serum phosphorus and calcium, the
products remained at levels 18, 19, and 19 yo, respectively, higher than
in the average of the control.
The degree of hyperphosphatemia was not the same in the NSH
horses. It was most severe in NSH 2, then NSH 3, and, last, NSH 1.
Horses NSH 2 and 3 were given dibasic sodium phosphate and NSH 1
monobasic sodium phosphate, but regardless of the source the imbalance
was made the same. With only three experimental horses and
no data on blood and urine pH and so forth, we will not attempt to
discuss what caused the differences in hyperphosphatemia. The important
point is that the degree of hypocalcemia and therefore the degree
of parathyroid hyperactivity (Table XlI, for analysis see Appendix
Table IV) and of roentgenologic changes was a direct function of the
degree of hyperphosphatemia.
Serum alkaline phosphatase. ALBRIGHT and REIFENSTEIN (1948)
stated: “In the absence of any other cause for a higher phosphatase
level such as liver disease or obstructive jaundice, a high serum phosphatase
level is probably indicative of increased osteoblastic activity.”
With regard to the cause of the increased osteoblastic activity in hyperparathyroidism
they wrote: “As the bones become weak they will be
7 Krook/Lowe
Downloaded from
vet.sagepub.com by guest on April 14, 2010