Nutritional Secondary Hyperparathyroidism in the Horse

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72 Expcrimcntal Nutritional Sccondary Hypcrparathyroidism in the Horse. . . It would seem, therefore, that an inverse relationship between calcium and phosphorus should not exist. An experiment by MCLEAN et al. (1946) offered the explanation. They introduced the term “biological solubility” and defined undersaturation, saturation, and supersaturation of calcium and phosphorus in blood serum on the basis of this term. “The limit of biological solubility is the point at which deposition of the bone salt just occurs in the matrix of rachitic cartilage in vitro.” Levels above this point were considered supersaturated and below this level undersaturated. MCLEAN et al. performed the following experiment: Adult dogs whose serum did not mineralize rachitic cartilage in vitro were given a large dose of parathormone at 0 and at 4 hours. The serum calcium rose rapidly and leached maximum level after 12 hours. A concurrent but slight rise in the serum phosphorus level was also recorded. At 4 hours the serum induced a slight mineralization of rachitic cartilage in vitro. After 8 hours the ion product of calcium and phosphorus of blood serum and in vitro mineralization tendency was still higher. They concluded, then, that at 4 hours the serum must have been at least saturated and, after 8 hours, supersaturated. According to these authors, the cause of supersaturation must be sought in the active intervention by the parathyroid hormone because “there is no way in which a solution of a salt, in contact with a solid phase, may become supersaturated by simple equilibrium with the solid”. The reports just mentioned concerned the interrelationship between calcium and phosphorus in noncompensatory, exogenous hyperparathyroidism. The results indicate, therefore, the effects of the parathyroid hormone on serum calcium and phosphorus. The interrelationship between calcium and phosphorus can be better demonstrated in the reverse condition, viz., the effect of different levels of serum calcium and phosphorus on the parathyroid glands. HAM et al. (1 940) showed conclusively that “hypocalcemia, instead of hyperphosphatemia, is the primary cause of physiological hypertrophy of the parathyroid glands”. Their results were confirmed by PATT and LUCKIIARUT (1942), STOERK and CARNES (1945), and EWGFELDT et al. (1954). Different ways have been employed to produce hypocalcemia leading to secondary hyperparathyroidism. I-IAM et al. simply underfed calcium to induce hypocalcemia, PATT and LUCKHARUT lowered serum calcium by intravenous injections of sodium oxalate, and COPP et al. (1962) used EDTA injections. With all these methods serum calcium alone was influenced, and regardless of the method the result was, as far Downloaded from vet.sagepub.com by guest on April 14, 2010
Scruin Phosphorus, Calciiiiii, and Alkalinc l’hosphatnsc 73 as the product of calcium and phosphorus is concerned, an /iiidwsut/irated serum. There is no reason to expect that a primary decrease in either ion would increase the other. On the other hand, a primary increase in either ion will decrease the other when the saturation point is reached. Experimental hyperparathyroidism due to hypocalcemia following excessive phosphorus feeding with continuous analyses of serum calcium and phosphorus has been reported in the swine and rat. LIEGEOIS and DERIVALJX (1951) fed pigs diets with calcium to phosphorus ratios varying from 1 : 5.5 to 1 : 11.6. Serum phosphorus rose from the second week through the fifth week and then fell to and remained within normal range. At their height serum phosphorus levels of close to 11 mg. per 100 ml. were recorded as compared to the initial 6.5. Serum calcium remained within normal range for 2 or even 5 weelis, then dropped as low as 6.5 mg. per 100 ml. in one case. Normalization occurred after 7 to 8 weelis. Hyperphosphaturia occurred a short time after the highest serum phosphorus and the lowest serum calcium levels had been observed. Thisexperiment showed the intimate relationship between serum calcium and phosphorus. Excessive phosphorus feeding resulted in hyperphosphatemia and, after some ddq, during which period saturation of serum occurred, serum calcium fell. Once the hyperparathyroidism was induced by hypocalcemia, the effects of increased parathyroid hormone levels influence the relationship between serum calcium and phosphorus, i.e. release of bone mineral, increased solubility of calcium and phosphorus in blood serum, and increased renal excretion of phosphorus. Supersaturation does not invalidate the law of constant ion product. In later stages when hyperphosphatemia is partly or completely compensated for, or even overcompensated for, the ion product may not reach saturation. Changes in one ion are then not reflected in the other, but this, of course, does not contradict the reciprocity of calcium and phosphorus in a saturated solution. ENGFELDT et al. (1 954) induced secondary hyperparathyroidism in rats by feeding diets with excessive amounts of phosphorus in proportion to calcium. They stated, “In our experiment it has not been possible to confirm the existence of a direct correlation between the content of calcium and phosphorus in the diet and the concentration of these substances in the blood. Further, it can be concluded that there is no inverse relationship between the blood-calcium and the blood-phosphorus, as has, previously, been pointed out by others”. Morphologic evidences of parathyroid hyperactivity were observed in rats after 60 Downloaded from vet.sagepub.com by guest on April 14, 2010
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Pathologia Veterinaria Online http:
Page 3 and 4:
Supplementum ad Vol. 1 (1964) Patho
Page 5 and 6:
V . Experimental Nritritional Secon
Page 7 and 8:
Introduction and Object of Investig
Page 9 and 10:
I. The Anatomy of the Parathyroid G
Page 11 and 12:
Comparative Aspects of the Embryolo
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The Aracroscopic Anatomy of the Equ
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The Microscopic Anatomy of the Equi
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'I'hc hlicroscopic Anatomy of the E
Page 19 and 20:
’The I\licroscopic Anatomy of the
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10 . 9 . a . 7 0 + 6 . 5 . 0 ’I
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‘The hl icroscopic Anatomy of the
Page 25 and 26:
’I’hc hlicroscopic Anatomy of t
Page 27 and 28: ‘I’lic ihlrcroscopic Anatomy of
Page 29 and 30: ‘I’hc Alicroscopic Anatomy of t
Page 31 and 32: Discussion 25 7bbic 1 .. Avcragc si
Page 33 and 34: Discussion 27 Table VZZ. Nuclear si
Page 35 and 36: 11. Nutritional Secondary Hyperpara
Page 37 and 38: The Nature of the Osteopathy 31 Fig
Page 39 and 40: ’The Nature of the Osteopathy 33
Page 41 and 42: Etiology 35 Experiments and clinica
Page 43 and 44: Clinical Pathology 37 Table X. Seru
Page 45 and 46: 111. Experimental Nutritional Secon
Page 47 and 48: Ration 41 Table XI/. Calcium and ph
Page 49 and 50: Necrops y 43 6. Necropsy The animal
Page 51 and 52: Clinical Observations 45 During wee
Page 53 and 54: Clinico-pathologic Determinations 4
Page 55 and 56: 90. *. 90. 90. 70. / . Clinico-path
Page 57 and 58: (:linico-pathologic Determinations
Page 59 and 60: Rocntgencilogic Observations 53 Fie
Page 61 and 62: lioentgcnologic Ohscrvntions 55 I,'
Page 63 and 64: Pathologic Anatomy 57 7bb/e XIS. Si
Page 65 and 66: Pathologic Anatomy 59 fhb/c. A’X.
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Page 71 and 72: Pathologic Anatoiny Downloaded from
Page 73 and 74: Pathologic Anatomy 67 Downloaded fr
Page 75 and 76: Pathologic Anatomy 69 Fiq. 37. Cont
Page 77: V. Experimental Nutritional Seconda
Page 81 and 82: Serum Phosphorus, Calcium, and Alka
Page 83 and 84: Serum Phosphorus, Calcium, and Alka
Page 85 and 86: The Parathyroid Glands 79 should be
Page 87 and 88: The Skeleton 81 5. The Skeleton The
Page 89 and 90: The Skeleton 83 ary hyperparathyroi
Page 91 and 92: Summary and Conclusions The thesis
Page 93 and 94: Siimmary and Conclusions 87 Rocntgc
Page 95 and 96: References 89 COILIP, J. B.: 'I'hc
Page 97 and 98: Refereiices 91 ~~CILAN, F. C. and U
Page 99 and 100: Appendix Tables and Statistical Ana
Page 101 and 102: Tables and Statistical Analyses 95
Page 103 and 104: ’Tablcs and Statistical Analyscs
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Nutritional Secondary Hyperparathyroidism in the Horse

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