Nutritional Secondary Hyperparathyroidism in the Horse

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50 Experimental Nutritional Secondary Hyperparathyroidism in the Horse. 6- 6. 4’ 4. Chart 8. Serum alkaline phosphatase in experimental nutritional secondary hyperparathyroidism. Phosphatase in sigma units on Y-axis, weeks on X-axis. Experi- mental animals as in Chart 5. Downloaded from vet.sagepub.com by guest on April 14, 2010
(:linico-pathologic Determinations 51 a) A diet with a calcium to phosphorus ratio of 1 : 3.68 immediately caused hyperphosphatemia. 13) Serum calcium first increased slightly and then decreased (NSH 1 and NSH 3) or decreased immediately (NSH 2). Hyperphosphatemia and hypocalcemia progressed for about 10 weelis. c) Clinicopathologic evidences of hyperparathyroidism were manifest at the 11th week (NSH 1 and 3) or at the 13th week (NSH 2). At week 11 the serum P dropped in NSH 1 and 3. In NSI-I 2 this did not occur, but the progressing hyperphosphatemia was partly arrested. As the serum phosphorus started to decrease, a rise in serum calcium occurred. During the next phase, covering the period from week 12 to week 23, serum phosphorus increased until it reached maximum and then decreased rapidly. During the same period serum calcium rose all the time, although compensation was not complete. At the end of this period the dietary calcium to phosphorus ratio was decreased from 1 : 3.68 to 1 : 6.19. Serum phosphorus then increased from week 23 through week 30, whereas serum calcium decreased during the same period of time. At week 30 the serum calcium reached its second minimum. The hyperparathyroidism now caused decreasing serum phosphorus and increasing serum calcium levels in all NSH horses. d) The product of total serum calcium and serum phosphorus described a triphasic curve over the experiment. The curves of these products were similar to those of serum phosphorus. The sequence of events was: i) Increase; hyperphosphatemia greater in degree than hypocalcemia. ii) Decrease ; hypocalcemia of relatively greater degree than hyperphosphatemia, which showed a temporary and partial compensation. iii) Increase; both phosphorus and calcium increasing; maximum product reached after 16, 20, and 20 weelis in NSH 1, 2, and 3, respectively. iv) Decrease ; hyperphosphatemia compensated for to a greater degree than hypocalcemia. In the middle of this phase the dietary ratio of calcium and phosphorus was decreased, resulting in increasing serum phosphorus levels but in still lower serum calcium levels; net result, thus, decreased product. 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
Page 13 and 14: The Aracroscopic Anatomy of the Equ
Page 15 and 16: The Microscopic Anatomy of the Equi
Page 17 and 18: 'I'hc hlicroscopic Anatomy of the E
Page 19 and 20: ’The I\licroscopic Anatomy of the
Page 21 and 22: 10 . 9 . a . 7 0 + 6 . 5 . 0 ’I
Page 23 and 24: ‘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: 90. *. 90. 90. 70. / . Clinico-path
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 and 78: V. Experimental Nutritional Seconda
Page 79 and 80: Scruin Phosphorus, Calciiiiii, and
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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