Nutritional Secondary Hyperparathyroidism in the Horse

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34 Nutritional Secondary Hyperparathyroidism in the Horse Table WII. Dietary calcium and calcium to phosphorus ratio in experimental nutritional secondary hyperparathyroidism in the horse G. Ca/day Ca : P Occurrence of symptoms ratio STURGESS and CRAWFORD (1927) 20.1 1 : 3.1 After more than 9 months NIIMI (1927) 1.5 1 : 8.1 After 5 months NIIMI and AOKI (1927) 2.6 1 : 8.1 After 5 months GROENEWALD (1937) 3.4 1 : 7.0 After 9 months Table ZX. Normal calcium and phosphorus requirement in the horse Growing horses (360 kg. mature weight) 8 months old 19 months old 44 months old Growing horses (540 kg. mature weight) 6 months old 14 months old 44 months old G. &/day Ca : P ratio 17 1.3 : 1 13 1 :1 9 1 : 1 15 1.3 : 1 14 1.2 : 1 11 1 :1 the exception of 22 severely affected animals, all showed improvement within 3 weeks. LANE corrected two other outbreaks in the same manner. INGLE (1909) developed a theory to explain the etiology based on LANE’S study of the disease in South Africa. INGLE was interested in the mineral constituents of horses’ diets, primarily calcium oxide and phosphorus pentoxide. He pointed out that oat hay and Indian corn, the basal diet for many South African horses and mules, resulted in a large excess of phosphorus over calcium. He noted that, although no experiments using diets with high phosphorus in proportion to calcium had been reported in horses, WEISKE (1891) had experimented with such diets in rabbits. Avery light-weight, fragile skeleton resulted. Calcium carbonate added to the diet prevented the fragile bones. INGLE then reviewed LANE’S method for treating the disease and concluded that the results occurred because LANE supplemented the diet with more calcium than phosphorus. INGLE thus concluded that a calcium source alone was needed to treat or prevent nutritional secondary hyperparathyroidism. Downloaded from vet.sagepub.com by guest on April 14, 2010
Etiology 35 Experiments and clinical studies since INGLE’S report have supported him fully. The optimum calcium to phosphorus ratio in the feed is now considered to be 1 : 1 [Natl. Acad. Sci. (1961)l. KINTNER and HOLT (1932) in feeding trials using affected horses found that excessive bone resorption was arrested when the ratio was 1.17 : 1 or above and that excessive resorption progressed when the ratio was decreased to 1 : 1.41 or below. The absolute amounts of calcium and ratios used in the experimental reproduction of the disease are summarized in Table VIII. In above reports as well as in that by KINTNER and HOLT, the ratios of calcium oxide and phosphorus pentoxide were given. The values given in the above list refer to calcium and phosphorus, instead. The normal requirement for the horse [Natl. Acad. Sci. (1961)l is given in Table IX. 3. Occurrence and Breed, Sex, and Age Predsposition Nutritional secondary hyperparathyroidism in the horse has been described, under varying terms, from countries all over the world according to the review by KINTNER and HOLT (1932). Mbcs~ (1959), however, referred to the disease as an “extra-European’’ osteodystrophy, which is surprising because the disease was first described in Switzerland [RYCHNER (1851)l and because the nature of the bone lesions was first revealed, as we have seen, in Germany [JOST (1910)l. The incidence varies considerable. Sporadic cases as well as “enzootic” outbreaks have been reported. STURGESS and CRAWFORD (1927) stated that at least 10% of all horses in Ceylon were affected to some degree. KINTNER and HOLT (1932) reported that about 15% of the U. S. Army horses on native feed in the Philippines were affected in 1930-1931. In the first six months of 1931 no less than 285 cases were diagnosed. The disease accounted for more than one-fourth of all hospitalized horses. YAMAGIWA and SATOH (1956) reported 499 cases from 1951 to 1956 at their pathology department in Japan, which certainly indicates a very high incidence. No breed predisposition has been reported, and sex is not a predisposing factor either. In accordance with the fact that the calcium requirement is higher during pregnancy [Natl. Acad. Sci. (1961)], KINTNER and HOLT (1932) showed that all investigators had agreed “that pregnancy may influence the development and/or the course of Downloaded from vet.sagepub.com by guest on April 14, 2010
Page 1 and 2: 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: ’The Nature of the Osteopathy 33
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 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
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References 89 COILIP, J. B.: 'I'hc
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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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