Nutritional Secondary Hyperparathyroidism in the Horse

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82 Experimental Nutritional Secondary Hyperparathyroidism in the Horse. Table XXII. Weight increases in some mammals Weight (function of birth weight) Birth 8 weeks of age 16 weeks of age Swine* 1 17 40 Dog** 1 8 24 Cat*** 1 7 - Goat** 1 3 5 Horse, Percheron* 1 2.5 3.7 Dairy cattle, Holstein* 1 1.7 2.8 Beef cattle* 1 1.6 2.2 *MUMFORD eta]., 1923; **SPECTOR, 1956; ***ALTMAN and DITTMER, 1962. (1957, 1959) among others]. Within 3 months the bone has almost disappeared. The osteitis fibrosa is of an extreme hypostotic type. Spontaneous cases of hyperostotic osteitis fibrosa have been described in the cat. In the cases described by BAUMANN (1941) and by LIEGEOIS (1946) the swelling of the jawbones was so severe as to interfere with mastication. Dietary data were not presented, but the progress of the disease was much slower than that in the experimental cases just referred to. ii) The importance of age is well known from spontaneous cases in thehorse (Chapter 111), cat,goat, swine, andmonkey [KROOK (1964)l. This is obviously due to the higher normal metabolic rate of bone in young then in old individuals. Old age does not prevent the disease, however [KINTNER and HOLT (1932), among others]. In renal secondary hyperparathyroidism the age factor is also important in the pathogenesis of the changes in bones. Young dogs with congenital renal anomalies more often develop hyperostotic osteitis fibrosa than old dogs with acquired chronic nephropathy [KROOK (1 964)]. iii) Species differences are very obvious. In the goat the great majority of reported cases have shown the hyperostotic type to be present [HINTZE (1909); ROSSWOG (1912); LESBOUYRIES and DRIEUX (1951); TAJIMA and OSHIMA (1951); and general descriptions by M6cs~ (1959), and COHRS (1961)], although the isostotic type may occur [CHRISTELLER (1923)l. The enlargement of the jaw is usually so prominent as to interfer with mastication. The swelling of the maxillary and nasal bones encroaches upon the upper respiratory passages with dyspnea as a result; hence the expressive German term Scbniiffeelkrankbeit (“sniffing disease”). Spontaneous nutritional second- Downloaded from vet.sagepub.com by guest on April 14, 2010
The Skeleton 83 ary hyperparathyroidism in the dog [WEBER (1929)] and in swine [M~CSY (1959) ; COHRS (1961)l again exemplifies hyperostotic osteitis fibrosa. In these two species the condition has been reproduced experimentally. WEBER and BECK (1932) induced J'ch;rziffehankheit in young dogs in 9 to 12 weeks. The dietary calcium to phosphorus ratio was not given; the bone lesions were hyperostotic. LIEGEOIS and DERIVAUX (1951) fed young pigs diets with calcium to phosphorus ratios varying from 1 : 5.5 to 1 : 11.6. Lameness occurred within 3 weeks, and at the end of the seventh week the maxillary swelling was severe enough to cause respiratory difficulties. Monkeys likewise are prone to develop hyperostotic generalized osteitis fibrosa, even with a moderately upset calcium to phosphorus balance in the feed [CORDY (1957); KROOIC and BARRETT (1962)l. In the horse the lesions develop relatively slowly and are usually hyperostotic (Chapter 11) but may be isostotic (this study). In cattle they are usually isostotic [TAMAGAWA (1956)l. The reasons for such species differences may be sought in differences in the normal growth rate (Table XXII). In our study clinical symptoms of general osteitis fibrosa occurred as early as after 12 weeks. Using a similar calcium to phosphorus imbalance in the diet, CRAWFORD and STURGESS (1927) recorded clinical symptoms only after 9 months. The explanation appears to be the age factor: our horses were about one-half year old at the beginning of the experiment; those of CRAWFORD and STURGESS were over 4 years of age. In the experiments by NIIMI (1927) and by NIIMI and AOKI (1927) in which a 1 : 8.1 calcium to phosphorus ratio was used, the high age of the horses seems to be the explanation for the late occurrence of the clinical symptoms, viz., at 5 months. The explanation for the isostotic or slightly hyperostotic osteitis fibrosa in our NSH horses, in contrast to the marked hyperostotic rype reported in other spontaneous and experimental series appears again to be the age factor. A less severe calcium to phosphorus imbalance in the feed of young horses with a normally high metabolic rate would cause a more severe resorption than a more severe imbalance in adult horses with a relatively low metabolic rate in the skeleton. The clinical picture was dominated by lameness. Several authors [VARNELL (1 860) ; LANE (1906); ICINTNER and HOLT (1932); GREENLEE (1939); among others] have described joint changes which would explain the lameness. Because of resorption of trabeculae supporting the articular cartilage, this cartilage loses its support and yields to pressure. VARNELL also described subchondral cysts. Cartilage irregu- 8 Krook/Lowe Downloaded from vet.sagepub.com by guest on April 14, 2010
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Pathologia Veterinaria Online http:
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Supplementum ad Vol. 1 (1964) Patho
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V . Experimental Nritritional Secon
Page 7 and 8:
Introduction and Object of Investig
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I. The Anatomy of the Parathyroid G
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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
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’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
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’I’hc hlicroscopic Anatomy of t
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‘I’lic ihlrcroscopic Anatomy of
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‘I’hc Alicroscopic Anatomy of t
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Discussion 25 7bbic 1 .. Avcragc si
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Discussion 27 Table VZZ. Nuclear si
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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 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: The Skeleton 81 5. The Skeleton The
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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