Nutritional Secondary Hyperparathyroidism in the Horse

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30 Nutritional Secondary Hyperparathyroidism in the Horse disease is hyperparathyroidism, of which there are two main types, primary and secondary. The primary form, caused by parathyroid neoplasia or primary hyperplasia, serves no purpose at all. The resulting generalized osteitis fibrosa is only the regrettable result of an uncontrolledexcessiveparathormone incretion. The primary role of the parathyroid(s) in VON RECKLINGHAUSEN’S disease was established in 1925 with MANDL’S surgical removal of a parathyroid adenoma which resulted in the healing of generalized osteitis fibrosa in a man. Secondary hyperparathyroidism, on the other hand, is of a compensatory nature. It is caused by hypocalcemia [HAM et al. (1940); PATT and LUCKHARDT (1942); STOERK and CARNES (1945); ENGFELDT et al. (1954); among others], and its purpose is to correct this hypocalcemia. The hypocalcemia may be secondary to hyperphosphatemia due to chronic renal insufficiency. Parathyroid hyperplasia of this origin was first described by BERGSTRAND in 1921. In this renal secondary hyperparathyroidism the bone lesions may predominate, especially in young individuals, and misleading terms such as renal rickets, renal dwarfism, and “rubber jaw disease” have therefore been introduced. Hypocalcemia can further result from low calcium feeding or, secondarily, from excessive phosphorus feeding. In both instances parathyroid hyperplasia will occur. If hypocalcemia results from low calcium feeding with normal (or low) phosphorus intake, rickets and generalized osteitis fibrosa may occur simultaneously [MAREK and WELLMAN (1 931)]. If, on the other hand, the hypocalcemia is secondary to excessive phosphorus intake, the ion product of calcium and phosphorus in the blood serum exceeds the normal. In this case the hyperparathyroidism is not accompanied by rickets. Nutritional secondary hyperparathyroidism is not known to cause generalized resorption of bone in man [BERGSTRAND (1956)l. In domesticated animals such a nutritional secondary hyperparathyroidism with generalized osteitis fibrosa, sometimes very severe, is of fairly common occurrence. It has been described in the horse, cow, goat, monkey, pig, dog, and cat. Our concepts of the metabolic bone diseases of the “too little mineralized bone” type are based on relatively recent research. It is therefore not surprising that the nomenclature applied to what should be called “nutritional secondary hyperparathyroidism” has been variable. The disease of horses under consideration has been known since ancient times. Probably it was this disease that was described as “animal osteomalacia” by VEGETIUS about 400 A. D. The first reliable Downloaded from vet.sagepub.com by guest on April 14, 2010
The Nature of the Osteopathy 31 Fig. 17. HAUBNER’S illustration of “osteoporosis of a peculiar nature.” Reproduced from .!Wag. ges. Thierhcilk., 1854. description appears to be that by RYCHNER in 1851. His case was a 2-year-old horse that had developed a slow, troubled chewing which was not related to the second dentition or a tooth disorder. Both maxillae showed a uniform swelling that extended backward to the level of the last molars. The entire mandible evidenced a moderate, diffuse swelling. The hyperostotic bones were somewhat warmer than normal and yielded to pressure. The swelling progressed rapidly, and the hollow percussion sound over the nasal and maxillary sinuses disappeared. The horse was destroyed. On post-mortem examination the skull bones were easily breakable, the cut surface showed multiple cysts filled with a semigelatinous, somewhat hemorrhagic fluid, and the teeth were freely movable in their alveoli. After maceration the 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: 11. Nutritional Secondary Hyperpara
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 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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