Nutritional Secondary Hyperparathyroidism in the Horse

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78 Experimental Nutritional Secondary Hyperparathyroidism in the Horse. . . greater and greater degree. Whether this initial resorption is brought about by some irritation of the osteocytes by the parathyroid hormone to cause RUTISHAUSER’S osteolysis or by stimulation of osteoclastic resorption is of minor importance in this connection. Regardless of the type of resorption, increased alkaline phosphatase levels will occur in blood serum. As the resorption continues, the hypocalcemia is gradually compensated for and the demand for calcium decreases. When, during the 23rd week of our experiment, hypocalcemia was induced once more by means of still greater phosphorus intake, the processes were repeated, both the decrease-increase in serum calcium and the increase-decrease in serum alkaline phosphatase. KINTNER and HOLT (1932) in single determinations in horses with nutritional secondary hyperparathyroidism found that serum calcium averaged 9% lower and serum phosphorus averaged 20% higher than in normal horses. GROENEWALD (1937) found no changes at all in a very limited number of horses. These reports emphasize the necessity of repeated determinations over a long period of time. It is quite possible to record almost normal values for serum calcium, phosphorus, and alkalinephosphatase evenwithsevere lesions of generalized osteitis fibrosa present. In our NSH horses serum phosphorus never returned to normal, whereas the calcium values came very close to the original ones after 23 weeks, just before the phosphorus intake was increased. 3. Roentgenologic Changes The roentgenologic changes, which grew quantitatively worse, were qualitatively similar to those described by KINTNER and HOLT (1932) and GROENEWALD (1937). The changes occurred at the same time as clinical symptoms were apparent. This relatively late appearance of radiographic changes is not surprising. ALBRIGHT and REIFENSTEIN (1948) stated that at least 30% of the bone minerals must be removed to cause changes in the roentgenogram. Nevertheless, great importance must be ascribed to the roentgenologic examination. Roentgenograms showed that the changes occurred earlier in the mandibles than in the metacarpus. The series of roentgenograms further showed that the changes progressed more rapidly and were more severe in the mandible than in the metacarpus. This is of direct clinical importance. In cases of lameness, when roentgenographic changes of limbs suggest excessive bone resorption, the mandible Downloaded from vet.sagepub.com by guest on April 14, 2010
The Parathyroid Glands 79 should be radiographed routinely. With the method we found to be superior, viz., a ventrodorsal view of the rostra1 end of the mandible, a positive or negative diagnosis of osteitis fibrosa should offer no great difficulties. The resorption of the laminae durae dentes is considered almost specific for generalized osteitis fibrosa since it does not occur in rickets or osteomalacia or even in advanced cases of osteoporosis [ALBRIGHT and REIFENSTEIN (1 948)]. 4. The Parathyroid Glands The weight increase, the morphology, and the functional evaluation of the parathyroid glands have conclusively shown parathyroid hyperplasia and cellular hypertrophy. Regarding the cell types the changes occurring in nutritional secondary hyperparathyroidism in the horse were disappearance of dark chief cells, predominance of light chief cells, and an increase in water-clear cells. Judging from the cytoplasm to nucleus ratio and the size of the nucleus of the dark and light chief cells, the latter indicate a more active state [EGER and VAN LESSEN (1954)l. The morphology of the light chief cells of NSH horses differed from that of the control and of the normal horses of Chapter I. The cells had undergone pronounced hypertrophy, the nucleus was significantly enlarged, and a corresponding increase in the cytoplasm was evidenced by an unchanged cytoplasm to nucleus ratio. EGER and VAN LESSEN (1954) also concluded that the small waterclear cells are the most active parathyroid cells and that the large water-clear cells represent early degeneration. CASTLEMAN and MALLORY (1935, 1937) stated that in primary hyperplasia of the parathyroids in man “a uniform direction of differentiation of all cells to the large water-clear cell type is the invariable finding”, whereas in renal secondary hyperplasia “such uniformity is lacking. Here the glands are composed almost completely of normal-sized chef cells, although a few small water-clear cells are occasionally present.” With regard to the functional state of the water-clear cells they wrote (1935) : “When the whole gland is composed of these cells, as in some cases of nephritis and hypertension, it is felt that hyperplasia is definite.” The intermediate stages during the transformation of light chief cells offer some information on the functional state of the end product, the large water-clear cell. The first thing that happens is a coalescence 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
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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
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 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: Serum Phosphorus, Calcium, and Alka
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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