Nutritional Secondary Hyperparathyroidism in the Horse

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86 Summary and Conclusions Part 11. Nutritional Secondary Hyperparathyroidism in the Horse Hyperparathyroidism was induced in three young horses by feeding them a diet with optimal calcium contents but with exccssive amounts of phosphorus. Wheat bran and sodium phosphate were used as additional phosphorus sources. A calcium to phosphorus ratio of 1 :3.68 was used during the first 23 weeks of the experiment and a ratio of 1 :6.19 during the last 18 weeks. The following observations and conclusions were made: I. Clinical Sympioms Insidious shifting lameness appeared from week 12 and progressed eon- tinuously. At the same time a "cardboard" sound occurred on percussion of the sinuses and it incrcased in degree likewise. Mild enlargement of the jawbones appeared later in the experiment. One horse suffered a distal epiphysiolysis of the radius. 2. Clinico-pathologic Obseruaiion.< All horses responded immediately with hyperphosphatemia, the severity of which varied in the horses. A corresponding hypocalcemia resulted, establishing the inverse relationship between calcium and phosphorus in saturated blood serum. Hypocalcemia induced hyperparathyroidism, the biochemical evidences of which appeared during the 11th week. A gradual, aIthough incomplete, compensation for the hypocalcemia occurred during the following 12-week period. The changes in scrum phosphorus during this period were decrease, increase, decrease. The decreasing values were interpreted as expressions of increased renal excretion of phosphorus due to hyperparathyroidism, whereas the increase, which occurred simultaneously with rising serum calcium levels, occurred in accordance with the supersaturating factor of the parathormone as discovercd by &{CLEAN et al. (1946). At the end of this period thc phosphorus intake was increased. Once again the serum phosphorus increased and serum calcium decreased. After 8 weeks the hyperparathyroidism overcame even this excessive dietary phosphorus, and partial compensation for hyperphosphatemia and hypocalcemia began. The inverse relationship bctwcen serum calcium and phosphorus was thus showm to hold true in supersaturated serum. Serum alkaline phosphatasc was inversely related to serum calcium; with each decrease in serum calcium an increase in serum alkaline phosphatase occurred, and vice versa. In accordance with the concepts of RUTISIIAUSER and his associates (1951), viz., that alkaline phosphatasc is not only the enzyme of bone apposition but also of bone resorption, the changes in serum alkaline phosphatase were interpreted as indicative of the degree of bone resorption. Downloaded from vet.sagepub.com by guest on April 14, 2010
Siimmary and Conclusions 87 Rocntgcnographic changes consisted of progrcssivc radiolucency and gra- dually appearing coarse tralicculation and miliary mottling of bonc. ‘The appcar- ance of these changes coincided with the clinical symptoms. The changes occurred first and rcachcd the most severe degrec in the mandible. A rcntrodorsal view of thc rostra1 cnd of the mandible, obtaincd by placing a nonscreen film in thc mouth of the animal, was found to be thc method of choice. ‘The rocntgcnograms wcre thus of limitcd value in thc detcction of carly bonc changes in nutritional secondary hyperparathyroidism, but thc importance of roetitgcnologic cxamination of the niandible iii cstablishing a diagnosis of Scncralizcd ostcitis fibrosa in clinical cases of lamcncss bascd on csccssivc bonc resorption xvas emphasized. 4. Necr0p.y 0b.rcrvafion.r ’T’hc parathyroid glands cshibitcd advanccd hypcrr rophy and liylmplasia die degree of which was directly proportional to thc degrec of hypocalccmia. No dark chief cclls werc prcsent. Thc histologic picture was dominated by very hypcr- tropliic light cliicf cclls. The numhcr of water-clear cells was markedly incrcascd. Oxyphil cclls did not occur. Bccausc of the dccrcascd sizc of the nucleus, the incrcascd cytoplasm to nucleus ratio, the staining propcrties of the cytoplasm, aid the increased nuinbcr of juxtanuclear bodics in the cytoplasm, the watcr-clear cclls xvcre interpretcci as cshaustcd cclls. Thc skeleton showed generalized ostcitis fibrosa to a degree corresponding to the parathyroid hypcrtrophp and hyperplasia of the different horses. Sites of predilection of osteoclastic rcsorption were as follo\cs: cancellous bone of the skull; cancellous bone of thc ribs and metaphvses of long bones; uuter circum- fcrential lamellac of long bones ; I-lavcrsian systems of compact bone including compact bone coating canccllous bonc; interstitial lainellac of compact bonc. In thc jawbones thc changes were of a inidly hypcrostotic type, but the classical external appearance of “highcad” was not prcscnt. With vcry much accelerated resorption processes, the fibrosis and ostwid apposition, which is thc morphologic basis for thc swo!len facc, did not have time to dcvclop niarkedly. Resorption of tbc outer circ,unifcrential lamcllac of cortical bone with loss of osscous support for the pcriosteuni was dcsigimtcd as of spccial importance in the pathogcncsis of lamcncss in nutritional secondary hypcrparathyroiclisin in the I70rsc. 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
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The Nature of the Osteopathy 31 Fig
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’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 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: Summary and Conclusions The thesis
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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