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1526  Section 13  Diseases of Bone and Joint

              concentrations are normal. Serum 1,25(OH) 2 D 3  concen­  Radiography can only give a qualitative indication of
  VetBooks.ir  trations may be normal to increased.           bone mineral density (BMD). DEXA or quantitative CT
                                                              is required for a quantitative measurement of BMD.
            Radiography
                                                              mild to moderate decreases in BMD, and would be useful
            The key radiographic change seen in animals with rick­  These techniques are also more sensitive in detecting
            ets is widening and increased lucency of the long bones   for monitoring response to treatment.
            physes (Figure 172.2). A 10‐point radiographic scoring
            method for rickets based on the severity of radiographic   Therapy
            changes in the wrists and knees, to produce a score indi­
            cating the severity of nutritional rickets, has been devel­  Animals with nutritional rickets should be placed on a
            oped for human patients. The key features of this scoring   commercial balanced  diet  with the  recommended 1:1
            system include widening of the growth plate, irregularity   Ca:P ratio and adequate levels of vitamin D. This may be
            of the physeal–metaphyseal interface, and concavity or   supplemented with additional calcium, phosphorus, and
            cupping of the metaphysis. Other radiographic changes   vitamin D as required. Care must be taken with vitamin
            may  include  swollen  costochondral  junctions,  infrac­  D  administration,  as  vitamin  D  is  toxic  at  high  doses,
            tions and other pathologic fractures, delayed appearance   leading to widespread soft tissue mineralization, so regu­
            of ossification centers, curving of long bones, metaphy­  lar monitoring of serum calcium and phosphorus con­
            seal sclerosis, and generalized osteopenia. Stress frac­  centrations is recommended. A recent study found that
            tures and decreased bone density are seen radiographically   treatment with 25OHD increased serum 25OHD faster
            in osteomalacia. In humans, the presence of Looser   than cholecalciferol (vitamin D) treatment, although
            zones is considered consistent with osteomalacia; these   sample numbers were small and a safe dosage was not
            are radiolucent areas surrounded by a zone of sclerosis in   determined. Other vitamin D metabolite options
            the cortex.                                       include dihydrotachysterol, calcitriol (1,25(OH) 2 D 3 ), and
                                                              alfacalcidol.
                                                                Vitamin D 2  or ergocalciferol may be used but large
                                                              doses are required initially, and its long half‐life means
                                                              that if an animal becomes hypercalcemic it takes up to
                                                              four weeks for the effects of ergocholecalciferol to wane.
                                                              Therefore, it is not considered an ideal treatment for
                                                              rickets in dogs and cats.
                                                                Dogs and cats with rickets will benefit from 3–4 weeks
                                                              of confinement in order to prevent further stress and
                                                              microfractures. Pain relief for those with microfractures
                                                              may be helpful.


                                                              Prognosis
                                                              The prognosis for dogs and cats with nutritional rickets
                                                              for return to normality is good, providing catastrophic
                                                              fracture does not occur and the predisposing reason
                                                              (such as malabsorption, total parenteral nutrition) is
                                                              removed. Once the poorly mineralized bone laid down
                                                              during the period of dietary deficiency is replaced
                                                                during remodeling, the bones will return to normal
                                                              strength.
            Figure 172.2  Radiographs of the carpus from a 5‐month‐old
            Pomeranian with hereditary vitamin D‐resistant rickets. There is   Inherited Rickets
            substantial widening of the radial and ulnar physes, irregularity of
            the physeal–metaphyseal interface and cupping of the   Inherited forms of rickets resulting from inborn errors in
            metaphyses. The metaphyseal‐epiphyseal bone of the radius and   metabolism have been diagnosed in both cats and dogs.
            ulna is flared. Source: Reproduced with permission from LeVine   There is confusion in the literature with regard to articles
            DN, Zhou Y, Ghiloni R, et al. Hereditary 1,25 dihydroxyvitamin    on inherited rickets; a number of reported cases are
            D‐resistant rickets in a Pomeranian dog caused by a novel
            mutation in the vitamin D receptor gene. J Vet Intern Med 2009;   more  consistent  with  a  diagnosis  of  nutritional  FOD
            23: 1278–83.                                      than inherited rickets. Care should be taken in making a
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