Page 1587 - Clinical Small Animal Internal Medicine
P. 1587

172  Metabolic Bone Diseases  1525

                 In humans, rickets and osteomalacia are described in   of the reported cases of rickets in the literature, puppies
  VetBooks.ir  patients with gastrointestinal  malabsorption disorders,   were fed a diet of milk and meat. Such a diet would likely
               due to failure to absorb fat‐soluble vitamins such as
                                                                  meet the calcium and phosphorus requirements for the
                 vitamin D, and reduced absorption of calcium. Rickets
                                                                  tion of milk is low.
               has been described in a 17‐week‐old male border collie   animals, but not vitamin D, as the vitamin D concentra­
               with extrahepatic biliary atresia.                   A case of rickets has occurred in a 10‐week‐old
                 Aluminium toxicity from chronic antacid administra­  Shetland sheepdog on a commercial renal failure diet.
               tion or long‐term total parenteral nutrition may also   Such diets are designed to be low in phosphorus and
               cause rickets and osteomalacia in humans.            protein in order to alleviate some of the clinical and bio­
                 Osteomalacia may occur in combination with FOD in   chemical changes associated with the disease. However,
               dogs and cats with chronic kidney disase. Hyperphos­  the  level  of  phosphorus  in  the  diet  fed  to  this  young
               phatemia results in increased plasma FGF23 concentra­  dog  was inadequate for a growing animal, leading to
               tions, leading to inhibition of the renal 1‐alpha‐hydroxylase   phosphorus deficiency and rickets. Similarly, osteomala­
               enzyme, causing decreased production of 1,25(OH) 2 D 3 .   cia has been reported in an adult dog with food allergies
               This combination of osteomalacia and FOD is often   fed an unbalanced elimination ration.
               termed renal osteodystrophy. As mentioned earlier,   Affected animals present with lameness, reluctance to
               while bone changes do occur in adult animals with   walk, and a failure to grow and gain weight. Animals may
               chronic kidney disease, the changes seldom result in   have angular limb deformities, particularly affecting the
               clinical signs.                                    forelimbs. Rickets most commonly affects rapidly grow­
                 Vitamin D also has an important role in the immune   ing physes, such as the distal radius, proximal tibia, distal
               system, and has been associated with many different dis­  femur, and proximal humerus. The metaphyses of long
               eases in both humans and animals. Low serum 25OHD   bones, particularly the distal radius, may be swollen.
               concentrations in dogs have been associated with   Animals may have swollen costochondral junctions,
               immune‐mediated  disorders,  various  types  of  cancer,   known as the rachitic rosary. Affected animals may have
               acute pancreatitis, progression of leishmania, chronic   pathologic fractures, and delayed eruption of teeth and
               enteropathy, chronic valvular heart disease, and poor   enamel  hypoplasia  may also be  seen.  In  animals  with
               outcome in congestive heart failure, while in cats, low   severe hypocalcemia, seizures may be the presenting
               serum 25OHD has been associated with inflammatory   clinical sign.
               bowel disease, intestinal small cell lymphoma, and myco­  Osteomalacia is reported rarely in dogs, and this may
               bacteriosis. However, care should be taken not to overin­  partly be due to the subtlety of the clinical signs. The
               terpret the role of vitamin D in these diseases. Correlation   most common clinical sign of osteomalacia in humans is
               is not causation, and randomized clinical trials are   bone pain, and in older dogs this may easily be mistaken
               required to determine the significance of vitamin D in   as reluctance to move due to chronic degenerative joint
               the pathogenesis of different diseases and whether   disease and not investigated further.
               changes in serum 25OHD are primary or occur second­
               ary to the disease.
                                                                  Diagnosis
                                                                  Biochemistry
               Signalment
                                                                  Animals  with rickets  due to vitamin D deficiency will
               Rickets occurs in young animals and cases of rickets in   have decreased or low normal serum calcium concentra­
               the literature have been reported in 10–14‐week‐old pup­  tion, hypophosphatemia, increased serum alkaline
               pies and kittens. Nutritional rickets has been reported     phosphatase activity, and increased plasma PTH concen­
               most commonly in greyhound litters, presumably because   tration. Serum vitamin D concentrations depend on the
               these animals are more likely to be fed unusual diets.  inciting cause of the rickets. In vitamin D deficiency
                 Rickets is extremely rare in cats, and naturally occur­    rickets, usually both serum 25OHD and 1,25(OH) 2 D 3
               ring nutritional rickets has not been reported in the   concentrations are decreased. However, confusingly in
                 literature.  However,  rickets  has been induced experi­  some cases, the increase in PTH as a result of hypocalce­
               mentally in both cats and dogs fed vitamin D‐deficient   mia leads to increased activity of the renal 1‐alpha‐
               diets.                                             hydroxylase and normal to increased serum 1,25(OH) 2 D 3
                                                                  concentrations.  Despite this, low serum 25OHD indi­
                                                                  cates there is insufficient vitamin D being obtained
               History and Clinical Signs
                                                                  from the diet.
               As with nutritional FOD, animals with rickets usually   In phosphorus deficiency rickets, animals have severe
               have a history of an unusual postweaning ration. In two   hypophosphatemia but serum calcium and 25OHD
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