Glycogen storage disease type Ia (GSDIa; von Gierke disease; MIM 232200) is caused by a deficiency in glucose-6-phosphatase-a. Patients with GSDIa are unable to maintain glucose homeostasis and suffer from severe hypoglycemia, hepatomegaly, hyperlipidemia, hyperuricemia, and lactic acidosis. The canine model of GSDIa is naturally occurring and recapitulates almost all aspects of the human form of disease. We investigated the potential of recombinant adeno-associated virus (rAAV) vector-based therapy to treat the canine model of GSDIa. After delivery of a therapeutic rAAV2/8 vector to a 1-day-old GSDIa dog, improvement was noted as early as 2 weeks posttreatment. Correction was transient, however, and by 2 months posttreatment the rAAV2/ 8-treated dog could no longer sustain normal blood glucose levels after 1 hr of fasting. The same animal was then dosed with a therapeutic rAAV2/1 vector delivered via the portal vein. Two months after rAAV2/1 dosing, both blood glucose and lactate levels were normal at 4 hr postfasting. With more prolonged fasting, the dog still maintained near-normal glucose concentrations, but lactate levels were elevated by 9 hr, indicating that partial correction was achieved. Dietary glucose supplementation was discontinued starting 1 month after rAAV2/1 delivery and the dog continues to thrive with minimal laboratory abnormalities at 23 months of age (18 months after rAAV2/1 treatment). These results demonstrate that delivery of rAAV vectors can mediate significant correction of the GSDIa phenotype and that gene transfer may be a promising alternative therapy for this disease and other genetic diseases of the liver.

Iron is an essential element for nearly all living organisms and disruption of iron homeostasis can lead to a number of clinical manifestations. Iron is used in the formation of both hemoglobin and myoglobin, as well as numerous enzyme systems of the body. Disorders of iron in the body include iron deficiency anemia, anemia of inflammatory disease, and iron overload. This article reviews normal iron metabolism, disease syndromes of iron imbalance, diagnostic testing, and treatment of either iron deficiency or excess. Recent advances in diagnosing iron deficiency using reticulocyte indices are reviewed.

Myelography and magnetic resonance imaging (MRI) were performed on a 4‐year‐old neutered female Rottweiler with bilateral pelvic limb paresis. On the myelogram, there was extradural spinal cord compression at the level of the Tll‐12 intervertebral disc. Inadvertent placement of epidural contrast medium also allowed identification of a 1‐cm circular filling defect in the epidural space dorsal to the compressed spinal cord. MRI showed partial loss of the nucleus pulposus signal of the T11–12 disc, a focal signal void within the vertebral canal at T11 compatible with a free disc fragment, and extradural masses compressing the spinal cord at T10–11 and T11–12. Hemorrhage within the masses was confirmed on T2*‐weighted images. A mixture of hematoma and mineralized disc material was found at surgery, and there was no histopathologic evidence of neoplasia. In this article, the appearance on MRI of hemorrhage associated with intervertebral disc herniation is discussed.

Tracheal collapse is common in middle age toy and miniature breed dogs. Cartilaginous defects have been identified histologically and are considered a form of chondromalacia. In addition to tracheal cartilaginous changes, concurrent lower airway histologic changes indicative of inflammation have been noted in dogs with tracheal collapse and these changes may lead t o concurrent bronchiectasis. The purpose of this study was to investigate the prevalence of bronchiectasis in dogs with a previous radiographic diagnosis of tracheal collapse. The thoracic radiographs of 60 dogs with tracheal collapse were evaluated for evidence of concurrent bronchiectasis. Eighteen of 60 (30%) dogs had evidence of bronchiectasis, and all were cylindrical in morphology. The signalment of affected dogs was similar to that previously reported. The occurrence of bronchiectasis in this group of dogs with tracheal collapse (18 dogs) was six times higher (P < 0.05) than the expected prevalence within a random sample population (three dogs). The results of this study provide evidence of a link between tracheal collapse and bronchiectasis. A finding of bronchiectasis with tracheal collapse should encourage further evaluation for chronic lower airway disease in these patients.

BackgroundThe urine protein:creatinine ratio (UPC) is used to quantify urine protein excretion and guide recommendations for monitoring and treatment of proteinuria.Hypothesis/ObjectivesHome urine samples will have lower UPCs than hospital samples. The objectives were to compare UPCs of samples collected in each setting and to determine whether environment of sample collection might affect staging, monitoring or treatment recommendations.AnimalsTwenty‐four client‐owned dogs.MethodsProspective, nonmasked study. Clients collected a urine sample from their dog at home and a second sample was collected at the hospital. Dogs receiving corticosteroids or angiotensin‐converting enzyme inhibitors were excluded, as were those with urine samples of inadequate volume, no protein on dipstick analysis, or active urine sediment. Samples were refrigerated after collection, dipstick and sediment evaluations were completed and each sample was frozen at −80°C within 12 hours. UPCs were performed on frozen samples within 2 months.ResultsFrom 81 paired samples, 57 were excluded. Of the remaining 24, 12/24 (50%) had higher hospital sample UPCs, 9/24 (38%) had identical UPCs, and 3/24 (12%) had lower hospital UPCs. The UPCs of hospital samples were higher than home samples for the total population (P = .005) and the subset with UPC > 0.5 (P = .001).ConclusionsSetting and related circumstances of urine collection in dogs is associated with UPC differences; results are usually higher in hospital than in home samples. This difference has the potential to affect clinical interpretation.