Background There is a paucity of veterinary literature on the safety or outcome of zoledronic acid (ZA) use in dogs for either bone pain or hypercalcemia. Hypothesis/Objectives The primary aim was to report the adverse events in dogs receiving intravenous administration of ZA. Animals Ninety‐five dogs with ZA use. Methods A retrospective cohort study was performed; all dogs that received at least 1 dose of ZA and had a serum biochemistry profile performed before and after treatment were reviewed. Diagnosis, indication for treatment, adverse events and survival times were recorded. Results Ninety‐five dogs met the inclusion criteria. Thirty‐one (33%) received multiple intravenous infusions of ZA (range, 2‐7), making a total of 166 administrations in all dogs. The dose range was 0.13 to 0.32 mg/kg, given at intervals of 4 to 6 weeks. Thirteen adverse events were recorded in 10 dogs: azotemia (n = 8), vomiting (n = 2), pancreatitis (n = 1), cutaneous ulceration (n = 1), and diarrhea (n = 1). Zoledronic acid could not be confirmed as the cause of azotemia in any case. The change in serum creatinine concentration from dose to dose was not related to the total dose received ( P = .46). Five dogs (5%) changed Veterinary Comparative Oncology Group Common Terminology Criteria (VCOG‐CTAE) renal/genitourinary grade after administration of ZA; their total dose 0.4 mg/kg (range, 0.26‐0.66) was not significantly different to the group which did not change VCOG‐CTAE renal/genitourinary grade 0.35 mg/kg (range, 0.2‐1.50; P = .93). Conclusions and Clinical Importance Multiple doses of ZA were well tolerated in dogs within this study. A small number of dogs developed progressive azotemia which was not associated with cumulative dose.
A 10‐year‐old crossbreed (labradoodle) was presented with an acute history of vomiting and diarrhoea, with supraventricular tachycardia and ventricular premature complexes. Physical examination revealed mild tachycardia, but no significant abnormalities otherwise. Investigations with echocardiogram and computed tomography identified a right atrial mass, nodular interstitial lung pattern, multiple nodules throughout the hepatic parenchyma and peritoneal effusion. Abdominocentesis confirmed a haemoabdomen. Treatment was declined and the dog was euthanased the same day. Histopathology of the cardiac mass confirmed a cardiac myxoma, which stained Alcian blue‐positive, demonstrating the mucin content of the tumour. The hepatic lesions were factor VIII‐positive, consistent with a visceral haemangiosarcoma.
Biopsies from 92 dogs with TCC were routinely processed for histopathology and graded into low grade or high grade, according to Meuten & Meuten (2017). DNAisolation from paraffin embedded material was performed with the use of commercially available sets. Exon 15 was examined for the presence of the BRAF variant c.1784T > A by TaqMan ® SNP Assay. RESULTS 64/92 TCCs were classified as high grade and 28/92 as low grade. BRAF mutation was found in 33/64 (51.5%) of the high grade and in 12/28 (42.8%) of low grade TCCs. STATEMENT (CONCLUSIONS) BRAF variant analysis is a new, highly specific diagnostic test for TCC. However, it is important to note that only identification of the mutation is diagnostic. It must be taken into consideration that histologically low grade TCCs showed the mutation in only about 40% of the cases. Further studies of clinical outcome are ongoing to evaluate the prognostic relevance of this finding. Additional factors, such as breed and anatomical site of the neoplasm may also influence the prevalence of BRAF mutation.
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