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10 hpf) is associated with outcome, though the appropriate cutoff value is not known. Ki67 staining is also associated with prognosis.
· KIT labelling pattern appears to be associated with prognosis as for dogs
· Multiple lesions: Unlike in dogs, multiple cutaneous tumours are associated with splenic involvement and worse outcomes than solitary tumours in cats in some studies, though other studies found no effect on prognosis.
· HIstologic margins may not predict recurrence, though evaluation of this factor in a group
of ‘high-risk’ MCT may be of more clinical significance.
· Recurrent tumours may be associated with a worse prognosis
I currently recommend evaluation of local lymph nodes in every cat and abdominal ultrasound and buffy
coat assessment in cats with multiple or high mitotic index MCT. For tumours with aggressive growth, more aggressive surgery is warranted, but given the benign behaviour of the majority of feline cutaneous MCT surgical margins of 1-2 cm seem reasonable.
· Splenic MCT may be solitary or associated with cutaneous tumours. Involvement of the liver
and bone marrow/peripheral blood is common. Splenectomy is the treatment of choice, even if liver involvement or mastocytemia is documented, as it is associated with the longest survival times (> 1 year median). The addition of chemotherapy should be considered for cats with evidence of more distant disease (liver involvement, persistent mastocytemia), though the best protocol, and whether or not it impacts outcome, is not known.
· Intestinal: Prognosis was previously thought to be poor because of extensive disease at diagnosis but a recent study suggests that the behaviour of these tumours is extremely variable. Based on this, my current recommendation is for surgical excision if possible. Chemotherapy could be considered for metastatic or unresectable tumours.
Systemic treatment in feline MCT:
Response rates of approximately 50-80% to CCNU and to toceranib are reported, and there are anecdotal/ case reports of responses to other such as vinblastine, chlorambucil and imatinib. For cats with gross disease, it would seem reasonable to start with CCNU or toceranib and consider the other drugs as alternatives if a good response was not seen.
References:
1. Krick EL, Billings AP, Shofer FS, Watanabe S, Sorenmo KU Cytological lymph node evaluation in dogs with mast cell tumours: association with grade and survival Vet Comp Oncol 2009;7:130-138
2. Weishaar KM, Thamm DH, Worley DR, Kamstock DA Correlation of nodal mast cells with clinical outcome in dogs with mast cell tumour and a proposed classification system for the evaluation of node metastasis J Comp Pathol 2014;151:329-338
3. Kry KL, Boston SE. Additional local therapy with primary re-excision or radiation therapy improves survival and local control after incomplete or close surgical excision of MCTs in dogs Vet Surg 2014;43:182-189
4. Miller RL, van Lelyveld S, Warland J, Dobson JM, Foale RD A retrospective review of treatment and response of high-risk MCTs in dogs Vet Comp Oncol 2016;14:361-370
WSV18-0091
GENETICS
WHAT PRACTITIONERS SHOULD KNOW ABOUT THE GENETICS OF HIP DYSPLASIA
J. Bell1
1Tufts Cummings School of Veterinary Medicine, Department of Clinical Sciences, N. Grafton- MA, USA
WHAT PRACTITIONERS SHOULD KNOW ABOUT THE GENETICS OF HIP DYSPLASIA
Jerold S Bell DVM, Adjunct Professor of Clinical Genetics
Tufts Cummings School of Veterinary Medicine, N. Grafton, MA USA
jerold.bell@tufts.edu
Canine hip dysplasia is a complexly inherited disorder that is seen in wolves and across all purebred and mixed-breed dogs. It is the number one cause of arthritis in all dogs. We observe this disorder in clinical practice as; hip pain/stiffness, decreased range of motion, altered hind limb gait, and later arthritis.
The diagnosis of hip dysplasia is through the phenotypic evaluation of the hips. While palpation may reveal
laxity or crepitus, the standard for diagnosis is through hip radiographs. The hip-extended ventrodorsal
hip radiograph under general anesthesia is the accepted standard in most of the world. Radiographic evaluation includes; subluxation, shallow acetabulae, bony remodeling – especially at the dorsal rim of
the acetabulum and femoral neck, and osteoarthritic changes. Different countries have different hip grading systems, including the OFA, BVA/KC, and FCI. PennHIP measures the difference between a hip compressed and hip distracted view and generates a distraction index (DI) representing passive laxity of the hip. The Dorsolateral Subluxation (DSL) test generates a score using a dorsoventral radiograph with the hips flexed and bearing weight at the stifles on the x-ray table. DSL is mostly used as a research tool and is not widely utilized in genetic screening.
The age of assessment for hip dysplasia is important, as it is not a congenital disorder and develops over time. PennHIP recommends evaluation for laxity beyond 4 months of age. The DSL test is recommended after 8 months of age. The BVA/KC and FCI require dogs to be 1 year of age. The OFA used to certify hips at 1 year of age, but found that 95% accuracy of diagnosis only occurred after 2 years of age. PennHIP describes an accurate early age diagnosis of hip dysplasia, but a study of early- age OFA preliminary ratings show a similar predictability. All of the different radiographic evaluations for hip dysplasia measure phenotypic aspects, and are all found to be correlated to each other.
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