SUPPORTIVE THERAPIES
In dogs with extensive tumor burden, ancillary therapies to minimize the systemic effects of mast cell degranulation should
be implemented. Mast cells are capable of liberating a wide range of preformed and newly synthesized inflammatory mediators,
which can cause marked patient morbidity and mortality. Histamine is one predominant inflammatory mediator released by degranulating
mast cells, so treatment with histamine-blocking agents may decrease the likelihood of undesirable paraneoplastic complications.
Blocking gastric H2 receptors with either cimetidine (5 to 10 mg/kg orally t.i.d. to q.i.d.), ranitidine (1 to 4 mg/kg orally b.i.d. to t.i.d.),
or famotidine (0.3 to 0.6 mg/kg orally b.i.d. to t.i.d.) should be implemented to minimize gastroduodenal irritation from
excessive parietal cell hydrochloric acid secretion. Occasionally, dogs not responding to H2 blockade may benefit from a proton-pump inhibitor such as omeprazole (0.5 to 1 mg/kg orally once a day). Blocking the H1 receptors with diphenhydramine (1 to 4 mg/kg orally t.i.d.) or hydroxyzine (2.2 mg/kg orally t.i.d.) may be indicated to
minimize complications derived from peripheral H1 receptor activation, such as hypotension, bronchospasms, local erythema, swelling, and pain.
CONCLUSION
Although mast cell tumors in dogs were described more than a century ago, our understanding of the etiopathogenesis for malignant
mast cell transformation is constantly expanding. Several treatment options exist for canine cutaneous mast cell tumors. Localized
mast cell tumors are often cured with surgery, radiation therapy, or a combination of the two. Successful management of nonresectable
mast cell tumors may be achieved with combination adjuvant therapies, with many patients experiencing high quality-of-life
scores and long survival times. Most important, the recent discovery of small molecule inhibitors such as SU11654, demonstrating
therapeutic efficacy against cutaneous mast cell tumors, may revolutionize cancer management in companion animals.
Timothy M. Fan, DVM, DACVIM (internal medicine, oncology)
Louis-Philippe de Lorimier, DVM
Department of Veterinary Clinical Medicine
College of Veterinary Medicine
University of Illinois
Urbana, Il 61802
REFERENCES
1. Brodey RS. Canine and feline neoplasia. Adv Vet Sci Comp Med 1970;14:309-354.
2. Patnaik AK, Ehler WJ, MacEwen EG. Canine cutaneous mast cell tumor: Morphologic grading and survival time in 83 dogs. Vet Pathol 1984;21:469-474.
3. Miller DM. The occurrence of mast cell tumors in young Shar-Peis. J Vet Diagn Invest 1995;7:360-363.
4. Gieger TL, Theon AP, Werner JA, et al. Biologic behavior and prognostic factors for mast cell tumors of the canine muzzle:
24 dogs (1990-2001). J Vet Intern Med 2003;17:687-692.
5. Simoes JPC, Schoning P, Butine M. Prognosis of canine mast cell tumors: A comparison of three methods. Vet Pathol 1994;31:637-647.
6. Turrel JM, Kitchell BE, Miller LM, et al. Prognostic factors for radiation treatment of mast cell tumors in 85 dogs. J Am Vet Med Assoc 1988;193:936-940.
7. Bostock DE, Crocker J, Harris K, et al. Nucleolar organiser regions as indicators of post-surgical prognosis in canine spontaneous
mast cell tumours. Br J Cancer 1989;59:915-918.
8. Abadie JJ, Amardeilh MA, Delverdier ME. Immunohistochemical detection of proliferating cell nuclear antigen and Ki-67 in
mast cell tumors from dogs. J Am Vet Med Assoc 1999;215:1629-1634.
9. Zemke D, Yamini B, Yuzbasiyan-Gurkan V. Mutations in the juxtamembrane domain of c-KIT are associated with higher grade mast
cell tumors in dogs. Vet Pathol 2002;39:529-535.
10. Webster JD, Kiupel M, Kaneene JB, et al. The use of KIT and tryptase expression patterns as prognostic tools for canine cutaneous
mast cell tumors. Vet Pathol 2004;41:371-377.
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