Page 569 - Small Animal Clinical Nutrition 5th Edition

590 Small Animal Clinical Nutrition

study revealed a lower prevalence of overweight and obese dogs BHD gene. Genetic analysis and pedigree evaluation support
VetBooks.ir with sarcomas and carcinomas, but no difference in distribution this mutation as causative for this cancer (Lingaas et al, 2003).
Point mutations, chromosomal translocations and gene ampli-
of BCS in dogs with round cell tumors compared to controls.
fication occur as spontaneous events in any dividing cell popula-
Overweight or obese body condition in dogs may also influ-
ence the risk of bladder cancer. Investigators have evaluated the tion.These changes accumulate over a lifetime, possibly explain-
role of diet in preventing bladder cancer in Scottish terriers, a ing why many cancers arise in mature or aged individuals.
breed predisposed to the development of transitional cell carci- Carcinogens can be found in many different aspects of the
noma of the urinary bladder. This survey-based study evaluat- environment. The most common biologic agents capable of
ed each dog’s diet for one year before diagnosis and compared inducing cancer are retroviruses, DNA tumor viruses and some
data to that from non-neoplastic counterparts. Results were parasites. Various chemical compounds, some naturally occur-
adjusted for age, sex and weight.There was a statistically signif- ring and some synthetic, are capable of inducing malignant
icant decreased risk of developing transitional cell carcinoma in neoplasia. In most cases, chemical carcinogens require repeated
dogs fed green leafy and yellow-orange vegetables and for dogs administration or exposure to demonstrate an effect. Physical
fed vegetables at least three times per week. Although the risk carcinogens include ultraviolet radiation, ionizing radiation and
of transitional cell carcinoma was lower in dogs fed cruciferous foreign materials (London and Vail, 1996).
vegetables, the finding was insignificant. These results suggest
diet may play a role in the prevention or management of blad- Cancer Cachexia
der cancer (Raghavan et al, 2005). Cancer cachexia is a complex paraneoplastic syndrome that
Currently, there is no common thread or single measurable adversely alters the functional status of the patient (Figure 30-
parameter that defines the population at risk for or experienc- 2). It manifests as weight loss, reduced food intake and systemic
ing cancer. Risk assessment for cachexia and nutritional support inflammation as a consequence of the cancer disease process
for cancer must be tailored to each patient with consideration (Fearon et al, 2006).This syndrome differs from simple starva-
for breed, age, tumor type and other factors. tion in that both protein and fat stores are lost almost simulta-
neously in cachectic patients. Initially in simple starvation, fat
Etiopathogenesis stores are lost preferentially followed later by loss of protein
There are three basic steps that ultimately lead to generation of stores.The time frame for onset of noticeable cachexia-induced
a cancer cell from a normal cell: 1) initiation, 2) promotion and weight loss in dogs and cats with cancer can vary. One survey-
3) progression (London and Vail, 1996). Initiating agents based study examined dogs as they were presented to the oncol-
induce permanent and irreversible changes in the DNA of ogy service (Michel et al, 2004). Body weight before cancer
affected cells. Promoting agents cause reversible tissue and cel- diagnosis was available for 64 of 100 dogs. Twenty-three per-
lular changes up to development of the first autonomous tumor cent had lost more than 10% of their body weight before diag-
cell. Promoting action generally occurs over a long latency peri- nosis. Body condition scoring, however, found only 4% of dogs
od and requires nearly continuous exposure to the promoting with cachexia and 15% with clinically evident muscle wasting;
agent. Progressing agents convert initiated cells, or cells under- 29% were markedly overweight (Michel et al, 2004). Although
going promotion, into cells that exhibit the malignant pheno- body condition scoring and changes in weight are good clinical
type capable of developing into a mature neoplasm. measures of body condition, they do not consider the complex-
Multi-step carcinogenesis occurs through five basic path- ity of factors influencing the cachectic state such as the meta-
ways; more than one pathway may be involved in the genera- bolic alterations that can occur even before any overt clinical
tion of a particular tumor (London and Vail, 1996). The five signs associated with cancer cachexia are identified (Ogilvie
carcinogenic pathways are: 1) heritable, 2) passive, 3) biologic, and Vail, 1996, 1992; Ogilvie and Moore, 1995).
4) chemical and 5) physical. Cancer cachexia may be partly due to negative energy bal-
Although little is known about breed-specific genetic alter- ance secondary to decreased energy intake or altered energy
ations that may predispose domestic pets to develop neoplastic expenditure (Lawson et al, 1982; Dempsey et al, 1984). Inves-
disease, certain breeds of dogs have a higher incidence of can- tigators have found alterations in basal metabolic rate and rest-
cer than others. Recent studies have examined breed-specific ing energy requirement (RER) that were associated with
predispositions to certain types and subtypes of cancer, such as altered carbohydrate, protein and lipid metabolism in human
lymphoma (Modiano et al, 2005). Breeds commonly overrep- patients with cancer cachexia (Lawson et al, 1982; Dempsey et
resented in tumor-bearing cohorts include boxers, rottweilers, al, 1984). Additionally, resting energy expenditure and caloric
German shepherd dogs, Scottish terriers and golden retrievers. requirements are increased in some tumor-bearing people and
Siamese cats appear to be at more risk than other feline breeds. animals when compared to healthy individuals (Dempsey et al,
Perhaps the best characterized genetic mutation suspected to 1986; Hansell et al, 1986; Fredrix et al, 1991; Zyliez et al, 1990;
cause a specific cancer is found in German shepherd dogs with Delarue et al, 1990).
renal cystadenocarcinoma and nodular dermatofibrosis. The Several studies have evaluated energy expenditure in dogs
chromosomal region that overlaps the human Birt-Hogg- with lymphoma and non-hematopoietic malignancies. Dogs
Dubé (BHD) locus responsible for a phenotypically similar with osteosarcoma have been compared to normal beagles to
syndrome in people, showed mutation of exon 7 of the canine evaluate metabolic alterations using indirect calorimetry (rest-