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Abstract

Objective

To determine whether apparently resting dogs with nonhematopoietic malignancies have increased resting energy expenditure (REE), compared with clinically normal dogs.

Animals

46 client-owned dogs with nonhematopoietic malignancies and 30 client-owned dogs that were clinically normal.

Procedure

Apparently resting, client-owned dogs with nonhematopoietic malignancies before (n = 46) and 4 to 6 weeks after (n = 30) surgical removal of tumors were compared with apparently resting, clinically normal, client-owned dogs (n = 30). An open flow indirect calorimetry system was used to determine the following: rate of oxygen consumption (ml/min/kg of body weight); rate of carbon dioxide production (mls/min/kg), REE (kcal/kg/d), and respiratory quotient. Because of the wide range of body weight, REE and oxygen consumption were also expressed per kg of body weight0.75.

Results

Surgical removal of the tumor did not significantly alter any of the variables measured when all dogs with tumors were assessed as a single group, or when the dogs were divided on the basis of having the following types of tumors: carcinomas and sarcomas, osteosarcomas, and mammary adenocarcinomas. None of the data obtained prior to surgical treatment from any of the dogs grouped by tumor type were significantly different from clinically normal dogs.

Conclusions

REE (54.4 ± 16 kcal/kg/d or 125 ± 19 kcal/kg0.75/d) and, presumably, caloric requirements of dogs with nonhematopoietic malignancies are not significantly different from those obtained from clinically normal dogs (53.9 ± 16 kcal/kg/d or 116 ± 32 kcal/kg0.75/d). Furthermore, these variables do not change significantly when the tumor is excised and the dog is reassessed after 4 to 6 weeks.

Clinical Relevance

Knowledge that REE in dogs with solid tumors is not significantly different from REE of clinically normal dogs may be of value when planning nutritional treatment for dogs with nonhematopoietic malignancies. (Am J Vet Res 1996;57:1463-1467)

Free access
in American Journal of Veterinary Research

Abstract

Objective

To determine whether alterations in carbohydrate metabolism exist in dogs with nonhematopoietic malignancies but without evidence of weight loss or cachexia.

Animals

90 dogs with nonhematopoietic malignancies and 18 control dogs.

Procedure

An intravenous glucose tolerance test was done in 90 dogs with previously untreated nonhematopoietic malignancies and in 18 clinically normal dogs. These dogs also had no evidence of unrelated diseases that would affect glucose metabolism. None of the dogs had evidence of cachexia. Samples were assayed for glucose, lactate, and insulin concentrations. This procedure was repeated for 45 of the tumor-bearing dogs from which all gross evidence of tumor was completely excised and evidence of diseases that would alter carbohydrate metabolism did not exist.

Results

The mean of all time points during the intravenous glucose tolerance test (ie, 0, 5, 15, 30, 45, and 60 minutes) for lactate (12.9 ± 6.7 mg/dl) and insulin (69.1 ± 44.9 µU/ml) concentrations in untreated dogs with nonhematopoietic malignancies were significantly higher than values for controls (lactate, 9.7 ± 4.3 mg/dl; and insulin, 31.7 ± 11.5 µU/ml). This increase in lactate and insulin values did not return to normal when the dogs were rendered free of all observable evidence of cancer after surgery.

Conclusions

Carbohydrate metabolism is altered in dogs with a variety of nonhematopoietic malignancies and these abnormalities do not abate when dogs are rendered free of gross evidence of malignant disease after surgery.

Clinical Relevance

Alterations in carbohydrate metabolism may result in decreased quality of life and may be associated with the paraneoplastic syndrome, cancer cachexia. (Am J Vet Res 1997;58:277–281)

Free access
in American Journal of Veterinary Research

Summary

Energy expenditure (ee) was determined, using an open-flow indirect calorimetry system in a group of 20 clinically normal, apparently resting, client-owned dogs. Five evaluations were performed over an 8-hour period to determine reliability of the method. The intraclass correlation coefficient was calculated as the ratio of within- and between-subject variances, using repeated-measures anova. When only the middle 3 evaluations were included, the intraclass correlation coefficient was 0.87, indicating good reliability. The first evaluation was higher than the subsequent 4 evaluations for rate of O2 consumption (Vo2/kg and Vo2/kg0.75; (P ≤ 0.01), and ee/kg and ee/kg0.75 (P ≤ 0.005). The respiratory quotients at the first (P = 0.004) and second (P = 0.013) evaluations were different from the respiratory quotient at the fourth evaluation. Therefore, the first evaluation may not be representative of the actual ee. The mean value of at least 3 subsequent evaluations after an adequate adaptation period (5 to 10 minutes) to the equipment will be useful for predicting energy requirements of apparently resting, clinically normal dogs.

Free access
in American Journal of Veterinary Research

Summary

Forty-four dogs with histologically confirmed malignant tumors were used in a prospective study to determine the toxicity of the chemotherapeutic agent mitoxantrone, when administered at dosages higher than what has been previously reported for use in dogs. After each dose was administered, dogs were evaluated for signs of toxicosis for 3 weeks or until the dog developed progressive disease, died, or was euthanatized. Forty dogs had been refractory to 1 or more treatment modalities (surgery, n = 26; chemotherapy other than mitoxantrone, n = 17; radiation, n = 2) prior to entering this study. Ten dogs were given mitoxantrone at a dosage of 5.5 mg/m2 of body surface, IV, every 3 weeks (39 total doses); 11 were given mitoxantrone at a dosage of 6.0 mg/m2, IV, every 3 weeks (26 total doses); and 23 were given mitoxantrone at a dosage of 6.5 mg/m2, IV, every 3 weeks (70 total doses).

The most common signs of toxicosis were vomiting, anorexia, diarrhea, lethargy, and sepsis secondary to myelosuppression. Two dogs, both of which received the highest dosage, died of complications attributable to mitoxantrone administration. The prevalence of toxicoses was not associated with age, breed, sex, tumor type, number of doses, or dosage. Dogs did develop myelosuppression 7 days after they were given mitoxantrone. Median neutrophil count for dogs that received mitoxantrone at a dosage of 6.5 mg/m2 was 2,800 cells/μl (range, 300 to 4,600 cells/μl); median neutrophil count for dogs that received mitoxantrone at a dosage of 6.0 mg/m2 was 3,800 cells/μl (range, 600 to 10,400 cells/μl); and median neutrophil count for dogs that received mitoxantrone at a dosage of 5.5 mg/m2 was 4,500 cells/μl (range, 1,700 to 16,100 cells/μl).

Free access
in Journal of the American Veterinary Medical Association

Summary

Serum α1-acid glycoprotein (α1 ag) concentrations were determined in 55 dogs with previously untreated, histologically confirmed, high-grade lymphoblastic lymphoma, and in 34 dogs with histologically confirmed nonhematopoietic malignancies (13 dogs with carcinomas and 21 dogs with sarcomas). Serum concentrations were again determined in 32 dogs with lymphoma that were in complete remission 3 weeks after 1 dose of doxorubicin (30 mg/m2 of body surface, iv) and in 22 dogs that were still in complete remission 3 weeks after a fourth dose of doxorubicin. For comparison, serum α1 ag concentrations were measured in 19 clinically normal (control) dogs of similar weight and age. Eight of the control dogs were given 1 dose of doxorubicin (30 mg/m2, iv), and serum α1 ag concentrations were measured 3 weeks later.

In control dogs, mean serum α1 ag concentration after treatment with doxorubicin was not significantly different from mean concentration before treatment. Mean α1 ag concentrations in untreated dogs with lymphoma, in dogs with sarcomas, and in dogs with carcinomas were all significantly higher than mean concentration for untreated control dogs. In addition, the mean concentration for dogs with osteosarcomas was significantly higher than mean concentration for untreated control dogs. There were no significant differences in mean serum α1 ag concentrations among dogs with different clinical stages of lymphoma (stage IIIa, stage IVa, stage Va). However, mean serum α1 ag concentrations were were significantly increased for dogs with stages IIIa,, IVa, and Va lymphoma, compared with mean concentration for untreated control dogs. Mean serum α1 ag concentrations were significantly decreased in dogs with lymphoma that were in complete remission after either 1 or 4 doses of doxorubicin, compared with mean concentration in dogs with lymphoma that had not been treated.

Free access
in Journal of the American Veterinary Medical Association

SUMMARY

Fifteen dogs were given doxorubicin, iv, at a dosage of 30 mg/m2 of body surface. A commercially available biological extract of Serratia marcescens (besm) was administered sc to 9 of these dogs (0.04 mg/kg of body weight every third day, n = 2; 0.08 mg/kg every other day, n = 2; and 0.08 mg/kg daily, n = 5), beginning the day after administration of doxorubicin, in an attempt to find an optimal dosage and schedule of administration of besm to reduce the duration and severity of chemotherapy-induced myelosuppression. Nine additional dogs were randomized into 3 groups of 3 dogs to receive 1 of the following dosages of besm sc: 0.08, 0.16, and 0.32 mg/kg. Serum was harvested immediately prior to treatment and at 2, 4, 6, 8, 12, 24, 48, and 72 hours from this latter group of dogs for subsequent analysis of canine granulocyte colony-stimulating factor (g-csf) by enzyme immunoassay. Increasing the dosage and schedule of administration of besm reduced the duration and severity of doxorubicin-induced myelosuppression. Neutrophil counts of the group of dogs given besmdaily at a dosage of 0.08 mg/kg and the controls were evaluated statistically. The neutrophil count increased significantly (P < 0.05) above pretreatment values in besm-treated dogs after day 7. Median neutrophil counts of the besm-treated dogs were never significantly lower than pretreatment values, whereas the median counts of the dogs treated with doxorubicin alone were significantly below normal for 6 days (days 7-12). The median counts decreased below normal (< 3,000 cells/μl) for 1 day in the dogs given besm and doxorubicin, and for 3 days in the dogs that were given only doxorubicin. Four of the 6 dogs not treated with besm and none of those given besm developed serious neutropenia (< 1,500/μl). There was an increase in canine g-csf 4 to 6 hours after besm was administered to dogs at dosages of 0.16 and 0.32 mg/kg. These findings demonstrate that besm is capable of reducing the duration and severity of doxorubicin-induced myelosuppression, and that this may be at least partially mediated by g-csf.

Free access
in American Journal of Veterinary Research

Summary:

A study was undertaken to determine the effect chemotherapy had when used to treat 45 dogs with measurable metastatic osteosarcoma. The primary tumor was histologically confirmed as an osteosarcoma in each case. Thirty-nine dogs had the primary tumor surgically removed. Twenty-four of these dogs were treated adjunctively with cisplatin (70 mg/m2 of body surface, IV, q 3 weeks; median 2 doses, range 1 to 6 doses) prior to the onset of metastasis. The remaining 6 dogs from which the primary tumor was not surgically removed were diagnosed as having metastatic osteosarcoma in addition to the primary tumor on initial examination.

The median time from initial examination until the development of metastatic disease was 115 days (range, 27 to 1,199 days). The location of the metastatic disease was lungs (31 dogs), bone (3 dogs), soft tissue (1 dog), and multiple sites including lungs, bone, and soft tissue sites (10 dogs). The metastatic lesions were confirmed by pretreatment biopsy (n = 8) or cytologic evaluation (n = 2) in 10 cases and at necropsy in 27 cases. The remaining 8 cases were diagnosed radiographically as multiple metastatic lesions in the lungs consistent with metastatic osteosarcoma.

The metastatic disease was treated with cisplatin in 31 dogs (70 mg/m2, IV, q 3 weeks; median 2 doses, range 1 to 4 doses), doxorubicin in 11 dogs (30 mg/m2, IV, q 3 weeks; median 2 doses, range 1 to 3 doses), and mitoxantrone in 3 dogs (5 mg/m2, IV, q 3 weeks; median 2 doses, range 1 to 3 doses). Eight dogs that had metastatic disease treated with cisplatin were also given doxorubicin; 2 dogs treated with either doxorubicin or mitoxantrone were treated subsequently with cisplatin. The extent of neoplastic disease was determined immediately before the first dose of chemotherapy, and then every 3 to 6 weeks thereafter unless the dog had signs compatible with progressive disease, in which case, an evaluation was done more frequently. Each dog was treated with one chemotherapeutic agent until the dog developed progressive disease, or until the dog's quality of life diminished to an unacceptable level as determined by the owner or attending veterinarian. One dog treated with doxorubicin achieved partial remission. The duration of the partial remission was 21 days, and the lesion was confirmed to be osteosarcoma on necropsy 159 days after the metastatic disease was diagnosed. The median survival time of the other 44 dogs that did not respond to treatment from the time the metastatic disease was diagnosed was 61 days (range, 14 to 192 days). Cisplatin, doxorubicin, and mitoxantrone chemotherapy appear to be ineffective for the treatment of measurable metastatic osteosarcoma in the dog.

Free access
in Journal of the American Veterinary Medical Association

Summary:

We evaluated the development of nephrotoxicosis in 64 dogs with malignant neoplasia given cisplatin during 4-hour saline solution diuresis. Cisplatin (70 mg/m2 of body surface area, iv, q 21 d) was given to 8 dogs once, 22 dogs twice, 9 dogs 3 times, and 25 dogs 4 times. For each treatment, cisplatin was given over a 20-minute period after saline (0.9% NaCl) solution was administered iv for 3 hours at a rate of 25 ml/kg/h. After cisplatin infusion, saline solution diuresis was continued at the same rate for 1 hour. Before each treatment with cisplatin, the dogs were evaluated by conducting a physical examination, cbc, and analysis of serum urea nitrogen and creatinine concentrations, and in most cases, serum phosphorus concentration and urine specific gravity were determined. Exogenous creatinine clearance also was evaluated in 8 dogs prior to 1 (n = 8), 2 (n = 8), 3 (n = 6), and 4 (n = 4) treatments. Five (7.8%) of 64 dogs developed clinically evident renal disease after two (n = 3) and three (n = 2) doses of cisplatin. Two of the 5 dogs had preexisting diseases of the urinary tract prior to the start of treatment. Survival time in dogs that developed renal disease (median, 114 days; range, 26 to 273 days) was similar to that of all dogs in this study (median, 145 days; range, 5 to 586 days), with 30 dogs still alive at the conclusion of the study. Three of the 5 dogs that developed renal disease were alive at the conclusion of the study, 1 died of tumor-related causes, and another died as a direct result of nephrotoxicosis. There was a significant (P < 0.05) decrease in median neutrophil counts and a significant (P < 0.05) increase in median creatinine concentrations prior to the third and fourth treatments, compared with pretreatment values. Therefore, the 4-hour saline solution diuresis protocol used in this study to administer up to 4 doses of cisplatin appeared to be effective in preventing clinically apparent nephrotoxicosis in dogs with tumors and without preexisting urinary tract disease.

Free access
in Journal of the American Veterinary Medical Association

SUMMARY

A study was undertaken to determine the toxic effects of cisplatin, an antineoplastic agent, when administered immediately after a 1-hour saline diuresis. Four treatments with cisplatin (70 mg/m2 of body surface, q 3 wk) were administered iv to 6 healthy dogs over a 20-minute period after 0.9% NaCl (saline) solution was administered iv for 1 hour at a volume of 132 ml (kg)0.75. Each dog vomited at least once within 8 hours after each treatment was administered. Clinical status, body weight, and food consumption were normal throughout the 12-week study for 5 of the 6 dogs. The sixth dog developed acute renal failure and became acutely blind and deaf within 3 days after the fourth treatment with cisplatin. Serum electrolyte, creatinine, and urea nitrogen values remained within established normal limits in all dogs immediately prior to each treatment, and in 5 of 6 dogs evaluated 3 weeks after the final treatment. The serum creatinine value (3.3 mg/dl) obtained from the Beagle euthanatized 2 weeks after the fourth treatment was above established normal values. Despite normalcy for all but 1 of the creatinine values, serum creatinine concentration obtained 3 weeks after the final treatment with cisplatin was significantly (P = 0.0001) higher than pretreatment values. When compared with data from all other evaluation periods, significant decreases in glomerular filtration rate, as determined by exogenous (P ≤ 0.0001) and endogenous (P ≤ 0.0001) creatinine clearance testing, were identified 3 weeks after the fourth treatment with cisplatin. Neutrophil counts decreased significantly below pretreatment values at the third (P = 0.009), fourth (P < 0.0001), and fifth (P < 0.0001) evaluation period. We concluded that cisplatin can be administered with biochemical evidence, but not necessarily clinical evidence, that renal dysfunction may develop after 4 treatments with cisplatin (70 mg/m2, iv) are administered to dogs, using a 1-hour diuresis protocol.

Free access
in American Journal of Veterinary Research