Effects of oral cisapride administration in chinchillas (Chinchilla lanigera) with experimentally induced fecal output reduction

BackgroundCisapride, a prokinetic drug, has been anecdotally recommended in chinchillas at a dose of 0.5 mg/kg PO q8-12h to treat gastrointestinal hypomotility. However, studies in other rodent species suggest that higher doses are necessary to be effective.MethodsIn two randomized, placebo-controlled, blinded, crossover studies, the effects of cisapride (10 mg/kg PO q12h for four doses), administered with or without concurrent syringe feeding of a critical care formula (25 mL/kg PO q12h for two doses) were evaluated in chinchillas following recovery from sedation induced by alfaxalone-butorphanol. Food intake and fecal output were quantified to assess the effects of cisapride on these parameters.ResultsOver the first 24 hours after recovery from sedation, animals that received cisapride and syringe feeding had the least reduction in fecal output (-27 ± 23%) compared to the control treatment (-48 ± 22%, P = 0.008) or to animals which received syringe feedings alone (-40 ± 23%, P = 0.12). Cisapride administered without concurrent syringe feedings had no effect on fecal output. No adverse effects were recorded following the administration of cisapride.Conclusions and clinical relevanceThe oral administration of cisapride at 10 mg/kg q12h in conjunction with syringe feeding resulted in a slight, but not clinically relevant, attenuation of fecal output reduction by ~13% compared to syringe feedings alone and by ~20% compared to no treatment. Without the concurrent administration of syringe feedings, cisapride had no effect on fecal output in chinchillas.     

Efficacy of a combination of febantel, pyrantel, and praziquantel for the treatment of kittens experimentally infected with Giardia species

This study evaluated the effect of two combination products containing febantel, pyrantel, and praziquantel (FPP) for the treatment of Giardia species in experimentally infected kittens. In experiment 1, five kittens were administered the United States (US) formulation of FPP at doses of 37.8 mg/kg, 7.56 mg/kg, and 7.56 mg/kg, respectively, PO, q24h, for 5 days and four kittens remained as controls. In experiment 2, five kittens were administered the European formulation of FPP at the doses of 12.5 mg/kg, 12 mg/kg, and 4.16 mg/kg, respectively, PO, q24h, for 5 days and four kittens remained as controls. In experiment 3, six kittens were administered the US formulation of FPP at 56.5 mg/kg, 11.3 mg/kg, 11.3 mg/kg, respectively, PO, q24h, for 5 days and five kittens remained as controls. Thirteen days after treatment, kittens testing negative for Giardia species cysts were administered 20 mg/kg methylprednisolone acetate, IM, weekly for a maximum of two injections. Feces were analyzed for Giardia species cysts using a direct immunofluorescence test. After experiment 3, four of the six treated kittens, but no control kittens, remained negative for Giardia species after the administration of methylprednisolone acetate.     

Effects of urine alkalization and activated charcoal on the pharmacokinetics of orally administered carprofen in dogs

OBJECTIVE: To investigate the effects of oral administration of activated charcoal (AC) and urine alkalinization via oral administration of sodium bicarbonate on the pharmacokinetics of orally administered carprofen in dogs. ANIMALS: 6 neutered male Beagles. PROCEDURES: Each dog underwent 3 experiments (6-week interval between experiments). The dogs received a single dose of carprofen (16 mg/kg) orally at the beginning of each experiment; after 30 minutes, sodium bicarbonate (40 mg/kg, PO), AC solution (2.5 g/kg, PO), or no other treatments were administered. Plasma concentrations of unchanged carprofen were determined via high-performance liquid chromatography at intervals until 48 hours after carprofen administration. Data were analyzed by use of a Student paired t test or Wilcoxon matched-pairs rank test. RESULTS: Compared with the control treatment, administration of AC decreased plasma carprofen concentrations (mean +/- SD maximum concentration was 85.9 +/- 11.9 mg/L and 58.1 +/- 17.6 mg/L, and area under the time-concentration curve was 960 +/- 233 mg/L x h and 373 +/- 133 mg/L x h after control and AC treatment, respectively). The elimination half-life remained constant. Administration of sodium bicarbonate had no effect on plasma drug concentrations. CONCLUSIONS AND CLINICAL RELEVANCE: After oral administration of carprofen in dogs, administration of AC effectively decreased maximum plasma carprofen concentration, compared with the control treatment, probably by decreasing carprofen absorption. Results suggest that AC can be used to reduce systemic carprofen absorption in dogs receiving an overdose of carprofen. Oral administration of 1 dose of sodium bicarbonate had no apparent impact on carprofen kinetics in dogs.     

A phase I clinical trial evaluating imatinib mesylate (Gleevec) in tumor-bearing cats

A phase I clinical trial evaluating the toxicity of orally-administered imatinib mesylate was performed in 9 tumor-bearing cats. Imatinib is a small molecule, tyrosine kinase inhibitor, which selectively blocks the function of overexpressed proteins associated with various malignancies. Cats included in the study had diagnoses of fibrosarcoma, squamous cell carcinoma, and mast cell tumor, and each cat was staged using CBC and serum biochemistry; urinalysis, thoracic radiographs, and abdominal ultrasonography were performed in some cats. Most cats were treated previously by surgery, radiation therapy, chemotherapy, or some combination of these treatments. None of the cats received any concurrent chemotherapy. Six cats were treated with imatinib mesylate at 1-2 mg/kg PO q24h. Dose escalations were made to 2, 4, and 10 mg/kg PO q24h in 5 cats. Two cats started therapy at 10 mg/kg PO q24h, and 1 cat started therapy at 15 mg/kg PO q24h; all 3 cats remained at these dosages. No signs of toxicity, as evaluated by CBC and serum biochemistry, were noted in 8 of the 9 cats, and minimal gastrointestinal toxicity was observed. Due to the low frequency of adverse effects, further evaluation of imatinib is ongoing at a dosage of 10 mg/kg PO q24h.     

Pharmacokinetics of metronidazole and its concentration in body fluids and endometrial tissues of mares.

Serum concentrations of metronidazole were determined in 6 healthy adult mares after a single IV injection of metronidazole (15 mg/kg of body weight). The mean elimination rate (K) was 0.23 h-1, and the mean elimination half-life (t1/2) was 3.1 hours. The apparent volume of distribution at steady state was 0.69 L/kg, and the clearance was 168 ml/h/kg. Each mare was then given a loading dose (15 mg/kg) of metronidazole at time 0, followed by 4 maintenance doses (7.5 mg/kg, q 6 h) by nasogastric tube. Metronidazole concentrations were measured in serial samples of serum, synovia, peritoneal fluid, and urine. Metronidazole concentrations in CSF and endometrial tissues were measured after the fourth maintenance dose. The highest mean concentration in serum was 13.9 +/- 2.18 micrograms/ml at 40 minutes after the loading dose (time 0). The highest mean synovial and peritoneal fluid concentrations were 8.9 +/- 1.31 micrograms/ml and 12.8 +/- 3.21 micrograms/ml, respectively, 2 hours after the loading dose. The lowest mean trough concentration in urine was 32 micrograms/ml. Mean concentration of metronidazole in CSF was 4.3 +/- 2.51 micrograms/ml and the mean concentration in endometrial tissues was 0.9 +/- 0.48 micrograms/g at 3 hours after the fourth maintenance dose. Two mares hospitalized for treatment of bacterial pleuropneumonia were given metronidazole (15.0 mg/kg, PO, initially then 7.5 mg/kg, PO, q 6 h), while concurrently receiving gentamicin, potassium penicillin, and flunixin meglumine IV. Metronidazole pharmacokinetics and serum concentrations in the sick mares were similar to those obtained in the healthy mares.     

Insulin-like growth factors and recurrent hypoglycemia associated with renal cell carcinoma in a horse

The case was examined at the Easter Bush Veterinary Hospital, The University of Edinburgh. A 520 kg, 6-year-old Thoroughbred gelding was referred for evaluation of acute onset profound depression, head pressing, and lack of response to external stimuli. The horse had a history of moderate weight loss over several months despite adequate nutrition and a good appetite. Previous episodes of weakness had been observed following administration of anthelmintics, namely, alternate doses of pyrantel and ivermectin, administered every 8 weeks. In an attempt to eliminate a possible parasitic cause of weight loss, over the 7 days prior to presentation, the referring veterinary surgeon treated the horse with a 5-day course of fenbendazole^a (7.5 mg/kg PO q24h) and moxidectin^b (0.4 mg/kg PO), 2 days later. A 5-day course of prednisolone^c (1 mg/kg PO q24h) was initiated on the same day as the fenbendazole. This dose was then tapered to 0.5 mg/kg PO q24h, and was still being administered at the time of presentation.     

The effect of dosing interval on the efficacy of misoprostol in the prevention of aspirin-induced gastric injury

The effect of twice-daily administration of misoprostol on aspirin-induced gastric injury was evaluated. Twenty-four random-source dogs were divided into groups that received aspirin and misoprostol as follows: group I, aspirin 25 mg/kg PO q8h and placebo PO q8h; group II, aspirin 25 mg/kg PO q8h and misoprostol 3 microg/kg PO q8h; group III, aspirin 25 mg/kg PO q8h, misoprostol 3 microg/kg PO q12h, and placebo PO q24h; and group IV, aspirin 25 mg/kg PO q8h, misoprostol 3 microg/kg PO q24h, and placebo PO q12h for 28 days. Gastroscopy was performed on days -9, 5, 14, and 28. Visible lesions were scored on a scale of 1 (mucosal hemorrhage) to 11 (perforating ulcer). No difference in total score was identified between groups I and IV on any day. Median total scores for groups II and III were significantly (P < or = .05) lower compared to groups I and IV on day 5. Group III had a significantly lower score (P < or = .05) than groups I, II, and IV on day 28. This study suggests that misoprostol 3 microg/kg PO q12h is as effective as misoprostol 3 microg/kg PO q8h in preventing aspirin-induced gastric injury in this model. However, misoprostol 3 microg/ kg PO q8h was less effective in preventing aspirin-induced gastric injury on days 14 and 28 than in previous studies. No difference among numbers of dog-days of vomiting, diarrhea, or anorexia was detected among groups.     

Semilobar holoprosencephaly in a Morgan horse

A6 1/2‐month‐old Morgan filly was examined because of a history of abnormal behavior, teeth grinding, hypothermia, and electrolyte disturbances when weaned. She was from a breeding farm with several other Morgan horses. The 11‐year‐old dam had been purchased the year before as a proven broodmare, which had several previous foals. Breeding, gestation, and birth of this foal were normal. She was raised with 4 other mares and their offspring on pasture with free access to shelter in an open barn. Supplementary feeding consisted of oats and timothy hay. The owners reported that the foal showed unusual behavior, such as lack of apprehension of people, lack of distress from maternal separation, and a higher activity level than other foals of the same age. The foal extensively chewed the dam's tail and mane, masticated oats slowly with rapid jaw movements without actually swallowing them, and ground her teeth. She frequently nibbled the handler's clothes without biting, ate pebbles, and played with the salt block in the paddock. At 4 1/2 months of age, she was treated for suspected gastroduodenal ulcers and weaned. The referring veterinarian examined her 5 days after weaning because of dull demeanor and excessive teeth grinding. The foal was in thin body condition, hypothermic (37°C, 98.6°F), and tachycardic (60 beats per minute [bpm]) and had decreased borborygmi. Major abnormalities on serum biochemistry were severe hypernatremia (166 mmol/L; reference range 136–144 mmol/L) and hyperchloremia (128 mmol/L; reference range 94–104 mmol/L), azotemia (urea, 11.3 mmol/L; reference range 4.2–8.9 mmol/L), and hyperfibrinogenemia (5.2 g/L, reference range 1.6–2.9 g/L). The only abnormality on the CBC was hemoconcentration (PCV, 0.57 L/L; reference range 0.28–0.44 L/L). The foal was treated with penicillin procaine G^a (20,000 IU/kg [9072 IU/1b] IM q12h) and rifampin^b (5 mg/kg [2.7 mg/1b] PO q8h). The next day the tachycardia worsened (120 bpm) and the foal was estimated to be 5–8% dehydrated. IV fluid therapy with lactated Ringer solution^c (LRS) was initiated, and the antibiotic was changed to ceftiofur^d (2 mg/kg [0.91 mg/1b] IV q12h). The foal and dam were rejoined, and the foal's clinical status improved with resumption of nursing. Serial laboratory testing showed persistent hypernatremia 160 mmol/L) and hyperchloremia (123 mmol/L), azotemia urea 11.3 mmol/L and creatinine 168 umol/L; reference range 80–130 μmol/L), hyperglycemia (8.7 mmol/L; reference range 3.7–6.7 mmol/L), high aspartate aminotranferase activity (662 U/L; reference range 259–595 U/L), and high creatine kinase (CK) activity (1,196 U/L; reference range 108–430 U/L). The foal's condition improved and IV fluids were discontinued. Ceftiofur administration was discontinued and trimethoprim‐sulfamethoxazole^e (25 mg/kg [11.3 mg/1b] PO q12h) was administered for 3 days. During the next month the foal was stable but the abnormal behavior persisted. She was weaned again, and within days marked behavior changes such as circling, throwing the head around compulsively, and severe hind‐end shivering recurred. At examination, the foal was dull, tachycardic (60 bpm), was hypothermic (33.6°C, 92.5°F), had dark red mucous membranes, and was estimated to be 5% dehydrated. Laboratory findings were similar to those of the previous tests except for high fibrinogen (7.1 g/L). The foal was again rejoined with the dam, treated with intramuscular penicillin, and referred     

Effect of insulin dosage on glycemic response in dogs with diabetes mellitus: 221 cases (1993-1998)

OBJECTIVE: To evaluate glycemic response to insulin treatment in dogs with diabetes mellitus. DESIGN: Retrospective study. ANIMALS: 221 dogs with diabetes mellitus. PROCEDURE: Type and dosage of insulin used, minimum and maximum blood glucose concentrations, time of blood glucose concentration nadir, and optimal duration of action of insulin were determined on the basis of data obtained prior to initial examination at the teaching hospital (127 dogs), at the time of initial examination (212 dogs), at the time a second follow-up blood glucose curve was performed (59 dogs), and at the time of clinical control of diabetes mellitus (83 dogs). RESULTS: Prior to examination, 69 of 127 dogs (54%) received 1 s.c. insulin injection daily. Thirty-one dogs (24%) received a high dose of insulin (i.e., > 1.5 U/kg [0.7 U/lb] of body weight); 27 of these dogs (87%) received 1 injection/d. Eleven of 16 dogs (69%) that were hypoglycemic (blood glucose concentration < 80 mg/dl) also received 1 injection/d. However, optimal duration of action of insulin was > 12 hours in only 5 of 83 dogs (6%) evaluated at the time diabetes mellitus was clinically controlled. At that time, only 1 dog (1%) received a high dose of insulin, and the dog received 2 injections/d. Moreover, 8 of 10 dogs (80%) with hypoglycemia received 1 injection/d. CONCLUSIONS AND CLINICAL RELEVANCE: Most dogs with diabetes mellitus are clinically regulated with 2 daily insulin injections. Administration of a high dose of insulin or development of hypoglycemia may be more common in diabetic dogs that receive insulin once daily, compared with dogs that receive insulin twice daily.     

Administration of acepromazine maleate to 31 dogs with a history of seizures

Objective: To retrospectively evaluate the incidence of seizures in dogs presenting with a history of seizures that were treated with acepromazine (ACE) during hospitalization. Design: Retrospective study. Setting: Privately owned emergency and referral hospital. Animals: Thirty‐one client‐owned dogs. Interventions: Administration of ACE. Measurements and main results: The medical records from dogs with an acute or chronic seizure history that received ACE were reviewed. Factors evaluated included presenting complaint, seizure history, ACE dosage, duration of observation, seizure activity, and other medications used. Thirty‐one dogs qualified for the study: 20 males and 11 females. Age range was 3 months to 14.9 years. Presenting complaint was seizure in 28/31 dogs. There was a prior history of seizures in 22/31 dogs, and 15/22 were currently on antiseizure medication. ACE was given 1–5 times per dog. Mean ACE dose was 0.029 mg/kg IV (range: 0.008–0.057 mg/kg; n=46), 0.036 mg/kg IM (range: 0.017–0.059 mg/kg; n=14), 0.53 mg/kg PO (n=2). Twenty‐seven dogs did not seizure after administration of ACE within the observation period (mean: 16.4 hours, range: 0.25–66 hours). Twenty‐five dogs received antiseizure medication before ACE. Eight seizure episodes occurred in 4 dogs (all of whom presented for seizures) within 0.3–10 hours after ACE administration. Conclusions: There was no observed correlation between ACE administration in dogs with a seizure history and the recurrence of seizure activity during hospitalization. The time from ACE administration to seizure activity was greater than expected for measurable effects to be seen in 1 dog (10 hour). Further studies with a larger group and alternative ACE doses are needed to more thoroughly evaluate the safety of short‐term ACE use in dogs with a seizure history.     

Delayed recurrence of nasal aspergillosis in a dog

A two-year-old, female spayed Australian cattle dog was diagnosed with nasal aspergillosis. The dog was treated topically with clotrimazole. Clinical signs recurred two months later and the clotrimazole treatment was repeated and 5 mg/kg itraconazole twice daily was added to it. The recommended dose of itraconazole for nasal aspergillosis is 5 mg/kg twice daily administered orally. The dog's symptoms completely resolved, but it developed an adverse febrile reaction to the Itraconazole. The Itraconazole was discontinued and the dog remained asymptomatic for four years. The dog then developed mucopurulent discharge from the right nostril and was diagnosed as having recurrent nasal aspergillosis. Itraconazole at 5 mg/kg twice daily was prescribed, which again induced a fever. When the itraconazole was decreased to 5 mg/kg once daily there were no fever episodes, but the nasal discharge was not completely resolved. The dog was then treated with topical clotrimazole Infusion, and maintained on 5 mg/kg itraconazole daily. To the authors' knowledge, this case is unique because of the delayed recurrence of nasal aspergillosis. Additionally, the idiosyncratic febrile reaction to the itraconazole has not previously been reported in the veterinary literature, but is similar to reports of drug-induced fever in humans.     

Effects of chronic oral amiodarone on left ventricular function,ECGs, serum chemistries,and exercise tolerance in healthy dogs

Amiodarone, a class III antiarrhythmic with beta-adrenergic blocking and antimuscarinic properties, has a wide spectrum of clinical use in humans. This study was conducted to establish the effects of a 25 mg/kg q12h loading dose and a 30 mg/kg q24h maintenance dose of amiodarone, each given PO for 3.5 weeks, on systemic arterial pressure, echocardiographic (ECHO) indices of left ventricular function, ECGs, exercise tolerance, and serum biochemistries in adult, clinically normal dogs. Means were calculated and were compared by analysis of variance with repeated measures. When a significant F statistic was identified, specific means were compared by Bonferroni's post hoc test. Body weight and heart rate (HR) decreased, and PQ, QT, and corrected QT (QTc) increased significantly (P < .05) for the weeks that the dogs received the loading dose, but all parameters returned to values the same as those in the pretest for the weeks when dogs received the maintenance dose. Serum activity of hepatic enzyme activities and cholesterol concentrations increased, and serum concentrations of thyroid hormones (triiodothyronine [T3] and thyroxine [T4]), phosphorous, and total carbon dioxide decreased. The changes in PQ, QT, and QTc are similar to those obtained previously, but the detailed ECG and ECHO observations have not been reported. A dose of 25 mg/kg q12h, but not 30 mg/kg q24h, is an appetite suppressant, and the lower dose produces neither ECG nor ECHO changes of clinical or toxicological significance in normal dogs.     

Pharmacokinetics of phenylbutazone in mature Holstein bulls: steady-state kinetics after multiple oral dosing

Six mature Holstein bulls were given an 8-day course of phenylbutazone (PBZ) orally (loading dose, 12 mg of PBZ/kg of body weight and 7 maintenance doses of 6 mg of PBZ/kg, q 24 h). Plasma concentration-vs-time data were analyzed, using nonlinear regression modeling. The harmonic mean +/- pseudo-SD of the biologic half-life of PBZ was 61.8 +/- 12.8 hours. The arithmetic mean +/- SEM of the total body clearance and apparent volume of distribution were 0.0021 +/- 0.0001 L/h/kg and 0.201 +/- 0.009 L/kg, respectively. The predicted mean minimal plasma concentration of PBZ with this dosage regimen was 75.06 +/- 4.05 micrograms/ml. The predicted minimal plasma drug concentration was compared with the observed minimal plasma drug concentration in another group of bulls treated with PBZ for at least 60 days. Sixteen mature Holstein bulls were given approximately 6 mg of PBZ/kg, PO, daily for various musculoskeletal disorders. The mean observed minimal plasma concentration of PBZ in the 16 bulls was 76.10 +/- 2.04 micrograms/ml, whereas the mean predicted minimal plasma concentration was 74.69 +/- 3.10 micrograms/ml. Dosages of 4 to 6 mg of PBZ/kg, q 24 h, or 10 to 14 mg of PBZ/kg, q 48 h, provided therapeutic plasma concentrations of PBZ with minimal steady-state concentrations between 50 and 70 micrograms/ml.     

The use of lithium carbonate to prevent lomustine-induced myelosuppression in dogs: a pilot study

This was a preliminary investigation of the use of lithium to prevent lomustine-induced myelosuppression. Four 10 to 11 kg beagles received lomustine 20 to 30 mg, PO, q3wk, with cephalexin prophylaxis. Two dogs also received lithium, 150 to 300 mg, PO, q12h. Lithium blood concentrations fluctuated in and out of therapeutic interval. Lithium was discontinued in one dog in week 13, and in the other dog in week 38, due to toxicoses. All dogs developed grade 1 to 4 neutropenia after each lomustine treatment. In dogs receiving lomustine only, platelet concentrations decreased from 274 and 293 × 10(9)/L in week 1, to 178 and 218 × 10(9)/L in weeks 38 and 13, respectively. In dogs receiving lomustine and lithium, platelet concentrations decreased from 351 and 288 × 10(9)/L in week 1, to 214 and 212 × 10(9)/L, in weeks 36 and 13, respectively. Lithium did not prevent lomustine-induced myelosuppression and had important side-effects.     

Disseminated aspergillosis in a dog with diskospondylitis and neurologic deficits.

A German shepherd dog was treated initially for signs of urinary tract infection; subsequently, signs of spinal pain and neurologic deficits developed. Fungal hyphae were found in the urine sediment, and spinal radiography revealed changes in the vertebrae and intervertebral disks at the levels of T3 to T8, T12 to T13, L3-4, and L5-6, consistent with diskospondylitis. Fungal cultures of urine and specimens from spinal lesions yielded Aspergillus terreus. Itraconazole (5 mg/kg of body weight, PO, q 24 h) was used to treat this infection, and locomotion improved. Sudden death occurred 4 weeks after treatment was initiated; this was attributed to exsanguination associated with a weakened renal artery. This dog was raised in Florida and resided in central Virginia. The disseminated aspergillosis found in this dog was not limited to the hot arid climates that some reports suggest are optimal conditions for growth.     

Dietary mannoheptulose does not alter glucose or lipid metabolism in adult Labrador Retrievers

Mannoheptulose (MH), a glycolytic inhibitor, has been preliminarily investigated as a novel functional food ingredient for dogs. This study aimed to determine the effects of dietary MH, delivered as an extract of un‐ripened avocados, on fatty acid and glucose kinetics in healthy adult Labrador Retriever dogs (n = 12 dogs). The study was a double‐blindcrossover with each dog receiving both dietary treatments, control (CON) and MH (400 mg/kg of diet), in random order. Glucose and glycerol plasma turnover (Ra) and oxidation (Ox) were measured in fasting and in response to repeated meal feeding (“fed”) with stable isotope tracers (U‐¹³C‐glucose, 1,1,2,3,3‐D₅‐glycerol) and indirect calorimetry. Palmitate Ra and Ox were examined during repeated meal feeding only using an oral bolus of U‐¹³C‐K₂‐palmitate and indirect calorimetry. MH had no discernible effect on fasting glucose Ra (677, 722 SEM 36 μmol/min, CON, MH) or Ox (107, 109 μmol/min, CON, MH SEM 10 μmol/min) or fed glucose Ra (2913, 3626 SEM 644 μmol/min, CON, MH) or Ox (951, 936 SEM 174 μmol/min, CON, MH). Glycerol Ra, an index of the rate of lipolysis, was not different between dietary treatments (Fast 162, 113 SEM 35 μmol/min CON, MH; Fed 172, 135 SEM 21 μmol/min, CON, MH). Similarly, palmitate oxidation was not impacted by MH feeding (1966, 2276 SEM 79 μmol/min, CON, MH). Together, these findings do not support MH as a novel functional food ingredient at least at the dietary dose tested.     

Suspected hypothyroid-associated neuropathy in a female rottweiler dog

A 7-year-old, 46-kg spayed female rottweiler dog was presented with sudden onset of disorientation, bilateral convergent strabismus, and enophthalmos. Diagnostic workup revealed hypothyroid-associated cranial neuropathy. Symptoms abated considerably upon treatment with levothyroxine-sodium (T4) at an initial dose of 800 μg/kg body weight (BW), PO, q12h, which was reduced 3 days later to 600 μg/kg BW, q12h due to severe agitation and panting. Two weeks later the dosage of the levothyroxine-sodium (T4) was reduced to 400 μg/kg BW in the morning and 600 μg/kg BW in the evening. Eight weeks after the initial presentation, the dog had recovered with only mild convergent strabismus in the right eye. This is the first case report of suspected hypothyroid-associated neuropathy resulting in these symptoms.     

Efficacy of Low‐ and High‐Dose Trilostane Treatment in Dogs (< 5 kg) with Pituitary‐Dependent Hyperadrenocorticism

Background

Trilostane is commonly used to treat pituitary‐dependent hyperadrenocorticism (PDH) in dogs. There are differing opinions regarding the dose and frequency of trilostane administration in dogs with PDH.

Objectives

To compare the efficacy of 2 trilostane protocols in the treatment of dogs with PDH.

Animals

Sixteen client‐owned dogs with PDH and a body weight <5 kg.

Methods

Prospective observational study. Group A (n=9; low‐dose treatment group) received 0.78 ± 0.26 mg of trilostane/kg PO every 12 h and group B (n = 7; high‐dose treatment group) 30 mg of trilostane/dog PO every 24 h. All of the dogs were reassessed at 2, 4, 8, 12, 16, and 24 weeks after the initiation of treatment.

Results

An improvement in both ACTH‐stimulated serum cortisol concentrations and clinical signs occurred more slowly in group A than in group B; however, after 20 weeks of treatment, 2/7 dog in group B had clinical signs and abnormal laboratory findings consistent with hypoadrenocorticism. At 24 weeks, an improvement in the clinical findings of all of the dogs in both groups was detected.

Conclusions and clinical importance

In dogs with PDH, twice‐daily administration of low‐dose trilostane is an effective approach to the management of PDH. In addition, our results suggest fewer potential adverse effects if trilostane is administered twice daily in the lower dose.     

Efficacy of omeprazole paste for prevention of gastric ulcers in horses in race training

OBJECTIVE: To determine the minimal effective dosage of omeprazole oral paste for the prevention of naturally occurring ulcers in horses starting race training. DESIGN: Prospective study. ANIMALS: 175 horses. PROCEDURE: Horses in the dose selection portion of the study were sham dose treated or received 1 mg (0.45 mg/lb) or 2 mg (0.9 mg/lb) of omeprazole/kg, PO, every 24 hours for 28 days or 4 mg of omeprazole/kg (1.8 mg/lb; loading dose), PO, every 24 hours for 4 days, then 1 or 2 mg of omeprazole/kg, PO, every 24 hours for 24 days. Horses in the dose confirmation portion of the study were sham dose treated or received 1 mg of omeprazole/kg, PO, every 24 hours for 28 days. Gastric ulcer scores at the beginning and end of the study were compared. RESULTS: Sham-dose-treated horses had significantly higher ulcer scores than did horses treated with any of the omeprazole dosages evaluated. Among horses treated with omeprazole, there was no significant interaction of dose (1 or 2 mg/kg) and loading dose; therefore, the lowest effective dose (1 mg/kg) was evaluated in the dose confirmation portion of the study. In the dose confirmation study, 4 of 39 (10%) sham-dose-treated horses remained ulcer free, which was significantly different from the proportion of horses (31/38 [82%]) receiving 1 mg of omeprazole/kg that remained ulcer free. CONCLUSIONS AND CLINICAL RELEVANCE; Results indicated that omeprazole administered at a dosage of 1 mg/kg, PO, every 24 hours for 28 days was effective for prevention of gastric ulcers in horses starting race training.