Familial stomatocytosis — hypertrophic gastritis (FSHG), a newly recognised disease in the dog (Drentse patrijshond)

Summary

A newly recognised disease, which we have given the provisional name of familial stomatocytosis‐hypertrophic gastritis (FSHG), is described in two families of dogs of the Drentse patrijshond breed. The affected dogs consisted of 3 females and 5 males, 3 to 19 (mean 9.5) months of age at admission. The main clinical problems were diarrhoea, icterus, and ataxia and paresis of the pelvic limbs. Laboratory evaluation revealed abnormal red cell shape (stomatocytosis), increased osmotic fragility, haemolytic anaemia, and increased liver enzymes and serum bilirubin. Gastroscopic and histopathologic examination of the gastric mucosa revealed hypertrophic gastritis resembling Ménétrier's disease in man. Histologic findings in the liver were suggestive of progressive liver disease. Cysts were found in the kidneys of the five oldest patients. Electroneurography in 2 dogs revealed polyneuropathy. In the parents of 2 patients (sister and brother), there were no clinical or laboratory abnormalities. An autosomal recessive hereditary defect of lipid metabolism is suspected.     

A retrospective study of clinical signs and epidemiology of chronic valve disease in a group of 207 Dachshunds in Poland

Background

Chronic mitral valve disease is frequently seen in the Dachshund. Dachshunds (n=207) made up 11.73% of the dogs admitted to the Cardiology Service at the Small Animal Clinic, Warsaw University of Life Sciences, Poland (first visits only).

Results

Of these, 35 dogs had no clinically detectable heart disease while 172 had chronic valve disease with the mitral valve affected most often (130 dogs), both mitral and tricuspid valves infrequently (39 dogs) and rarely the tricuspid valve (3 dogs). Males were affected more frequently than females and the average age of dogs with chronic valve disease was 11.9 years for females and 11.3 years for males. A majority of the diseased Dachshunds were classified as ISACHC 2 (79), followed by ISACHC 1 (60). Most frequent clinical signs noted by owners included coughing, exercise intolerance, dyspnea and tachypnea. Heart murmurs were generally louder with increased disease severity; however there were 20 dogs in the ISACHC 1 group with no audible heart murmurs. The most frequent electrocardiographic abnormalities included an increased P wave and QRS complex duration, increased R wave amplitude and tachycardia. With increased disease severity, echocardiography revealed an increase in heart size. A higher ISACHC class was related to increased heart size (based on echocardiography) and increased percentage of patients exhibiting enlargement of both left atrium and left ventricle (based on radiography).

Conclusions

The Dachshund is often affected by chronic mitral valvular disease with a late onset of associated clinical signs and few cardiac complications.     

Chronic active hepatitis in 26 Doberman pinschers

Chronic active hepatitis with increased hepatic copper concentration was diagnosed in 25 female and 1 male Doberman Pinscher dogs. Common clinical signs included polyuria/polydipsia, weight loss, anorexia, icterus, and ascites. Increased liver enzyme activities and abnormal liver function test results were the most consistent clinicopathologic changes. The dogs were assigned to 3 groups on the basis of clinical course of the disease. Group 1 dogs (n = 12) had clinical signs of advanced liver failure and died within one week. Group 2 dogs (n = 7) had less severe clinical signs of liver disease and died within one month. Group 3 dogs (n = 5) did not have clinical signs of illness or had mild clinical signs of liver disease and died 1 to 42 months after initial evaluation. One dog could not be reevaluated and another dog was alive 3 months after initial examination. Treatments consisted of supportive care for dogs in group 1, and dietary manipulations and corticosteroids for dogs in groups 2 and 3. The association of increased liver copper concentration and chronic active hepatitis is not known.     

Liver histopathology and liver and serum alanine aminotransferase and alkaline phosphatase activities in epileptic dogs receiving phenobarbital

Phenobarbital (PB) therapy is frequently associated with elevated serum alanine aminotransferase (ALT) and alkaline phosphatase (AP) activities in dogs without clinical signs of liver disease. The goal of this study was to determine if increased serum ALT and AP activities in clinically healthy PB-treated epileptic dogs are due to hepatic enzyme induction or to subclinical liver injury. Liver biopsies were obtained from 12 PB-treated dogs without clinical signs of liver disease but with elevated serum ALT and/or AP activities or both. Liver biopsies were obtained from eight healthy control dogs not receiving PB. Biopsies were evaluated histopathologically (all dogs) and liver homogenates were assayed for ALT (all dogs) and AP (six treated dogs, all controls) activities. As a positive control, liver cytochrome P4502B, an enzyme known to be induced by PB, was measured by benzyloxyresorufin-O-dealkylase activity and immunoblotting (five treated dogs, all controls). Serum AP isoenzyme analyses were performed. Results showed that ALT and AP activities in liver homogenates were not increased in treated dogs compared with controls, whereas the positive control for induction, CYP2B, was dramatically increased in treated dogs. Histopathological examination of liver biopsies revealed more severe and frequent abnormalities in treated dogs compared to controls, but similar types of abnormalities were found in both groups. Serum AP isoenzyme analyses in treated dogs demonstrated increased corticosteroid-induced and liver isoenzyme activities compared to controls. Results do not support induction of ALT or AP in the liver as the cause of elevated serum activities of these enzymes due to PB.     

Hepatotoxicity associated with CCNU (lomustine) chemotherapy in dogs

One hundred seventy-nine tumor-bearing dogs were treated with 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU) between 1995 and 2001. CCNU was given as a single dose of 50-110 mg/m2 body surface area PO. Treatment interval varied, but the minimal interval between CCNU doses was 3 weeks. After treatment, 11 dogs (6.1%) developed hepatic toxicity. The median number of CCNU doses and the median total cumulative CCNU dose were significantly higher in dogs that developed hepatic toxicity (4 doses; 350 mg/m2) than in dogs without hepatic damage (3 doses; 230 mg/m2). Median duration to detection of hepatic toxicity from the last dose of CCNU was 11 weeks (range 2-49 weeks). Common biochemical abnormalities were abnormally high serum liver enzyme activities and hypoalbuminemia. Six dogs with CCNU-associated hepatic toxicity had ascites, and 3 dogs had concurrent pleural effusion. Serum concentrations of bile acids were abnormally high in 4 of 5 dogs tested. Percutaneous ultrasound-guided liver biopsies were performed in 10 dogs, and findings were nonspecific and chronic in nature. Seven dogs were euthanized because of progressive liver failure, and their median survival from diagnosis of liver disease was 9 weeks. Three dogs died of other causes and 1 dog of unknown cause. Although clinical signs resolved in 3 dogs, biochemical abnormalities and histopathologic lesions persisted 4 to 38 months from the time of diagnosis of liver disease. Our findings suggest that CCNU can cause delayed, cumulative dose-related, chronic hepatotoxicity that is irreversible and can be fatal.     

Congenital dilatation of the bile ducts (Caroli's disease) in young dogs

We describe 8 young dogs with congenital dilatation of the intra- and extrahepatic bile ducts and diffuse cystic kidney disease, compatible with Caroli's disease in humans. The dogs were referred between 1980 and 2000 because of chronic disease at an age of 6 months to 3 years. These dogs included 3 Collies, 2 Frisian Stabyhouns, 2 Jack Russell Terriers, and 1 mixed-breed dog. The most common signs were vomiting (6/6), polyuria and polydipsia (4/6), and anorexia (4/6). Ascites was a common finding (4/6). Clinicopathologic abnormalities were available for 6 dogs. All had increased plasma alkaline phosphatase activity and fasting bile acids: increased alanine aminotransferase activity and urea and creatinine concentrations were present in 50% of dogs. Ultrasound examination of the liver showed severely dilated bile ducts without evidence of obstruction, and calcification in all cases but 1. Postmortem examination revealed severe dilatation of the larger intra- and extrahepatic bile ducts. The common bile duct and gall bladder were normal, and the bile system was patent. The ducts contained a clear viscid fluid often with calcified material. Microscopically, marked portal fibrosis was present, often with abnormally structured dilated bile ducts lined with columnar or cuboid epithelium and regularly small calcifications. The lesion was complicated by ascending cholangitis in 1 dog. The kidneys showed marked cortical and medullary fibrosis with a diffuse radial cystic pattern; only slight renal fibrosis was found in the oldest dog. Seven dogs were euthanized without treatment; the oldest dog was alive and well 5 months after diagnosis and was maintained on a protein-restricted diet.     

Response of canine cutaneous epitheliotropic lymphoma to lomustine (CCNU): a retrospective study of 46 cases (1999-2004)

BACKGROUND: Epitheliotropic lymphoma (ELSA) is an uncommon cutaneous canine malignancy of T lymphocytes. A consensus regarding the therapeutic standard of care is lacking, warranting evaluation of chemotherapeutic agents traditionally employed against canine nodal lymphoma in the treatment of ELSA. HYPOTHESIS: The purpose of this retrospective, multi-institutional study was to evaluate the efficacy of 1-(2-chloroethyl)-3-cyclohexyl-l-nitrosourea (CCNU) in the treatment of ELSA. ANIMALS: Forty-six dogs with adequate follow-up and treatment response information. METHODS: All cases were diagnosed histopathologically. Immunohistochemisty (CD3, CD79a) was performed on 42/46 samples. RESULTS: Presenting skin lesions included generalized scales (25/46), plaques or nodules (22/46), mucocutaneous lesions (14/ 46), and corneal involvement (1/46). Lymph node involvement and Sézary syndrome were documented in 7 and 2 dogs, respectively. The median number of CCNU treatments was 4 (range, 1-11), with a median starting dose of 60 mg/m(2) (range, 30-95). Of the 46 dogs, 15 achieved complete remission, 23 achieved partial remission, 5 had stable disease, and 3 had progressive disease, for an overall response rate of 83%. The median number of treatments to achieve a response was 1 (range, 1-6). The overall median duration of response was 94 days (range, 22-282). Sixteen dose reductions were required because of neutropenia (10/46), thrombocytopenia (1/46), anemia (1/46), increased liver enzyme activity (3/46), or unspecified reasons (1/46). CONCLUSIONS AND CLINICAL IMPLICATIONS: Given the high response rate and well tolerated protocol, prospective studies are warranted to investigate the utility of CCNU alone or in multi-agent protocols for the treatment of ELSA.     

Pulmonary Abnormalities in Dogs with Leptospirosis

Background: Leptospirosis in dogs is a multiorgan disease affecting mostly kidneys and liver. Objectives: The objective was to characterize prevalence, clinical, and radiological features and outcome of dogs with leptospirosis and pulmonary abnormalities. Animals: Fifty dogs with leptospirosis. Methods: Medical records of dogs diagnosed with leptospirosis at the Small Animal Clinic, Berlin, were reviewed. Diagnosis was based on microscopic agglutination test, blood or urine polymerase chain reaction, and histopathology. Based on clinical and/or radiological signs, patients were grouped into dogs with lung abnormalities (group 1) or without (group 2). Severity of respiratory distress was scored as mild to moderate (grade 1) or severe (grade 2). Thoracic radiographs were scored based on pulmonary changes and location as grade 1 (caudal interstitial pattern), 2 (generalized mild to moderate reticulonodular interstitial pattern), or 3 (generalized severe reticulonodular interstitial pattern with patchy alveolar consolidations). Results of CBC and biochemistry were compared between groups. Results: Thirty‐five dogs had radiological pulmonary changes (grade 1: 5; grade 2: 14; grade 3: 16); 31 of them had pulmonary distress (grade 1: 13, grade 2: 18). Sixty‐seven percent of the dogs with dyspnea grade 2 were mainly euthanized because of respiratory distress. Fifteen percent of the dogs with dyspnea grade 1 and 21% without clinical respiratory signs were euthanized because of acute renal failure or sepsis. Conclusions and Clinical Importance: In 70% of dogs with leptospirosis pulmonary changes were detected. Lung involvement represented a severe complication causing increased case fatality depending on the severity of respiratory distress.     

Hepatotoxicosis in dogs consuming a diet of camel meat contaminated with indospicine

Background Four dogs presented with clinical signs of severe hepatic disease after consuming a commercial camel meat diet. Methods Laboratory investigation revealed evidence of severe liver disease, including markedly increased serum alanine aminotransferase (ALT) activity and total bilirubin concentration, and prolonged clotting times. Results Two dogs deteriorated despite supportive therapy and were euthanased. Histologically, both livers appeared similar, with the main lesion being extensive periacinar necrosis and haemorrhage. Indospicine, a toxic amino acid of plant origin, was detected in the serum and/or plasma from all four dogs, as well as in tissues of a dog that was necropsied and in a sample of the camel meat fed to this animal. Serum biochemistry tests using blood samples collected from 15 additional dogs identified as having eaten the diet detected indospicine was in the serum of 14 and 3 had increased ALT activity. One of the latter dogs subsequently developed clinical signs of severe liver disease and was euthanased. Conclusion To the authors' knowledge, this is the first published report of the detection of indospicine residues in camel meat and the occurrence of severe, sometimes fatal, liver disease in dogs that consumed this contaminated meat.     

Copper-associated chronic hepatitis in Labrador Retrievers

This study summarizes the clinical and pathologic findings in 15 Labrador Retrievers with copper-associated chronic hepatitis (CACH). Our hypothesis was that this form of hepatitis is caused by a defect in hepatic copper metabolism, which most likely originates from a genetic defect. Affected Labradors consisted of 11 female and 4 male Labrador Retrievers. Eight family members of 2 of these patients were examined prospectively, as were 6 unrelated healthy Labrador Retrievers. All dogs were registered at the breed club. The average age at clinical presentation was 7 years (range, 2.5-10.5 years). All dogs were presented for anorexia, which was associated with vomiting in 8 patients. The diagnosis of CACH was based on histologic examination of liver biopsy specimens in all dogs, including semiquantitation of copper. A disproportionate increase in alanine aminotransferase (ALT) activity relative to alkaline phosphatase (ALP) activity, as well as the centrolobular localization of copper and the association of copper accumulation with hepatic lesions, suggested a primary copper storage disease rather than primary cholestatic liver disease causing copper accumulation. Mean hepatic copper concentration measured in related Labradors was 1,317 microg/g dry weight liver (range, 402-2,576 microg/g). Mean hepatic copper concentration of unrelated normal Labradors was 233 microg/g dry weight liver (range, 120-304 microg/g). Our findings support the hypothesis that a hereditary form of hepatitis occurs in Labrador retrievers and is caused by a defect in hepatic copper metabolism.     

Pancreatic abscess in dogs: six cases (1978-1986)

Pancreatic abscess was diagnosed by exploratory celiotomy in 6 dogs. The most common clinical signs included acute onset of lethargy (n = 5), anorexia (n = 6), vomiting (n = 5), and diarrhea (n = 2). Physical examination revealed pain response to abdominal palpation (n = 5), depression (n = 5), icterus (n = 3), fever (n = 3), and cranial abdominal mass (n = 2). Consistent preoperative clinicopathologic abnormalities included leukocytosis with left shift, observance of toxic neutrophils on the blood smear, hyperlipasemia, hyperamylasemia, hyperbilirubinemia, and increased serum alkaline phosphatase activity. In 5 of 6 dogs, abdominal radiography revealed increased soft tissue density in the cranial portion of the abdomen. Ultrasonography performed on 4 dogs confirmed pancreatic mass. In all dogs, exploratory celiotomy revealed a cavitary pancreatic mass that contained sterile, mucopurulent material. Histopathologic diagnoses included acute necrotizing or chronic-active pancreatitis and steatitis. Two dogs were euthanatized at the time of diagnosis, and the remaining 4 were treated by use of pancreatic debridement(s), open abdominal drainage, and intensive administration of fluids and antibiotics. One dog was euthanatized 4 days after surgery, because of progressive pancreatic abscessation. Three dogs recovered and were discharged.     

HEPATIC VOLUME ESTIMATION USING QUANTITATIVE COMPUTED TOMOGRAPHY IN DOGS WITH PORTOSYSTEMIC SHUNTS

The purpose of this study was to use quantitative computed tomography (CT) to estimate liver volume in dogs with a portosystemic shunt and to compare the liver volume in normal dogs to dogs with a shunt. Twenty-one dogs with a portosystemic shunt underwent contrast-enhanced abdominal CT for shunt characterization and preoperative planning. Six dogs without clinical signs relating to liver disease were used as a control group. In addition, liver volume was compared before and 2-4 months after surgical shunt attenuation in three dogs. All studies followed established clinical imaging protocols. Liver margins were defined on each image using an operator-defined region of interest and hepatic volume renderings were produced from which the liver volume was quantitatively estimated. There was a statistically significant association between liver volume and body weight in control and shunt dogs (r = 0.909 and 0.899, respectively, P < 0.01). Liver volume normalized to body weight was 15.5 +/- 5.2 cm3/kg in affected dogs and 24.5 +/- 5.6 cm3/kg in control dogs. Based on postligation CT studies in three affected dogs, liver volume increased by 43%, 51%, and 62%. Hepatic volume estimation may be a clinically useful parameter in the initial and postsurgical evaluation of dogs with portosystemic shunts.     

Idiopathic lymphoplasmacytic rhinitis in dogs: 37 cases (1997-2002)

OBJECTIVE: To determine clinical signs and rhinoscopic, computed tomographic, and histologic abnormalities in dogs with idiopathic lymphoplasmacytic rhinitis. DESIGN: Retrospective case series. ANIMALS: 37 dogs. PROCEDURE: Clinical information was obtained from medical records. Nasal computed tomographic images and histologic slides of biopsy specimens were reviewed. RESULTS: Dogs ranged from 1.5 to 14 years old (mean, 8 years); most (28) were large-breed dogs. Nasal discharge was unilateral in 11 of 26 (42%) dogs and bilateral in 15 of 26 (58%) dogs. In dogs with unilateral disease, duration of clinical signs ranged from 1.5 to 36 months (mean, 8.25 months; median, 2 months), and in dogs with bilateral disease, duration of signs ranged from 1.25 to 30 months (mean, 6.5 months; median, 4 months). Computed tomography (n = 33) most often revealed fluid accumulation (27/33 [82%]), turbinate destruction (23/33 [70%]), and frontal sinus opacification (14/33 [42%]). Rhinoscopy (n = 37) commonly demonstrated increased mucus and epithelial inflammation; turbinate destruction was detected in 8 of 37 (22%) dogs. Bilateral biopsy specimens from all 37 dogs were examined. Four dogs had only unilateral inflammatory changes. The remaining 33 dogs had bilateral lesions; in 20, lesions were more severe on 1 side than the other. CONCLUSIONS AND CLINICAL RELEVANCE: Findings suggest that idiopathic lymphoplasmacytic rhinitis is a key contributor to chronic nasal disease in dogs and may be more common than previously believed. In addition, findings suggest that idiopathic lymphoplasmacytic rhinitis is most often a bilateral disease, even among dogs with unilateral nasal discharge.     

Liver glutathione concentrations in dogs and cats with naturally occurring liver disease

OBJECTIVE: To determine total glutathione (GSH) and glutathione disulfide (GSSG) concentrations in liver tissues from dogs and cats with spontaneous liver disease. SAMPLE POPULATION: Liver biopsy specimens from 63 dogs and 20 cats with liver disease and 12 healthy dogs and 15 healthy cats. PROCEDURE: GSH was measured by use of an enzymatic method; GSSG was measured after 2-vinylpyridine extraction of reduced GSH. Concentrations were expressed by use of wet liver weight and concentration of tissue protein and DNA. RESULTS: Disorders included necroinflammatory liver diseases (24 dogs, 10 cats), extrahepatic bile duct obstruction (8 dogs, 3 cats), vacuolar hepatopathy (16 dogs), hepatic lipidosis (4 cats), portosystemic vascular anomalies (15 dogs), and hepatic lymphosarcoma (3 cats). Significantly higher liver GSH and protein concentrations and a lower tissue DNA concentration and ratio of reduced GSH-to-GSSG were found in healthy cats, compared with healthy dogs. Of 63 dogs and 20 cats with liver disease, 22 and 14 had low liver concentrations of GSH (micromol) per gram of tissue; 10 and 10 had low liver concentrations of GSH (nmol) per milligram of tissue protein; and 26 and 18 had low liver concentrations of GSH (nmol) per microgram of tissue DNA, respectively. Low liver tissue concentrations of GSH were found in cats with necroinflammatory liver disease and hepatic lipidosis. Low liver concentrations of GSH per microgram of tissue DNA were found in dogs with necroinflammatory liver disease and cats with necroinflammatory liver disease, extrahepatic bile duct occlusion, and hepatic lipidosis. CONCLUSIONS AND CLINICAL RELEVANCE: Low GSH values are common in necroinflammatory liver disorders, extrahepatic bile duct occlusion, and feline hepatic lipidosis. Cats may have higher risk than dogs for low liver GSH concentrations.     

Clinical and imaging findings in five dogs with intracranial blastomycosis (Blastomyces dermatiditis)

Fungal infections affecting the central nervous system are rare. The purpose of this study was to describe clinical and imaging findings in dogs with intracranial blastomycosis (Blastomyces dermatiditis). The radiology database was searched retrospectively for patients with a diagnosis of intracranial blastomycosis which had computed tomography performed as part of their diagnostic work-up. Medical records and imaging studies were reviewed. Five dogs met the inclusion criteria. Major presenting complaints were stertor/nasal discharge (n=2), exophthalmos (n=1), and seizures (n=2). Clinical and laboratory findings were variable. Computed tomographic examination revealed a single contrast-enhancing intra-axial mass (n=1), a nasal mass disrupting the cribriform plate (n=3), and an intracranial mass extending into the orbit and nasal cavity (n=1). Findings in intracranial blastomycosis in dogs are variable, and the disease may mimic other inflammatory disorders or neoplasia.     

Canine congenital portosystemic encephalopathy

The case records of 21 dogs with congenital portosystemic encephalopathy are reviewed. The disorder was most common in Australian cattledogs (blue heelers; 8 cases), Old English sheepdogs (3 cases) and Maltese terriers (3 cases). Extra-hepatic shunts occurred in small breeds, with the exception of 1 cattledog, while intra-hepatic shunts occurred in the medium to large breeds. The most common clinical pathology abnormalities were abnormal ammonia tolerance, mild to moderate increases in plasma alanine aminotransferase or alkaline phosphatase concentrations, decreased total serum protein concentrations, increased fasting ammonia concentrations and ammonium biurate crystalluria. Radiological examination revealed that all the dogs had a small liver. The kidneys were enlarged in 5 of 10 dogs in which kidney size could be estimated. Surgical ligation of an extra-hepatic shunt was successful in 2 of 4 dogs in which it was attempted. Medical management resulted in alleviation of clinical signs in 5 of 8 dogs. The period of successful treatment ranged from a few months to over a year.     

Clinical outcome of congenital extrahepatic portosystemic shunt attenuation in dogs aged five years and older: 17 cases (1992-2005)

OBJECTIVE: To assess the outcome of extrahepatic portosystemic shunt (EHPSS) treatment in dogs aged 5 years and older. DESIGN: Retrospective case series. ANIMALS: 17 client-owned dogs. PROCEDURES: Medical records for dogs (> or = 5 years old) that underwent surgical attenuation of an EHPSS (1992 through 2005) were evaluated; data, including clinical signs, clinicopathologic findings, surgical procedure, and outcome, were recorded. Follow-up information was obtained via patient examination or telephone interview with veterinarians and owners. RESULTS: Dogs (5 to 9 years old [median age, 6.6 years]) had neurologic (n = 12), urinary tract (8), and gastrointestinal tract (6) EHPSS-associated clinical signs. Serum bile acids and ammonia concentrations were abnormal in all evaluated dogs. Treatment of EHPSSs included complete (n = 6 dogs) or partial (2) suture attenuation or ameroid constrictor placement (9). Two dogs died following surgery. Follow-up information (6 to 120 months) was available for 13 dogs. Deaths were attributable to heart failure (n = 1), bacterial hepatitis (2; with pyelonephritis in 1 dog), and unknown causes (3). At a median of 23 and 25 months, serum bile acids concentrations had almost normalized in 5 of 8 dogs and ammonia concentrations were within reference limits in 3 of 5 dogs, respectively; dogs with abnormal liver function test results had no associated clinical signs. Median long-term survival time was 72 months. CONCLUSIONS AND CLINICAL RELEVANCE: Attenuation of EHPSS in > or = 5-year-old dogs ameliorated signs of liver dysfunction in surviving dogs, although return of normal liver function occurred less frequently than expected.     

A retrospective study of juvenile- and adult-onset generalized demodicosis in dogs (1986–91)

Abstract The medical records of 81 dogs (47 juvenile, 34 adult) with generalized demodicosis were reviewed. There was a significant difference in the distribution of breeds (juvenile P < 0.002, adult P < 0.001; chi squared) presented for demodicosis compared with the distribution of the same breeds presented to our practice during the same time period. Cocker Spaniels and mixed-breed dogs were likely to be under-represented in both the adult- and juvenile-onset groups. Significantly more miticidal treatments were required to achieve clinical remission in adult dogs with pustular demodicosis compared with juvenile dogs with pustular disease (P < 0.05; Kruskall-Wallis). Concurrent disease and associated drug administration were assessed for adult dogs with demodicosis. Of dogs with concurrent conditions (n=15), administration of corticosteroids and endogenous hyperadrenocorticism were recognized most often (10/15). Concurrent neoplastic, infectious, parasitic or metabolic disease was uncommon in dogs with adult-onset demodicosis. Résumé— Les dossiers médicaux de 81 chiens présentant des démodécies généralisées (47 formes juvéniles, 34 formes adultes) ont été analysés. Il existait une différence significative (forme juvénile P < 0.002, forme adulte P < 0.001) dans la distribution des races présentées pour démodécie par rapport aux mêmes races présentées à notre consultation à la même époque. Les cockers spaniels et les chiens métissés sont sous - représentés dans les deux groupes. Le nombre de traitements acaricides nécessaires pour obtenir une rémission clinique était significativement plus élevé chez les chiens adultes présentant une démodécie pustulcuse que chez les jeunes (P < 0.05; Kruskall-Wallis). La présence de pathologies intercurrentes ou iatrogènes a été recherchée chez les chiens adultes. Chez les chiens présentant une pathologie intercurrente (n=15), les diagnostics les plus fréquents (10/15), étaient l'administration de corticoïdes ou un hypercorticisme endogène. Une pathologie intercurrente de type néoplasique, infectieuse, parasitaire ou métabolique est rarement associée à la forme adulte de démodécie canine. [Lemarié, S.L., Hosgood G., Foil C.S. A retrospective study of juvenile- and adult-onset generalized demodicosis in dogs (1986–91) (Analyse retrospective de formes juveniles et de formes adultes de demodecie generalisee chez le chien (1986–91). Veterinary Dermatology 1996; 7 : 3–10.] Resumen Se revisó la historia médica de 81 perros (47 jóvenes, 34 adultos) con demodicosis generalizada. Habia diferencias significativas en la distribución de razas (jóvenes P < 0.002, adulto P < 0.001; chi cuadrado) con una presentación de demodicosis comparado con la distribución de las mismas razas que se presentaron en nuestra consulta durante el mismo período. Los Cocker Spaniel y los cruzados tenían menos posibilidades de presentarse tanto en el grupo de perros jóvenes como en el de adultos. Se necesitaron tratamientos significativamente más miticidas para consequir curación clínica en los perros adultos con demodicosis pustular comparado con los perros jóvenes con presentación pustular (P < 0.05; Kruskall-Wallis). Se detectaron con mayor frecuencia enfermedades concomitantes (n = 15), administración de corticosteroides e hiperadrenocorticismo endógeno (10/15). Fueron poco frecuentes las enfermedades neoplásicas, infecciosas, parasíticas o metabólicas en los casos de demodicosis del adulto. [Lemarié, S.L., Hosgood G., Foil C.S. A retrospective study of juvenile- and adult-onset generalized demodicosis in dogs (1986–91) (Estudio retrospectivo de la demodicosis canina en el adulto y en el perro joven (1986–91). Veterinary Dermatology 1996; 7 : 3–10.] Zusammenfassung— Die Krankenblätter von 81 Hunden (47 juvenil, 34 adult) mit generalisierter Demodikose kamen zur Auswertung. Es bestand einer signifikanter Unterschied in der Verteilung der Rassen (juvenil P < 0,002, adult P < 0,001; Chi-quadrat), die wegen Demodikose vorgestellt wurden, im Vergleich zur der Verteilung der selben Rassen, die während des gleichen Zeitabschnitts in unserer Praxis kamen. Cockerspaniel und Mischlinge schienen unterrepräsentiert sowohl in der Adult- wie in der Juvenil-Demodikosegruppe. Es wurden signifikant mehr akarizide Behandlungen für das Erreichen einer klinischen Remission bei adulten. Hunden mit pustulärer Demodikose benötigt im Vergleich zu juvenilen Hunden mit pustulärer Erkrankung (P < 0,05; Kruskall-Wallis). Bestehende Krankheit und die damit verbundene Arzneimittelanwendung wurden bei adulten Hunden mit Demodikose ausgewertet. Bei Hunden mit bestehenden Krankheitsbildern (n = 15) wurde am häufigsten die Verabreichung von Kortikosteroiden und endogener Hyperadrenokortizismus festgestellt (10/15). Gleichzeitige neoplastische, infektiöse, parasitäre oder stoffwechselbedingte Erkrankung war bei Hunden mit adult-beginnender Demodikose selten. [Lemarié, S.L., Hosgood G., Foil C.S. A retrospective study of juvenile- and adult-onset generalized demodicosis in dogs (1986–91) (Retrospektive Studie über juvenil- und adult-beginnende Demodikose beim Hund (1986–91). Veterinary Dermatology 1996; 7 : 3–10.]     

Effects of long-term phenobarbital treatment on the liver in dogs

Long-term administration of phenobarbital has been reported to cause hepatic injury in dogs. Phenobarbital induces hepatic enzymes, and it may be difficult to distinguish the effect of enzyme induction on serum liver enzyme activities from actual hepatic damage. The hepatotoxicity of phenobarbital and the impact of enzyme induction on serum liver enzyme activity were investigated prospectively in 12 normal dogs. Phenobarbital was administered for 29 weeks at 5 mg per kilogram of body weight (range, 4.8— 6.6 mg/kg) PO q12h, resulting in therapeutic serum phenobarbital concentrations (20–40 μg/mL). Serum alkaline phosphatase (ALP), alanine transaminase (ALT), aspartate transaminase (AST), γ-glutamyltransferase (GGT), fasted bile acids (fBA), total bilirubin, and albumin were determined before and during treatment. Lateral abdominal radiographs, abdominal ultrasounds, and histopathologic examinations of liver tissue obtained by ultrasound-guided biopsy were performed before and during treatment. Radiographs revealed a moderate increase in liver size in most dogs. Ultrasonographic examination revealed no change in liver echogenicity or architecture. No evidence of morphologic liver damage was observed histopathologically. ALP and ALT increased significantly ( P < .05), GGT increased transiently, and albumin decreased transiently during the study. There were no significant changes in AST, bilirubin, and fBA. These results suggest that increases in serum ALP, ALT, and GGT may reflect enzyme induction rather than hepatic injury during phenobarbital treatment in dogs. Serum AST, fBA, and bilirubin, and ultrasonographic evaluation of the liver are not affected by the enzyme-inducing effect of phenobarbital and can therefore be helpful to assess liver disease in dogs treated with the drug.     

Myopathy and alterations in serum 3-methylhistidine in dogs with liver disease

Liver disease can influence the metabolism of various other organs. Regarding the influence of liver diseases on muscles, only a few studies done on people exist. The goal of our study was to investigate the influence of liver diseases on muscles in dogs. Twenty-eight dogs with different liver diseases were investigated in this study. The diagnosis of muscle alteration was based on electromyography (EMG), creatine kinase serum activity, 3-methylhistidine serum concentration and a muscle biopsy in some cases. Our results suggest that liver diseases in dogs can be accompanied with muscle alteration. 3-Methylhistidine serum concentration as a new parameter for muscle destruction in dogs was significantly increased compared to clinical healthy dogs and was comparable to those concentrations in dogs with histologically confirmed myopathy of different types. The differentiation of the liver diseases into severe hepatitis, moderate hepatitis and liver tumours showed a significant elevation of 3-methylhistidine serum concentration in cases of liver tumours (P=0.03) and a tendency in cases of severe hepatitis (P=0.07). Based on our study we can conclude that liver diseases have an influence on muscles in dogs and 3-methylhistidine could be a useful parameter for muscle destruction.