Clinical and pathological aspects of progressive hyperphosphatasemia associated with vacuolar hepatopathy and hepatocellular carcinoma in a Scottish Terrier bitch / Aspectos clínicos e patológicos da hiperfosfatasemia progressiva associada à hepatopatia vacuolar e carcinoma hepatocelular em uma cadela da raça Scottish Terrier

ABSTRACT: Hyperphosphatasemia refers to an increase in alkaline phosphatase serum activity, and Scottish Terriers (STs) are predisposed to develop this condition of uncertain pathogenesis. This study describes a case of progressive hyperphosphatasemia with vacuolar hepatopathy and hepatocellular carcinoma (HCC) in a ST bitch. This dog had a five-year clinical follow-up with progressive hyperphosphatasemia (up to 5503 U/L) and with ultrasound findings and histologic diagnosis of vacuolar hepatopathy, in addition to posterior onset of HCC. A steroidogenic adrenal panel revealed an increase of adrenocortical hormones, especially progesterone and androstenedione, consistent with a subdiagnosed hypercortisolism. Euthanasia was elected and at necropsy, multinodular, yellow to red masses were observed in the liver, which were histologically and immunohistochemically defined as HCC. The association of the clinical, imaging, biochemical, adrenal panel and pathologic findings allowed to characterize and confirm a progressive disorder in this ST bitch associated with elevated adrenocortical hormones.

RESUMO: Hiperfosfatasemia é o aumento sérico de fosfatase alcalina, sendo que Scorrish Terriers estão predispostos a desenvolverem essa condição de patogênese desconhecida. Este trabalho descreve um caso de hiperfosfatasemia progressiva com hepatopatia vacuolar e carcinoma hepatocelular em um canino da raça Scottish Terrier. Uma cadela Scottish Terrier foi acompanhada clinicamente por cinco anos devido à hiperfosfatasemia persistente (até 5503 U/L), com achados ultrassonográficos e histológicos compatíveis com hepatopatia vacuolar, além de posterior desenvolvimento de carcinoma hepatocelular. O painel esteroidogênico realizado indicou aumento dos hormônios adrenocorticais, principalmente progesterona e androstenediona, consistente com diagnóstico de hipercortisolismo subdiagnosticado "atípico". Devido ao prognóstico desfavorável, a eutanásia foi realizada e na necropsia, massas amarelas a vermelhas e multinodulares foram observadas no fígado, com diagnóstico de carcinoma hepatocelular pela análise histológica e imuno-histoquímica. A associação dos achados clínicos, de imagem, bioquímicos, do painel androgênico e patológicos permitiram caracterizar e confirmar um distúrbio progressivo no canino da raça Scottish Terrier associado ao aumento dos hormônios adrenocorticais.

Clinical and pathological aspects of progressive hyperphosphatasemia associated with vacuolar hepatopathy and hepatocellular carcinoma in a Scottish Terrier bitch / Aspectos clínicos e patológicos da hiperfosfatasemia progressiva associada à hepatopatia vacuolar e carcinoma hepatocelular em uma cadela da raça Scottish Terrier

Hyperphosphatasemia refers to an increase in alkaline phosphatase serum activity, and Scottish Terriers (STs) are predisposed to develop this condition of uncertain pathogenesis. This study describes a case of progressive hyperphosphatasemia with vacuolar hepatopathy and hepatocellular carcinoma (HCC) in a ST bitch. This dog had a five-year clinical follow-up with progressive hyperphosphatasemia (up to 5503 U/L) and with ultrasound findings and histologic diagnosis of vacuolar hepatopathy, in addition to posterior onset of HCC. A steroidogenic adrenal panel revealed an increase of adrenocortical hormones, especially progesterone and androstenedione, consistent with a subdiagnosed hypercortisolism. Euthanasia was elected and at necropsy, multinodular, yellow to red masses were observed in the liver, which were histologically and immunohistochemically defined as HCC. The association of the clinical, imaging, biochemical, adrenal panel and pathologic findings allowed to characterize and confirm a progressive disorder in this ST bitch associated with elevated adrenocortical hormones.

Hiperfosfatasemia é o aumento sérico de fosfatase alcalina, sendo que Scorrish Terriers estão predispostos a desenvolverem essa condição de patogênese desconhecida. Este trabalho descreve um caso de hiperfosfatasemia progressiva com hepatopatia vacuolar e carcinoma hepatocelular em um canino da raça Scottish Terrier. Uma cadela Scottish Terrier foi acompanhada clinicamente por cinco anos devido à hiperfosfatasemia persistente (até 5503 U/L), com achados ultrassonográficos e histológicos compatíveis com hepatopatia vacuolar, além de posterior desenvolvimento de carcinoma hepatocelular. O painel esteroidogênico realizado indicou aumento dos hormônios adrenocorticais, principalmente progesterona e androstenediona, consistente com diagnóstico de hipercortisolismo subdiagnosticado "atípico". Devido ao prognóstico desfavorável, a eutanásia foi realizada e na necropsia, massas amarelas a vermelhas e multinodulares foram observadas no fígado, com diagnóstico de carcinoma hepatocelular pela análise histológica e imuno-histoquímica. A associação dos achados clínicos, de imagem, bioquímicos, do painel androgênico e patológicos permitiram caracterizar e confirmar um distúrbio progressivo no canino da raça Scottish Terrier associado ao aumento dos hormônios adrenocorticais.

Impact of atrazine and nitrate on liver and kidney of egyptian toad Sclerophrys regularis: bioindicator alarming on ecosystem

Atrazine and nitrate have been shown to act as potent oxidative stressors in amphibians either alone or in combination under stable laboratory conditions, causing histopathological alternations in liver and kidney structures at the sub-lethal concentrations. A control group and three treatments groups were tested; atrazine, nitrate, atrazine-nitrate treatments with doses of 300 µg L-1, 200 mg L-1 and their combination respectively. Sever distortion in liver and kidney tissues were shown related to the different treatments. The most hepatic lesions were observed depletion in glycogen content, degeneration of hepatocytes, hemorrhage, necrosis, vasodilatation, congestion in blood vessels, cloudy swelling in the hepatocytes and aggregation of melanomacrophage cells in between the hepatocytes that increased in combination treatment group. In kidney, the most lesions were represented in degeneration of renal tubules, fibrosis, hemorrhage, leucocytes infiltration, thickness in the wall of the renal capsule, atrophy of glomerulus, deformation of Bowman's epithelium. These negative impacts may be a bioindicator alarming the ecosystem disrupting caused by the uncontrolled apply of these chemicals in agriculture.(AU)

Hemochromatosis-like disease in Brazilian tapirs (Tapirus terrestris) in Pará state, Brazil / Hemocromatose símile em antas brasileiras (Tapirus terrestris) no estado do Pará, Brasil

We report two cases of hemochromatosis-like disease in captive Brazilian tapirs, Tapirus terrestris in Pará state, Brazil. Both animals presented symptoms of chronic hepatopathy associated with marked accumulation of hemosiderin. The coloration of Perls demonstrated pronounced iron accumulation in macrophages in the portal space, Kupffer cells, and, to a lesser extent, in the hepatocytes of the periportal region. Marked portal fibrosis was evidenced by Masson's trichrome. The pathological mechanisms of this disease in tapirs are not yet well established. It has been suggested that the species may have different mechanisms of iron absorption and elimination, rendering them sensitive to elevation in dietary levels of this metal. Two previous reports of this disease in T. terrestris exist from zoos in Australia and Scotland. This is the first report of this disease in tapirs in Brazil based on histopathological and histochemical findings.(AU)

Relatamos dois casos de hemocromatose símile em antas brasileiras, Tapirus terrestris mantidas em cativeiro no estado do Pará, Brasil. Ambas apresentavam lesões de hepatopatia crônica e acentuada, associadas a acúmulo acentuado de hemossiderina. A coloração de Perls demonstrou acúmulo acentuado de ferro nos macrófagos do espaço porta, células de Kupffer e, em menor extensão, hepatócitos na região periportal. Havia, ainda, fibrose portal marcada evidenciada por tricrômico de Masson. Os mecanismos patológicos da doença em antas ainda não estão bem estabelecidos e tem sido sugerido que a espécie apresenta diferentes mecanismos de absorção e eliminação de ferro, sendo sensíveis à elevação dos níveis dietéticos desse metal. Existem dois relatos anteriores da doença em T. terrestres em zoológicos na Austrália e na Escócia. Este é o primeiro relato da doença em antas no Brasil.(AU)

Acute necrotic hepatotoxicity caused by Lantana camara L. ingestion in dairy cattle / Hepatotoxicidade necrótica aguda por ingestão de Lantana camara L. em bovinos leiteiros

This study describes an outbreak of acute necrotic hepatopathy associated with spontaneous poisoning by Lantana camara L. in dairy cattle. A herd of 15 cows and heifers was introduced into a native pasture with limited food supply, and, sixteen days later, eight animals had spontaneous nasal hemorrhage, fever, lethargy, jaundice, and dry, dark stools with mucus and blood. The clinical course varied from two to five days. In the pasture where the cattle were kept, abundant adult specimens of L. camara L. with evident signs of consumption were observed. In total, seven cattle died and necropsy was performed in three of them. All animals had moderate jaundice, hemorrhage in the subcutaneous tissue and on the surface of different organs. The liver was slightly enlarged, with orange discoloration and enhanced lobular pattern. Histologically, multifocal areas of coagulative necrosis of hepatocytes in the centrilobular area, occasionally extending to the midzonal area, were observed, as well as marked hepatocellular degeneration and prominent cholestasis. The current study suggests that L. camara L. poisoning should be considered a differential diagnosis of acute and necrotic hepatotoxicity in cattle, despite the absence of photosensitization.(AU)

Esse estudo descreve um surto de hepatopatia necrótica aguda associada a intoxicação espontânea por Lantana camara L. em bovinos leiteiros. Um lote de 15 vacas e novilhas foram introduzidas em um piquete com campo nativo, com escassa oferta de alimento. Após dezesseis dias, oito animais manifestaram epistaxe, febre, apatia, icterícia, fezes ressecadas e escuras com muco e sangue. A evolução do quadro clínico variou de dois a cinco dias. No piquete em que os bovinos estavam alojados havia grande quantidade de L. camara L. com sinais evidentes de consumo. No total, sete bovinos morreram, e destes, o exame post mortem foi realizado em três. Os bovinos exibiam moderada icterícia, hemorragias no tecido subcutâneo e na superfície de diferentes órgãos. O fígado estava discretamente aumentado, com coloração alaranjada e padrão lobular evidente. As lesões histológicas consistiam em acentuada necrose de coagulação de hepatócitos em região centrolobular, por vezes se estendendo a região mediozonal, além de acentuada degeneração dos hepatócitos e evidente Colestase. O presente trabalho alerta para que intoxicação por L. camara L. seja levada em consideração nos diagnósticos diferenciais de hepatotoxicidade necrótica aguda em bovinos, mesmo sem indícios de fotossensibilização.(AU)

Acute necrotic hepatotoxicity caused by Lantana camara L. ingestion in dairy cattle / Hepatotoxicidade necrótica aguda por ingestão de Lantana camara L. em bovinos leiteiros

This study describes an outbreak of acute necrotic hepatopathy associated with spontaneous poisoning by Lantana camara L. in dairy cattle. A herd of 15 cows and heifers was introduced into a native pasture with limited food supply, and, sixteen days later, eight animals had spontaneous nasal hemorrhage, fever, lethargy, jaundice, and dry, dark stools with mucus and blood. The clinical course varied from two to five days. In the pasture where the cattle were kept, abundant adult specimens of L. camara L. with evident signs of consumption were observed. In total, seven cattle died and necropsy was performed in three of them. All animals had moderate jaundice, hemorrhage in the subcutaneous tissue and on the surface of different organs. The liver was slightly enlarged, with orange discoloration and enhanced lobular pattern. Histologically, multifocal areas of coagulative necrosis of hepatocytes in the centrilobular area, occasionally extending to the midzonal area, were observed, as well as marked hepatocellular degeneration and prominent cholestasis. The current study suggests that L. camara L. poisoning should be considered a differential diagnosis of acute and necrotic hepatotoxicity in cattle, despite the absence of photosensitization.(AU)

Esse estudo descreve um surto de hepatopatia necrótica aguda associada a intoxicação espontânea por Lantana camara L. em bovinos leiteiros. Um lote de 15 vacas e novilhas foram introduzidas em um piquete com campo nativo, com escassa oferta de alimento. Após dezesseis dias, oito animais manifestaram epistaxe, febre, apatia, icterícia, fezes ressecadas e escuras com muco e sangue. A evolução do quadro clínico variou de dois a cinco dias. No piquete em que os bovinos estavam alojados havia grande quantidade de L. camara L. com sinais evidentes de consumo. No total, sete bovinos morreram, e destes, o exame post mortem foi realizado em três. Os bovinos exibiam moderada icterícia, hemorragias no tecido subcutâneo e na superfície de diferentes órgãos. O fígado estava discretamente aumentado, com coloração alaranjada e padrão lobular evidente. As lesões histológicas consistiam em acentuada necrose de coagulação de hepatócitos em região centrolobular, por vezes se estendendo a região mediozonal, além de acentuada degeneração dos hepatócitos e evidente Colestase. O presente trabalho alerta para que intoxicação por L. camara L. seja levada em consideração nos diagnósticos diferenciais de hepatotoxicidade necrótica aguda em bovinos, mesmo sem indícios de fotossensibilização.(AU)

Neurobehavioral and hepatic complications induced by acute inhalation exposure to abamectin in female rats of the Wistar strain treated with ginger (Zingiber officinale)

The study we conducted aimed to evaluate the acute toxicity of abamectin (ABM) (pesticide) on liver function and neurobehavioral by using the open field test. As a therapy, we have opted for a treatment based on natural antioxidants ginger extract (Zingiber officinale) mixed with olive oil to see the restorative effects during the experiment. The study was conducted on female Wistar rats. The latter was given an inhalation exposure of abamectin (ABM) at a dose CL50 > 5.04mg/L/1hr each morning for one week. The effects of this exposure showed a drop in body weight gain (g), a significant decrease in the relative and absolute weights liver (gm/100 gm body weight) accompanied by hepatic impairment indicating a significant disturbance of transaminases (AST/ALT), alkaline phosphatase (ALP) activity and significant behavioral changes. Administration of ginger (Zingiber officinale) extract at a dose of 3 ml mixed with olive oil at a dose of 1 ml/kg for 7 days orally (gavages) after inhalation indicates that ginger has a more remarkable and rapid effect on physical and mental health, it acts as a major means of defense and hepato-protective against toxicity.(AU)

Neurobehavioral and hepatic complications induced by acute inhalation exposure to abamectin in female rats of the Wistar strain treated with ginger (Zingiber officinale)

The study we conducted aimed to evaluate the acute toxicity of abamectin (ABM) (pesticide) on liver function and neurobehavioral by using the open field test. As a therapy, we have opted for a treatment based on natural antioxidants ginger extract (Zingiber officinale) mixed with olive oil to see the restorative effects during the experiment. The study was conducted on female Wistar rats. The latter was given an inhalation exposure of abamectin (ABM) at a dose CL50 > 5.04mg/L/1hr each morning for one week. The effects of this exposure showed a drop in body weight gain (g), a significant decrease in the relative and absolute weights liver (gm/100 gm body weight) accompanied by hepatic impairment indicating a significant disturbance of transaminases (AST/ALT), alkaline phosphatase (ALP) activity and significant behavioral changes. Administration of ginger (Zingiber officinale) extract at a dose of 3 ml mixed with olive oil at a dose of 1 ml/kg for 7 days orally (gavages) after inhalation indicates that ginger has a more remarkable and rapid effect on physical and mental health, it acts as a major means of defense and hepato-protective against toxicity.(AU)

Neurobehavioral and hepatic complications induced by acute inhalation exposure to abamectin in female rats of the Wistar strain treated with ginger (Zingiber officinale)

The study we conducted aimed to evaluate the acute toxicity of abamectin (ABM) (pesticide) on liver function and neurobehavioral by using the open field test. As a therapy, we have opted for a treatment based on natural antioxidants ginger extract (Zingiber officinale) mixed with olive oil to see the restorative effects during the experiment. The study was conducted on female Wistar rats. The latter was given an inhalation exposure of abamectin (ABM) at a dose CL50 > 5.04mg/L/1hr each morning for one week. The effects of this exposure showed a drop in body weight gain (g), a significant decrease in the relative and absolute weights liver (gm/100 gm body weight) accompanied by hepatic impairment indicating a significant disturbance of transaminases (AST/ALT), alkaline phosphatase (ALP) activity and significant behavioral changes. Administration of ginger (Zingiber officinale) extract at a dose of 3 ml mixed with olive oil at a dose of 1 ml/kg for 7 days orally (gavages) after inhalation indicates that ginger has a more remarkable and rapid effect on physical and mental health, it acts as a major means of defense and hepato-protective against toxicity.

Gynura segetum induces hepatic sinusoidal obstruction syndrome in mice by impairing autophagy

ABSTRACT Purpose: To investigate the underlying mechanism of hepatic sinusoidal obstruction syndrome (HSOS) induced by Gynura segetum by measuring autophagy in mouse models. Methods: The model group was administered G. segetum (30 g/kg/d) by gavage, while the normal control group was administered an equal volume of saline daily for five weeks. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), hepatic histopathological examinations, and Masson staining were performed to evaluate liver injury. Liver intercellular adhesion molecule-1 (ICAM-1) and P-selectin were evaluated by immunohistochemistry. Hepatocellular apoptosis was assessed using the terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay. Protein expression levels of autophagy markers were measured using Western blot analysis. Results: Gynura segetum was found to significantly induce liver injury compared with control mice, as evidenced by the increase of serum transaminases, a decrease in triglyceride levels, and histopathological changes in mice. Gynura segetum remarkably induced hepatocellular apoptosis and upregulated the expressions of ICAM-1 and P-selectin and also downregulated the protein expression levels of LC3, Atg12 and cytoplasmic polyadenylation element binding protein. Conclusions: Our results suggested that G. segetum induced liver injury with HSOS, and it was partly due to its ability to impair the autophagy pathway.

Acute necrotic hepatotoxicity caused by Lantana camara L. ingestion in dairy cattle

ABSTRACT: This study describes an outbreak of acute necrotic hepatopathy associated with spontaneous poisoning by Lantana camara L. in dairy cattle. A herd of 15 cows and heifers was introduced into a native pasture with limited food supply, and, sixteen days later, eight animals had spontaneous nasal hemorrhage, fever, lethargy, jaundice, and dry, dark stools with mucus and blood. The clinical course varied from two to five days. In the pasture where the cattle were kept, abundant adult specimens of L. camara L. with evident signs of consumption were observed. In total, seven cattle died and necropsy was performed in three of them. All animals had moderate jaundice, hemorrhage in the subcutaneous tissue and on the surface of different organs. The liver was slightly enlarged, with orange discoloration and enhanced lobular pattern. Histologically, multifocal areas of coagulative necrosis of hepatocytes in the centrilobular area, occasionally extending to the midzonal area, were observed, as well as marked hepatocellular degeneration and prominent cholestasis. The current study suggests that L. camara L. poisoning should be considered a differential diagnosis of acute and necrotic hepatotoxicity in cattle, despite the absence of photosensitization.

RESUMO: Esse estudo descreve um surto de hepatopatia necrótica aguda associada a intoxicação espontânea por Lantana camara L. em bovinos leiteiros. Um lote de 15 vacas e novilhas foram introduzidas em um piquete com campo nativo, com escassa oferta de alimento. Após dezesseis dias, oito animais manifestaram epistaxe, febre, apatia, icterícia, fezes ressecadas e escuras com muco e sangue. A evolução do quadro clínico variou de dois a cinco dias. No piquete em que os bovinos estavam alojados havia grande quantidade de L. camara L. com sinais evidentes de consumo. No total, sete bovinos morreram, e destes, o exame post mortem foi realizado em três. Os bovinos exibiam moderada icterícia, hemorragias no tecido subcutâneo e na superfície de diferentes órgãos. O fígado estava discretamente aumentado, com coloração alaranjada e padrão lobular evidente. As lesões histológicas consistiam em acentuada necrose de coagulação de hepatócitos em região centrolobular, por vezes se estendendo a região mediozonal, além de acentuada degeneração dos hepatócitos e evidente Colestase. O presente trabalho alerta para que intoxicação por L. camara L. seja levada em consideração nos diagnósticos diferenciais de hepatotoxicidade necrótica aguda em bovinos, mesmo sem indícios de fotossensibilização.

Infecção verdadeira por Capillaria hepatica em cão / True infection by Capillaria hepatica in a dog

Background: Capillaria hepatica is a nematode, zoonotic, with worldwide distribution. The main hosts are rodents, nevertheless other mammals can be affected. Although the parasite has high affinity for the liver, it rarely causes a hepaticdisease in domestic animals and humans. The diagnosis is difficult and usually a biopsy is required. The treatment is difficult and is based in anti-helminthic and corticoid, but prevention is the best strategy against the disease. The aim of thepresent report is to describe a case of hepatic capillariosis in a dog approaching the clinical signs, diagnosis and therapeutic.Case: A 12-year-old Brazilian Terrier bitch, with a history of visit to the farm and regular hunting of rats, frogs, birds andother wild animals, was attended with hyporexia and apathy. At the physical exam the dog presented elevation of rectaltemperature, intense jaundice and abdominal pain. In the biochemical exams was noticed a slight increase in globulins anda sharp increase in alkaline phosphatase (AP), total, direct and indirect bilirubin, suggesting a liver injury. In the ultrasonographic exam, hepatomegaly with dispersed hyperechoic areas were observed, suggesting hepatic steatosis. The patientwas treated with ursodesoxicolic acid and S-adenosil metionin for 30 consecutive days, showing a clinic improvement.Two months after the end of the treatment the animal worsened, showing jaundice, ascites, motor incoordination, weakness, difficulty in food and water ingestion and changes in the mental state. In the complete blood count was observed amacrocytic hypochromic regenerative anemia, leukocytosis with neutrophilia and monocytosis and thrombocytopenia.In biochemical exams was detected decrease in creatinine and albumin and increase in alanine aminotransferase and AP,suggesting hepatopathy by biliary obstruction. There were performed exams for leishmania and ehrlichiosis that testednegative. In the ultrasonographic exam it...

Infecção verdadeira por Capillaria hepatica em cão / True infection by Capillaria hepatica in a dog

Background: Capillaria hepatica is a nematode, zoonotic, with worldwide distribution. The main hosts are rodents, nevertheless other mammals can be affected. Although the parasite has high affinity for the liver, it rarely causes a hepaticdisease in domestic animals and humans. The diagnosis is difficult and usually a biopsy is required. The treatment is difficult and is based in anti-helminthic and corticoid, but prevention is the best strategy against the disease. The aim of thepresent report is to describe a case of hepatic capillariosis in a dog approaching the clinical signs, diagnosis and therapeutic.Case: A 12-year-old Brazilian Terrier bitch, with a history of visit to the farm and regular hunting of rats, frogs, birds andother wild animals, was attended with hyporexia and apathy. At the physical exam the dog presented elevation of rectaltemperature, intense jaundice and abdominal pain. In the biochemical exams was noticed a slight increase in globulins anda sharp increase in alkaline phosphatase (AP), total, direct and indirect bilirubin, suggesting a liver injury. In the ultrasonographic exam, hepatomegaly with dispersed hyperechoic areas were observed, suggesting hepatic steatosis. The patientwas treated with ursodesoxicolic acid and S-adenosil metionin for 30 consecutive days, showing a clinic improvement.Two months after the end of the treatment the animal worsened, showing jaundice, ascites, motor incoordination, weakness, difficulty in food and water ingestion and changes in the mental state. In the complete blood count was observed amacrocytic hypochromic regenerative anemia, leukocytosis with neutrophilia and monocytosis and thrombocytopenia.In biochemical exams was detected decrease in creatinine and albumin and increase in alanine aminotransferase and AP,suggesting hepatopathy by biliary obstruction. There were performed exams for leishmania and ehrlichiosis that testednegative. In the ultrasonographic exam it...(AU)

Intoxicação espontânea por brotos de Xanthium spp. em bovinos no sul do Rio Grande do Sul / Spontaneous poisoning by sprouts of Xanthium spp. in cattle in southern Rio Grande do Sul

Background: Xanthium spp., the cockleburs, are invasive plants found on riverbanks, lakeshores, and floodplains. Ingestion of Xanthium sprouts or fruit causes cocklebur toxicosis, which is characterized clinically and pathologically by acuteliver failure. The main lesion observed is an accentuation of the lobular pattern of the liver (nutmeg appearance), whichis microscopically characterized by coagulation necrosis in the centrilobular region, hepatocyte degeneration in otherregions of the hepatic parenchyma, and sinusoidal congestion. The objective of this study was to describe an outbreak ofspontaneous cattle poisoning by ingestion of Xanthium spp. sprouts in the southern region of Rio Grande do Sul, Brazil.Case: In September 2018, a beef cattle farm located in Rio Grande county, Rio Grande do Sul, Brazil, reported significantmortality of cattle in a short period of time. There were 700 cattle on the property, divided by class into three differentherds, all kept under extensive conditions in native wetlands. All fields were heavily infested by cocklebur, with mostplants in the budding stage. Twenty animals developed muscle tremors, salivation, aggression, and recumbency. Theclinical course lasted 24 to 48 h, with a lethal outcome in all cases. An 18-month-old male crossbreed bovine was sent tothe Regional Diagnostic Laboratory of the Universidade Federal de Pelotas (UFPel) School of Veterinary Medicine fornecropsy. Gross examination revealed ascites and accentuation of the lobular pattern of the liver. Organ fragments wereharvested and fixed in 10% buffered formalin. Microscopically, the liver exhibited marked coagulation necrosis in thecentrilobular region and vacuolization of the hepatocyte cytoplasm in the midzonal and periportal regions. In the brain,there was perineuronal edema, cytoplasmic shrinkage and basophilia, gliosis, and satellitosis...

Intoxicação espontânea por brotos de Xanthium spp. em bovinos no sul do Rio Grande do Sul / Spontaneous poisoning by sprouts of Xanthium spp. in cattle in southern Rio Grande do Sul

Background: Xanthium spp., the cockleburs, are invasive plants found on riverbanks, lakeshores, and floodplains. Ingestion of Xanthium sprouts or fruit causes cocklebur toxicosis, which is characterized clinically and pathologically by acuteliver failure. The main lesion observed is an accentuation of the lobular pattern of the liver (nutmeg appearance), whichis microscopically characterized by coagulation necrosis in the centrilobular region, hepatocyte degeneration in otherregions of the hepatic parenchyma, and sinusoidal congestion. The objective of this study was to describe an outbreak ofspontaneous cattle poisoning by ingestion of Xanthium spp. sprouts in the southern region of Rio Grande do Sul, Brazil.Case: In September 2018, a beef cattle farm located in Rio Grande county, Rio Grande do Sul, Brazil, reported significantmortality of cattle in a short period of time. There were 700 cattle on the property, divided by class into three differentherds, all kept under extensive conditions in native wetlands. All fields were heavily infested by cocklebur, with mostplants in the budding stage. Twenty animals developed muscle tremors, salivation, aggression, and recumbency. Theclinical course lasted 24 to 48 h, with a lethal outcome in all cases. An 18-month-old male crossbreed bovine was sent tothe Regional Diagnostic Laboratory of the Universidade Federal de Pelotas (UFPel) School of Veterinary Medicine fornecropsy. Gross examination revealed ascites and accentuation of the lobular pattern of the liver. Organ fragments wereharvested and fixed in 10% buffered formalin. Microscopically, the liver exhibited marked coagulation necrosis in thecentrilobular region and vacuolization of the hepatocyte cytoplasm in the midzonal and periportal regions. In the brain,there was perineuronal edema, cytoplasmic shrinkage and basophilia, gliosis, and satellitosis...(AU)

Dieta hiperlipídica induz danos hepáticos associados à dhgna sem desequilíbrio redox no fígado de camundongos Swiss / Hyperlipid diet induces NAFLD associated liver damage without redox imbalance in Swiss mice liver

A doença hepática gordurosa não alcoólica (DHGNA) é uma doença de prevalência crescente e fortemente associada ao desequilíbrio redox e à perda da homeostase glicêmica. O desenvolvimento de modelos in vivo que mimetizem características fisiopatológicas da mesma é essencial para a descoberta e o desenvolvimento de estratégias terapêuticas. Validar um modelo de DHGNA associado ao desequilíbrio redox e à intolerância à glicose, induzida por dieta hiperlipídica, de baixo custo e fácil reprodutibilidade. Dezesseis camundongos Swiss receberam dieta hiperlipidica, durante 10 semanas. Durante todo o experimento foram avaliados peso corporal, tolerância à glicose, marcadores do estresse oxidativo e morfologia hepática. A dieta hiperlipídica promoveu um aumento significativo dos níveis de triglicerídeos (p<0,05) e do peso do tecido hepático (p<0,01), além de severa inflamação, necrose e esteatose dos hepatócitos. Os animais que seguira a DH (dieta hiperlipídica) apresentaram ainda, uma menor tolerância à glicose (p <0,05), entretanto não apresentaram redução dos grupamentos tióis. O modelo de DHGNA, induzida por DH, foi associada a danos histológicos hepáticos e à intolerância à glicose, entretanto não apresentou desequilíbrio redox, sendo um modelo inviável para estudos com tratamentos com antioxidantes. O trabalho teve por objetivo validar um modelo de DHGNA induzido por dieta hiperlipídica associada a alterações na resposta glicêmica e sem modificações na homeostase redox em camundongos.

Non-alcoholic fatty liver disease (NAFLD) is an increasingly prevalent disease strongly associated with redox imbalance and loss of glycemic homeostasis. The development of in vivo models that mimics its pathophysiological characteristics is essential for the discovery and development of therapeutic strategies. To validate a NAFLD model associated with redox imbalance and low-fat diet-induced glucose intolerance and easily reproducible. Sixteen Swiss mice received a high fat diet for 10 weeks. Throughout the experiment, body weight, glucose tolerance, oxidative stress markers and liver morphology were evaluated. The hyperlipid diet promoted a significant increase in triglyceride levels (p<0.05) and liver tissue weight (p <0.01), in addition to severe inflammation, necrosis and steatosis of hepatocytes. The animals that followed the hyperlipidic diet (HD) still had a lower glucose tolerance (p<0.05), ), however it did not show reduction of thiol groups. The HD-induced NAFLD model was associated with liver histological damage and glucose intolerance, however it did not present redox imbalance, being an unfeasible model for studies with antioxidant treatments. The study aimed to validate a model of NAFLD induced by a highfat diet associated with changes in the glycemic response and without changes in redox homeostasis in mice.

Dieta hiperlipídica induz danos hepáticos associados à dhgna sem desequilíbrio redox no fígado de camundongos Swiss / Hyperlipid diet induces NAFLD associated liver damage without redox imbalance in Swiss mice liver

A doença hepática gordurosa não alcoólica (DHGNA) é uma doença de prevalência crescente e fortemente associada ao desequilíbrio redox e à perda da homeostase glicêmica. O desenvolvimento de modelos in vivo que mimetizem características fisiopatológicas da mesma é essencial para a descoberta e o desenvolvimento de estratégias terapêuticas. Validar um modelo de DHGNA associado ao desequilíbrio redox e à intolerância à glicose, induzida por dieta hiperlipídica, de baixo custo e fácil reprodutibilidade. Dezesseis camundongos Swiss receberam dieta hiperlipidica, durante 10 semanas. Durante todo o experimento foram avaliados peso corporal, tolerância à glicose, marcadores do estresse oxidativo e morfologia hepática. A dieta hiperlipídica promoveu um aumento significativo dos níveis de triglicerídeos (p<0,05) e do peso do tecido hepático (p<0,01), além de severa inflamação, necrose e esteatose dos hepatócitos. Os animais que seguira a DH (dieta hiperlipídica) apresentaram ainda, uma menor tolerância à glicose (p <0,05), entretanto não apresentaram redução dos grupamentos tióis. O modelo de DHGNA, induzida por DH, foi associada a danos histológicos hepáticos e à intolerância à glicose, entretanto não apresentou desequilíbrio redox, sendo um modelo inviável para estudos com tratamentos com antioxidantes. O trabalho teve por objetivo validar um modelo de DHGNA induzido por dieta hiperlipídica associada a alterações na resposta glicêmica e sem modificações na homeostase redox em camundongos.(AU)

Non-alcoholic fatty liver disease (NAFLD) is an increasingly prevalent disease strongly associated with redox imbalance and loss of glycemic homeostasis. The development of in vivo models that mimics its pathophysiological characteristics is essential for the discovery and development of therapeutic strategies. To validate a NAFLD model associated with redox imbalance and low-fat diet-induced glucose intolerance and easily reproducible. Sixteen Swiss mice received a high fat diet for 10 weeks. Throughout the experiment, body weight, glucose tolerance, oxidative stress markers and liver morphology were evaluated. The hyperlipid diet promoted a significant increase in triglyceride levels (p<0.05) and liver tissue weight (p <0.01), in addition to severe inflammation, necrosis and steatosis of hepatocytes. The animals that followed the hyperlipidic diet (HD) still had a lower glucose tolerance (p<0.05), ), however it did not show reduction of thiol groups. The HD-induced NAFLD model was associated with liver histological damage and glucose intolerance, however it did not present redox imbalance, being an unfeasible model for studies with antioxidant treatments. The study aimed to validate a model of NAFLD induced by a highfat diet associated with changes in the glycemic response and without changes in redox homeostasis in mice.(AU)

Hepatopatia esteroidal em gatas após terapia com prednisolona: aspectos laboratoriais, tomográficos e histopatológicos / [Steroid hepatopathy in cats after prednisolone use: laboratory, tomographic, and histopathologic aspects]

Glicocorticoides são amplamente utilizados na clínica de pequenos animais, entretanto seu uso contínuo pode causar efeitos colaterais. Os gatos são considerados menos susceptíveis a esses efeitos do que outras espécies, mas existem poucos trabalhos abordando os efeitos adversos em felinos. O objetivo deste estudo foi avaliar possíveis alterações laboratoriais, histopatológicas e do grau de atenuação radiográfica do parênquima hepático de gatas submetidas à terapia com prednisolona. Um ensaio clínico foi realizado em quatro gatas hígidas, as quais receberam prednisolona, por via oral, na dose de 3mg/kg, durante 60 dias consecutivos. Nos achados histopatológicos após 60 dias de tratamento, observou-se desorganização dos cordões de hepatócitos e degeneração vacuolar, além de necrose de hepatócitos, porém não foram observados sinais de fibrose no parênquima hepático. Os dados da tomografia computadorizada demonstram aumento do grau de atenuação do parênquima hepático a partir do 30º dia da administração de prednisolona, que persistiu até o final do experimento. No presente estudo, foi possível caracterizar a existência de hepatopatia esteroidal em gatos em estágios precoces da terapia com prednisolona.(AU)

Glucocorticoids are widely used medications in small animal practice; however, its continuous use can have side effects. Cats are considered less susceptible than other species, however, the literature does not usually address adverse effects in felines. The objective of this study was to evaluate possible laboratory and histopathologic changes, as well as changes to the degree of radiographic attenuation of the hepatic parenchyma in cats treated with prednisolone. A clinical trial was done in four healthy cats, who received prednisolone orally at 3mg/kg during 60 consecutive days. In the histopathologic findings at 60 days of treatment, there were disorganized hepatocyte chords and vacuolar degeneration, as well as hepatocyte necrosis, however, there were no signs of fibrosis in the hepatic parenchyma. Data obtained via computed tomography showed increase of the degree of attenuation in the hepatic parenchyma from day 30 of prednisolone therapy, which persisted until the end of the experiment. In the present study, it was possible to characterize the existence of steroidal hepathopathy in cats in the early stages of prednisolone therapy.(AU)

Hepatopatia esteroidal em gatas após terapia com prednisolona: aspectos laboratoriais, tomográficos e histopatológicos / [Steroid hepatopathy in cats after prednisolone use: laboratory, tomographic, and histopathologic aspects]

Glicocorticoides são amplamente utilizados na clínica de pequenos animais, entretanto seu uso contínuo pode causar efeitos colaterais. Os gatos são considerados menos susceptíveis a esses efeitos do que outras espécies, mas existem poucos trabalhos abordando os efeitos adversos em felinos. O objetivo deste estudo foi avaliar possíveis alterações laboratoriais, histopatológicas e do grau de atenuação radiográfica do parênquima hepático de gatas submetidas à terapia com prednisolona. Um ensaio clínico foi realizado em quatro gatas hígidas, as quais receberam prednisolona, por via oral, na dose de 3mg/kg, durante 60 dias consecutivos. Nos achados histopatológicos após 60 dias de tratamento, observou-se desorganização dos cordões de hepatócitos e degeneração vacuolar, além de necrose de hepatócitos, porém não foram observados sinais de fibrose no parênquima hepático. Os dados da tomografia computadorizada demonstram aumento do grau de atenuação do parênquima hepático a partir do 30º dia da administração de prednisolona, que persistiu até o final do experimento. No presente estudo, foi possível caracterizar a existência de hepatopatia esteroidal em gatos em estágios precoces da terapia com prednisolona.(AU)

Glucocorticoids are widely used medications in small animal practice; however, its continuous use can have side effects. Cats are considered less susceptible than other species, however, the literature does not usually address adverse effects in felines. The objective of this study was to evaluate possible laboratory and histopathologic changes, as well as changes to the degree of radiographic attenuation of the hepatic parenchyma in cats treated with prednisolone. A clinical trial was done in four healthy cats, who received prednisolone orally at 3mg/kg during 60 consecutive days. In the histopathologic findings at 60 days of treatment, there were disorganized hepatocyte chords and vacuolar degeneration, as well as hepatocyte necrosis, however, there were no signs of fibrosis in the hepatic parenchyma. Data obtained via computed tomography showed increase of the degree of attenuation in the hepatic parenchyma from day 30 of prednisolone therapy, which persisted until the end of the experiment. In the present study, it was possible to characterize the existence of steroidal hepathopathy in cats in the early stages of prednisolone therapy.(AU)

Cirrose hepática associada à ingestão de Cycas revoluta em canino / Hepatic cirrhosis associated with ingestion of Cycas revoluta in canine

Background: Cycas revoluta (“sago palm”) is a toxic ornamental plant which, when ingested, can cause hepatotoxic effects, gastrointestinal signs, and neurological alterations. Albeit rarely, C. revoluta ingestion can culminate with chronic severe hepatitis associated with hepatic fibrosis. The objective of this work is to report a case of hepatic cirrhosis consequent to ingestion of C. revoluta in a dog and describe the clinical and pathological aspects that accompany the development of chronic hepatopathy, as a way to provide information that may help diagnosis of this condition. Case: A 9-month-old male mongrel dog was presented for examination with a history of increased abdominal volume and anorexia 20 days after ingesting the seeds of Cycas revoluta. Laboratory exams revealed hypochromic microcytic anemia, neutrophilic leukocytosis, monocytosis, thrombocytopenia, decreased albumin, and elevation of the enzymes alanine aminotransferase and alkaline phosphatase. Ultrasound scanning showed presence of hepatomegaly, a heterogeneous hepatic parenchyma, and free fluid in the peritoneum. The animal was treated and was discharged from the hospital. Twenty days later, the patient returned to the hospital exhibiting prostration, vomiting, ascites, and pale mucous membranes. The alterations observed in the previous laboratory exams persisted except for thrombocytopenia, which was absent. A new treatment was administered, and the animal was discharged three days later. However, the patient returned once again exhibiting hyporexia, hemorrhagic diarrhea, and slight prostration that progressed to severe prostration, lateral decubitus and death approximately two months after ingesting the plant. Necropsy revealed a markedly poor body condition, slight icterus, limb edema, ascites and hydrothorax, and an atrophied liver with a yellowish color and an irregular, but firm, capsule surface. Additional alterations included...