Resultado da pesquisa (3)
Termo utilizado na pesquisa cirrhosis
#1 - Cirrose hepática em cães: 80 casos (1965-2003), p.471-480
Abstract in English:
ABSTRACT.- Silva M.C., Fighera R.A., Brum J.S., Graça D.L., Kommers G.D., Irigoyen L.F. & Barros C.S.L. 2007. [Hepatic cirrhosis in dogs: 80 cases (1965-2003).] Cirrose hepática em cães: 80 casos (1965-2003). Pesquisa Veterinária Brasileira 27(11):471-480. Departamento de Patologia, Universidade Federal de Santa Maria, Camobi, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br
A retrospective study in 80 cases of canine hepatic cirrhosis was carried out at the Veterinary Pathology Laboratory of the Federal University of Santa Maria, Rio Grande do Sul, Brazil. Considering those cases in which the sex and age of the dogs were informed in the necropsy reports, males comprised 53.8% of the cases and 46.2% were females; while 50.0% of these dogs were aged, 48.6% were adults and 1.4% were puppies. The main observed clinical signs include ascites (39/80 [48.8%]), icterus (19/80 [23.8%]), anorexia (13/80 [16.2%]), neurological disturbances (12/80 [15.0%]), dyspnea (12/80 [15.0%]) and subcutaneous edema (10/80 [12.5%]). In 63 dogs for which there was a description of gross morphology in the necropsy reports, 76.2% had macronodular and 23.8% had micronodular cirrhosis. In 14 cases in which the histopathology of the liver was reviewed different degrees of fibrosis were observed: mild in 57.2%, moderate in 21.4%, or marked in 21.4%; in these cases there were no correlation with the degree of fibrosis and other associated histological changes such as lipidosis, biliary ducts hyperplasia, inflammation, bilestasis, hemosiderosis and random hepatocellular necrosis. Extra hepatic changes included ascites (39/63 [61.9%]), icterus (19/63 [30.2%]), status spongiosus (15/63 [23.8%]), hydrothorax (12/63 [19.0%]), subcutaneous edema (10/63 [15.9%]), portosystemic shunts (11/63 [17.5%]), gastric our duodenal ulceration (11/63 [17.5%]) and cholemic nephrosis (4/63 [6.3%]).
Abstract in Portuguese:
ABSTRACT.- Silva M.C., Fighera R.A., Brum J.S., Graça D.L., Kommers G.D., Irigoyen L.F. & Barros C.S.L. 2007. [Hepatic cirrhosis in dogs: 80 cases (1965-2003).] Cirrose hepática em cães: 80 casos (1965-2003). Pesquisa Veterinária Brasileira 27(11):471-480. Departamento de Patologia, Universidade Federal de Santa Maria, Camobi, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br
A retrospective study in 80 cases of canine hepatic cirrhosis was carried out at the Veterinary Pathology Laboratory of the Federal University of Santa Maria, Rio Grande do Sul, Brazil. Considering those cases in which the sex and age of the dogs were informed in the necropsy reports, males comprised 53.8% of the cases and 46.2% were females; while 50.0% of these dogs were aged, 48.6% were adults and 1.4% were puppies. The main observed clinical signs include ascites (39/80 [48.8%]), icterus (19/80 [23.8%]), anorexia (13/80 [16.2%]), neurological disturbances (12/80 [15.0%]), dyspnea (12/80 [15.0%]) and subcutaneous edema (10/80 [12.5%]). In 63 dogs for which there was a description of gross morphology in the necropsy reports, 76.2% had macronodular and 23.8% had micronodular cirrhosis. In 14 cases in which the histopathology of the liver was reviewed different degrees of fibrosis were observed: mild in 57.2%, moderate in 21.4%, or marked in 21.4%; in these cases there were no correlation with the degree of fibrosis and other associated histological changes such as lipidosis, biliary ducts hyperplasia, inflammation, bilestasis, hemosiderosis and random hepatocellular necrosis. Extra hepatic changes included ascites (39/63 [61.9%]), icterus (19/63 [30.2%]), status spongiosus (15/63 [23.8%]), hydrothorax (12/63 [19.0%]), subcutaneous edema (10/63 [15.9%]), portosystemic shunts (11/63 [17.5%]), gastric our duodenal ulceration (11/63 [17.5%]) and cholemic nephrosis (4/63 [6.3%]).
#2 - Intoxicação por Crotalaria retusa (Fabaceae) em eqüídeos no semi-árido da Paraíba
Abstract in English:
Nobre V.M.T., Riet-Correa F., Barbosa Filho J.M., Dantas A.F.M., Tabosa I.M. & Vasconcelos J.S. 2004. [Poisoning by Crotalaria retusa (Fabaceae) in Equidae in the semiarid region of Paraíba.] Intoxicação por Crotalaria retusa (Fabaceae) em eqüídeos no semi-árido da Paraíba. Pesquisa Veterinária Brasileira 24(3):132-143. Depto Clínicas Veteri-nárias, Universidade Federal de Campina Grande, Patos, PB 58700-000, Brazil. E-mail: verônica.nobre@uol.com.br
From 2000 to 2003 eight cases of poisoning by Crotalaria retusa L. were observed in horses on 8 farms in the semiarid region of Paraíba and Ceará. C. retusa was found in all farms. The main clinical signs were characteristic of hepatic encephalopathy, with dullness or hyperexcitability, head pressing, compulsive walking or circling and, occasionally, violent uncontrollable galloping. Decreased cranial nerve reflexes, ataxia and weakness were also observed. Other clinical signs were anorexia, weight loss, photosensitization and jaundice. The clinical manifestation period varied from 4 to 40 days, but most horses had a previous history of weight loss. At necropsy the livers were hard, with irregular surface and white areas mixed with dark red areas and increased lobular pattern. Mild jaundice, ascitis, hydropericardium and hydrothorax were also observed. Edema and moderate congestion were seen in the lungs. Histologic changes of the liver were characterized by fibrosis, mainly periportal, megalocitosis and bile duct cell proliferation. Multifocal areas of centrilobular or midzonal hemorrhages were also observed. Centrilobular hemorrhagic necrosis was present in two horses. Alzheimer type II astrocytes were observed, isolated or in groups, mainly in the caudate nucleus and cortex in 4 horses. The poisoning was experimentally produced in 1 adult horse and 3 adult donkeys. The horse received daily 100 g of C. retusa seeds and died 52 days after the beginning of the experiment. The dried whole C. retusa was mixed with grass and given to the 3 experimental donkeys at daily doses of 10g/kg, 5g/kg and 2.5g/kg, respectively. The donkey treated with 5g per kg died 48 days after beginning of the experiment and the other two were sacrificed at 120 days. Clinical signs and pathology were similar to those observed in spontaneous cases, but Alhzeimer type II astrocytes were observed only in the donkey that died 48 days after the beginning of ingestion of the plant material. The concentration of monocrotaline in the whole plant given to the donkeys was 0.5%.
Abstract in Portuguese:
Nobre V.M.T., Riet-Correa F., Barbosa Filho J.M., Dantas A.F.M., Tabosa I.M. & Vasconcelos J.S. 2004. [Poisoning by Crotalaria retusa (Fabaceae) in Equidae in the semiarid region of Paraíba.] Intoxicação por Crotalaria retusa (Fabaceae) em eqüídeos no semi-árido da Paraíba. Pesquisa Veterinária Brasileira 24(3):132-143. Depto Clínicas Veteri-nárias, Universidade Federal de Campina Grande, Patos, PB 58700-000, Brazil. E-mail: verônica.nobre@uol.com.br
From 2000 to 2003 eight cases of poisoning by Crotalaria retusa L. were observed in horses on 8 farms in the semiarid region of Paraíba and Ceará. C. retusa was found in all farms. The main clinical signs were characteristic of hepatic encephalopathy, with dullness or hyperexcitability, head pressing, compulsive walking or circling and, occasionally, violent uncontrollable galloping. Decreased cranial nerve reflexes, ataxia and weakness were also observed. Other clinical signs were anorexia, weight loss, photosensitization and jaundice. The clinical manifestation period varied from 4 to 40 days, but most horses had a previous history of weight loss. At necropsy the livers were hard, with irregular surface and white areas mixed with dark red areas and increased lobular pattern. Mild jaundice, ascitis, hydropericardium and hydrothorax were also observed. Edema and moderate congestion were seen in the lungs. Histologic changes of the liver were characterized by fibrosis, mainly periportal, megalocitosis and bile duct cell proliferation. Multifocal areas of centrilobular or midzonal hemorrhages were also observed. Centrilobular hemorrhagic necrosis was present in two horses. Alzheimer type II astrocytes were observed, isolated or in groups, mainly in the caudate nucleus and cortex in 4 horses. The poisoning was experimentally produced in 1 adult horse and 3 adult donkeys. The horse received daily 100 g of C. retusa seeds and died 52 days after the beginning of the experiment. The dried whole C. retusa was mixed with grass and given to the 3 experimental donkeys at daily doses of 10g/kg, 5g/kg and 2.5g/kg, respectively. The donkey treated with 5g per kg died 48 days after beginning of the experiment and the other two were sacrificed at 120 days. Clinical signs and pathology were similar to those observed in spontaneous cases, but Alhzeimer type II astrocytes were observed only in the donkey that died 48 days after the beginning of ingestion of the plant material. The concentration of monocrotaline in the whole plant given to the donkeys was 0.5%.
#3 - Experimental poisoning of cattle by Senecio brasiliensis (Compositae)
Abstract in English:
In experimental studies with Senecio brasiliensis (Spreng.) Lessing, 14 young bovines received orally the aerial parts of the dried plant collected during sprouting. In one part of the experiments, the dried plant was given once in amounts as the equivalent of 5 to 35 g of the fresh plant per kg of body weight; in the other part, the dried plant was given repeatedly during 1 to 8 months, either daily at doses as the equivalent of 0.31 to 5 g/kg of the fresh plant, or weekly in doses corresponding to 7·daily doses (0.31 g/kg x 7 to 1.25 g/kg x 7). The experiments demonstrated the toxicity of S. brasiliensis for cattle. The course of the poisoning was classified as acute, subacute and chronic, according to the period of time that elapsed since the administration, or the beginning of the administration of the plant, and the type of liver lesions. The clinical manifestations, post-mortem findings and histopathological changes were similar, in general, to those observed in poisoning caused by other species of Senecia, due to its hepatotoxic action. When the. poisoning followed an acute course, which occurred whert. The animals received once arnounts corresponding to 17.5 and 35 g/kg of the fresh plant, anorexia, paralysis of. the rumen, blood in the feces, and increased heart and respiratory rates were observed. These symptoms became apparent from 6 to 22 hours·after the plant was given, and lasted from 22 to 25 hours, terminating in death. The main post-mortem findings were a nutmeg appearance of the cut surface of the liver, edema of the gall bladder wall and hemorrhages in various tissues and organs. Histopathological e-xamination revealed a severe centrolobular necrosis with congestion and hemorrhages in the liver as the rnost important lesion. When the course of the poisoning was chronic, which occurred when the animals received single doses of 5 and 10 g/kg of the plant (all doses given here correspond to the fresh plant) or daily. repeated doses from 0,625 to 5 g/kg, at the total of 75 to 150 g/kg, or weekly doses equivalent to 7 daily doses, from 2,1875 g/kg (= 0,3125 g/kg x 7) to 8,75 g/kg (= 1,25 g/kg x 7), at the total of 61,25 to 78,75 g/kg, during 1 to 8 months, the main symptoms were prógressive anorexia,· associated with loss of weight, dry feces, occasional diarrhea, strong abdominal contractions during the last days of life, and, at times, icterus. Marked nervous symptoms were only observed in two animals. The first clinical sings appeared between the 12th and 246th day after the administration, or beginning of the administration of the plant; in one animal clinical manifestations were observed on the 133rd day of the experiment and 66 days after the last administration. The symptoms lasted from 2 to 92 days. In all these experiments the animals died, with exçeption of the bovine which received a single dose corresponding to 10 g/kg. of the fresh plant, which never showed symptorfis, but when euthanized 9 months after the start of the experiment, lesions of chronic poisoning (hepatic cirrhosis) were found. The main post-mortem findings were generalized icterus, edema of the mesenterium, increased amount of liquid in the peritoqeal cavity, edema of the mucosa of the abomasum and the gall bladder, hemorrhages in the epi- and endocardium, and cirrhotic liver lesions- the liver was lighter in color or yellowish grey, sometimes with red areas, was firmer than normal, the cut surface had yellowish grey areas which alternated with others of reddish color, and had in most cases a delicate whitish pattern. The main histopathologic changes were also those of cirrhosis: there were moderate to large arnounts of collagen, especially in the portal spaces and the centre of the lobules, but also as bundles subdividing the liver lobules and in smallar amounts surrounding the hepatic cells, with proliferation of fibroblasts and the epitelial cells of the bile ducts, vacuolar degeneration of hepatic cells, and discrete to moderate megalocytosis. The amounts of S. brasiliensis which caused acute poisoning corresponded to those of other species of the genus Senecio. However, the amounts required for the chronic course of poisoning were somewhat smaller, indicating that S. brasiliensis belongs to the group of the more toxic species of Senecio. The bovines which received the weekly accumulated doses, developed symptoms of poisoning more quickly and the animals died earlier then those receiving the sarne total amounts in daily administrations. The importance of S. brasiliensis as a cause of naturally occuring poisoning of cattle in Brazil has not yet been defined. However, since animals in the chronic course of the disease might die several months after having eaten the plant, it is quite likely that cases of poisoning by S. brasiliensis have remained hitherto unrecognized.
Abstract in Portuguese:
Em estudo experimental com Senecio brasiliensis (Spreng.) Lessing, da família Compositae, foram administradas a 14 bovinos jovens desmamados as partes aéreas da planta dessecada, coletada em fase de brotação no Rio Grande do Sul. Os experimentos consistiram na administração de doses únicas, correspondentes a 5-35 g da planta verde fresca por kg de peso do animal, e de doses repetidas durante 1 a 8 meses, tanto diárias, correspondentes a 0,3125 - 5 g/kg da planta verde fresca, como semanais, com doses equivalentes a 7 doses diárias. Os experimentos reveleram que S. brasiliensis possui ação tóxica para bovinos. Foram observados, de acordo com o período que decorreu desde a administração da planta, nos casos de dose única, ou desde o início dela nos de doses repetidas, e sobretudo pelas lesões observadas no fígado, quadros agudo, crônico e subagudo de intoxicação. Os achados clínicos, de necropsia e histopatológicos da intoxicação experimental estão, em linhas gerais, de acordo com os produzidos por outras espécies de Senecio, isto é, relacionados com a ação hepatotóxica da planta. Na intoxicação aguda, produzida por doses únicas correspondentes a 17,5 e 35 g/kg da planta verde fresca, foram observadas anorexia, paralisação do rúmen, eliminação de sangue nas fezes, freqüências cardíaca e respiratória aumentadas. Esses sintomas começaram de 6 a 22 horas após a ingestão da planta pelos animais e a evolução foi de 22 a 25 horas, findando com a morte. Os principais achados de necropsia foram o aspecto de noz-moscada da superfície de corte do fígado, edema da parede da vesícula biliar e hemorragias em diversos tecidos e órgãos. Os exames histopatológicos revelaram, como lesão mais importante, acentuada necrose centrolobular, acompanhada de congestão e hemorragia centrolobulares no fígado. Na intoxicação crônica, produzida pela administração de doses únicas de 5 e 10 g/kg da planta (todos os valores aqui indicados correspondem sempre a planta verde fresca); ou de doses repetidas diariamente de 0,625 a 5 g/kg, no total de 75 a 150 g/kg, ou por administrações semanais de doses equivalentes a 7 doses diárias, de 2,1875 g/kg ( = 0,3125 g/kg x 7) a 8,75 g/kg ( = 1,25 g/kg x 7), no total de 61,25 a 78,75 g/kg, durante 1 a 8 meses, os principais sintomas observados fora.-n anorexia progressiva, acompanhada de perda de peso, fezes ressequidas, às vezes diarréicas, contrações abdominais fortes nos últimos dias de vida, às vezes icterícia; sintomas nervosos bem evidentes (andar sem rumo, pressão da cabeça contra a parede do box) foram observados somente em 2 animais. Os sintomas apareceram entre o 12º e o 246º dias após a administração, ou início dela, correspondendo, em um animal, a 66 dias após o término da administração, 133º dia desde o início do experimento. A duração dos sintomas variou entre 2 e 92 dias. Em todos esses experimentos os animais morreram, com exceção do bovino que recebeu uma única dose corrrespondente a 10 g/kg da planta verde fresca, que nunca adoeceu, mas quando sacrificado 9 meses após o início do experimento, à necrópsia apresentou lesões de intoxicação crônica (cirrose hepática). Os principais achados de necropsia na intoxicação crônica foram icterícia generalizada, edema do mesentério, aumento do líquido na cavidade abdominal, edema da mucosa do coagulador e da parede da vesícula biliar, hemorragias do epi e endocárdio, e sobretudo lesões de cirrose hepática - o fígado tinha coloração mais clara que o normal, ou coloração amarelo-acinzentada, às vezes com áreas avermelhadas, ao corte era mais duro que o normal e a superfície de corte apresentava áreas de coloração amarelo-acinzentada alternadas com outras de coloração avermelhada, na maioria dos casos com fino desenho esbranquiçado sob forma de arborização. As principais alterações histopatológicas eram também as de cirrose hapática, traduzidas principalmente por presença de moderada a grande quantidade de colágeno especialmente nos espaços porta e no centro dos lóbulos, e também sob forma de focos e feixes dentro dos lóbulos hepáticos, subdividindoos, e entre as trabéculas e as células hepáticas, com proliferação de fibroblastos e das células epiteliais das vias biliares, processos degenerativos vacuolares das células hepáticas e megalocitose de discreta a moderada. As quantidades de S. brasiliensis necessárias para causar intoxicação experimental aguda correspondem às descritas para outras espécies tóxicas do gênero Senecio de outros países, porém, para causar intoxicação crônica, equivalem às doses mínimas, e até menores que essas, indicando que S. brasiliensis é uma das espécies mais tóxicas de Senecio até agora estudadas. Nos bovinos que receberam doses semanais equivalentes a 7 doses diárias, os primeiros sintomas de intoxicação apareceram mais precocemente e a morte dos animais ocorreu sempre mais cedo que nos que receberam a mesma quantidade em dosagens diárias. Não se conhece ainda bem a importância de Senecio brasiliensis· como causa de intoxicações naturais em bovinos no Brasil; vale notar que, na intoxicação-crônica, podendo o animal morrer até vários meses após ter ingerido a planta, muitos casos de intoxicação podem, facilmente; passar despercebidos.
