ABSTRACT
Senna occidentalis may be accidently ingested by humans and animals. In this study, the percentages of S. occidentalis seeds necessary for experimental reproduction of hepatic encephalopathy were determined in a pig model and the biochemical and microscopic pathology is described in detail, with emphasis on the astrocytes. The experimental groups (G1, G2 and G3) were fed rations containing 5%, 7.5% and 10% of S. occidentalis seeds for 7-11 days. Pigs from the three experimental groups showed incoordination, ataxia, disorientation, head pressing, anorexia, recumbency and depression. In addition, the enzymes aspartate aminotransferase, alkaline phosphatase and creatine phosphokinase increased in all treated animals, which also showed higher serum total bilirubin and ammonia levels than in the control group (C). Microscopically, all experimental animals revealed acute hepatocellular swelling, multifocal coagulative necrosis in the pancreas, necrosis in the cardiac muscle, severe spongiosis in brain white and grey matter, and Alzheimer type II astrocytes in grey matter of the cerebral cortex. These cells were glial fibrillary acidic protein (GFAP) negative in G3. In white matter, a decrease in the positive area occupied by GFAP-immunolabelling and in the number of astrocytes per immunoreactive area was observed in G3 animals (5.35 ± 1.14% and 410 ± 45 cells/mm2, respectively) compared to the C animals (13.93 ± 1.59% and 581 ± 36 cells/mm2, respectively). This loss of GFAP was accompanied by alterations in astrocyte morphology, such as shrinkage of the cell body and retraction of the extending processes. This pig model of ammonia-mediated astrocyte damage could be used to study not only poisoning by S. occidentalis, but also other medical conditions resulting in hepatoencephalopathy.
Subject(s)
Hepatic Encephalopathy , Poisons , Senna Plant , Animals , Astrocytes , Glial Fibrillary Acidic Protein , Hepatic Encephalopathy/chemically induced , Seeds , SwineABSTRACT
Objetivo : To evaluate the therapeutic agents used during metabolic crises and in long-term management of patients with propionic acidemia (PA).Materials and methods : The records of PA patients were retrospectively evaluated.Results : The study group consisted of 30 patients with 141 admissions. During metabolic crises, hyperammonemia was found in 130 (92%) admissions and almost all patients were managed with normal saline, ≥ 10% dextrose, and restriction of protein intake. In 56 (40%) admissions, management was done in intensive care unit, 31 (22%) with mechanical ventilation, 10 (7%) with haemodialysis, 16 (11%) with vasopressor agents, and 12 (9%) with insulin. In the rescue procedure, L-carnitine was used in 135 (96%) patients, sodium bicarbonate in 116 (82%), sodium benzoate in 76 (54%), and metronidazole in 10 (7%), biotin in about one-quarter, L-arginine in one third, and antibiotics in three-quarter of the admissions. Blood/packed RBCs were used in 28 (20%) patients, platelets in 26 (18%), fresh frozen plasma in 8 (6%), and granulocyte-colony stimulating factors in 10 (7%) admissions. All patients were managed completely/partially with medical nutrition formula plus amino acid mixture, vitamins and minerals. For long-term management 24 (80%) patients were on L-carnitine, 22 (73%) on sodium benzoate, 6 (20%) on biotin, one half on alkaline therapy and 4 (13%) on regular metronidazole use. Almost all patients were on medical formula and regular follow-up.Conclusion : Aggressive and adequate management of acute metabolic crises with restriction of protein intake, stabilization of patient, reversal of catabolism, and removal of toxic metabolites are essential steps. Concerted efforts to ensure adequate nutrition, to minimize the risk of acute decompensation and additional therapeutic advances are imperative to improve the outcome of PA patients. Arq Bras Endocrinol Metab. 2014;58(3):237-42.
Objetivo : Avaliar os agentes terapêuticos usados durante as crises metabólicas e para o manejo de longo prazo de pacientes com academia propiônica (AP).Materiais e métodos : Avaliação retrospectiva das fichas médicas de pacientes com AP.Resultados : O grupo estudado consistiu de 30 pacientes com 141 hospitalizações. Durante as crises metabólicas, a hiperamonemia foi observada em 130 (92%) pacientes hospitalizados e quase todos foram tratados com solução salina regular, ≥ 10% dextrose e restrição da ingestão de proteína. Em 56 (40%) das hospitalizações, o manejo foi feito na unidade de terapia intensiva, 31(22%) com ventilação mecânica, 10 (7%) com hemodiálise, 16 (11%) com vasopressores e 12 (9%) com insulina. Para o resgate, a L-carnitina foi usada em 135 (96%) pacientes, o bicarbonato de sódio em 116 (82%), o benzoato de sódio em 76 (54%), o metronidazole em 10 (7%), a biotina em cerca de um quarto, a L-arginina em um quarto e antibióticos em três quartos dos pacientes hospitalizados. Sangue/concentrado de hemácias foram usados em 28 (20%), plaquetas em 26 (18%), plasma fresco congelado em 8 (6%) e fatores estimulantes de colônias de granulócitos em 10 (7%) pacientes hospitalizados. Todos os pacientes foram manejados completamente/parcialmente com fórmula de nutrição hospitalar mais uma mistura de aminoácidos, vitaminas e minerais. Para o manejo de longo prazo, 24 (80%) dos pacientes foram tratados com L-carnitina, 22 (73%) com benzoato de sódio, 6 (20%) com biotina, a metade com tratamento alcalino e 4 (13%) com uso regular de metronidazole. Quase todos os pacientes foram tratados com fórmulas médicas e acompanhamento regular.Conclusão : O manejo adequado e agressivo de crises metabólicas com restrição da ingestão de proteína, ...