Fulminant hepatitis: a clinical review of 11 years

24 cases of fulminant hepatitis (FH) hospitalized in the Clínica de Doenças Infecciosas e Parasitárias do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo during the period from January 1976 to December 1986 were reviewed from their clinical, epidemiological and laboratorial aspects. 88% of the patients died; 20 patients (83%) presented hemorrhages and, of these, 19 died. Bacterial infections occurred in 14 patients (58%) all of whom died. Ascitis was noted in 3 cases; cerebral edema was present in 16 cases. Maximal ALT levels for each patient during hospitalization ranged widely from 81 to 4,460 UI/l. Thirteen patients presented high creatinine levels (54%). Prothrombin time activity ranged from 2.1% to 67%. Fever was present in 20 cases (83%). Encephalopathy occurred within the first 2 weeks of illness in 72% of the cases. In 7 cases other illnesses were present. The etiology could not be determined in 13 cases. In 3 cases it was due to yellow fever and 6 cases were caused by viruses other than yellow fever. In one case the cause was drug usage and in another case, possibly alcohol. The authors believe that the clinical definition of FH requires further discussion before it is established. In this study FH is a young person's disease. The mortality found was similar to that by other authors. Factors that contributed to death were: hemorrhages and bacterial infection. Factors that worsened the prognosis of hepatitis were: associated illnesses and surgical procedure. The levels of ALT during hospitalization did not correlate well with the severity of the hepatitis. The authors believe that yellow fever should be considered a cause of FH where the clinical picture meets the criteria for such, although its mechanisms of encephalopathy remain obscure. The clinical details of the 3 cases of yellow fever are presented.Vinte e quatro casos de hepatite fulminante (HF), internados na Clínica de Doenças Infecciosas e Parasitárias do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo durante o período de janeiro de 1976 a dezembro de 1986, foram revistos para a obtenção de dados clínicos, epidemiológicos e laboratoriais. 88% dos pacientes morreram. Vinte (83%) dos pacientes apresentaram hemorragias, dentre os quais 19 morreram (95%). Infecções bacterianas secundárias ocorreram em 14 pacientes (58%) todos os quais faleceram. Ascite foi notada em 3 casos e edema cerebral em 16 casos. Os valores máximos de ALT obtidos para cada paciente durante a internação variaram de 81 a 4.460 UI/l. Treze pacientes tiveram elevação de creatinina (54%). A atividade do tempo de protrombina variou de 2,1% a 67%. A febre esteve presente em 20 casos (83%). A encefalopatia surgiu durante as 2 primeiras semanas de doenças em 72% dos casos. Em 7 casos havia doenças associadas à hepatite. A etiologia não pode ser determinada em 13 casos; 3 casos foram por febre amarela; e 6 casos por outros vírus. Em 1 caso a causa foi drogas e em um caso, possivelmente, foi álcool. Os autores acreditam que a definição de HF merece discussão antes de ser totalmente aceita. Neste estudo, a HF foi uma doença que acometeu principalmente jovens. A letalidade encontrada foi semelhante a de outros estudos. Fatores que contribuíram para o óbito foram hemorragias e infecções bacterianas secundárias. Fatores de piora do prognóstico da hepatite foram a presença de outras doenças associadas e de procedimento cirúrgico. Os níveis de ALT durante a internação não refletiram a gravidade da hepatite. Os autores acreditam que a febre amarela deve ser considerada um agente etiológico de HF quando o seu quadro clínico seja compatível com tal, embora os mecanismos fisiopatológicos da encefalopatia sejam ainda obscuros. Os dados clínicos dos 3 casos de febre amarela são apresentados à parte

Ação, "in vitro". Da violeta de genciana sobre formas evolutivas do plasmodium falciparum

In order to investigate whether gentian violet exhibited "in vitro" inhibitory activity against Plasmodium falciparum, the Authors have carried out 20 sensitivity tests according to the microtechnique described by RIECK MANN et al.5. Results have shown inhibition of schizonts'maturation at the following concentration: 1/1000; 1/1500; 1/2000; 1/2500; 1/3000 and 1/4000, thus demonstrating inhibitory activity of the tested dye against asexual blood parasites. The present data suggest gentain violet may be possibly used in the prophylaxis of transfusion-acquired malaria.Utilizando a técnica de RIECKMANN e col.5, os autores realizaram 20 microtestes de sensibilidade, procurando verificar a capacidade da violeta de genciana em impedir, na cultura "in vitro", o desenvolvimento habitual do Plasmodium falciparum. Os resultados mostraram que houve inibiçáo da evolução do protozoário nas concentrações de 1/1000, 1/1500, 1/2000, 1/2500, 1/3000 e 1/4000, significando que nas condições da experiência o corante atuou sobre as formas sangüíneas assexuadas do protozoário. Estas verificações sugerem que a violeta de genciana poderia ser usada na profilaxia da malária transfusional

Neurotoxicity of oxamniquine in the treatment of human infection due to S. mansoni

One hundred and eighty patients from the "Clínica de Doenças Infecciosas e Parasitárias do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo" with mansonic schistosomiasis have been treated with oxamniquine (single oral dose 12.5 15 mg or 16-20 mg/kg body weight, respectively to patients younger or older than 15 years old). The patients were 5 to 65 years old and the predominant clinical forms were intestinal and hepato-intestinal disease. The main neuropsychiatric side effects were: drowsiness (50.6%), dizziness (41.1%), headache (16.1%), temporary amnesia (2.2%), behaviour disturbances (1.7%), chills (1.1%), seizures (1.1%). In 20 patients the neurotoxicity associated with the drug has been evaluated comparing the electroencephalogram before and after the treatment. Alterations have been detected in 3 (15%) but were not associated with neuropsychiatric manifes- tations. The results show that oxamniquine determines toxic side effects in the neuropsychiatric area.Foram tratados com oxamniquine (dose oral única de 12,5 a 15 mg e 15 a 20 mg/kg de peso, para maiores e menores de 15 anos respectivamente) 180 indivíduos com esquistossomose mansoni, matriculados na Clínica de Doenças Infecciosas e Parasitárias do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo. As idades variaram de 5 a 65 anos e as formas clínico-evolutivas prevalentes foram a intestinal e hepatointestinal. Os principais efeitos colaterais neuropsiquiátricos foram: sonolência (50,6%), tontura (41,1%), cefaléia (16,1%), amnésia transitória (2,2%), alterações de comportamento (1,7%), tremores (1,1%) e convulsão (1,1%). Em 20 indivíduos foi avaliada a neurotoxicidade da droga através de eletroencefalografia, antes e após o tratamento. Em 3 (15%), foram detectados alterações no traçado, sem contudo apresentarem manifestações clínicas neuropsiquiátricas. Os resultados demonstram ser o oxamniquine determinante de efeitos tóxico-colaterais na esfera neuropsiquiátrica

Vena cavae compression syndrome in paracoccidioidomycosis

The Authors report the first description of an inferior vena cavae compression syndrome due to paracoccidioidomycosis. The clinical course of the disease, laboratory and ultrasonographic findings are summarized, providing evidence to the diagnosis of inferior vena cavae compression.Os Autores registram o primeiro caso de síndrome de compressão da veia cava inferior devida a paracoccidioidomicose. Resumem a evolução clínica do paciente, tratamento e os achados laboratoriais e ultrassonográficos que evidenciaram o diagnóstico de compressão da veia cava inferior

Fulminant hepatitis: a clinical review of 11 years

24 cases of fulminant hepatitis (FH) hospitalized in the Clínica de Doenças Infecciosas e Parasitárias do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo during the period from January 1976 to December 1986 were reviewed from their clinical, epidemiological and laboratorial aspects. 88% of the patients died; 20 patients (83%) presented hemorrhages and, of these, 19 died. Bacterial infections occurred in 14 patients (58%) all of whom died. Ascitis was noted in 3 cases; cerebral edema was present in 16 cases. Maximal ALT levels for each patient during hospitalization ranged widely from 81 to 4,460 UI/l. Thirteen patients presented high creatinine levels (54%). Prothrombin time activity ranged from 2.1% to 67%. Fever was present in 20 cases (83%). Encephalopathy occurred within the first 2 weeks of illness in 72% of the cases. In 7 cases other illnesses were present. The etiology could not be determined in 13 cases. In 3 cases it was due to yellow fever and 6 cases were caused by viruses other than yellow fever. In one case the cause was drug usage and in another case, possibly alcohol. The authors believe that the clinical definition of FH requires further discussion before it is established. In this study FH is a young person's disease. The mortality found was similar to that by other authors. Factors that contributed to death were: hemorrhages and bacterial infection. Factors that worsened the prognosis of hepatitis were: associated illnesses and surgical procedure. The levels of ALT during hospitalization did not correlate well with the severity of the hepatitis. The authors believe that yellow fever should be considered a cause of FH where the clinical picture meets the criteria for such, although its mechanisms of encephalopathy remain obscure. The clinical details of the 3 cases of yellow fever are presented

Mitochondrial physiology

As the knowledge base and importance of mitochondrial physiology to evolution, health and disease expands, the necessity for harmonizing the terminology concerning mitochondrial respiratory states and rates has become increasingly apparent. The chemiosmotic theory establishes the mechanism of energy transformation and coupling in oxidative phosphorylation. The unifying concept of the protonmotive force provides the framework for developing a consistent theoretical foundation of mitochondrial physiology and bioenergetics. We follow the latest SI guidelines and those of the International Union of Pure and Applied Chemistry (IUPAC) on terminology in physical chemistry, extended by considerations of open systems and thermodynamics of irreversible processes. The concept-driven constructive terminology incorporates the meaning of each quantity and aligns concepts and symbols with the nomenclature of classical bioenergetics. We endeavour to provide a balanced view of mitochondrial respiratory control and a critical discussion on reporting data of mitochondrial respiration in terms of metabolic flows and fluxes. Uniform standards for evaluation of respiratory states and rates will ultimately contribute to reproducibility between laboratories and thus support the development of data repositories of mitochondrial respiratory function in species, tissues, and cells. Clarity of concept and consistency of nomenclature facilitate effective transdisciplinary communication, education, and ultimately further discovery

Mitochondrial physiology

As the knowledge base and importance of mitochondrial physiology to evolution, health and disease expands, the necessity for harmonizing the terminology concerning mitochondrial respiratory states and rates has become increasingly apparent. The chemiosmotic theory establishes the mechanism of energy transformation and coupling in oxidative phosphorylation. The unifying concept of the protonmotive force provides the framework for developing a consistent theoretical foundation of mitochondrial physiology and bioenergetics. We follow the latest SI guidelines and those of the International Union of Pure and Applied Chemistry (IUPAC) on terminology in physical chemistry, extended by considerations of open systems and thermodynamics of irreversible processes. The concept-driven constructive terminology incorporates the meaning of each quantity and aligns concepts and symbols with the nomenclature of classical bioenergetics. We endeavour to provide a balanced view of mitochondrial respiratory control and a critical discussion on reporting data of mitochondrial respiration in terms of metabolic flows and fluxes. Uniform standards for evaluation of respiratory states and rates will ultimately contribute to reproducibility between laboratories and thus support the development of data repositories of mitochondrial respiratory function in species, tissues, and cells. Clarity of concept and consistency of nomenclature facilitate effective transdisciplinary communication, education, and ultimately further discovery