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      Micetismos: Parte 2: Síndromes con sintomatología demorada y latencia muy larga

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          Abstract

          En este trabajo se analizan los micetismos menos comunes, caracterizados por la aparición demorada de síntomas y por tiempos de latencia muy largos. Estas intoxicaciones son provocadas por especies de hongos ectomicorrícicos poco comunes. Se analizan: a) Toxíndrome nefrotóxico demorado o retrasado. Micetismo orellánico o por orellanina. b) Toxíndrome con rabdomiólisis. Micetismos por Tricholoma equestre y Tricholoma terreum. c) Toxíndrome encefalopático o neurotóxico retrasado. Micetismo por Pleurocybella porrigens. d) Toxíndrome cardiovascular. Micetismo por Trogia venenata. Se discuten el tiempo de incubación, las características sintomatológicas, el curso clínico, las toxinas responsables de cada micetismo y su mecanismo de acción, y el tratamiento que ha resultado efectivo para la recuperación de los pacientes.

          Translated abstract

          Less common mycetisms, characterized by delayed-onset and very long latency times are analyzed. These intoxications are caused by rare ectomycorrhizal fungal species. The following syndromes have been taken into account: (a) Delayed nephrotoxic syndrome. Orellanic mycetism or mycetism due to orellanin. (b) Syndrome with rhabdomyolysis. Mycetisms by Tricholoma equestre, and Tricholoma terreum. (c) Delayed encephalopathic or neurotoxic syndrome. Mycetism by Pleurocybella porrigens. (d) Cardiovascular syndrome. Mycetism by Trogia venenata. The incubation time, symptom characteristics, clinical course, toxins responsible for each mycetism and their mechanism of action, and treatment that has shown to be effective for patient recovery are discussed.

          Translated abstract

          Neste trabalho, analisam-se micetismos menos comuns, caracterizados pelo aparecimento retardado de sintomas e tempos de latência muito longos. Essas intoxicações são causadas por espécies raras de fungos ectomicorrízicos. São analisados os seguintes: (a) síndrome de toxicidade nefrotóxica retardada ou atrasada. Micetismo orelânico ou micetismo por orelanina. (b) Toxíndrome com rabdomiólise. Micetismo por Tricholoma equestre e Tricholoma terreum. (c) Toxicidade tardia encefalopática ou neurotóxica. Micetismo por Pleurocybella porrigens. (d) Síndrome cardiovascular. Miceticismo por Trogia venenata. O tempo de incubação, as características sintomatológicas, o curso clínico, as toxinas responsáveis por cada micetismo e seu mecanismo de ação e o tratamento efetivo para a recuperação dos pacientes são discutidos.

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          Most cited references138

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          Hypoglycemia, functional brain failure, and brain death.

          Hypoglycemia commonly causes brain fuel deprivation, resulting in functional brain failure, which can be corrected by raising plasma glucose concentrations. Rarely, profound hypoglycemia causes brain death that is not the result of fuel deprivation per se. In this issue of the JCI, Suh and colleagues use cell culture and in vivo rodent studies of glucose deprivation and marked hypoglycemia and provide evidence that hypoglycemic brain neuronal death is in fact increased by neuronal NADPH oxidase activation during glucose reperfusion (see the related article beginning on page 910). This finding suggests that, at least in the setting of profound hypoglycemia, therapeutic hyperglycemia should be avoided.
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            Genetic and biophysical basis of sudden unexplained nocturnal death syndrome (SUNDS), a disease allelic to Brugada syndrome.

            Sudden unexplained nocturnal death syndrome (SUNDS), a disorder found in southeast Asia, is characterized by an abnormal electrocardiogram with ST-segment elevation in leads V1-V3 and sudden death due to ventricular fibrillation, identical to that seen in Brugada syndrome. We screened patients with SUNDS for mutations in SCN5A, the gene known to cause Brugada syndrome, as well as genes encoding ion channels associated with the long-QT syndrome. Ten families were enrolled, and screened for mutations using single-strand DNA conformation polymorphism analysis, denaturing high-performance liquid chromatography and DNA sequencing. Mutations were identified in SCN5A in three families. One mutation, R367H, lies in the first P segment of the pore-lining region between the DIS5 and DIS6 transmembrane segments of SCN5A. A second mutation, A735V, lies in the first transmembrane segment of domain II (DIIS1) close to the first extracellular loop between DIIS1 and DIIS2, whereas the third mutation, R1192Q, lies in domain III. Analysis of these mutations in Xenopus oocytes showed that the R367H mutant channel did not express any current and the likely effect of this mutation is to depress peak current due to the loss of one functional allele. The A735V mutant expressed currents with steady state activation voltage shifted to more positive potentials. The R1192Q mutation accelerated the inactivation of the sodium channel current. Both mutations resulted in reduced sodium channel current (I(Na)) at a time corresponding to the end of phase 1 of the action potential, as described previously in the Brugada syndrome. Based upon these observations we suggest that SUNDS and Brugada syndrome are phenotypically, genetically and functionally the same disorder.
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              The epidemiology of selenium deficiency in the etiological study of endemic diseases in China.

              K Ge, G. Yang (1993)
              The distribution of chemical elements in rocks and soils varies widely. Selenium is one of the elements that has remarkable regional variations in distribution and bioavailability. This paper reviews the epidemiology of selenium deficiency in China in connection with the etiology of human selenium-responsive diseases, the well-defined Keshan disease (KD) and the less-well-defined Kashin-Beck disease (KBD).
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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Journal
                abcl
                Acta bioquímica clínica latinoamericana
                Acta bioquím. clín. latinoam.
                Federación Bioquímica de la Provincia de Buenos Aires (La Plata, Buenos Aires, Argentina )
                0325-2957
                1851-6114
                March 2019
                : 53
                : 1
                : 79-107
                Affiliations
                [03] orgnameUniversidad de Buenos Aires orgdiv1Hospital de Clínicas José de San Martín orgdiv2División Alergia e Inmunología
                [01] Buenos Aires orgnameUniversidad de Buenos Aires orgdiv1Hospital de Clínicas José de San Martín orgdiv2Área Hematología Argentina
                [02] orgnameUniversidad de Buenos Aires orgdiv1Facultad de Medicina orgdiv2Microbiología I
                Article
                S0325-29572019000100014
                97b6ccb9-1fb1-4d4d-b3ae-b7d0408f3ea5

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

                History
                : 23 November 2018
                : 16 August 2018
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 149, Pages: 29
                Product

                SciELO Argentina

                Categories
                Toxicología

                Micetismos,Mycetisms,Delayed-onset syndromes,Toxidromes,Cortinarius,Tricholoma,Pleurocybella,Trogia,Toxins,Treatment,Síndromes demorados,Toxíndromes,Toxinas,Tratamiento,Miscetismos,Síndromes retardadas,Tratamento

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