Requisits del transport de mostres de diagnòstic per garantir l’estabilitat de les seves propietats biològiques

Mostres de diagnòstic; Conservació i transport; NormativaMuestras de diagnóstico; Conservación y transporte; NormativaDiagnostic samples; Conservation and transport; RegulationsAquest document s’aplica a les mostres de diagnòstic que es trameten entre un mòdul d’obtenció de mostres fins als laboratoris clínics processadors i també entre dos laboratoris. El document dóna una sèrie de recomanacions sobre les condicions adequades per al transport de les mostres de diagnòstic amb aquests objectius: • Preservar la integritat de les mostres de diagnòstic amb la finalitat de mantenir l’estabilitat de les propietats biològiques que les componen. Per aquest motiu, al document es troben una sèrie de consideracions sobre les variables mediambientals que poden afectar-les, com disminuir la seva influència i les referides al temps i la forma de transport, des de l’obtenció de la mostra, fins al processament al laboratori clínic destinatari. • Exposar una sèrie de requisits referits a la preparació i col·locació dels diferents tipus de contenidors, i les condicions idònies d’embalatge, etiquetatge i senyalització, de manera que formen part del conjunt de mesures organitzatives i de bona praxi. • Referir-se al contingut documental i dels registres que s’haurien de preparar i adjuntar a les mostres de diagnòstic, amb la finalitat de demostrar la traçabilitat del procediment de transport des del moment de la obtenció de la mostra fins a la recepció final al laboratori clínic processador, respectant la llei de confidencialitat de les dades. • Acomplir les condicions i els requisits de seguretat per disminuir o minimitzar el risc que pot comportar als manipuladors implicats en el transport de les mostres, ja sigui personal transportista, la societat o el medi ambient davant d’un accident mentre es porta a terme el transport de les mostres de diagnòstic

Reversible mitochondrial respiratory chain impairment during symptomatic hyperlactatemia associated with antiretroviral therapy

Direct evidence confirming the hypothesis that a dysfunction of the mitochondrial respiratory chain (MRC) underlies the pathogenesis of hyperlactatemia associated with highly active antiretroviral therapy (HAART) is scarce. We studied mitochondrial DNA (mtDNA) content and MRC function in the skeletal muscle of an HIV-infected patient during an episode of symptomatic hyperlactatemia. Skeletal muscle biopsy was performed during the episode when the patient was symptomatic and 3 months later when the patient was clinically recovered. Assessment of mitochondria was performed using histological, polarographic, spectrophotometrical, and Southern blot and real time PCR DNA quantification methods. The histological study disclosed extensive mitochondrial impairment in the form of ragged-red fibers or equivalents on oxidative reactions. These findings were associated with an increase in mitochondrial content and a decrease in both mitochondrial respiratory capacity and MRC enzyme activities. Mitochondrial DNA content declined to 53% of control values. Mitochondrial abnormalities had almost disappeared later when the patient became asymptomatic. Our findings support the hypothesis that MRC dysfunction stands at the basis of HAART-related hyperlactatemia

Reversible mitochondrial respiratory chain impairment during symptomatic hyperlactatemia associated with antiretroviral therapy

Direct evidence confirming the hypothesis that a dysfunction of the mitochondrial respiratory chain (MRC) underlies the pathogenesis of hyperlactatemia associated with highly active antiretroviral therapy (HAART) is scarce. We studied mitochondrial DNA (mtDNA) content and MRC function in the skeletal muscle of an HIV-infected patient during an episode of symptomatic hyperlactatemia. Skeletal muscle biopsy was performed during the episode when the patient was symptomatic and 3 months later when the patient was clinically recovered. Assessment of mitochondria was performed using histological, polarographic, spectrophotometrical, and Southern blot and real time PCR DNA quantification methods. The histological study disclosed extensive mitochondrial impairment in the form of ragged-red fibers or equivalents on oxidative reactions. These findings were associated with an increase in mitochondrial content and a decrease in both mitochondrial respiratory capacity and MRC enzyme activities. Mitochondrial DNA content declined to 53% of control values. Mitochondrial abnormalities had almost disappeared later when the patient became asymptomatic. Our findings support the hypothesis that MRC dysfunction stands at the basis of HAART-related hyperlactatemia