RESUMO
Presentar en una serie de casos los posibles errores técnicos durante el bloqueo epidural, ya que se pueden prevenir y corregir durante el procedimiento. Materiales y métodos: Se evaluaron retrospectivamente, entre enero de 2013 y abril de 2014, 118 pacientes con dolor lumbar y/o radicular tratados con antiinflamatorio/analgésico mínimamente invasivo mediante una inyección selectiva guiada por tomografía computada (TC) en el espacio epidural. En todos los casos se utilizó una aguja espinal 21 G, y se inyectó esteroide de depósito (betametasona 3 mg) y anestésicos (lidocaína 1 ml al 2% + bupivacaína 0,5 ml al0,5%) o solo esteroide en los pacientes con sospecha de duramadre perforada. Se seleccionaron únicamente aquellos casos en los que hubo errores de técnica durante el procedimiento. Resultados: Cinco pacientes (4,23%) tuvieron complicaciones técnicas durante el bloqueo epidural. Estas se observaron luego de una inadecuada posición del extremo de la aguja (perforación de la duramadre y falta de acceso al espacio epidural) y se objetivaron por la aspiración directa del líquido cefalorraquídeo (LCR) o por la disposición del aire, utilizado como trazador antes de la inyección del medicamento. Los errores se detectaron y corrigieron con rapidez, sin mayores inconvenientes ni necesidad de tratamientos complementarios. Conclusión: El bloqueo epidural es una práctica frecuentemente usada en el manejo del dolor lumbar crónico. Los errores técnicos y las complicaciones del procedimiento son poco comunes, pero para su manejo y posterior corrección es importante conocerlos y contar con un médico experimentado...
Assuntos
Humanos , Analgesia Epidural , Dor , Ética , Erros de Medicação , Manejo da Dor , RadiculopatiaRESUMO
BACKGROUND: Adoptive immunotherapy with autologous and donor-derived cytotoxic T lymphocytes (CTL) has recently been used to treat Epstein Barr virus (EBV)-positive posttransplant lymphoproliferative disease (PTLD). METHODS AND RESULTS: We report complete regression of EBV-positive PTLD in an 18-month-old small bowel and liver transplant recipient after one infusion of partially human leukocyte antigen (HLA)-matched EBV-specific CTL grown ex vivo from an EBV seropositive unrelated blood donor. No infusion-related toxicity or evidence of graft-versus-host disease was observed. The tumor showed signs of regression within 1 week and EBV load in peripheral blood dropped to undetectable levels. Limiting dilution analyses (LDA) detected no EBV-specific CTL precursor (CTLp) cells before the infusion, and high numbers of CTLp at 4 hr and 24 hr post-CTL infusion. There was a reversal of the CD4/8 ratio in peripheral blood and an increase in HLA-DR positive CD8 cells. The patient has been in complete remission for 24 months. CONCLUSION: If this success is repeated in more PTLD patients, then stored CTL could be used for antiviral and antitumor therapies in immunocompromised patients.
Assuntos
Herpesvirus Humano 4/imunologia , Imunoterapia Adotiva , Intestino Delgado/transplante , Transplante de Fígado/efeitos adversos , Transtornos Linfoproliferativos/terapia , Complicações Pós-Operatórias/terapia , Linfócitos T Citotóxicos/imunologia , Antígenos HLA-DR/genética , Células-Tronco Hematopoéticas/imunologia , Teste de Histocompatibilidade , Humanos , Lactente , MasculinoRESUMO
By inactivating potent glucocorticoid hormones (cortisol and corticosterone), 11 beta-hydroxysteroid dehydrogenase type 2 (11 beta-HSD2) plays an important role in the placenta by controlling fetal exposure to maternal glucocorticoids, and in aldosterone target tissues by controlling ligand access to co-localized glucocorticoid and mineralocorticoid receptors. Amino acid sequence from homogeneous human placental 11 beta-HSD2 was used to isolate a 1897 bp cDNA encoding this enzyme (predicted M(r) 44126; predicted pI 9.9). Transfection into mammalian (CHO) cells produces 11 beta-HSD2 activity which is NAD(+)-dependent, is without reductase activity, avidly metabolizes glucocorticoids (Km values for corticosterone, cortisol and dexamethasone of 12.4 +/- 1.5, 43.9 +/- 8.5 and 119 +/- 15 nM respectively) and is inhibited by glycyrrhetinic acid and carbenoxolone (IC50 values 10-20 nM). Rabbit antisera recognizing 11 beta-HSD2 have been raised to an 11 beta-HSD2-(370--383)-peptide-carrier conjugate. Recombinant 11 beta-HSD2, like native human placental 11 beta-HSD2, is detectable with affinity labelling and anti-11 beta-HSD2 antisera, and appears to require little post-translational processing for activity. 11 beta-HSD2 mRNA (approximately 1.9 kb transcript) is expressed in placenta, aldosterone target tissues (kidney, parotid, colon and skin) and pancreas. In situ hybridization and immunohistochemistry localize abundant 11 beta-HSD2 expression to the distal nephron in human adult kidney and to the trophoblast in the placenta. 11 beta-HSD2 transcripts are expressed in fetal kidney (but not lung, liver or brain) at 21-26 weeks, suggesting that an 11 beta-HSD2 distribution resembling that in the adult is established by this stage in human development.
Assuntos
Anticorpos , Hidroxiesteroide Desidrogenases/genética , Hidroxiesteroide Desidrogenases/imunologia , Placenta/enzimologia , 11-beta-Hidroxiesteroide Desidrogenases , Adulto , Sequência de Aminoácidos , Animais , Sequência de Bases , Células CHO , Clonagem Molecular , Cricetinae , Primers do DNA/genética , DNA Complementar/genética , Feminino , Feto/enzimologia , Humanos , Hidroxiesteroide Desidrogenases/metabolismo , Hibridização In Situ , Masculino , Dados de Sequência Molecular , Estrutura Molecular , Reação em Cadeia da Polimerase , Gravidez , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Coelhos , Homologia de Sequência de Aminoácidos , Distribuição Tecidual , TransfecçãoRESUMO
11 beta-hydroxysteroid dehydrogenase type 2 (11 beta-HSD2) efficiently inactivates potent glucocorticoid hormones (cortisol and corticosterone), leaving aldosterone unmetabolized. Abundant 11 beta-HSD2 activity in human placenta plays a central role in controlling fetal glucocorticoid exposure, which if excessive is harmful and may predispose to low birth weight and hypertension in adulthood. Similar 11 beta-HSD2 activity in the distal nephron protects mineralocorticoid receptors from glucocorticoids and appears to be important in normal blood pressure control. We have purified human placental 11 beta-HSD2 16000-fold, to homogeneity, and determined over 100 residues of the internal amino acid sequence. Purification was assisted by a novel technique allowing highly specific (single spot on two-dimensional electrophoresis) photoaffinity labelling of active 11 beta-HSD2 in crude tissue extracts by its glucocorticoid substrates. This work reveals that 11 beta-HSD2 is a member of the short-chain alcohol dehydrogenase superfamily (apparent monomer M(r) approximately 40,000). It is a very basic (apparent pI = 9.1) intrinsic membrane protein, requiring as yet undefined membrane constituents for full stability. Affinity chromatography and affinity labelling studies suggest that 11 beta-HSD2 has a compulsory ordered mechanism, with NAD+ binding first, followed by a conformational change allowing glucocorticoid binding with high affinity.
