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Postdiarrheal Shiga Toxin-Mediated Hemolytic Uremic Syndrome Similar to Septic Shock Translated title: Síndrome urémico hemolítico símil shock séptico, posterior a diarrea mediada por toxina shiga

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      Abstract

      The inflammatory response of host endothelial cells is included in the development of vascular damage observed in enterohemorrhagic Escherichia coli (EHEC) infection, resulting in hemolytic uremic syndrome (HUS). The response to a non-conventional treatment for a group of D+ HUS (diarrhea positive HUS) patients, with clinical hemodynamic parameters of septic shock was evaluated in this prospective study (1999-2003). Twelve children 2.8 ± 0.6 years old, with D+ HUS produced by E. coli infection with serological evidence of Shiga toxin, presenting severe unstable hemodynamic parameters and neurological dysfunction at onset, were studied. The protocol included fresh frozen plasma infusions, methylprednisolone pulses (10mg/k/day) for three consecutive days and plasma exchange for five days, starting after admission to the intensive care unit (ICU). The twelve patients with increased pediatric risk of mortality (PRISM) score: 18 ± 2 after admission to intensive care unit (ICU), required dialysis for 17.4 ± 4 days, mechanical ventilator assistance for 10 ± 1 days and early inotropic drugs support for 10.5 ± 1 days. Neurological dysfunction included generalized tonic-clonic seizures lasting for 5.4 ± 1 days, n:8. Focal seizures were present in the remaining patients. Dilated cardiomyopathy was present in 6 children. Eight children suffered hemorrhagic colitis. Nine patients survived. Within one year of the injury, neurological sequelae, Glasgow outcome scale (GOS) 3 and 4, were present in two patients, chronic renal failure in one patient. We suggest that early introduction of this protocol could benefit D+ HUS patients with hemodynamic instability and neurological dysfunction at onset. Further studies are likely to elucidate the mechanisms involved in this early adverse clinical presentation of D+ HUS patients.

      Translated abstract

      La respuesta inflamatoria de la célula endotelial se incluye en el desarrollo del daño vascular observado en la infección por Escherichia coli enterohemorrágica que deviene en Síndrome Urémico Hemolítico (SUH). Se evaluó en forma prospectiva, entre 1999 y 2003, la respuesta a un tratamiento no convencional, en doce pacientes, edad 2.8 ± 0.6 años, que desarrollaron SUH con presencia de diarrea sanguinolenta (SUH D+) y evidencia serológica de toxina Shiga, los cuales en fase inicial presentaron parámetros hemodinámicos compatibles con shock séptico y compromiso neurológico grave. El protocolo incluyó transfusión de plasma fresco, pulsos de metilprednisolona (10mg/k/día) por tres días consecutivos y plasmaféresis por cinco días, iniciados en las primeras 48 horas. Los doce pacientes ingresaron en terapia intensiva, presentando una puntuación de riesgo de mortalidad pediátrica (PRISM): 18 ± 2, con requerimiento de diálisis por 17.4 ± 4 días, asistencia ventilatoria mecánica por 10 ± 1días y soporte temprano con drogas inotrópicas por un período de 10.5 ± 1 días. La disfunción neurológica se presentó con convulsiones tónico-clónicas generalizadas por 5.4 ± 1 días en 8 pacientes y con convulsiones focalizadas en los restantes. Seis pacientes desarrollaron miocardiopatía dilatada y 8 presentaron colitis hemorrágica. Sobrevivieron a la etapa aguda de la enfermedad 9 pacientes. Al finalizar el primer año de seguimiento, dos de ellos presentaban secuelas neurológicas (escala de seguimiento de Glasgow; GOS 3 y 4 respectivamente) y uno, fallo renal crónico. La introducción temprana de este protocolo podría beneficiar a pacientes con SUH D+ con inestabilidad hemodinámica grave y disfunción neurológica al inicio. Los mecanismos involucrados en esta temprana presentación clínica adversa de SUH D+ permanecen aún sin dilucidar.

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      Most cited references 48

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      How I treat patients with thrombotic thrombocytopenic purpura-hemolytic uremic syndrome.

       Daniel George (2000)
      Thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS) are, in adults, clinically and pathologically indistinguishable except for the severity of renal failure. They are best described as a single disorder, TTP-HUS, because the diagnostic evaluation and initial management are the same. Treatment with plasma exchange, available for more than 20 years, has dramatically altered the course of disease in adults with TTP-HUS. Plasma exchange has improved survival rates from 10% to between 75% and 92%, creating urgency for the initiation of treatment. This has resulted in decreased stringency of diagnostic criteria, which in turn has resulted in a broader spectrum of disorders for which the diagnosis of TTP-HUS is considered. Long-term follow-up has revealed increasing frequencies of relapse and of chronic renal failure. Although the increased survival rate is dramatic and recent advances in understanding the pathogenesis of these syndromes are remarkable, clinical decisions remain empirical. Therefore, the management decisions for patients with suspected TTP-HUS rely on individual experience and opinion, resulting in many different practice patterns. Multipractice clinical trials are required to define optimal management. (Blood. 2000;96:1223-1229)
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        Regulation of cytokine and cytokine receptor expression by glucocorticoids.

        Glucocorticoids (GCS) profoundly inhibit several aspects of T cell immunity largely through inhibition of cytokine expression at the transcriptional and posttranscriptional levels. GCS were also reported to act indirectly by inducing transforming growth factor-beta expression, which in turn blocks T cell immunity. In exerting their antiproliferative effects, GCS diffuse into target cells where they bind their cytoplasmic receptor, which in turn translocates to the nucleus where it inhibits transcription of cytokine genes through direct binding to the glucocorticoid response elements (GRE), which are located in the promoter region of cytokine genes or, alternatively, through antagonism of the action of transcription factors required for optimal transcriptional activation. In contrast to their inhibitory effects on cytokine expression, GCS up-regulate cytokine receptor expression that correlates with enhanced cytokine effects on target cells. In this review, we summarize the current state of knowledge of the mechanism of action of GCS, including the phenomenon of steroid-induced rebound, which ensues upon GCS withdrawal.
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          Corticosteroids for septic shock.

           D Annane (2001)
          To gather the data to provide a rationale for using replacement therapy with hydrocortisone in septic shock patients. The Medline and the Cochrane Library databases. Studies in animals and in humans were considered when significant data were available about the mechanisms of action of corticosteroids or about their use in severe sepsis. Corticosteroids were the first anti-inflammatory drugs tested in septic patients. Randomized trials clearly showed that a short course of a large dose of anti-inflammatory steroids is ineffective and potentially harmful in patients with severe sepsis. Recent demonstrations of altered hypothalamic-pituitary-adrenal axis response to septic insult have led to a reappraisal of the use of steroids in septic shock. Randomized trials in catecholamine-dependent septic shock patients strongly suggest that replacement therapy with hydrocortisone may alleviate the symptoms of systemic inflammatory response, reduce the duration of shock, and favorably affect survival. Current evidence that the therapeutic interest of replacement therapy with corticosteroids increases suggests that low doses of hydrocortisone should be offered to patients with catecholamine-dependent septic shock.
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            Author and article information

            Affiliations
            [1 ] Universidad Nacional de Cuyo Argentina
            [2 ] Universidad Nacional de Cuyo Argentina
            Contributors
            Role: ND
            Role: ND
            Role: ND
            Role: ND
            Role: ND
            Role: ND
            Role: ND
            Journal
            medba
            Medicina (Buenos Aires)
            Medicina (B. Aires)
            Fundación Revista Medicina (Ciudad Autónoma de Buenos Aires )
            1669-9106
            October 2005
            : 65
            : 5
            : 395-401
            S0025-76802005000500003

            http://creativecommons.org/licenses/by/4.0/

            Product
            Product Information: SciELO Argentina
            Categories
            MEDICINE, GENERAL & INTERNAL

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