RESUMEN
Las resinas de intercambio iónico forman parte del tratamiento habitual de la hiperkaliemia, especialmente en pacientes con insuficiencia renal crónica. Estas resinas se han asociado en muchas ocasiones a lesiones del tracto digestivo, especialmente en el caso del poliestireno sulfonato sódico (Kayexalato) asociado a sorbitol. Presentamos el caso de un paciente con una hemorragia digestiva secundaria a colitis isquémica asociada a cristales de poliestireno sulfonato cálcico (Kalimato) sin sorbitol (AU)
Cation-exchange resins are used in the management of hyperkalemia, particularly in patients with end-stage renal disease. These resins were associated with gastrointestinal tract lesions, especially sodium polystyrene sulfonate (Kayexalate) mixed with sorbitol. We present a case of colonic necrosis after the administration of calcium polystyrene sulfonate (Kalimate) not suspended in sorbitol (AU)
Asunto(s)
Humanos , Masculino , Adulto , Intercambio Iónico , Resinas/métodos , Seudohipoaldosteronismo/diagnóstico , Hiperpotasemia/diagnóstico , Hiperpotasemia/terapia , Tracto Gastrointestinal , Tracto Gastrointestinal/lesiones , Hemorragia Gastrointestinal/complicaciones , Hemorragia Gastrointestinal/diagnóstico , Hemorragia Gastrointestinal/tratamiento farmacológico , Seudohipoaldosteronismo/terapia , Insuficiencia Renal/complicaciones , Hiperpotasemia/complicaciones , Insuficiencia Renal/diagnóstico , Insuficiencia Renal/terapia , Metanosulfonato de Etilo/uso terapéutico , Polianetolsulfonato/uso terapéutico , Sorbitol/uso terapéutico , Colitis/complicaciones , Colitis/diagnósticoRESUMEN
Myotonic dystrophy type 1 (DM1) is caused by the expansion of a (CTG).(CAG) repeat in the DMPK gene on chromosome 19q13.3. At least 17 neurological diseases have similar genetic mutations, the expansion of DNA repeats. In most of these disorders, the disease severity is related to the length of the repeat expansion, and in DM1 the expanded repeat undergoes further elongation in somatic and germline tissues. At present, in this class of diseases, no therapeutic approach exists to prevent or slow the repeat expansion and thereby reduce disease severity or delay disease onset. We present initial results testing the hypothesis that repeat deletion may be mediated by various chemotherapeutic agents. Three lymphoblast cell lines derived from two DM1 patients treated with either ethylmethanesulfonate (EMS), mitomycin C, mitoxantrone or doxorubicin, at therapeutic concentrations, accumulated deletions following treatment. Treatment with EMS frequently prevented the repeat expansion observed during growth in culture. A significant reduction of CTG repeat length by 100-350 (CTG).(CAG) repeats often occurred in the cell population following treatment with these drugs. Potential mechanisms of drug-induced deletion are presented.