Máculas hiperpigmentadas y prolapso rectal, ¿qué debemos sospechar? / Hyperpigmented macules and rectal prolapse, what should we suspect?

El síndrome de Peutz-Jeghers (SPJ) es un síndrome autosómico dominante con una incidencia de 1 de cada 200 000 nacidos vivos. Las manifestaciones clínicas más frecuentes son las máculas hiperpigmentadas típicamente localizadas en la mucosa oral y la presencia de pólipos en el tracto gastrointestinal. A diferencia de la edad adulta, en Pediatría es excepcional el desarrollo de patología tumoral maligna. Sin embargo, en la edad pediátrica hay que tener un elevado índice de sospecha ante un paciente con diagnóstico de SPJ que presenta dolor abdominal compatible con una invaginación intestinal, ya que esta complicación es relativamente frecuente y precisa tratamiento quirúrgico urgente. Una vez realizado el diagnóstico de esta enfermedad, se deberán llevar a cabo controles periódicos mediante endoscopias a partir de los ocho años de edad (AU)

Peutz-Jeghers syndrome (PJS) is an autosomal dominant syndrome with an incidence of 1 in 200,000 live births. The most frequent clinical manifestations are hyperpigmented macules typically located on the oral mucosa and the presence of polyposis in the gastrointestinal tract.Unlike adulthood, in pediatrics the development of malignant tumor pathology is exceptional. However, in the pediatric age group, a high index of suspicion must be maintained when faced with a patient diagnosed with PJS who presents with abdominal pain compatible with intussusception, since this complication is relatively frequent and requires urgent surgical treatment. Once the diagnosis of this disease has been made, periodic controls should be carried out by means of endoscopies starting at eight years of age. (AU)

Potential role of tedizolid phosphate in the treatment of acute bacterial skin infections.

Tedizolid phosphate (TR-701), a prodrug of tedizolid (TR-700), is a next-generation oxazolidinone that has shown favorable results in the treatment of acute bacterial skin and skin-structure infections in its first Phase III clinical trial. Tedizolid has high bioavailability, penetration, and tissue distribution when administered orally or intravenously. The activity of tedizolid was greater than linezolid against strains of Staphylococcus spp., Streptococcus spp., and Enterococcus spp. in vitro studies, including strains resistant to linezolid and those not susceptible to vancomycin or daptomycin. Its pharmacokinetic characteristics allow for a once-daily administration that leads to a more predictable efficacy and safety profile than those of linezolid. No hematological adverse effects have been reported associated with tedizolid when used at the therapeutic dose of 200 mg in Phase I, II, or III clinical trials of up to 3 weeks of tedizolid administration. Given that the clinical and microbiological efficacy are similar for the 200, 300, and 400 mg doses, the lowest effective dose of 200 mg once daily for 6 days was selected for Phase III studies in acute bacterial skin and skin-structure infections, providing a safe dosing regimen with low potential for development of myelosuppression. Unlike linezolid, tedizolid does not inhibit monoamine oxidase in vivo, therefore interactions with adrenergic, dopaminergic, and serotonergic drugs are not to be expected. In conclusion, tedizolid is a novel antibiotic with potent activity against Gram-positive microorganisms responsible for skin and soft tissue infections, including strains resistant to vancomycin, linezolid, and daptomycin, thus answers a growing therapeutic need.