Abstract:Background and purpose
Cancer patients treated with targeted therapies (e.g., epidermal growth factor receptor inhibitors) are susceptible to dermatologic adverse events (AEs) including secondary skin infections. Whereas infections such as paronychia and cellulitis have been reported, nasal vestibulitis (NV) has not been described with the use of these agents. The aim of our study was to characterize NV in cancer patients treated with targeted therapies.
Methods
We utilized a retrospective chart review of ca… Show more
“…The rates of bacterial superinfection reported here (21 %) are consistent with those reported by Eilers et al in 2009 (29 %) [7]. In addition to folliculitis and furunculosis, other bacterial superinfections of the skin such as nasal vestibulitis also appear to occur at a higher frequency in patients receiving EGFR inhibitors or other targeted chemotherapies [33].…”
The EGFR inhibitor-induced papulopustular eruption has a stereotypical time course and occurs in a characteristic distribution affecting the central face, upper chest, and back. Bacterial superinfections more frequently affect the extremities, abdomen, and groin and may occur at any point during EGFR therapy.
“…The rates of bacterial superinfection reported here (21 %) are consistent with those reported by Eilers et al in 2009 (29 %) [7]. In addition to folliculitis and furunculosis, other bacterial superinfections of the skin such as nasal vestibulitis also appear to occur at a higher frequency in patients receiving EGFR inhibitors or other targeted chemotherapies [33].…”
The EGFR inhibitor-induced papulopustular eruption has a stereotypical time course and occurs in a characteristic distribution affecting the central face, upper chest, and back. Bacterial superinfections more frequently affect the extremities, abdomen, and groin and may occur at any point during EGFR therapy.
“…Approximately 30% of healthy adults carry SA asymptomatically at any given moment, regardless of environment, with higher carriage rates and clinical infections in children and those with diabetes, obesity, or certain genetic polymorphisms or drug regimens affecting innate immunity. 1 – 6 The primary reservoir for SA in humans is the nasal vestibule, and it is now realized that clinical and methicillin-resistant SA (MRSA) strains are nasally carried by the general public. 7 – 9 Since nasal carriers of SA easily transmit their infectious strains and are themselves at risk for extra-nasal SA infections with their nasally carried strain, 10 , 11 factors controlling the duration of nasal colonization warrant further investigation.…”
Human Staphylococcus aureus (SA) nasal carriage provides a reservoir for the dissemination of infectious strains; however, factors regulating the establishment and persistence of nasal colonization are mostly unknown. We measured carriage duration and nasal fluid inflammatory markers after nasally inoculating healthy participants with their previously isolated SA strains. Ten out of 15 studies resulted in rapid clearance (9±6 days) that corresponded with upregulated chemokines, growth factors, and predominantly Th1-type cytokines, but not IL-17. Nasal SA persistence corresponded with elevated baseline levels of MIP-1β, IL-1β, and IL-6, no induction of inflammatory factors post-inoculation, and decreased IL-1RA:IL-1β ratio. SA-expressed staphylococcal protein A (SpA) levels correlated positively with carriage duration. Competitive inoculation studies revealed that isogenic SpA knockout (ΔSpA) strains were cleared faster than wild-type only in participants with upregulated inflammatory markers post-inoculation. The remaining participants did not mount an inflammatory response and did not clear either strain. ΔSpA strains demonstrated lower growth rates in carrier nasal fluids and lower survival rates when incubated with neutrophils. Collectively, the presented studies identify innate immune effectors that cooperatively modulate nasal carriage duration, and confirm SpA as a bacterial co-determinant of SA nasal carriage.
“…La vestibulitis nasal corresponde a la infección aguda localizada de la región pilosa del vestíbulo nasal 35 , se diferencia de la foliculitis por presentar un compromiso difuso no circunscrito al folículo piloso asociado a la presencia de costras 36 . Es producido por S. aureus meticilino sensible (MSSA) hasta en el 43%-81% de los casos, adicionalmente se han reportado casos con cultivos positivos para MRSA, Prevotella spp y N. dassonvillei en menor frecuencia 35,37,38 . El mecanismo por el cual se produce esta patología implica la existencia de dos factores, la existencia de una disrupción de la barrera epitelial que permite el paso de microorganismos hacia las estructuras subyacentes, asociado a la colonización por estos agentes, en especial por S. aureus; ambos factores presentes gatillan la producción de una respuesta inflamatoria que explica la sintomatología 39 .…”
Section: Vestibulitis Nasalunclassified
“…La vestibulitis nasal es considerada una patología frecuente, sin embargo, en el último tiempo sólo se han reportado datos epidemiológicos en población oncológica, con tasas de incidencias de hasta 45% 40 , destacando la ausencia de datos epidemiológicos en pacientes no oncológicos. Se han postulado algunos factores predisponentes para desarrollar esta patología, entre ellos factores ambientales (baja humedad y alteraciones del pH), mecánicos (rinorrea, manipulación de la nariz, cuerpos extraños, trauma y sonarse la nariz de forma excesiva), propios del individuo (enfermedades sistémicas, inmunosupresión, cirugías y tabaquismo), infecciones y el uso de medicamentos (diuréticos, isotretinoína y quimioterapia, principalmente en base a taxanos, Avastin y anticuerpos antifactor de crecimiento epidermal) 37,40 .…”
Section: Vestibulitis Nasalunclassified
“…Clínicamente, la vestibulitis nasal se presenta con dolor localizado en el vestíbulo y punta nasal, asociado a eritema, edema y en algunas ocasiones a epistaxis. En el examen físico típicamente se puede observar enrojecimiento de la piel del vestíbulo, sensibilidad a la manipulación y la presencia de costras amarillentas 25,37 . En relación al manejo no existen guías clínicas, en la práctica se suele realizar un manejo escalonado según la severidad del cuadro clínico, de esta forma en casos leves el tratamiento se realiza de forma ambulatoria en base a humectantes y antibióticos tópicos 35,37 , mientras que, frente a casos severos, o mala respuesta al tratamiento, signos de celulitis o formación de abscesos es recomendable un manejo hospitalizado, asociado al uso de antibióticos sistémicos en conjunto al tratamiento tópico previamente descrito, lo cual permitiría un mejor control del cuadro infeccioso 25,35,37 .…”
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