RESUMEN
In this article, we describe the first, to our knowledge, reported case of severe bacteremic upper urinary tract infection with pyonephrosis-in the context of prior chronic urinary tract disease-caused by community-acquired methicillin-resistant Staphylococcus aureus (MRSA). The patient presented with fever and constitutional symptoms, and computed tomography revealed extensive renal parenchymal infection along with a staghorn calculus and dilatation of the pyelocalyceal system. His clinical condition rapidly deteriorated, and he developed uncontrollable sepsis, necessitating an emergent nephrectomy. Significant pyonephrosis was noted during surgery. Blood cultures yielded MRSA, and molecular analysis (by polymerase chain reaction) of the MRSA strains from blood and wound fluid showed that they were Panton-Valentine leukocidin positive and they also possessed SCCmecA type IV. Postoperatively, the patient was treated with intravenous vancomycin for 3 weeks and had a favorable outcome.
Asunto(s)
Infecciones Comunitarias Adquiridas/microbiología , Staphylococcus aureus Resistente a Meticilina/aislamiento & purificación , Pielonefritis/diagnóstico , Pielonefritis/microbiología , Pionefrosis/diagnóstico , Pionefrosis/microbiología , Infecciones Estafilocócicas/microbiología , Anciano de 80 o más Años , Antibacterianos/uso terapéutico , Infecciones Comunitarias Adquiridas/complicaciones , Humanos , Masculino , Pielonefritis/tratamiento farmacológico , Pionefrosis/tratamiento farmacológico , Infecciones Estafilocócicas/complicaciones , Infecciones Estafilocócicas/tratamiento farmacológico , Vancomicina/uso terapéuticoRESUMEN
AIM: To study the association of the frequency and pattern of KIT and PDGFRA mutations and clinicopathological factors in a group of patients with gastrointestinal stromal tumors (GIST). METHODS: Thirty patients with GIST were examined. Exons 9, 11, 13, and 17 of the KIT and exons 12 and 18 of the PDGFRA gene were analyzed for the presence of mutations by PCR amplification and direct sequencing. RESULTS: KIT or PDGFRA mutations were detected in 21 of the 30 patients (70%). Sixteen patients had mutations within KIT exon 11, three within KIT exon 9, and two within PDGFRA exon 18. GISTs with KIT exon 9 mutations were predominantly located in the small intestine, showed a spindle cell phenotype, and were assessed as potentially malignant. GISTs with KIT exon 11 mutations were located in the stomach and intestine, showed mainly a spindle cell phenotype, and were scored as potentially malignant (P < 0.05). Tumors with KIT exon 11 codon 557/558 deletion/insertion mutations were found to be associated with a potentially malignant clinical behaviour (P < 0.003). GISTs with PDGFRA mutations located in stomach showed a mixed cell phenotype and were classified as of very low or low moderate malignant potential. CONCLUSION: Determination of KIT and PDGFRA mutations should be additional parameters for the better prediction of GISTs clinical behaviour. Tumors with deletion/insertion mutations affecting codons 557/558 of the KIT gene seem to represent a distinct subset of malignant GISTs.
Asunto(s)
Exones , Tumores del Estroma Gastrointestinal , Mutagénesis Insercional , Proteínas Proto-Oncogénicas c-kit/genética , Receptor alfa de Factor de Crecimiento Derivado de Plaquetas/genética , Eliminación de Secuencia , Anciano , Anciano de 80 o más Años , Secuencia de Aminoácidos , Análisis Mutacional de ADN , Femenino , Tumores del Estroma Gastrointestinal/genética , Tumores del Estroma Gastrointestinal/patología , Humanos , Masculino , Persona de Mediana Edad , Datos de Secuencia Molecular , Fenotipo , Proteínas Proto-Oncogénicas c-kit/metabolismo , Receptor alfa de Factor de Crecimiento Derivado de Plaquetas/metabolismo , Estudios RetrospectivosRESUMEN
AIM: To investigate the incidence of KIT immunohistochemical staining in (GI) stromal tumors (GISTs), and to analyze the clinical manifestations of the tumors and prognostic indicators. METHODS: We retrospectively analyzed 50 cases of previously diagnosed GISTs. Tissue samples were assessed with KIT (CD117 antigen), CD34, SMA, desmin, S-100, NSE, PCNA, Ki-67, and BCL-2 for immunohistochemical study and pathological characteristics were analyzed for prognostic factors. RESULTS: Fifteen tumors (30%) were negative in KIT staining. A significant association was observed between gender (male patients: 14/15) and KIT-negative staining (P = 0.003).The patients's mean age was 56.6 years. Tumors developed in stomach (n = 8), small intestine (n = 5), large intestine (n = 1) and oesophagus (n = 1). The mean tumor size was 5.72 cm. The mitotic count ranged from 0-29/50 HPF (mean: 3.4) and 73% of tumors showed no necrosis. The majority of the tumors (67%) had dual or epithelioid differentiation. Tumors were classified as very low or low risk (n = 7), intermediate risk (n = 5), and high risk (n = 3) groups. Twelve (80%) patients were alive without evidence of residual tumor for an average period of 40.25 mo (12-82 mo); three patients developed metastatic disease to the liver and eventually died within 2-12 mo (median survival: 8.6 mo). CONCLUSION: A small subgroup of GISTs fulfils the clinical and morphological criteria of these tumors, and lacks KIT expression. These tumors predominantly developed in the stomach, being dual or epithelioid in morphology, which are classified as low risk tumors and presented a better survival status than KIT-positive tumors. The ability to diagnose GISTs still depends on immunohistochemical staining but the research should extend in gene mutations.