Conjuntivitis postnatal en un paciente premature causada por cytomegalovirus / Cytomegalovirus induced postnatal conjunctivitis in a premature patient

El citomegalovirus (CMV) constituye en la actualidad el principal virus causante de infecciones congénitas, neonatales y perinatales en la población pediátrica sana. La conjuntivitis por CMV es una entidad muy poco frecuente apenas recogida en la literatura. Se presenta ocasionalmente en niños inmunodepremidos con procesos leucémicos. También se ha podido detectar la presencia de CMV en las lágrimas de pacientes con mononucleosis por CMV, enfermos de SIDA y pacientes sometidos a trasplante renal. Se presenta un caso de conjuntivitis neonatal en un paciente con presencia del virus en el tracto respiratorio y orina. Debido a que el proceso inflamatorio y el aislamiento viral sólo se detectó en un ojo, se postula la posibilidad de que el proceso de autoinoculación a través de las manos del paciente sea la causa del proceso (AU)

Cytomegalovirus (CMV) is actually the principal viral etiological agent of congenital, neonatal and perinatal infections in healthy pediatric patients. The conjunctivitis caused by CMV is an infrequent pathology described in the literature. This entity has been occasionally described inimmunossuppresed children with leukemic processes. The virus could be detected in the tears of CMV mononucleosis children, AIDS patients and patients with kidney transplants. We report a neonatal CMV conjunctivitis in a child with this virus in the respiratory tract and urine. Because the inflammatory process and the viral isolation could be detected in one eye only, we postulated that the auto-inoculation, with hands, could be the cause of the conjunctivitis process (AU)

[Surgical management in subfoveal choroidal neovascularization in high myopia. Analysis of results]. / Tratamiento quirúrgico de la neovascularización coroidea subfoveolar en el miope magno. Análisis de los resultados.

PURPOSE: To analyse results obtained from treatment of choroidal neovascular membranes (CNM) in patients with high myopia after vitrectomy and CNM extraction. MATERIAL AND METHOD: A prospective study including 9 eyes (9 patients) suffering from high myopia (higher than 6 diopters of myopia and/or axial length of more than 26 mm) and subfoveal CNM treated with vitrectomy and membrane extraction. Mean age was 43.11 S.D. 9.02 years of age (range: 32-58). Mean follow up time was 28.44 S.D. 7.65 months (range: 14-39 months). RESULTS: Preoperatory best corrected visual acuity (BCVA) was 0.09 S.D. 0.05 (range: 0.01-0.2). Postoperatory BCVA resulted in 0.15 S.D. 0.09 (range: 0.1-0.4). Differences did not show statistical signification (p= 0.09, Student T test). One case of membrane recurrence was observed, one case developed increased intraocular pressure and cataract requiring extraction; another presented increased intraocular pressure in the early postoperative period. CONCLUSION: Extraction of CNM in high myopia using vitrectomy does not show significant improvements in BCVA.

Tratamiento quirúrgico de la neovascularización coroidea subfoveolar en el miope magno. Análisis de los resultados / Surgical management in subfoveal choroidal neovascularization in high myopia. Analysis of results

Objetivos: Analizar los resultados obtenidos en el tratamiento de la membrana neovascular (MNV) subretiniana en el miope magno mediante vitrectomía y extracción de la MNV. Método: Analizamos prospectivamente 9 ojos de 9 pacientes con miopía magna (mayor de 6 dioptrías y/o longitud axial superior a 26 mm) con MNV subretiniana subfoveolar tratados mediante vitrectomía y extracción de MNV. La edad media era de 43,11 D.S. 9,O2 años (rango: 32-58 años). El seguimiento medio ha sido de 28,44 D.S. 7,65 meses (rango: 14-39 meses).Resultados: La agudeza visual corregida (AVC) preoperatoria era de 0,09 D.S. 0,05 (rango: 0,01-0,2). Tras el tratamiento la AVC fue de 0,15 D.S. 0,09 (rango: 0,1-0,4), diferencia sin significación estadística (p = 0,09, t de Student datos apareados). En un caso la MNV recidivó, un caso desarrolló hipertensión ocular y catarata que requirió su extracción y en otro caso apareció una hipertensión ocular en el postoperatorio inmediato. Conclusiones: El tratamiento de las MNV subfoveolar en el miope magno mediante su extracción por vitrectomía no logra mejoría significativa de la AVC (AU)

High frequency of Ki-ras amplification and p53 gene mutations in adenocarcinomas of the human esophagus.

Mutated ras genes have been found to be conspicuously absent from primary tumors of the esophagus, although high expression of ras p21 oncoprotein in some esophageal squamous cell carcinomas and mutations of the Ki- and Ha-ras genes in esophageal carcinoma cell lines have been reported. In this study, we found amplification of the Ki-ras gene in four of 10 esophageal adenocarcinomas (40%). No such amplification was observed among 61 squamous cell carcinomas, one pseudosarcomatous carcinoma, and eight esophageal cell lines, nor in six adenocarcinomas of the stomach. In two samples on which immunohistochemical analysis could be performed, we found overexpression of Ki-ras proteins when compared with normal samples. This Ki-ras amplification in esophageal tumors did not correlate with any pathological feature of the tumors, with the survival of the patients, or with the presence of other genetic alterations. These findings provide the first evidence for amplification of the Ki-ras gene in human esophageal cancer, which is restricted to adenocarcinomas. We also found that six of eight adenocarcinomas had point mutations in the p53 gene; this is a considerably higher prevalence than that reported for esophageal squamous cell carcinomas. These results strongly suggest that esophageal adenocarcinomas differ from squamous cell carcinomas in their molecular genetic characteristics.

Possible role of activated ras genes in human esophageal carcinogenesis.

Activation by point mutation of the H-, K- and N-ras genes is found in many tumors. However, no such mutation has yet been found in human esophageal carcinomas from various parts of the world. We have confirmed the absence of mutation at codons 12, 13 and 61 of K- and N-ras and at codons 12 and 61 of H-ras in 25 primary tumors obtained in France. In contrast, among 7 human esophageal carcinoma cell lines (TE1, TE2, TE3, TE8, TE9, TE10, TE13) with different degrees of tumorigenicity in nude mice, 3 highly tumorigenic lines (TE1, TE2 and TE8) exhibited activation of ras oncogenes; 2 showed a G35 to A35 transition of K-ras gene and one a H-ras G35 to T35 transversion. Since these cell lines had been established from tumors of Japanese patients from Sendai, we examined 3 primary esophageal tumors from Tokyo and 19 from Sendai, including the primary tumors from which the TE cell lines had been derived. No ras mutation was detected, which suggests that the ras gene mutations in the TE cell lines are either due to their long-term culture or that only a small portion of the original tumors contained such mutations. In order to directly examine the effect of ras gene mutation, one of the non-tumorigenic cell lines, TE13, was transfected with a plasmid coding for a mutated H-ras gene (G35 to T35). Transfected clones expressing high levels of mutated ras gene were able to induce tumors in nude mice. Thus, although no primary human esophageal tumor contained mutated ras genes, our studies do not exclude a significant role of mutated ras genes in cell proliferation and malignant transformation of human esophageal cells.

Amplification of epidermal growth factor receptor gene but no evidence of ras mutations in primary human esophageal cancers.

Primary esophageal squamous cell carcinomas from 41 patients were analyzed for the presence of proto-oncogene alterations associated with this malignancy. The occurrence of activating ras gene mutations in 25 tumors was determined using oligomer hybridization of target sequences amplified by polymerase chain reaction. We found no evidence for mutations in codons 12 and 61 of the H-ras, K-ras, and N-ras genes, nor in codon 13 of the K-ras and N-ras loci in any of these tumors. The apparent absence of activated ras oncogene in esophageal cancers represents a possible exception to the presence of these mutations found consistently in numerous other types of human malignancies, and is in striking contrast to the 40% prevalence of ras mutations in human colorectal cancers. Southern blot hybridization experiments with DNAs from tumors demonstrated amplification of the epidermal growth factor receptor gene (c-erbB) in two of 25 carcinomas. No amplification of the structurally related c-erbB2 (neu) gene was detected. In three out of 12 carcinomas, the level of epidermal growth factor receptor RNA was significantly higher than in normal esophageal mucosal tissue. Our results suggest that enhanced transcription of the epidermal growth factor receptor gene is associated with the development of some esophageal cancers.