Hiperplasia epitelial focal / Focal epithelial hyperplasia

La hiperplasia epitelial focal (HEF) o enfermedad de Heck es una patolog¡a poco frecuente de la mucosa oral, caracterizada por una proliferaci¢n benigna del epitelio debida a la infecci¢n por el papilomavirus humano (PVH) tipos 13 y 32. El nombre enfermedad de Heck deriva del nombre del m‚dico que evalu¢ al primer paciente, en M‚xico, en 1961. Sin embargo, una revisi¢n de la literatura latinoamericana revela publicaciones previas realizadas por Estrada, en 1956, quien observ¢ esta entidad en indios colombianos. Algunos a¤os despu‚s, Soneira y Fonseca realizaron la primera descripci¢n completa de la enfermedad, y se¤alaron sus caracter¡sticas cl¡nicas e histol¢gicas y, adem s, sugirieron el posible origen viral. Finalmente, en 1965, Archard y col. la denominaron HEF, aunque en la actualidad se sugiere utilizar el nombre de hiperplasia multifocal del epitelio, que describe mejor las caracter¡sticas cl¡nicas y microsc¢picas de la enfermedad. La HEF, aunque.

The focal epithelial hyperplasia (HEF) or Heck's disease is a rare disease of the oral mucosa, characterized by benign epithelial proliferation due to infection with human papillomavirus (HPV) ttypes 13 and 32. The disease name derives Heck the name of the doctor who evaluated the first patient in Mexico in 1961. However, a review of Latin American literature reveals previous publications by Estrada, in 1956, who observed this entity in Colombian Indians. Some years later, Soneira and Fonseca made the first complete description of the disease, noting their clinical and histological features and also suggested the possible viral origin. Finally in 1965, Archard et al. HEF called it, although at present it is suggested to use the name multifocal epithelial hyperplasia, which best describes the clinical and microscopic features of the disease. The HEF is presented with a clear predominance of Americans, Eskimos and Indians some communities in South Africa, although isolated cases in other ethnic groups. In South America it is more common in the Amazon basin of Peru, Venezuela, Colombia, Bolivia, Brazil and Paraguay.

Falla terapéutica y hepatotoxicidad de los esquemas de tratamiento endovenoso e intramuscular con estibogluconato de sodio en pacientes con leishmaniasis cutánea / Therapeutic failure and hepatotoxicity with schemes intravenous and intramuscular sodium stibogluconate treatment in patients with cutaneous leishmaniasis

OBJETIVO. Describir la falla terapéutica y hepatotoxicidad de los esquemas de tratamiento endovenoso e intramuscular con estibogluconato de sodio en pacientes con leishmaniasis cutánea. MATERIAL y MÉTODOS. Estudio de cohorte única retrospectivo. Los pacientes fueron tratados con estibogluconato de sodio con el esquema endovenoso continuo por 20 días en una sola dosis, los que presentaron falla terapéutica recibieron un segundo curso de estibogluconato de sodio con el esquema intramuscular dosis dividido en series de la días de tratamiento con intervalos de 7 días de descanso por 3 series. Se revisó las historias clínicas y se evaluó en ambos grupos la falla terapéutica y hepatotoxicidad. RESULTADOS. Cumplieron los criterios de inclusión/exclusión 64 pacientes, todos varones. Leishmania braziliensis fue la especie de leishmania infectante en 96,4 % de casos. La cura fue de 48,4 % en el esquema endovenoso, L. braziliensis fue la única especie identificada en los pacientes con falla terapéutica. La hepatotoxicidad fue de 28,1 % en el esquema endovenoso y 6,3 % en el esquema intramuscular. El grupo de pacientes que falló con el esquema endovenoso y repitió el tratamiento pero con el esquema intramuscular (32 pacientes) tuvo un porcentaje de cura de 100 %; solo 2 pacientes (6,3 %) que recibieron el esquema intramuscular desarrollaron hepatotoxicidad durante el tratamiento. CONCLUSIONES. Existe una alta frecuencia de falla terapéutica y hepatotoxicidad en pacientes con Leishmaniasis cutánea tratados con estibogluconato de sodio con el uso del esquema endovenoso. Los pacientes tratados con el esquema intramuscular no presentan falla terapéutica y tienen una baja frecuencia de hepatotoxicidad.

OBJECTIVE. Describe the therapeutic failure and hepatotoxicity schemes intravenous and intramuscular sodium stibogluconate treatment in patients with cutaneous leishmaniasis (CL). MATERIAL AND METHODS. Retrospective single cohort study. Patients were treated with sodium stibogluconate with continuous intravenous scheme for 20 days in a single dose; those with therapeutic failure received a second course of sodium stibogluconate with intramuscular scheme doses divided into sets of 10 days of treatment with intervals 7 days off per 3 series. The medical records were reviewed and evaluated in both groups treatment failure and hepatotoxicity. RESULTS. They met the inclusion/exclusion of 64 patients, all males. The specie of leishmania was present in 96,4 % of cases was the Leishmania braziliensis. Curing was 48,4 % for the intravenous scheme, L. braziliensis was the only species identified in patients with therapeutic failure. Hepatotoxicity was 28,1% in the scheme intravenous and intramuscular 6,3 % in the scheme. The group of patients who failed with the scheme and repeated intravenous treatment but with the intramuscular scheme (32 patients) had a cure rate of 100 %; only 2 patients (6,3 %) who received intramuscular scheme developed hepatotoxicity during treatment. CONCLUSIONS. There is a high rate of treatment failure and hepatotoxicity in patients treated with CL with sodium stibogluconate intravenous use scheme. Patients treated with intramuscular scheme have no therapeutic failure and have a low frequency of hepatotoxicity.

Inocencias mutiladas: la explotación sexual comercial como forma de violencia contra la niña y la adolescente en Panamá / Mutilated innocences: the commercial sexual exploitation as a way of violence against the girl and the adolescent in Panama

Presenta la problemática de la explotación sexual contra las niñas y adolescentes, una forma de violencia de género, las implicaciones jurídicas en Panamá

Arthropod-Borne viral Diseases in Peru

Arthropode-Borne viral diseases have been a significant cause of morbidity and mortality for several decades in Peru. Epidemics and epizootics of Venezuelan equine encephalitis (VEE), subtype IAB virus occurred among humans and equine at intermittent intervals from 1925 through 1973 along the Pacific coastal plains, extending southward from the most northern Departament of Tumbes to the Departament of Ica. While the VEE IAB virus has not been detected since 1973, several isolates of VEE ID and an isolate VEE IIIC were obtained during 1971 and 1975 from mosquitoes and/or sentinel hamster in Quistococha, northeastern Amazon region. In 1994, the first human cases, associated with VEE virus ID were diagnosed among Peruvian soldiers near Pantoja, northern Amazon region, and during 1995, primarily among students and military personnel in Iquitos, northastern Amazon region. As early as 1913 , a disease resembling yellow fever was recognized in the Amazon region Peru. Outbreaks of this disease have continued to occur, apparently at annual interval, with the most recent and the largest sylvan outbreak ever recorded in Peru being documented during 1995 along the eastern foothills of the Andes Mountains. In 1990, dengue (DEN) 1 and DEN4 were first isolated in Peru during an outbreak of DEN fever among residents of the city of Iquitos, northeastern Amazon basin region. Seroepidemiological and case surveillance studies conducted 1992 through 1995 documented that DEN 1 continued to cause cases of DEN fever in Iquitos, and in 1995, an outbreak was associated with the introduction of DEN 2 into the community. Outbreaks of DEN fever, associated with DEN 1 occurred during 1994 and 1995 in the northern coastal cities of Tumbes and Piura, and in Pucallpa, Amazon basin region. In 1995, the first isolations of DEN 2 were obtained from febriles cases in Tumbes, Piura and Pucallpa. Although 2 serotypes of DEN were associated with human infection, none of the cases presented with hemorragic manifestations. The first isolations of Oropouche (ORO) fever virus were obtained during 1992 from febrile patients in Iquitos. The virus was isolated during 1994 from febrile cases and serological results revealed that ORO was the cause of an outbreak in the southeastern Amazon region. A single isolate of ORO virus was obtained during 1995 from a febrile patient in Iquitos