ARTICLE
TITLE

Peritonitis pelviana secundaria a malformación ginecológica en niña de 13 años. Presentación de un caso. Pelvic peritonitis secondary to a gynecological malformation in a 13 year-old girl. A case ReportPeritonitis pelviana secundaria a malformación ginecológica en niña de 13 años. Presentación de un caso. Pelvic peritonitis secondary to a gynecological malformation in a 13 year-old girl. A case ReportSe presentó una paciente en edad pediátrica con antecedentes de salud anterior, con dolor abdominal de varios días de evolución, vómitos y fiebre elevada. Al examen físico nos encontramos un abdomen ligeramente distendido fundamentalmente en hipogastrio, doloroso a los golpes de tos, a la palpación se encuentra una marcada reacción peritoneal, diagnosticándose cuadro de abdomen agudo por cuadro peritoneal, se le realizó laparotomía exploradora de urgencia con diagnostico presuntivo de Apendicitis Aguda Perforada, se comprobó la presencia de una malformación ginecológica consistente en 2 úteros separados y una duplicación vaginal, se corrigió anomalía vaginal, la paciente fue dada de alta y después de un ciclo menstrual se evaluó evolucionando satisfactoriamente y sin complicaciones. DeCS: ANOMALIAS, PERITONITIS, PELVIS, GINECOLOGIA.ABSTRACT A patient was presented in pediatric age with history of previous health with abdominal pain during several days, vomiting and high fever. At physical examination, we found a slightly distended abdomen mainly in the hypogastric region painful when coughing. At palpation a significant peritoneal reaction is seen, diagnosing acute abdomen picture for peritoneal picture, an urgent exploring laparotomy was performed with presumptive diagnosis of perforated acute appendicitis, it was documented the presence of gynecological malformation consistent in two separate uteri and a vaginal duplication, the vaginal abnormality was corrected, the patient was discharged from hospital and after a menstrual cycle she was evaluated evolving adequately and uneventfully.DeCS: ABNORMALITIES, PERITONITIS, PELVIS, GYNECOLOGY.

SUMMARY

DeCS: ABNORMALITIES, PERITONITIS, PELVIS, GYNECOLOGY.

PAGES
pp. Pág(s):83 - 92

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Déficit de 21-hidroxilasa: aspectos actuales / Deficiency of 21-hydroxylase: current aspectsDéficit de 21-hidroxilasa: aspectos actuales / Deficiency of 21-hydroxylase: current aspectsLa hiperplasia suprarrenal congénita (HSC) es una de las alteraciones autosómicas recesivas más frecuentes, caracterizada por un defecto enzimático en la síntesis de cortisol, la causa es en el 95% de los casos, la deficiencia de la enzima 21-hidroxilasa (21-OH). La 17-OH progesterona, precursor del cortisol, presenta valores elevados, marcadores del diagnóstico. Esta enfermedad presenta diferentes formas clínicas: las clásicas o graves comienzan desde el período neonatal, con síntomas debidos al exceso de andrógenos suprarrenales como virilidad y ambigüedad de los genitales externos de las niñas afectadas. En más del 70% de los casos se asocia con pérdida salina (deficiencia de aldosterona), potencialmente letal en varones que no se diagnostican precozmente. Resumimos las diferentes formas de presentación de la deficiencia de 21-OH, y describimos el diagnóstico y tratamiento. Los programas de detección precoz evitan la asignación incorrecta de sexo en la recién nacida y pueden salvar la vida de los varones con formas graves y pérdida salina. Comentamos el diagnóstico genético-molecular del CYP21A2 (cromosoma 6p 21.3). Revisamos las directrices futuras para el estudio y el tratamiento de esta enfermedad, incluyendo diversos tratamientos como la hormona de crecimiento, los antagonistas de las gonadotropinas y otros. El diagnóstico y tratamiento prenatales del feto femenino afectado son posibles, y los resultados son alentadores. Comentamos también, el abordaje hacia la transición y edad adulta, y la relevancia del control de la mujer con HAC durante la gestación. Palabras clave: Hiperplasia/diagnóstico/genética, esteroide 21-hodroxilasa/metabolismo, genitales/anomalías. ABSTRACT Congenital adrenal hyperplasia (CAH) is one of the most frequent autosomal recessive disorders. It is characterized by a deficiency of an enzyme involved in cortisol synthesis and in 95% of patients the cause is 21-hydroxylase deficiency. A diagnostic marker is elevated levels of 17-hydroxyprogesterone, a precursor of cortisol. CAH has several clinical forms, and classical or severe forms manifest in the neonatal period with symptoms due to excess adrenal androgen production such as virilization and ambiguity of the external genitalia in affected girls. In more than 70% of patients, there is associated salt wasting (aldosterone deficiency), which can be fatal in males without an early diagnosis. We summarize the various forms of presentation of 21-hydroxylase deficiency and describe diagnosis and treatment. Screening programs avoid incorrect sex assignment in the newborn and can save the lives of males with severe forms and salt wasting. We discuss the genetic-molecular diagnosis of CYP21A2 (chromosome 6p 21.3). We review future recommendations for the study and management of this disease, including several treatments such as, growth hormone, and gonadotrophin antagonists. Prenatal diagnosis and treatment in affected female fetuses are feasible and the results are encouraging. We also discuss the management of the transition to adulthood and the importance of follow-up of women with CAH during pregnancy.Key Words: Hyperplasia/diagnose/genetics, 21-steroid-hydroxylase/metabolism, genitals/anomalies.

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