Síndrome de Valentino: una causa no común de abdomen agudo. Reporte de un caso / Valentino Syndrome: an uncommon cause of acute abdomen. Case Report.

INTRODUCCIÓN: El síndrome de Valentino es la perforación de una úlcera péptica a nivel gástrico o duodenal, en donde el paciente se presenta de forma atípica, con un cuadro clínico sugerente de apendicitis aguda, asociado a peritonitis localizada. Al ser una entidad con escasos reportes a nivel mundial y con ningún caso documentado en el Ecuador, es fundamental difundir el presente caso clínico para conocimiento de la comunidad médico-científica. CASO CLÍNICO: Paciente masculino de 63 años, acudió a servicio de emergencia con dolor abdominal de 12 horas de evolución localizado en fosa iliaca derecha asociado a signos de irritación peritoneal y descompensación hemodinámica, sugestivo de peritonitis. Se realizó laparotomía exploratoria. EVOLUCIÓN: En el procedimiento quirúrgico no se evidenciaron cambios inflamatorios en el apéndice y tras la exploración de la cavidad abdominal se encontró una úlcera gástrica perforada; se realizó rafia primaria en dos planos, apendicectomía incidental, más lavado de cavidad abdominal. Paciente con recuperación exitosa, se indicó alta médica al séptimo día de hospitalización. CONCLUSIÓN: La perforación de una úlcera péptica puede generar un cuadro clínico de dolor en fosa ilíaca derecha, que puede confundirse con una apendicitis aguda debido a su similitud clínica. El equipo médico debe considerar al Síndrome de Valentino como un diagnóstico diferencial importante durante la evaluación del paciente que llega a la emergencia con cuadro clínico de dolor abdominal sugestivo de apendicitis aguda.

BACKGROUND: Valentino's syndrome is secondary to a perforated peptic ulcer, which could be located in the stomach or the duodenum, patients present with clinical features that suggest acute appendicitis, with localized peritonitis. There are few case reports about this syndrome worldwide and no one submitted in Ecuador. It is essential to transmit this clinical case for the knowledge of the medical- scientific community. CASE REPORT: A 63-year-old male patient came to the emergency department with abdominal pain, located in the right iliac fossa, that began 12 hours ago, associated to peritoneal irritation signs and hemodynamic decompensation; suggestive of peritonitis. An exploratory laparotomy was performed. EVOLUTION: During exploratory laparotomy, no inflammatory changes were identified in the appendix. After abdominal cavity exploration, a perforated gastric ulcer was found. Primary raffia was stitched in two planes, incidental appendectomy and lavage of the abdominal cavity were performed. The patient had a successful recovery; and was discharged after 7 days at hospitalization. CONCLUSION: The perforation of a peptic ulcer can generate right iliac fossa pain, simulating acute appendicitis due to its clinical similarity. The medical team should consider Valentino's Syndrome as an important differential diagnosis during the evaluation of a patient that arrives to the emergency room with abdominal pain, suggestive of appendicitis.

Expression and bioregulation of the kallikrein-related peptidases family in the human neutrophil.

The family of kallikrein-related peptidases (KLKs) has been identified in a variety of immunolabeled human tissue sections, but no previous study has experimentally confirmed their presence in the human neutrophil. We have investigated the expression and bioregulation of particular KLKs in the human neutrophil and, in addition, examined whether stimulation by a kinin B(1) receptor (B1R) agonist or fMet-Leu-Phe (fMLP) induces their secretion. Western blot analysis of neutrophil homogenates indicated that the MM of the KLKs ranged from 27 to 50 kDa. RT-PCR showed that blood neutrophils expressed only KLK1, KLK4, KLK10, KLK13, KLK14 and KLK15 mRNAs, whereas the non-differentiated HL-60 cells expressed most of them, with exception of KLK3 and KLK7. Nevertheless, mRNAs for KLK2, KLK5, KLK6 and KLK9 that were previously undetectable appeared after challenging with a mixture of cytokines. Both kinin B(1)R agonist and fMLP induced secretion of KLK1, KLK6, KLK10, KLK13 and KLK14 into the culture medium in similar amounts, whereas the B(1)R agonist caused the release of lower amounts of KLK2, KLK4 and KLK5. When secreted, the differing proteolytic activity of KLKs provides the human neutrophil with a multifunctional enzymatic capacity supporting a new dimension for its role in human disorders of diverse etiology.