Anisakiasis múltiple / No disponible

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[Portal and mesenteric thrombosis associated with protein S deficiency]. / Trombosis portal y mesentérica asociada al déficit de la proteína S.

INTRODUCTION: liver cirrhosis is the main cause of portal thrombosis (PT), while hypercoagulability syndromes are rarely found as the etiology of PT. We report a case of portal and mesenteric thrombosis secondary to protein S deficiency. CASE REPORT: a 74-year-old woman was admitted with melena secondary to upper gastrointestinal bleeding. She reported mild, diffuse abdominal pain in the last 2 weeks. Endoscopy revealed ruptured esophageal varices. Doppler ultrasonography and CT demonstrated a heterogeneous liver, splenomegaly and ascites, and complete non-occlusive PT involving the hilum and portal branches, as well as the superior mesenteric vein, with portosystemic collaterals. At this point a complete study for cirrhosis etiologies was negative, including a liver biopsy that showed nonspecific architectural changes secondary to diminished blood flow, which suggested non-cirrhotic portal hypertension. The search for hypercoagulability states determined a deficiency of S protein, with total pS = 107% and free pS = 56%. The patient was started on anticoagulant treatment and no other thrombotic events occurred. DISCUSSION: PT usually manifests without specific symptoms. The most common presentation is upper gastrointestinal bleeding, as occurred in our patient. Liver cirrhosis is one of the most frequent cause of PT. Up to 65% of these patients present an associated prothrombotic state, including protein S deficiency. Our case reminds us of the importance of a systematic search for hipercoagulability syndromes in patients with TP, even when the etiology can be conferred to liver cirrhosis.

Trombosis portal y mesentérica asociada al déficit de la proteína S / No disponible

Introducción: la causa más frecuente de trombosis portal (TP)es la cirrosis hepática, mientras que los estados hipercoagulables sonraramente identificados como etiología de la TP. Presentamos uncaso de TP y mesentérica secundaria al déficit de la proteína S (pS).Caso clínico: paciente mujer de 74 años, que debuta con dolorabdominal difuso de 2 semanas de evolución y hemorragia digestivaalta tipo melena secundaria a varices esofágicas. En el estudiose objetiva un hígado heterogéneo, esplenomegalia y ascitis,así como una trombosis portal completa no oclusiva del hilio hepáticoy de sus ramas y de la vena mesentérica superior con circulacióncolateral. El estudio etiológico de hepatopatía fue negativo,incluyendo una biopsia hepática que mostraba cambios arquitecturalessecundarios al flujo hemático disminuido compatible conhipertensión portal no cirrótica. El estudio de hipercoagulabilidadfue positivo para un déficit de proteína S. pS libre 56%, pS total107%. Desde entonces se inició tratamiento anticoagulante sinpresentar descompensaciones posteriores.Discusión: la trombosis portal suele manifestarse con síntomasinespecíficos, siendo la forma de presentación más frecuentela hemorragia digestiva alta como el caso que nos ocupa. La cirrosises una de las causas más frecuentes de trombosis portal, sinembargo existe hasta un 65% de estos pacientes que tienen unaenfermedad protrombótica asociada, como es el déficit de proteínaS. Nuestro caso remarca la importancia de realizar estudios defactores trombogénicos en pacientes con TP, incluso cuando laetiología se puede atribuir a una cirrosis

Introduction: liver cirrhosis is the main cause of portalthrombosis (PT), while hypercoagulability syndromes are rarelyfound as the etiology of PT. We report a case of portal andmesenteric thrombosis secondary to protein S deficiency.Case report: a 74-year-old woman was admitted with melenasecondary to upper gastrointestinal bleeding. She reported mild, diffuseabdominal pain in the last 2 weeks. Endoscopy revealed rupturedesophageal varices. Doppler ultrasonography and CT demonstrateda heterogeneous liver, splenomegaly and ascites, andcomplete non-occlusive PT involving the hilum and portal branches,as well as the superior mesenteric vein, with portosystemic collaterals.At this point a complete study for cirrhosis etiologies was negative,including a liver biopsy that showed nonspecific architecturalchanges secondary to diminished blood flow, which suggested noncirrhoticportal hypertension. The search for hypercoagulabilitystates determined a deficiency of S protein, with total pS = 107%and free pS = 56%. The patient was started on anticoagulant treatmentand no other thrombotic events occurred.Discussion: PT usually manifests without specific symptoms.The most common presentation is upper gastrointestinal bleeding,as occurred in our patient. Liver cirrhosis is one of the mostfrequent cause of PT. Up to 65% of these patients present an associatedprothrombotic state, including protein S deficiency. Ourcase reminds us of the importance of a systematic search forhipercoagulability syndromes in patients with TP, even when theetiology can be conferred to liver cirrhosis (AU)