Extensive Hepatic Infarction due to Polycythemia Vera.

Polycythemia vera (PV) is one of the three BCR-ABL1-negative myeloproliferative neoplasms characterized by activating mutations in JAK2, which clinically presents as erythrocytosis and has an increased risk of both thromboembolic events and progression to myelofibrosis and acute myeloid leukemia. Splanchnic vein thrombosis is a rare manifestation of venous thromboembolism involving one or more abdominal vessels and is strongly associated with PV. We herein report a case in which hepatic infarction due to PV was saved by conservative treatment.

Hypereosinophilic syndrome with massive liver infarction: A case report.

RATIONALE: Liver infarction caused only by hepatic artery occlusion is rare. Elevated levels of eosinophils in the blood and tissue can have devastating consequences. PATIENT CONCERNS: Male, 21 years old, presented with persistent abdominal distension and discomfort for more than ten days without an apparent cause. Laboratory findings showed an eosinophil percentage of 32.5% (normal range 0.5%-5%). Computed tomographic angiography of the hepatic artery and its branches did not show any enhancement, only the common hepatic artery was visible. DIAGNOSIS: The patient in this case had a peripheral blood eosinophil count of ≥1.5 × 109/L in multiple examinations over 6 months, and eosinophilic leukemia and secondary causes such as parasitic infections, allergic diseases, or tumors were ruled out, confirming the diagnosis of hypereosinophilic syndrome (HES). INTERVENTIONS: The patients were treated with interventional therapy, glucocorticoid pulse therapy and anti-infection therapy. OUTCOMES: After interventional therapy, glucocorticoid pulse therapy, and anti-infection treatment, the patient was reexamined 2 months later. The CT scan showed that the range of the original infarction in the liver had shrunk compared to before, and the remaining liver had enlarged with good compensation; Laboratory tests improved compared with baseline: eosinophil percentage of 0.1%. LESSONS: This article discusses a rare case of hepatic artery occlusion and liver infarction in a young male patient with HES. The cause of hepatic artery embolism and hepatic infarction may be related to the abnormal increase in eosinophils, which can lead to hypercoagulation and thrombus formation. The article emphasizes the importance of timely diagnosis and treatment of HES to prevent life-threatening thrombotic events and describes the successful management of the patient condition through anticoagulation, anti-infection, liver protection, and glucocorticoid therapy.

Sífilis congénita e infarto hepático, una asociación no reportada. Descripción de un caso pediátrico / Congenital syphilis and hepatic infarction, a not previously reported association. A pediatric case report

La sífilis congénita es causada por la infección del feto con Treponema pallidum durante el embarazo. Los síntomas son variables. Si bien es común el daño endotelial, no suele estar presente en los casos congénitos. Reportamos el caso de un lactante de 42 días de vida hospitalizado por masa abdominal. Las imágenes confirmaban la presencia de una lesión en el lóbulo hepático izquierdo sin efecto de masa. Las biopsias mostraron cambios compatibles con infarto y hepatitis neonatal. Las serologías del paciente y de su madre confirmaron el diagnóstico de sífilis congénita, y recibió tratamiento con penicilina intravenosa. El hígado se encuentra protegido de los daños isquémicos gracias a su doble irrigación, pero la acumulación de noxas puede haber provocado dicha presentación inusual. Tres meses más tarde, el paciente se encontraba libre de síntomas y la resonancia de control mostró atrofia del lóbulo izquierdo, mientras el resto del parénquima no presentaba alteraciones.

Congenital syphilis is caused by Treponema pallidum infection of the fetus during pregnancy. Symptoms are variable. While endothelial damage is common, it is not usually present in congenital cases. Here we report the case of a 42-day-old infant hospitalized due to an abdominal mass. Imaging studies confirmed the presence of an injury in the left lobe of the liver without mass effect. Biopsies showed changes compatible with infarction and neonatal hepatitis. The patient's and his mother's serologies confirmed the diagnosis of congenital syphilis, and he was treated with intravenous penicillin. The liver protected from ischemic injury by its double irrigation, but the accumulation of harmful agents may have caused this unusual presentation. Three months later, the patient was symptom-free, and the control MRI showed atrophy of the left lobe, while the rest of the parenchyma was unchanged.

Comments and illustrations of the WFUMB CEUS liver guidelines: Rare vascular pathology, part II.

In this second part of the topic the hepatic pseudoaneurysm, hepatic infarction, and pylephlebitis are discussed as acute and potentially life-threatening hepatic vascular diseases. The focus is on their appearance on B-mode ultrasonography, duplex ultrasonography, and contrast-enhanced ultrasonography. Zahn's pseudo infarction is an important differential diagnosis to wedge-shaped hepatic infarction in this context. Knowledge of the data should help raise awareness of these rare findings, to come up with relevant differential diagnoses in the corresponding clinical situation, to interpret the ultrasound images correctly and thus to initiate the appropriate diagnostic and therapeutic steps in time.

Acute Hepatopathy in a Dog Secondary to Hypothyroidism-Induced Atherosclerotic Infarction and Necrosis.

A 7 yr old male beagle was examined because of lethargy, anorexia, and cranial abdominal discomfort. Significant clinicopathologic abnormalities included severe liver enzyme elevations and hypercholesterolemia. Abdominal imaging identified vascular compromise of the left lateral liver lobe and a gallbladder mucocele. Following liver lobectomy and cholecystectomy, the dog's clinical signs resolved, and liver enzymes substantially improved. Diffuse hepatocellular infarction and necrosis secondary to multifocal atherosclerosis was present on histopathology of the liver. Hypothyroidism was subsequently diagnosed. Restoration of euthyroidism with oral levothyroxine therapy resolved the remaining liver enzyme elevations and hypercholesterolemia. To the author's knowledge, this is the first case report of hypothyroidism resulting in a clinically apparent and resolvable acute hepatopathy due to atherosclerosis. Clinicians should include atherosclerosis as a differential diagnosis for dogs with an acute hepatopathy and investigate dogs for hypothyroidism if atherosclerosis is diagnosed on liver biopsy.

A case of segmental hepatic necrosis complicating oxaliplatin and capecitabine chemotherapy A case report and review of the literature.

Chemotherapy is associated with different patterns of histopathological changes of the non-tumor-bearing liver. Hepatic infarction represents a relatively rare condition; the prevalence in several series of consecutive autopsies is 1.1%. To the best of our knowledge, no cases of liver infarction secondary to chemotherapy have been reported to date. We report a case of segmental hepatic infarction following the adjuvant chemotherapy with Oxaliplatin and Capecitabine in a patient who had undergone total gastrectomy and distal esophagectomy for gastric cancer. Liver infarction is usually managed by conservative therapy; interventional procedures such as percutaneous imaging-guided drainage or surgical evacuation should be reserved in cases where septic complications occur, with development of a hepatic abscess from the necrotic area. It is important to avoid misdiagnoses with liver metastases in order to define the most appropriate clinical management strategy. KEY WORDS: Adjuvant chemotherapy, Gastric cancer, Liver infarction, Hepatic necrosis.

A case of massive hepatic infarction in severe preeclampsia as part of the HELLP syndrome.

Hepatic infarction is a rare and fatal complication associated with hemolysis, elevated liver enzymes and low platelets syndrome. It can develop into fulminant liver failure and lead to death in 16% of cases. A 25-year-old woman, with unremarkable prenatal history, was sent to gynecological emergency unit for management of severe preeclampsia at 30 weeks and 4 days of pregnancy. Initial laboratory studies revealed aspartate aminotransferase at 290 U/L, alanine aminotransferase at 193 U/L and a normal value of hemoglobin, platelets and the prothrombin time. Behind the persistence of high blood pressure despite dual therapy, an emergent cesarean section was performed. However, two days after surgery, the patient accused an epigastric pain and was subsequently noted to have developed HELLP syndrome: thrombocytopenia (77000 /ul), anemia (hemoglobin 9.1 g/dL) and worsened liver injury (aspartate aminotransferase 2809 U/L; alanine aminotransferase 2502 U/L). A thoraco-abdominopelvic computed tomography (CT) was performed, which revealed massive hepatic infarction more marked on the right lobe, by showing the existence of diffuse hypodense plaques, poorly limited, not enhanced after injection, interesting all hepatic segments. The vascular permeability of the portal and subhepatic was preserved. During the surveillance, the laboratory tests worsened (hemoglobin = 4,6 g/dl; platelets count = 20000 /ul; WBC = 26000 /ul; CRP = 340 mg/l; albumin = 16 g/l, prothrombin time (PT) = 50%). The patient received antibiotics, she was transfused by red blood cells and platelets concentrates, she also received albumin with the pleural effusion drainage. The damaged hepatic areas stayed stable in control CT and the patient gradually improved here biological test, to become normal at 11 days after delivery. Hepatic infarction is an extraordinarily rare complication of preeclampsia. The diagnosis should be suspected by noting elevated liver enzymes, thrombocytopenia and typical images of hepatic infarction on abdominal CT. Early recognition and multidisciplinary management is necessary to prevent hepatic failure and death.

Cell-specific regulatory effects of CXCR2 on cholestatic liver injury.

The CXC chemokine receptor 2 (CXCR2) is critical for neutrophil recruitment and hepatocellular viability but has not been studied in the context of cholestatic liver injury following bile duct ligation (BDL). The present study sought to elucidate the cell-specific roles of CXCR2 on acute liver injury after BDL. Wild-type and CXCR2-/- mice were subjected BDL. CXCR2 chimeric mice were created to assess the cell-specific role of CXCR2 on liver injury after BDL. SB225002, a selective CXCR2 antagonist, was administrated intraperitoneally after BDL to investigate the potential of pharmacological inhibition. CXCR2-/- mice had significantly less liver injury than wild-type mice at 3 and 14 days after BDL. There was no difference in biliary fibrosis among groups. The chemokines CXCL1 and CXCL2 were induced around areas of necrosis and biliary structures, respectively, both areas where neutrophils accumulated after BDL. CXCR2-/- mice showed significantly less neutrophil accumulation in those injured areas. CXCR2Liver+/Myeloid+ and CXCR2Liver-/Myeloid- mice recapitulated the wild-type and CXCR2-knockout phenotypes, respectively. CXCR2Liver+/Myeloid+ mice suffered higher liver injury than CXCR2Liver+/Myeloid- and CXCR2Liver-/Myeloid+; however, only those chimeras with knockout of myeloid CXCR2 (CXCR2Liver+/Myeloid- and CXCR2Liver-/Myeloid-) showed reduction of neutrophil accumulation around areas of necrosis. Daily administration of SB225002 starting after 3 days of BDL reduced established liver injury at 6 days. In conclusion, neutrophil CXCR2 guides the cell to the site of injury, while CXCR2 on liver cells affects liver damage independent of neutrophil accumulation. CXCR2 appears to be a viable therapeutic target for cholestatic liver injury.NEW & NOTEWORTHY This study is the first to reveal cell-specific roles of the chemokine receptor CXCR2 in cholestatic liver injury caused by bile duct ligation. CXCR2 on neutrophils facilitates neutrophil recruitment to the liver, while CXCR2 on liver cells contributes to liver damage independent of neutrophils. CXCR2 may represent a viable therapeutic target for cholestatic liver injury.

Liver infarction in a patient with Clostridium Difficile colitis. A possible connection?

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"Bright Band Sign" A Grayscale Ultrasound Finding in Hepatic Infarction.

Hepatic infarction is infrequent due to the dual blood supply of the liver and the compensatory relationship between the hepatic artery and portal vein. Most cases occur in liver transplants due to vascular complications. Grayscale sonography combined with color and spectral wave Doppler can assess for vessel patency and parenchymal abnormalities. Liver infarctions appear as hypoechoic nonvascular regions on conventional and Doppler sonography. Here, we describe a grayscale ultrasound feature within liver infarctions in 2 liver transplants and in 1 native liver due to iatrogenic complication. This feature is similar to those described recently in the literature within splenic infarcts.