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 Liver Infarct with a Superimposed Liver Abscess as a Consequence of Hypercoagulable State in a Patient with COVID-19 without Respiratory Manifestations.

COVID-19 infection has been associated, particularly in severely ill patients requiring hospitalization, with a hypercoagulable state. The case presented herein was a 66-year-old man with SARS-CoV-2 infection who did not have any respiratory symptoms. He presented with the following clinical manifestations: portal vein and hepatic artery thrombosis, liver infarction, and a superimposed abscess of the liver. In this case, early detection and the administration of anticoagulants and antibiotics led to a significant improvement within weeks of the diagnosis. We encourage physicians to be aware of COVID-19-associated hypercoagulable state and its potential complications, regardless of the acuity of the presentation or the absence of respiratory symptoms.

Conservative Treatment of Huge Hepatic Subcapsular Hematoma Complicated with Hepatic Infarction after Cesarean Section Caused by HELLP Syndrome - a Case Report and Literature Review.

Hepatic subcapsular hematoma and hepatic infarction in labor are mostly secondary to HELLP syndrome and preeclampsia. There are few reported cases with a complicated diagnosis and treatment and high mortality. Here, we present a case of a huge hepatic subcapsular hematoma complicated with hepatic infarction after cesarean section that was secondary to HELLP syndrome and the patient was treated conservatively. Further, we have discussed the diagnosis and treatment of hepatic subcapsular hematoma and hepatic infarction caused by HELLP syndrome.

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

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 is 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.

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.

Assessment of Clinical Outcomes, Clinical Manifestations, and Risk Factors for Hepatic Infarction After Transjugular Intrahepatic Portosystemic Shunt Placement (TIPS): A Retrospective Comparative Study.

PURPOSE: To describe the imaging findings of hepatic infarction after transjugular intrahepatic portosystemic shunt (TIPS) placement and identify risk factors, clinical manifestations, and outcomes of infarction after TIPS. MATERIALS AND METHODS: In this retrospective analysis of a TIPS registry (1995-2021), cirrhotic patients with hepatic infarction (n = 33) and control patients without infarct (n = 33) after TIPS were identified. Laboratory values, ultrasound findings, and clinical variables were compared between groups to identify risk factors and differences in outcomes. A Cox proportional hazards regression model with propensity score was used to assess the effect of hepatic infarction on mortality and acute-on-chronic liver failure (ACLF) score. RESULTS: Hepatic infarction involved the right posterior segments (segments VI or VII) in 32 of 33 patients. Prolonged vasopressor requirement (p = 0.003) and intensive care unit stay (p = 0.001) were seen in patients with hepatic infarct, as well as trends toward lower post-TIPS portosystemic pressure gradient (p = 0.061) and higher risk of ACLF (p = 0.056). Procedure-related portal vein thrombosis or hepatic artery injury was identified in 12 and 5 patients with infarct, respectively. Patients with infarct had higher postprocedural aspartate aminotransferase (p < 0.001) and alanine aminotransferase (p < 0.001) levels, higher international normalized ratio (p = 0.016), lower platelet count (p = 0.042), and a greater decrease in hemoglobin level (p = 0.003). CONCLUSION: Hepatic infarction most frequently affects the right posterior hepatic segments after TIPS and results in a worse postprocedural course. Procedure-related complications and critically low portosystemic pressure gradient may contribute to TIPS-associated hepatic infarct.

Liver infarctions as the first manifestation of antiphospholipid antibody syndrome in pregnancy: a case report.

BACKGROUND: The differential diagnosis of abdominal pain in pregnant women is broad. Liver diseases as the origin of abdominal pain in pregnancy are rare, and severe forms occur in less than 0.1% of pregnancies. Some disorders, such as hemolysis, elevated liver enzymes, low platelets (HELLP) syndrome and preeclampsia, are unique to pregnancy, while others, such as antiphospholipid antibody syndrome, may manifest in pregnancy but have consequences beyond the current pregnancy. All of them require prompt identification and treatment. CASE PRESENTATION: A 27-year-old Caucasian woman who was 15+1 weeks pregnant reported to the emergency department twice due to stabbing right-upper-quadrant abdominal pain. Initial laboratory testing revealed mild leukocytosis and slightly elevated liver enzymes. On second presentation, the patient was febrile and had an increased C-reactive protein concentration. Over the course of the next days, nonhemolytic anemia and thrombocytopenia emerged with elevated liver enzymes. Coagulation studies also revealed a prolongation of activated partial thromboplastin time. Magnetic resonance imaging showed nonspecific alterations in the right liver lobe, possibly corresponding to infection or infarction. A hepatic viral infection was ruled out. At that time, the most likely diagnosis was cholangitis with liver abscess formation, and antibiotic therapy was started. Further worsening of the anemia and thrombocytopenia, development of proteinuria, together with a miscarriage on the fourth day of hospitalization resulted in the tentative diagnosis of (triple-positive) antiphospholipid antibody syndrome, which was confirmed 12 weeks after the initial investigation. Treatment consisted of prompt anticoagulation with heparin and later on with a vitamin K antagonist as well as high-dose glucocorticoid therapy. There was no need for intravenous immunoglobulin therapy or plasma exchange, although we suspected a catastrophic form of antiphospholipid antibody syndrome due to infarctions of the liver, placenta, and possibly kidneys (proteinuria). The outcome was favorable. CONCLUSION: We report a 27-year-old pregnant woman whose abdominal pain was caused by liver infarctions as the first manifestation of catastrophic antiphospholipid antibody syndrome. The antiphospholipid antibody syndrome was possibly secondary to hitherto clinically silent systemic lupus erythematosus since the antinuclear antibodies were increased later on. Hydroxychloroquine therapy was initiated to prevent antiphospholipid antibody syndrome recurrence in a future pregnancy.

Hepatic infarction, hematoma, and rupture in HELLP syndrome: support for a vasospastic hypothesis.

Purpose: HELLP syndrome is a relatively uncommon pregnancy-related condition characterized by hemolysis, elevated liver function tests, and low platelets. It can be accompanied by life-threatening hepatic complications including hepatic infarction, hematoma formation, and hepatic rupture. HELLP syndrome occurs in approximately 0.2% of pregnancies. Major hepatic complications occur in less than 1% of HELLP patients suggesting an incidence of 1/50,000. The pathogenesis is incompletely understood and in particular, it is difficult to understand a disorder with both major thrombotic and bleeding manifestations.Methods: Literature review.Results: On the basis of reports in the published literature, and our own clinical experience, we suggest that vasospasm is one of the principal drivers with hepatic ischemia, infarction, and hemorrhage as secondary events. It is known that vasoactive substances are released by the failing placenta. We suggest these cause severe vasospasm, most likely affecting the small post-sinusoidal hepatic venules. This leads to patchy or confluent hepatic ischemia and/or necrosis with a resultant increase in circulating liver enzymes. Reperfusion is associated with a fall in platelet count and microvascular hemorrhage if the microvasculature is infarcted. Blood tracks to the subcapsular space causing hematoma formation. If the hematoma ruptures the patient presents with severe abdominal pain, intra-abdominal hemorrhage, and shock.Conclusions: We suggest that hepatic and other complications associated with HELLP syndrome including placental abruption, acute renal failure, and posterior reversible encephalopathy syndrome (PRES) may also be due to regional vasospasm.

Pterostilbene alleviates liver ischemia/reperfusion injury via PINK1-mediated mitophagy.

Hepatic ischemia/reperfusion (I/R) injury contributes to morbidity and mortality during liver resection or transplantation, with limited effective treatments available. Here, we investigated the potential benefits and underlying mechanisms of pterostilbene (Pt), a natural component of blueberries and grapes, in preventing hepatic I/R injury. Male C57BL/6 mice subjected to partial warm hepatic I/R and human hepatocyte cell line L02 cells exposed to anoxia/reoxygenation (A/R) were used as in vivo and in vitro models, respectively. Our findings showed that pretreatment with Pt ameliorated hepatic I/R injury by improving liver histology, decreasing hepatocyte apoptosis, and reducing plasma ALT and AST levels. Likewise, cell apoptosis, mitochondrial membrane dysfunction, and mitochondrial ROS overproduction in L02 cells triggered by the A/R challenge in vitro were reduced due to Pt administration. Mechanistically, Pt treatment efficiently enhanced mitophagy and upregulated PINK1, Parkin, and LC3B expression. Notably, the protective effect of Pt was largely abrogated after cells were transfected with PINK1 siRNA. Moreover, Pt pretreatment promoted hepatocyte proliferation and liver regeneration in the late phase of hepatic I/R. In conclusion, our findings provide evidence that Pt exerts hepatoprotective effects in hepatic I/R injury by upregulating PINK1-mediated mitophagy.

Hepatic Artery Embolization for Postoperative Hemorrhage: Importance of Arterial Collateral Vessels and Portal Venous Impairment.

PURPOSE: To investigate the association between hepatic ischemic complications and hepatic artery (HA) collateral vessels and portal venous (PV) impairment after HA embolization for postoperative hemorrhage. MATERIALS AND METHODS: From October 2003 to November 2019, 42 patients underwent HA embolization for postoperative hemorrhage. HA collateral vessels were classified according to visualization after embolization (grade 1, none; grade 2, 1-4 segmental HA; and grade 3, ≥4 segmental HA). Transhepatic portal vein stent placements were performed in the same session for 5 patients (11.9%) with poor HA collateral vessels (grade 1 or 2) and compromised PV flow (>70% stenosis). Hepatic ischemic complications were analyzed for relevance to HA collateral vessels and PV compromise. RESULTS: After HA embolization, HA flow was found to be preserved (grade 3) through intra- and/or extrahepatic collateral vessels in 23 patients (54.8%), and hepatic complications did not occur regardless of PV flow status (0%). Of the 19 patients (45.2%) with poor HA collateral vessels (grade 1 or 2), segmental hepatic infarction occurred in 2 of 15 patients (13.3%) with preserved PV flow (10 naïve and 5 stented). The remaining 4 patients with poor HA collateral vessels and untreated compromised PV flow experienced multisegmental hepatic infarction (n = 3) or hepatic failure (n = 1) (100%) (P < .005). CONCLUSIONS: After HA embolization, preserved HA flow (≥4 segmental HA) lowered the risk of hepatic complications regardless of the PV flow. Based on these findings, transhepatic PV stent placement seems to be an effective intervention for the prevention of hepatic complications in cases of poor HA collateral vessels and compromised PV flow.

99mTc-Mebrofenin SPECT/CT in Hepatic Infarction.

A 68-year-old man with hereditary hypercoagulability was referred to nuclear medicine for elevated aminotransferases after a recent living-donor liver transplant. A hepatic infarction was suspected. A Tc-mebrofenin SPECT/CT was performed and showed decreased radiotracer uptake in a wedge-shaped distribution in the anterior liver suggestive of a hepatic infarction. Subsequently, an enhanced MRI corroborated the diagnosis. Oral anticoagulation therapy was then initiated, and aminotransferases soon normalized.

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.

Not hepatic infarction: Cold quadrate sign.

A 50-year-old male presented with bilateral lower extremity plain is found to have a wedge-shape hypodense region in the hepatic quadrate lobe. The hypoenhancement was thought to be a result of systemic-portal venous shunting due to IVC obstruction, a "cold" version of the classically described hot quadrate sign. Follow-up CT confirmed the diagnosis. Venous drainage pathway for both hot and cold quadrate signs is discussed.

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.