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.

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.