lenvatinib and Hemorrhage

The subject was a man in his late 70s who was seeing a family physician for diabetes and dyslipidemia on an outpatient basis. A routine medical checkup revealed liver dysfunction, prompting an abdominal ultrasound. As a result, a large hepatic tumor was discovered, prompting a thorough examination. The patient was diagnosed with hepatocellular carcinoma and multiple liver metastases, as well as tumor shadows that could indicate pulmonary metastases, after a thorough examination at our hospital. Due to the patient not having viral hepatitis or any drinking history and had formerly been confirmed as having fatty liver, a diagnosis of cirrhosis and hepatocellular carcinoma caused by NASH (nonalcoholic steatohepatitis) was given. A Child-Pugh score of 5 (A) and modified albumin-bilirubin (mALBI) grade 2 were used to maintain liver function. As a result, a 12-mg/day Lenvatinib treatment regimen was initiated. From the 6th day of the start of oral administration, the patient developed right hypochondralgia and loss of appetite. Blood samples showed increased levels of liver enzymes and inflammatory reaction, requiring hospitalization for closer examination. Intratumoral hemorrhage from hepatocellular carcinoma was discovered by dynamic CT scans. The patient's general condition was stable, and an angiogram was performed on the 3rd day of admission. As a result, persistent extravasation was discovered, necessitating transcatheter arterial embolization (TAE) treatment of the lesion for tumor vessel embolization. Thereafter, transient deterioration of the liver function occurred but an immediate improvement was seen. The patient was discharged without a recurrence of hemorrhage. An outpatient follow-up was performed, with blood test results indicating that liver function was maintained with a Child-Pugh score of 6 (A), and a dynamic CT showing that intratumoral hemorrhage was under control, allowing for readministration. Readministration of Lenvatinib was started at 4mg/day, one level lower, because the patient's body weight had dropped below 60kg. There are few reports on Lenvatinib-induced intratumoral hemorrhage, and this is a unique case worthy of reporting, with previous literary references, in which the entire process from intratumoral hemorrhage to readministration of Lenvatinib after embolization treatment has been documented.

Topics: Carcinoma, Hepatocellular; Embolization, Therapeutic; Hemorrhage; Humans; Liver Neoplasms; Male; Phenylurea Compounds; Quinolines

Lenvatinib has been approved as a systemic therapy for patients with unresectable hepatocellular carcinoma (HCC). We recently experienced lenvatinib-induced tumor-related hemorrhage in patients with HCC. The full details of tumor-related hemorrhage as a lenvatinib-related adverse event have not been elucidated.. This was a retrospective single-center study that enrolled consecutive patients treated with lenvatinib for unresectable HCC from April 2018 to February 2020.. Sixty-eight consecutive patients were enrolled in this study. Among them, 5 cases developed intraperitoneal or intratumoral hemorrhages. The patients with hemorrhage had larger tumors (maximum tumor size, 97.5 ± 46.4 and 38.2 ± 28.8 mm, respectively; p = 0.009) than the patients without hemorrhage. The dosing period of lenvatinib (median, 3 and 93 days, respectively; p < 0.001) and the survival time from initial administration of lenvatinib (median, 77 and 495 days, respectively; p < 0.001) of the patients with hemorrhage were shorter than those of the patients without hemorrhage. Especially, in 4 cases with large HCCs (maximum tumor diameter was >90 mm), tumor hemorrhage with vascular lake-like phenomenon was evident, although most tumor blood flow was suppressed.. It becomes clear that lenvatinib treatment brings about tumor-related hemorrhages despite rapid suppression of tumor blood flow. We speculate that lenvatinib quickly blocks the feeding circulation, resulting in tumor hemorrhage by necrosis. Clinicians should pay careful attention to the development of life-threatening hemorrhages when treating large HCCs with lenvatinib.

Topics: Aged; Aged, 80 and over; Antineoplastic Agents; Carcinoma, Hepatocellular; Computed Tomography Angiography; Female; Hemorrhage; Humans; Liver Neoplasms; Male; Middle Aged; Phenylurea Compounds; Protein Kinase Inhibitors; Quinolines; Retrospective Studies; Treatment Outcome

Topics: Antineoplastic Agents; Carcinoma, Hepatocellular; Chemical and Drug Induced Liver Injury; Hemorrhage; Humans; Liver; Liver Function Tests; Liver Neoplasms; Phenylurea Compounds; Quinolines

Topics: Aged, 80 and over; Antineoplastic Agents; Carcinoma, Hepatocellular; Hemorrhage; Humans; Liver Neoplasms; Male; Middle Aged; Phenylurea Compounds; Quinolines; Tomography, X-Ray Computed

Lenvatinib has become an important treatment option for advanced thyroid cancer. Fistula and tumor-related bleeding are life-threatening adverse effects that are triggered by tumor shrinkage. The aim of this study was to evaluate basic parameters, such as time and tumor shrinkage level, and analyze patient characteristics that might be related to onset of complications.. A retrospective study of 16 patients who received lenvatinib for thyroid cancer treatment was performed.. Fistula was observed in two patients (12.5%), while tumor-related bleeding was observed in one (6.3%). Complications were found to appear at 10.4 weeks from initiation and with tumor decrease of 19.2%. Risk factors for complications were identified as anaplastic histological type, tumor invasion, and leukocytopenia induced by lenvatinib.. Individual dose adjustment is needed with respect to these features in order to manage severe adverse effects induced by lenvatinib.

Topics: Aged; Aged, 80 and over; Antineoplastic Agents; Female; Fistula; Hemorrhage; Humans; Male; Middle Aged; Phenylurea Compounds; Protein Kinase Inhibitors; Quinolines; Thyroid Neoplasms

Topics: Aged; Antineoplastic Agents; Cell Differentiation; Dose-Response Relationship, Drug; Hemorrhage; Humans; Male; Phenylurea Compounds; Precision Medicine; Protein Kinase Inhibitors; Quinolines; Thyroid Neoplasms