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Sudden-onset gallbladder rupture due to Ceftriaxone-associated pseudolithiasis in a patient with acquired hemophilia
Naonori Harada1, Ikumi Shibano2, Daiki Mukai2
1Department of Hematology, Fuchu Hospital, Osaka, Japan; Hematology, Graduate School of Medicine, Osaka Metropolitan University, Japan.
We herein report a 76-year-old man with acquired hemophilia A (AHA) who developed gallbladder rupture due to Ceftriaxone (CTRX)-associated pseudolithiasis. The patient was admitted for an examination of systemic subcutaneous bleeding. A blood test showed a prolonged activated partial thromboplastin time and sequentially revealed low factor VIII activity (<1%) and a high factor VIII inhibitor level of 143 BU/mL. The patient was thus diagnosed with AHA. After admission, he developed a high-grade fever and was administered intravenous CTRX, considering the possibility of psoas abscess or cellulitis. Although his high-grade fever was improved, computed tomography incidentally showed a high-density lesion in the gallbladder, suggestive of CTRX-associated pseudolithiasis without clinical symptoms. Despite cessation of CTRX, the pseudolithiasis never disappeared, and the patient suddenly died after rapid progression of abdominal bloating. An autopsy revealed that the gallbladder was severely swollen and had ruptured with hemorrhaging because of hemorrhagic cholecystitis, caused by CTRX-associated pseudolithiasis with AHA. Our case demonstrated that CTRX-associated pseudocholelithiasis can unexpectedly induce gallbladder hemorrhaging and rupture in a patient with a bleeding diathesis, including AHA. CTRX-associated pseudocholelithiasis can cause a fatal outcome in patients with a bleeding disorder, even if CTRX is ceased as soon as pseudocholelithiasis is detected.
We herein report a 76-year-old man with acquired hemophilia A (AHA) who developed gallbladder rupture due to Ceftriaxone (CTRX)-associated pseudolithiasis. The patient was admitted for an examination of systemic subcutaneous bleeding. A blood test showed a prolonged activated partial thromboplastin time and sequentially revealed low factor VIII activity (<1%) and a high factor VIII inhibitor level of 143 BU/mL. The patient was thus diagnosed with AHA. After admission, he developed a high-grade fever and was administered intravenous CTRX, considering the possibility of psoas abscess or cellulitis. Although his high-grade fever was improved, computed tomography incidentally showed a high-density lesion in the gallbladder, suggestive of CTRX-associated pseudolithiasis without clinical symptoms. Despite cessation of CTRX, the pseudolithiasis never disappeared, and the patient suddenly died after rapid progression of abdominal bloating. An autopsy revealed that the gallbladder was severely swollen and had ruptured with hemorrhaging because of hemorrhagic cholecystitis, caused by CTRX-associated pseudolithiasis with AHA. Our case demonstrated that CTRX-associated pseudocholelithiasis can unexpectedly induce gallbladder hemorrhaging and rupture in a patient with a bleeding diathesis, including AHA. CTRX-associated pseudocholelithiasis can cause a fatal outcome in patients with a bleeding disorder, even if CTRX is ceased as soon as pseudocholelithiasis is detected.
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