Infectious mononucleosis due to Epstein-Barr virus reactivation in an immunocompromised 60-year-old patient with COVID-19.

Epstein-Barr virus (EBV) reactivation in COVID-19 patients has been reported, but studies on its clinical significance are lacking. We herein report the occurrence of infectious mononucleosis (IM) due to EBV reactivation in a 60-year-old man with rheumatoid arthritis being treated with methotrexate and tocilizumab. The patient presented with a fever and tested positive for COVID-19. Laboratory findings revealed an increased atypical lymphocyte count, decreased platelet count, and elevated liver enzyme levels. Flow cytometry showed predominant expansion of reactive T cells. EBV reactivation was confirmed using real-time polymerase chain reaction. The patient was treated with remdesivir, and clinical improvement was observed after 10 days of treatment. Follow-up showed a gradual decrease in the EBV-DNA load with no recurrence of atypical lymphocytes. These findings suggest that COVID-19 in immunocompromised patients may lead to unexpected EBV reactivation and IM, even for patients outside the age at which IM is likely to occur.

Sudden-onset gallbladder rupture due to Ceftriaxone-associated pseudolithiasis in a patient with acquired hemophilia A.

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.

Pharmacokinetics of ibrutinib in a patient with chronic lymphocytic leukemia on hemodialysis.

Ibrutinib, an oral Bruton's tyrosine kinase inhibitor, is a key drug for the treatment of chronic lymphocytic leukemia (CLL). It is primarily metabolized by cytochrome P450 3A. However, there are no data on the pharmacokinetics of ibrutinib in patients with severe renal impairment or on hemodialysis (HD). We evaluated the pharmacokinetics of ibrutinib in a patient with CLL undergoing HD. An 84-year-old man on HD was diagnosed with CLL and was started on ibrutinib 140 mg daily. The second day of ibrutinib administration was an HD day, and its plasma concentrations before and 1, 2, 4, and 24 hours after administration were measured and found to be 0, 6.9, 28.4, 57.1, and 0 ng/mL, respectively. The maximum plasma concentration (Cmax) and time taken to reach Cmax (tmax) on days 14 and 15 of ibrutinib treatment were 64.8 ng/mL (4 hours) and 48.1 ng/mL (2 hours), respectively. Thus, we concluded that HD did not have a significant effect on the pharmacokinetics of ibrutinib in this patient. Therefore, dose adjustment of ibrutinib between HD and non-HD days is not recommended. Interestingly, we found that tmax of the drug was prolonged, and Cmax was higher on HD days compared to those on non-HD days.