ABSTRACT
This editorial commented on an article in the World Journal of Gastroenterology titled "Risks of Reactivation of Hepatitis B Virus in Oncological Patients Using Tyrosine Kinase-Inhibitors: Case Report and Literature Analysis" by Colapietro et al. In this editorial, we focused on providing a more comprehensive exploration of hepatitis B virus reactivation (HBVr) associated with the usage of tyrosine kinase inhibitors (TKIs). It includes insights into the mechanisms underlying HBV reactivation, the temporal relationship between TKIs and HBV reactivation, and preventive measures. The aim is to understand the need for nucleos(t)ide analogs (NAT) and serial blood tests for early recognition of reactivation and acute liver injury, along with management strategies. TKIs are considered to be an intermediate (1%-10%) of HBVr. Current guidelines stipulate that patients receiving therapy with high or moderate risks of reactivation or recent cancer diagnosis must have at least tested hepatitis B surface antigen, anti-hepatitis B core antigen (HBc), and anti-hepatitis B surface antibody. Anti-HBc screening in highly endemic areas means people with negative tests should be vaccinated against HBV. Nucleoside or nucleotide analogs (NAs) like entecavir (ETV), tenofovir disoproxil fumarate (TDF), and tenofovir alafenamide (TAF) form the basis of HBV reactivation prophylaxis and treatment during immunosuppression. Conversely, lamivudine, telbivudine, and adefovir are generally discouraged due to their reduced antiviral efficacy and higher risk of fostering drug-resistant viral strains. However, these less effective NAs may still be utilized in cases where ETV, TDF, and TAF are not feasible treatment options.
Subject(s)
Antiviral Agents , Hepatitis B virus , Neoplasms , Protein Kinase Inhibitors , Virus Activation , Humans , Virus Activation/drug effects , Hepatitis B virus/drug effects , Hepatitis B virus/immunology , Hepatitis B virus/isolation & purification , Antiviral Agents/therapeutic use , Antiviral Agents/adverse effects , Protein Kinase Inhibitors/adverse effects , Protein Kinase Inhibitors/therapeutic use , Neoplasms/drug therapy , Hepatitis B/diagnosis , Hepatitis B/virology , Hepatitis B/drug therapy , Risk Factors , Antineoplastic Agents/adverse effects , Antineoplastic Agents/therapeutic use , Protein-Tyrosine Kinases/antagonists & inhibitors , Hepatitis B Surface Antigens/bloodABSTRACT
Drug-induced acute pancreatitis is a potentially ignored diagnosis that must be precisely valued. Drug-induced acute pancreatitis can be considered the third common cause of acute pancreatitis after ruling out alcohol and gallstones. Levofloxacin belongs to a class of fluoroquinolone antibiotics used for treating various infections. Besides photosensitivity and liver toxicity, levofloxacin can induce acute pancreatitis, although rarely described. We highlight a case of acute pancreatitis in a female induced by levofloxacin. She presented with typical signs and symptoms of acute pancreatitis and had been taking levofloxacin for urinary tract infections for the last 3 days. After ruling out all other possible causes, her clinical picture, laboratory results, and imaging findings confirmed acute pancreatitis induced by levofloxacin.
ABSTRACT
Kawasaki illness is an inflammatory condition of small- to medium-sized vessels that primarily affects children. It affects the lymph nodes, skin, mucous membranes, and heart, especially the coronary arteries. Patients who lack the comprehensive clinical manifestations of classic Kawasaki disease (KD) are typically evaluated for incomplete KD. Such patients have persistent fever and lack one or more characteristic clinical signs. Here, we present a case of a 16-month-old baby presented with fever for nine days, excessive crying and irritability for four days, and refusal to feed for one day with pallor and developed lip cracking, mucositis, bilateral edema, and redness in the palms and soles followed by periungual desquamation. Lab evaluations revealed anemia, elevated white cell count, and c-reactive protein along sterile pyuria. Since the child became afebrile after ten days of illness, inflammatory marker levels decreased, and no coronary artery abnormalities were detected on 2D echocardiography, and the child was diagnosed with incomplete KD based on the clinical, laboratory, and radiological evaluations after ruling out all other possible causes. He was managed conservatively with low-dose aspirin, and the child was doing well on a two-month follow-up.