Hypersensitivity reactions (HSRs) to iodinated contrast media (ICM) can range from mild cutaneous symptoms to life-threatening anaphylaxis. In patients with a history of ICM hypersensitivity, avoidance of the culprit agent is generally recommended. This case report describes a successful desensitization in a 56-year-old man with recurrent HSRs to multiple agents including ioversol, iohexol, iobitridol, and iopamidol. Intradermal testing was performed to identify potentially safe alternatives; however, all tested agents, including iohexol, ioversol, iobitridol, iopamidol, iodixanol, iomeprol, and iopromide, yielded positive results. Given the clinical necessity of transcatheter arterial chemoembolization, a 13-step rapid desensitization protocol with iodixanol was implemented. The procedure was completed without any breakthrough reactions. This case highlights desensitization as a feasible and effective strategy for patients with hypersensitivity to multiple ICM agents.

Dihydrocodeine is an effective antitussive agent that inhibits the cough reflex by interacting with opioid receptors in the brain. It is easily available in pharmacies without a prescription, which may contribute to a lack of awareness about potential drug hypersensitivity reactions. In the first reported case in Korea, a 29-year-old man developed acute generalized exanthematous pustulosis (AGEP) after consuming an over-the-counter cold medicine containing dihydrocodeine. He was admitted to the Emergency Department with high fever and full-body skin rashes that appeared 3 hours after taking the medicine. His EuroSCAR AGEP score was 9, with symptoms improving upon discontinuation of dihydrocodeine and the application of topical steroids. AGEP caused by dihydrocodeine, including codeine, is very rare, with 3 cases reported worldwide. By analyzing AGEP cases due to dihydrocodeine or codeine, we identified that risk factors for the development of AGEP from dihydrocodeine include a history of psoriasis and the presence of an IL36RN mutation, which result in the activation of Th17 in the blood or the skin. In cases of AGEP caused by dihydrocodeine, it is also recommended to discontinue codeine due to cross-reactivity with dihydrocodeine. Additionally, patients with AGEP due to dihydrocodeine may be able to use other opioid classes, such as morphine or tramadol, due to low cross-reactivity.

Dihydrocodeine is an effective antitussive agent that inhibits the cough reflex by interacting with opioid receptors in the brain. It is easily available in pharmacies without a prescription, which may contribute to a lack of awareness about potential drug hypersensitivity reactions. In the first reported case in Korea, a 29-year-old man developed acute generalized exanthematous pustulosis (AGEP) after consuming an over-the-counter cold medicine containing dihydrocodeine. He was admitted to the Emergency Department with high fever and full-body skin rashes that appeared 3 hours after taking the medicine. His EuroSCAR AGEP score was 9, with symptoms improving upon discontinuation of dihydrocodeine and the application of topical steroids. AGEP caused by dihydrocodeine, including codeine, is very rare, with 3 cases reported worldwide. By analyzing AGEP cases due to dihydrocodeine or codeine, we identified that risk factors for the development of AGEP from dihydrocodeine include a history of psoriasis and the presence of an IL36RN mutation, which result in the activation of Th17 in the blood or the skin. In cases of AGEP caused by dihydrocodeine, it is also recommended to discontinue codeine due to cross-reactivity with dihydrocodeine. Additionally, patients with AGEP due to dihydrocodeine may be able to use other opioid classes, such as morphine or tramadol, due to low cross-reactivity.

Dihydrocodeine is an effective antitussive agent that inhibits the cough reflex by interacting with opioid receptors in the brain. It is easily available in pharmacies without a prescription, which may contribute to a lack of awareness about potential drug hypersensitivity reactions. In the first reported case in Korea, a 29-year-old man developed acute generalized exanthematous pustulosis (AGEP) after consuming an over-the-counter cold medicine containing dihydrocodeine. He was admitted to the Emergency Department with high fever and full-body skin rashes that appeared 3 hours after taking the medicine. His EuroSCAR AGEP score was 9, with symptoms improving upon discontinuation of dihydrocodeine and the application of topical steroids. AGEP caused by dihydrocodeine, including codeine, is very rare, with 3 cases reported worldwide. By analyzing AGEP cases due to dihydrocodeine or codeine, we identified that risk factors for the development of AGEP from dihydrocodeine include a history of psoriasis and the presence of an IL36RN mutation, which result in the activation of Th17 in the blood or the skin. In cases of AGEP caused by dihydrocodeine, it is also recommended to discontinue codeine due to cross-reactivity with dihydrocodeine. Additionally, patients with AGEP due to dihydrocodeine may be able to use other opioid classes, such as morphine or tramadol, due to low cross-reactivity.

Dihydrocodeine is an effective antitussive agent that inhibits the cough reflex by interacting with opioid receptors in the brain. It is easily available in pharmacies without a prescription, which may contribute to a lack of awareness about potential drug hypersensitivity reactions. In the first reported case in Korea, a 29-year-old man developed acute generalized exanthematous pustulosis (AGEP) after consuming an over-the-counter cold medicine containing dihydrocodeine. He was admitted to the Emergency Department with high fever and full-body skin rashes that appeared 3 hours after taking the medicine. His EuroSCAR AGEP score was 9, with symptoms improving upon discontinuation of dihydrocodeine and the application of topical steroids. AGEP caused by dihydrocodeine, including codeine, is very rare, with 3 cases reported worldwide. By analyzing AGEP cases due to dihydrocodeine or codeine, we identified that risk factors for the development of AGEP from dihydrocodeine include a history of psoriasis and the presence of an IL36RN mutation, which result in the activation of Th17 in the blood or the skin. In cases of AGEP caused by dihydrocodeine, it is also recommended to discontinue codeine due to cross-reactivity with dihydrocodeine. Additionally, patients with AGEP due to dihydrocodeine may be able to use other opioid classes, such as morphine or tramadol, due to low cross-reactivity.

Dihydrocodeine is an effective antitussive agent that inhibits the cough reflex by interacting with opioid receptors in the brain. It is easily available in pharmacies without a prescription, which may contribute to a lack of awareness about potential drug hypersensitivity reactions. In the first reported case in Korea, a 29-year-old man developed acute generalized exanthematous pustulosis (AGEP) after consuming an over-the-counter cold medicine containing dihydrocodeine. He was admitted to the Emergency Department with high fever and full-body skin rashes that appeared 3 hours after taking the medicine. His EuroSCAR AGEP score was 9, with symptoms improving upon discontinuation of dihydrocodeine and the application of topical steroids. AGEP caused by dihydrocodeine, including codeine, is very rare, with 3 cases reported worldwide. By analyzing AGEP cases due to dihydrocodeine or codeine, we identified that risk factors for the development of AGEP from dihydrocodeine include a history of psoriasis and the presence of an IL36RN mutation, which result in the activation of Th17 in the blood or the skin. In cases of AGEP caused by dihydrocodeine, it is also recommended to discontinue codeine due to cross-reactivity with dihydrocodeine. Additionally, patients with AGEP due to dihydrocodeine may be able to use other opioid classes, such as morphine or tramadol, due to low cross-reactivity.

Drug desensitization is a treatment strategy for patients with hypersensitivity to essential drugs without alternatives. The gradual increase in the drug dosage from low doses to therapeutic levels induces a transient immune tolerance to the culprit drug. Although desensitization has traditionally been recommended for IgE-mediated immediate hypersensitivity, this indication has recently been expanded to include non-IgE-mediated immediate responses, nonimmunological responses, and T-cell-mediated delayed hypersensitivity reactions. Although the exact mechanism behind desensitization remains unclear, the process is thought to attenuate various intracellular signals in target cells through Fcɛ receptor 1 internalization, alteration in signaling pathways in mast cells and basophils, reduction in Ca 2+ influx, and production of anti-drug IgG4 blocking antibody. Desensitization can be used for the safe administration of anti-neoplastic agents, antibiotics, aspirin, and nonsteroidal anti-inflammatory drugs. Various desensitization protocols have been proposed for each drug. The optimization of drug concentration, target dosage, administration interval, and route of administration is key to successful desensitization. In addition, the desensitization protocol should be individualized for each patient with consideration of the severity of the initial hypersensitivity response, the characteristics of the culprit drug, and the nature of the breakthrough reactions.

As imaging technologies have become essential for diagnosing various diseases, the use of contrast agents is rapidly expanding. As a result, hypersensitivity reactions (HSRs) to contrast agents have also increased. However, protocols for managing, diagnosing, and preventing these reactions are not fully established yet. Since the guidelines for contrast agent hypersensitivity suggested by domestic and international academic societies are not standardized and sometimes difficult to follow in medical facilities, there is a need for practical recommendations in a real-world setting. This review introduces the strategy to manage, diagnose, and prevent HSRs to contrast agents, which have been successfully implemented at Seoul National University Hospital for a decade. First, every single HSRs should be documented in the medical records because a previous history of hypersensitivity to contrast agents is the most significant risk factor for developing HSR to iodinated contrast media. Secondly, avoidance of culprit agents is the main strategy for preventing recurrences of HSRs to contrast agents. Thirdly, it is important to identify nonsensitized contrast agents using skin tests for future exposure to contrast media. In addition to skin testing, side chains of iodinated contrast media may provide a clue to reactive contrast agents. Fourthly, provocation tests can be performed in selected cases with a nonreactive agent based on the skin testing and side chain commonness. Prior to performing imaging studies, premedication can be applied stratified to the severity of the index HSR. All of these procedures are safe and prove to be executable in the medical facilities.

Desensitization therapy can help overcome severe hypersensitivity reactions and allow continuing administration of the culprit agents. However, this is time- and labor-intensive due to a prolonged infusion time and the serial adjustment of infusion rate between steps. Therefore, simplified protocols using fewer steps have been tested, although currently there is no established standard strategy. Cetuximab plays an important role in the treatment of metastatic colorectal cancer. Although cetuximab is well tolerated, severe infusion reactions occur in 1.1% of patients, and most occur within 1 hour of receiving the first dose. Here, we report a recent attempt to shorten the steps of gradual cetuximab desensitization. A 57-year-old male patient diagnosed with obstructive sigmoid colon cancer received cetuximab chemotherapy and experienced immediate anaphylaxis at the first cycle. A one-bag, 17-step desensitization protocol was applied to cetuximab administration. After the first successful desensitization cycle, the process of desensitization was shortened 1–2 step(s) per cycle, down to 2 steps, without a breakthrough reaction. The patient ultimately received regular infusions. Shortening of the rapid desensitization protocol can be considered if the previous cycle is well-tolerated, even in a patient who suffered previous anaphylaxis to cetuximab.

Methods: We enrolled 40 patients who underwent either MISS (M group, 20 patients) or open posterior instrumentation surgery (O group, 20 patients) for the treatment of traumatic unstable burst fractures. Clinical outcomes were evaluated based on postoperative back pain, operation time, blood loss, hospital stay duration, and perioperative complications. For radiologic evaluation, preoperative magnetic resonance imaging and plain radiography were performed before and after the surgery to evaluate the changes in the kyphotic angle and fracture union. Results: The change in the kyphotic angle was −8.2°±5.8° in the M group and −8.0°±7.8° in the O group. No significant difference was noted in terms of the change in the kyphotic angle (p=0.94, t-test) after 12 months of surgery. The Visual Analog Scale score was 1.5±0.7 points in the M group, while it was 5.2±1.4 points in the O group. In the M group, back pain has significantly decreased (p<0.01, t-test). The estimated blood loss was 195.5 mL in the M group and 1,077.5 mL in the O group; the operation time was significantly decreased in the O group from 290.7 to 120.7 minutes in the M group (p<0.05, t-test) (p=0.36, t-test). The average duration of hospital stay was 36.0 days in the M group and 41.9 days in the O group (p=0.36, t-test). Conclusions For the treatment of unstable burst fractures, MISS showed significant differences in terms of postoperative back pain, operation time, and blood loss as compared to open posterior instrumentation surgery.