Background/Aims: Standard triple therapy (STT; proton pump inhibitor [PPI]+clarithromycin+amoxicillin) used for Helicobacter pylori (H. pylori) eradication has shown low treatment success rates in recent years, which is most likely attributable to increased clarithromycin resistance. In this study, we compared treatment success rates of tailored therapy (TT) using real-time polymerase chain reaction (RT-PCR) and empirical STT. Methods: This retrospective study included 650 patients with H. pylori infection, who visited Eunpyeong St. Mary’s Hospital in Korea; 343 patients received TT based on RT-PCR assays, and 307 patients received STT. Eradication success was defined as a negative 13C-urea breath test result 4~8 weeks after treatment completion. Patients who failed first-line therapy and those with clarithromycin resistance received bismuth-containing quadruple therapy (BQT; PPI+bismuth+metronidazole+tetracycline). Results: Intention-to-treat analysis showed that H. pylori eradication rates were higher in patients who received RT-PCR–based TT than in those who were treated using empirical STT (80.5% [190/236] vs. 70.4% [216/307], P=0.069). Per-protocol (PP) analysis showed similar results (84.4% [190/225] vs. 74.7% [216/289], P=0.007). PP analysis showed that 7-day TT treatment was associated with a higher eradication rate than that observed with 10- to 14-day STT (85.2% [178/209] vs. 73.8% [59/80], P=0.029). The clarithromycin resistance rate was 27.9% (87/312). The eradication success rate was 89.2% (74/83) in patients with clarithromycin resistance, who received BQT as first-line therapy. Conclusions The treatment success rate was higher in patients who received 7-day RT-PCR–based TT than in those who were administered 10- to 14-day empirical treatment.

Background/Aims: Based on the Kyoto classification of gastritis, mucosal atrophy, endoscopic intestinal metaplasia, fold enlargement, nodularity, and diffuse redness may be associated with gastric cancer and Helicobacter pylori (H. pylori) infection. In this study, we investigated the association between Kyoto scores based on the aforementioned five variables and current H. pylori infection. Materials and Methods: We reviewed medical records of consecutive patients who underwent endoscopic biopsies between January and June 2019. The study included 687 patients (370 and 317 patients with H. pylori-negative and -positive results, respectively). The Kyoto score was evaluated by the endoscopist who performed the test and was reconfirmed by another endoscopist. The total Kyoto score was analyzed using a receiver operating characteristic (ROC) curve for each score from 0 to 8. Multivariate analysis was used to determine the variables associated with H. pylori infection. Results: The maximum value of the Youden index (which reflects the ideal cut-off score of the Kyoto score on the ROC curve) was a Kyoto score of 2 points (Youden index 0.5905). Nodularity (OR 24.69, 95% CI 8.57~71.16, P<0.001) and diffuse redness (1 point: OR 18.29, 95% CI 10.29~32.52, P<0.001 and 2 points: OR 30.82, 95% CI 14.07~67.52, P<0.001) showed the highest OR on multivariate analysis. Conclusions A Kyoto classification cut-off score of 2 points was suggestive of H. pylori infection, and mucosal nodularity and diffuse redness were most significantly associated with the risk of infection.

Enchondromas are common benign bone tumors of the hand and are typically located in the medullary cavity of the metaphysis of the tubular bones. Typical radiological findings reveal cartilage lobules with ring and arc calcifications and entrapped normal medullary fat. The regression of an existing enchondroma, in which the cartilage lobules are replaced by fatty marrow, is considered unusual. Only a few studies have been reported on long tubular bones. Herein, we report an unusual case of a 73-year-old man with an enchondroma in the hand. In this case, a histologic appearance of the enchondroma exhibited loss of matrix mineralization, which corresponded to replacement by marrow fat revealed by magnetic resonance imaging.

Enchondromas are common benign bone tumors of the hand and are typically located in the medullary cavity of the metaphysis of the tubular bones. Typical radiological findings reveal cartilage lobules with ring and arc calcifications and entrapped normal medullary fat. The regression of an existing enchondroma, in which the cartilage lobules are replaced by fatty marrow, is considered unusual. Only a few studies have been reported on long tubular bones. Herein, we report an unusual case of a 73-year-old man with an enchondroma in the hand. In this case, a histologic appearance of the enchondroma exhibited loss of matrix mineralization, which corresponded to replacement by marrow fat revealed by magnetic resonance imaging.

Autoimmune encephalitis (AE) is a category of immune-mediated disorders of the central nervous system (CNS) affecting children and adults. It is characterized by the subacute onset of altered mentation, neurocognitive issues, refractory seizures/ drug-resistant epilepsy, movement disorders, and/or autonomic dysfunction. AE is mediated by autoantibodies targeting specific surface components or intracytoplasmic antigens in the CNS, leading to functional or structural alterations. Multiple triggers that induce autoimmunity have been described, which are mainly parainfectious and paraneoplastic. The imaging features of AE often overlap with each other and with other common causes of encephalitis/encephalopathy (infections and toxic-metabolic etiologies). Limbic encephalitis is the most common imaging finding shared by most of these entities. Cortical, basal ganglia, diencephalon, and brainstem involvement may also be present. Cerebellar involvement is rare and is often a part of paraneoplastic degeneration. Owing to an improved understanding of AE, their incidence and detection have increased. Hence, in an appropriate setting, a high degree of suspicion is crucial when reporting clinical MRIs to ensure prompt treatment and better patient outcomes. In this review, we discuss the pathophysiology of AE and common etiologies encountered in clinical practice.

Autoimmune encephalitis (AE) is a category of immune-mediated disorders of the central nervous system (CNS) affecting children and adults. It is characterized by the subacute onset of altered mentation, neurocognitive issues, refractory seizures/ drug-resistant epilepsy, movement disorders, and/or autonomic dysfunction. AE is mediated by autoantibodies targeting specific surface components or intracytoplasmic antigens in the CNS, leading to functional or structural alterations. Multiple triggers that induce autoimmunity have been described, which are mainly parainfectious and paraneoplastic. The imaging features of AE often overlap with each other and with other common causes of encephalitis/encephalopathy (infections and toxic-metabolic etiologies). Limbic encephalitis is the most common imaging finding shared by most of these entities. Cortical, basal ganglia, diencephalon, and brainstem involvement may also be present. Cerebellar involvement is rare and is often a part of paraneoplastic degeneration. Owing to an improved understanding of AE, their incidence and detection have increased. Hence, in an appropriate setting, a high degree of suspicion is crucial when reporting clinical MRIs to ensure prompt treatment and better patient outcomes. In this review, we discuss the pathophysiology of AE and common etiologies encountered in clinical practice.

Enchondromas are common benign bone tumors of the hand and are typically located in the medullary cavity of the metaphysis of the tubular bones. Typical radiological findings reveal cartilage lobules with ring and arc calcifications and entrapped normal medullary fat. The regression of an existing enchondroma, in which the cartilage lobules are replaced by fatty marrow, is considered unusual. Only a few studies have been reported on long tubular bones. Herein, we report an unusual case of a 73-year-old man with an enchondroma in the hand. In this case, a histologic appearance of the enchondroma exhibited loss of matrix mineralization, which corresponded to replacement by marrow fat revealed by magnetic resonance imaging.

Autoimmune encephalitis (AE) is a category of immune-mediated disorders of the central nervous system (CNS) affecting children and adults. It is characterized by the subacute onset of altered mentation, neurocognitive issues, refractory seizures/ drug-resistant epilepsy, movement disorders, and/or autonomic dysfunction. AE is mediated by autoantibodies targeting specific surface components or intracytoplasmic antigens in the CNS, leading to functional or structural alterations. Multiple triggers that induce autoimmunity have been described, which are mainly parainfectious and paraneoplastic. The imaging features of AE often overlap with each other and with other common causes of encephalitis/encephalopathy (infections and toxic-metabolic etiologies). Limbic encephalitis is the most common imaging finding shared by most of these entities. Cortical, basal ganglia, diencephalon, and brainstem involvement may also be present. Cerebellar involvement is rare and is often a part of paraneoplastic degeneration. Owing to an improved understanding of AE, their incidence and detection have increased. Hence, in an appropriate setting, a high degree of suspicion is crucial when reporting clinical MRIs to ensure prompt treatment and better patient outcomes. In this review, we discuss the pathophysiology of AE and common etiologies encountered in clinical practice.

Enchondromas are common benign bone tumors of the hand and are typically located in the medullary cavity of the metaphysis of the tubular bones. Typical radiological findings reveal cartilage lobules with ring and arc calcifications and entrapped normal medullary fat. The regression of an existing enchondroma, in which the cartilage lobules are replaced by fatty marrow, is considered unusual. Only a few studies have been reported on long tubular bones. Herein, we report an unusual case of a 73-year-old man with an enchondroma in the hand. In this case, a histologic appearance of the enchondroma exhibited loss of matrix mineralization, which corresponded to replacement by marrow fat revealed by magnetic resonance imaging.

Autoimmune encephalitis (AE) is a category of immune-mediated disorders of the central nervous system (CNS) affecting children and adults. It is characterized by the subacute onset of altered mentation, neurocognitive issues, refractory seizures/ drug-resistant epilepsy, movement disorders, and/or autonomic dysfunction. AE is mediated by autoantibodies targeting specific surface components or intracytoplasmic antigens in the CNS, leading to functional or structural alterations. Multiple triggers that induce autoimmunity have been described, which are mainly parainfectious and paraneoplastic. The imaging features of AE often overlap with each other and with other common causes of encephalitis/encephalopathy (infections and toxic-metabolic etiologies). Limbic encephalitis is the most common imaging finding shared by most of these entities. Cortical, basal ganglia, diencephalon, and brainstem involvement may also be present. Cerebellar involvement is rare and is often a part of paraneoplastic degeneration. Owing to an improved understanding of AE, their incidence and detection have increased. Hence, in an appropriate setting, a high degree of suspicion is crucial when reporting clinical MRIs to ensure prompt treatment and better patient outcomes. In this review, we discuss the pathophysiology of AE and common etiologies encountered in clinical practice.