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BackgroundInternet gaming disorder has been a controversial topic for nearly a decade. Although internet addiction has been studied in medical students, there is a paucity of evidence regarding internet gaming disorder. Previous studies in Indonesia explored only the prevalence rate and characteristics. ObjectiveThis study aimed to determine the prevalence rate of internet gaming disorder and correlations between internet gaming disorder, temperament, and psychopathology among Indonesian medical students. MethodsA cross-sectional study was performed from August 2019 to September 2019 using total and convenience sampling at a private university and a public university, respectively. The study variables were measured using the Indonesian version of the 10-item Internet Gaming Disorder Test, the Temperament and Character Inventory, and the Symptoms Checklist 90. Chi-square and logistic regression analyses were conducted to examine the relationships between demographic factors, temperament, psychopathology, and the presence of internet gaming disorder. ResultsAmong the 639 respondents, the prevalence rate of internet gaming disorder was 2.03% (n=13), with a mean age of 20.23 (SD 0.13) years and an average gaming duration of 19.0 (SD 0.96) hours/week. Up to 71.2% respondents played using their mobile phones, and respondents with internet gaming disorder reported experiencing all psychopathologies assessed, except phobic anxiety. Bivariate analysis demonstrated that internet gaming disorder was associated with gender, gaming duration, gaming community affiliation, and 9 out of 10 domains of psychopathology. In a logistic regression model, internet gaming disorder was correlated with weekly gaming hours ≥20 hours (odds ratio [OR] 4.21, 95% CI 1.08-16.38, P=.04). ConclusionsThese findings suggest that the prevalence of internet gaming disorder among medical students in Jakarta, Indonesia is similar to that in other populations of Asian countries. The predisposing factor for internet gaming disorder was weekly gaming duration, while other demographic, temperament, and psychopathology variables acted as probable moderators. Strategies should, therefore, be developed and integrated into medical curriculum to screen and aid individuals with these predisposing factors.

Gastric outlet obstruction (GOO) is an uncommon but serious problem caused by benign causes. The incidence of GOO caused by peptic ulcer disease (PUD) is decreasing due to successful Helicobacter pylori treatment. Hence, these aggressive cases are rare. We present a case of a man who experienced intermittent abdominal pain and constipation for a week but acutely worsened in the last five days. He complained of intractable nausea and vomiting, leading to intolerable oral intake. Physical examination revealed abdominal distention, tenderness in epigastrium and right hypochondrium, and hypoactive bowel sounds. Laboratory results revealed leukocytosis with neutrophilia. Gastroscopy showed erosive esophagitis, pangastritis, and large duodenal ulcer causing stricture of duodenum pars I. An open distal gastrectomy, Roux-en-Y reconstruction, and fundoplication was then performed. The patient's general condition improved after ninth day of care and was discharge on the eleventh day of care. PUD is a major cause of GOO, but incidence has decreased to 5% with the use of proton pump inhibitors. If the distal stomach or duodenum is significantly obstructed, GOO should be considered. The gold standard for diagnosis is endoscopy. Initially, conservative and supportive therapy should be done followed by endoscopic treatment in appropriate cases. If there is no improvement, surgical interventions should be done. This case demonstrated the need for definitive invasive procedures in the intervention of GOO caused by PUD. When conservative measures fail, this case also adds support to the direct anatomic treatment of duodenal strictures. [ABSTRACT FROM AUTHOR]

Some proportions of populations, such as immunocompromised patients and organ transplant recipients might have inadequate immune responses to the vaccine for coronavirus disease 2019 (COVID‐19). For these groups of populations, administering monoclonal antibodies might offer some additional protection. This review sought to analyze the effectiveness and safety of tixagevimab‐cilgavimab (Evusheld) as pre‐exposure prophylaxis against COVID‐19. We used specific keywords to comprehensively search for potential studies on PubMed, Scopus, Europe PMC, and ClinicalTrials.gov sources until 3 September 2022. We collected all published articles that analyzed tixagevimab‐cilgavimab on the course of COVID‐19. Review Manager 5.4 was utilized for statistical analysis. Six studies were included. Our pooled analysis revealed that tixagevimab‐cilgavimab prophylaxis may decrease the rate of SARS‐CoV‐2 infection (OR: 0.24; 95% CI: 0.15–0.40, p < 0.00001, I2 = 75%), lower COVID‐19 hospitalization rate (OR: 0.13; 95% CI: 0.07–0.24, p < 0.00001, I2 = 0%), decrease the severity risk (OR: 0.13; 95% CI: 0.07–0.24, p < 0.00001, I2 = 0%), and lower COVID‐19 deaths (OR: 0.17; 95% CI: 0.03–0.99, p = 0.05, I2 = 72%). In the included studies, no major adverse events were reported. This study proposes that tixagevimab‐cilgavimab was effective and safe for preventing COVID‐19. Tixagevimab‐cilgavimab may be offered to those who cannot be vaccinated or have inadequate immune response from the COVID‐19 vaccine to give additional protection. [ABSTRACT FROM AUTHOR]

Objective: Unknown etiology Background: Many drugs have been reported to cause immune-mediated adverse drug reactions (IM-ADRs) in human immunodeficiency virus (HIV) patients; the most common is cutaneous adverse drug reaction (CADR). Immune thrombocytopenia purpura (ITP) is frequent in HIV patients, and it can be caused HIV, opportunistic infections, or drugs. Although drugs can cause immune thrombocytopenia, termed drug-induced immune thrombocytopenia (DIIT), there has been no study on DIIT in HIV patients. Case Report: A 33-year-old male patient was admitted to our hospital with pruritic skin lesion over the entire body, which started 7 days before. He was diagnosed with HIV infection, brain toxoplasmosis, and pulmonary tuberculosis 2 weeks before admission, and was given trimethoprim sulphamethoxazole, isoniazid, rifampicin, pyrazinamide, and ethambutol. Clindamycin was added 10 days before admission. Skin examination revealed generalized erythematous macules with palpable petechiae and purpura. The platelet count was 141 000/μL when he was diagnosed with HIV, and it was 2000/μL at the time of admission. Clindamycin was discontinued and he was given steroids and platelet transfusion. The skin lesions improved along with an increased platelet count. He was discharged on the 10th day of admission, with platelet count of 42 000/μL. When he returned to the outpatient clinic on the 15th day, his platelet was 54 000/μL. The skin lesions had resolved completely and become hyperpigmented, and no purpura or petechiae were seen. Conclusions: We present a case of an HIV patient with IM-ADR in the form of DIIT in conjunction with CADR that might have been caused by clindamycin. [ABSTRACT FROM AUTHOR]