https://journals.bohrpub.com/index.php/bjog <p><strong>BOHR Journal of Gastroenterology (BJG)</strong> is a peer reviewed open-access journal dedicated to fostering innovation and advancing knowledge in the field of Surgical Gastroenterology. Our journal aims to provide a forum for researchers, clinicians, and professionals to share their insights, discoveries, and advancements in various topics of Surgical Gastroenterology<strong>. </strong>Authors are solicited to contribute to the journal by submitting articles that illustrate high-quality research and contributes to the understanding, diagnosis, treatment, and prevention of diseases.</p> <p> </p> <p> </p> en-US BOHR Journal of Gastroenterology <p>Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a <a href="https://creativecommons.org/licenses/by/4.0/">Creative Commons Attribution 4.0 International License</a> that allows others to share the work with an acknowledgment of the work’s authorship and initial publication in this journal.</p> https://journals.bohrpub.com/index.php/bjog/article/view/616 <p>Background: Acute hepatitis due to hepatitis A virus infection is a self-limiting mild disease. Sometimes, it may have an atypical course in few percentages. We reviewed with characteristics, response to steroid therapy, and outcome of prolonged cholestatic jaundice in hepatitis A virus infection. Case summary: We analyzed acute hepatitis with a prolonged cholestatic course due to hepatitis A virus infection in an adolescent with preexisting hemoglobin E disease. Bilirubin was gradually increasing, the maximum total bilirubin was 48.3 mg/dl, and direct 46.6 mg/dl at day 50 of symptoms onset. After that, the steroid was started along with ursodeoxycholic acid. The patient gradually improved clinically and biochemically. Conclusion: Hepatitis A virus infection may cause prolonged cholestatic severe jaundice in a patient with preexisting congenital hemolytic disease. Steroid therapy may induce early recovery.</p> Afsana Yasmin Lutful Latif Chowdhury Copyright (c) 2024 BOHR Journal on Gastroenterology 2024-03-14 2024-03-14 1 1 https://journals.bohrpub.com/index.php/bjog/article/view/617 <p>It is currently believed that the cause of superior mesenteric artery syndrome (SMAS) is compression of the duodenum in the angle between the aorta and superior mesenteric artery (SMA). It is recognized that a decrease in aortomesenteric angle (AMA) &lt;25 and intervascular distance &lt;8 mm, caused by fat loss, is characteristic of SMAS. Based on these statements, surgeons operate on patients with symptoms of dyspepsia only based on a reduction of AMA. This study is devoted to the analysis of the literature, including four own studies on this issue.</p> <p>Results: Measurement of the length of the constriction in the third part of the duodenum on radiograms from available sources showed that its true length ranged from 2.5 to 4.2 (3.30 _ 0.15) cm and began a few centimetres cranial to the AMA. Therefore, it could not have been caused by compression in the AMA. In terms of length (3.20 _ 0.15 cm) and location, this constriction corresponded to Ochsner’s sphincter, which normally short-term contracts to prevent the penetration of an acid bolus into the jejunum. Conscientious studies have shown that AMA is proportional to BMI, i.e., a decrease in AMA is observed in all thin people. An analysis of 211 cases of SMAS made it possible to differentiate two types of diseases. In 101 patients, the disease occurred acutely 1–53 (8.2 _ 1.9) days after stressful situations, accompanied by a catabolic reaction and hypersecretion of hydrochloric acid. In 110 patients, SMAS developed 3 Michael D. Levin Copyright (c) 2024 BOHR Journal on Gastroenterology 2024-03-14 2024-03-14 1 1 5 12