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Proper mitochondrial function and adequate cellular ATP are necessary for normal pancreatic protein synthesis and sorting, maintenance of intracellular organelles and enzyme secretion. Inorganic phosphate is required for generating ATP and its limited availability may lead to reduced ATP production causing impaired Ca(2+) handling, defective autophagy, zymogen activation, and necrosis, which are all features of acute pancreatitis. We hypothesized that reduced dietary phosphate leads to hypophosphatemia and exacerbates pancreatitis severity of multiple causes. We observed that mice fed a low-phosphate diet before the induction of pancreatitis by either repeated caerulein administration or pancreatic duct injection as a model of pressure-induced pancreatitis developed hypophosphatemia and exhibited more severe pancreatitis than normophosphatemic mice. Pancreatitis severity was significantly reduced in mice treated with phosphate. In vitro modeling of secretagogue- and pressure-induced pancreatic injury was evaluated in isolated pancreatic acini using cholecystokinin and the mechanoreceptor Piezo1 agonist, Yoda1, under low and normal phosphate conditions. Isolated pancreatic acini were more sensitive to cholecystokinin- and Yoda1-induced acinar cell damage and mitochondrial dysfunction under low-phosphate conditions and improved following phosphate supplementation. Importantly, even mice on a normal phosphate diet exhibited less severe pancreatitis when treated with supplemental phosphate. Thus, hypophosphatemia sensitizes animals to pancreatitis and phosphate supplementation reduces pancreatitis severity. These appear to be direct effects of phosphate on acinar cells through restoration of mitochondrial function. We propose that phosphate administration may be useful in the treatment of acute pancreatitis. NEW & NOTEWORTHY Impaired ATP synthesis disrupts acinar cell homeostasis and is an early step in pancreatitis. We report that reduced phosphate availability impairs mitochondrial function and worsens pancreatic injury. Phosphate supplementation improves mitochondrial function and protects against experimental pancreatitis, raising the possibility that phosphate supplementation may be useful in treating pancreatitis.

Background Viral resistance-associated substitutions (RASs) can develop in the setting of DAAs therapy (i.e., emerging RASs). Long-term monitoring of fibrosis regression after achieving SVR to simiprevir (SMV)/sofosbuvir (SOF) is essential. The aim of this study was to determine the prevalence of baseline and emerging NS34A RASs in chronic HCV patients in Upper Egypt and to assess the impact of SMV/SOF therapy on liver stiffness. Results The enrolled 59 patients had HCV genotype 4a without any baseline RASs in the NS34A region. 96.6% (57/59) of patients achieved sustained virological response (SVR12). Of the two patients who failed to achieve SVR12, one of them developed emerging RASs Q80K in the NS34A region. Seventy-two weeks after SMV/SOF therapy, the percentage of patients with liver fibrosis stage (F2, F3, and F4) decreased from 75.4% before treatment to 42.1% after treatment. The combination of SOF and SMV appeared to be well tolerated. Conclusions All patients had HCV genotype 4a without any baseline RASs in the NS34A region. In addition, there was improvement of non-invasive measures of liver fibrosis in patients who achieved SVR, 72 weeks after SMV/SOF therapy.

Background& aim: HCV infection is one of the major health problems in our country. Prevalence of DM is higher among patients with chronic HCV infection. Insulin resistance (IR) is common in such and its impact on sustained virological response (SVR) is not well studied. This work was designed to assess impact of IR on SVR. Patients & methods: Between July 2016 and June 2017; 200 patients with chronic HCV infection were enrolled in a prospective study. Exclusion criteria included decompensated cirrhosis, hepatocellular carcinoma or extrahepatic malignancy, co-infection with HBV or HIV infection. HOMA and IR were assessed at baseline of therapy and 3-months post-therapy. Patients received sofosbuvir and daclatasvir for 3 months (chronic hepatitis) and for 6 months in (liver cirrhosis). Results: Mean age of patients was 49.89 ± 9.01 years, 111 (55.5%) patients were male and 180 (90%) achieved SVR. Baseline IR had insignificant difference between responders and non-responders (93% v. 90%; P = 0.45), while baseline HOMA was significantly higher in non-responders (10.11 ± 3.03 vs. 8.48 ± 2.98; P = 0.01). Also, post-therapy IR had insignificant difference between both groups (73.3% vs. 85%; P = 0.05), while post-therapy HOMA was significantly higher in non-responders (7.12 ± 2.31 vs. 5.06 ± 1.34; P = 0.01). Predictors of non-responders were age (> 40 years), low serum albumin and post-therapy IR. Conclusion: Baseline IR had no impact on SVR but it showed significant improvement in presence of SVR.

OBJECTIVE: The current study was conducted to evaluate the performance and screening effectiveness of commercially available rapid screening kits in comparison with chemiluminescence immunoassay (CLIA) and polymerase chain reaction (PCR). MATERIALS AND METHODS: This single-center, cross-sectional study was conducted at the Department of Pathology and Blood Transfusion Services, Shaheed Zulfiqar Ali Bhutto Medical University, PIMS, Islamabad, from January to April 2019. A total of 10 commercially available immunochromatographic test (ICT) devices and one CLIA kit (LIAISON XL) were tested for their sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), and accuracy using 100 positive and 100 negative samples each for HBV and HCV, respectively. RESULTS: The sensitivities and specificities of ICT kits for hepatitis B surface antigen were 65% and 70% (Hightop), 67% and 85% (RightSign), 62% and 73% (Wondfo), 70% and 80% (Accu-Chek), 68% and 77% (Fastep), 73% and 85% (Abon), 77% and 83% (ImmuMed), 80% and 90% (Insta-Answer), 67% and 81% (BioCheck), and 72% and 83% CTK Biotech, respectively. Similarly, the sensitivities and specificities of different ICT kits for HCV were 69% and 80% (Hightop), 76% and 83% (RightSign), 69% and 81% (Wondfo), 78% and 79% (Accu-Check), 68% and 68% (Fastep), 63% and 73% (Abon), 71% and 70% (ImmuMed), 79% and 68% (Insta-Answer), 62% and 66% (BioChek), and 69% and 78% CTK Biotech, respectively. The sensitivity and specificity of Diasorin Liaison Murex assay for both HBV and HCV were found to be 100% when compared with PCR. The PPV, NPV and Accuracy were determined accordingly.CONCLUSION: Rapid testing ICT devices for both HBV and HCV available in Pakistan were found to have a variable degree of sensitivity and specificity when compared with CLIA and PCR. Comparatively expensive but quality methods are more reliable as compared to rapid devices.

Background Changes in hematological parameters, such as neutrophils, leukocytes, neutrophil-lymphocyte ratio, platelet lymphocyte ratio, and mean platelet volume, have been observed during laparoscopic surgeries. Objectives The objectives of this research were to assess the changes in hematological parameters and liver enzymes during laparoscopic cholecystectomy (LC). Methods This prospective observational study included patients undergoing laparoscopic cholecystectomy for symptomatic cholelithiasis. Patients with comorbidities, including hepatitis, diabetes, and where laparoscopic cholecystectomy was converted to open cholecystectomy, were excluded. Preoperative and postoperative baseline hematological parameters and liver function tests (LFTs) were recorded. Characteristics like age, gender, body mass index (BMI), indication for surgery, duration of surgery, the pressure of pneumoperitoneum, and the duration of hospital stay were noted. A paired sample t-test was applied to assess the difference between the mean pre and postoperative values of different hematological parameters. Results It was observed that hemoglobin (Hb), hematocrit (Hct), platelets, and alkaline phosphatase (ALP) decreased postoperatively. However, mean corpuscular volume (MCV), mean platelet volume (MPV), leukocytes, and alanine transaminase (ALT) increased postoperatively. The difference in mean Hb, MCV, Hct, leukocytes, MPV, and ALT was statistically significant (p

Prognostic markers are needed to understand the disease course and severity in patients with Covid-19. There is evidence that Covid-19 causes gastrointestinal symptoms and abnormalities in liver enzymes. We aimed to determine if hepatobiliary laboratory data could predict disease severity in patients with Covid-19. In this retrospective, single institution, cohort study that analyzed patients admitted to a community academic hospital with the diagnosis of Covid-19, we found that elevations of Aspartate Aminotransferase (AST), Alanine Aminotransferase (ALT) and Alkaline Phosphatase (AP) at any time during hospital admission increased the odds of ICU admission by 5.12 (95% CI: 1.55–16.89; p = 0.007), 4.71 (95% CI: 1.51–14.69; p = 0.01) and 4.12 (95% CI: 1.21–14.06, p = 0.02), respectively. Hypoalbuminemia found at the time of admission to the hospital was associated with increased mortality (p = 0.02), hypotension (p = 0.03), and need for vasopressors (p = 0.02), intubation (p = 0.01) and hemodialysis (p = 0.002). Additionally, there was evidence of liver injury: AST was significantly elevated above baseline in patients admitted to the ICU (54.2 ± 15.70 U/L) relative to those who were not (9.2 ± 4.89 U/L; p = 0.01). Taken together, this study found that hypoalbuminemia and abnormalities in hepatobiliary laboratory data may be prognostic factors for disease severity in patients admitted to the hospital with Covid-19.

INTRODUCTION: Prognostic markers are needed to understand the disease course and severity in patients with Covid-19, a viral respiratory illness that causes systemic symptoms However, there is no model to date that evaluates the complexity of this illness We hypothesized that the MELD-Na score would be associated with disease severity in patients with Covid-19 METHODS: This is an IRB approved, retrospective, single institution, cohort study that analyzed patients admitted to a community academic hospital with the diagnosis of Covid-19 between March, 1st 2020 and June 11th, 2020 The primary outcome was mortality at 30 days based on MELD-Na score calculated at the time of admission Secondary outcomes included the development of an Acute Kidney Injury (AKI), need for hemodialysis (HD), need for vasopressor hemodynamic support, need for intubation and hospital stay lasting longer than 7 days RESULTS: The sample size consisted of 99 patients: admission data to calculate a MELD-Na score was available for 63 patients (63%) The MELD-Na score was found to be significantly higher in those who died at 30 days (14 38±6 92) after discharge relative to those who survived (9 68±5 69;P = 0 03);the odds of death at 30 days with a MELD-Na score greater than 10 was 9 00 (95% CI: 2 29, 35 50;P = 0 001) Patients with a MELD-Na score greater than 10 were more likely to have an AKI by an odds ratio (OR) of 3 31 (95% CI: 1 08, 10 17, P = 0 03), need HD by an OR of 9 69 (95% CI: 1 74, 53 96, P = 0 007), need vasopressor support by an OR of 4 55 (95% CI: 1 22, 16 99, P = 0 02) and stay in the hospital longer than 7 days by an OR of 4 17 (95% CI: 1 05, 16 47;P = 0 03) CONCLUSION: The MELD-Na score was found to be higher in patients with Covid-19 who died relative to those who survived at 30 days after discharge A MELD-Na score greater than 10 was prognostic of multiple clinical outcomes, including 30-day all cause mortality, development of an AKI, need for HD, need for vasopressors and longer hospital stay Thus, the MELD-Na score serves as a useful clinical scoring system for prognosis in patients admitted to the hospital with Covid-19 (Table Presented)

INTRODUCTION: Prognostic markers are needed to understand the disease course and severity in patients with Covid-19, a respiratory viral illness There is evidence that Covid-19 causes gastrointestinal symptoms and abnormalities in liver enzymes We aimed to determine if hepatobiliary laboratory data could predict disease severity in patients with Covid-19 METHODS: This is an IRB approved, retrospective, single institution, cohort study that analyzed patients admitted to a community academic hospital with the diagnosis of Covid-19 between March, 1st 2020 and May 5th, 2020 The primary outcome was the need for Intensive Care Unit (ICU) admission based on elevations in transaminases, Alkaline Phosphatase (AP) and Total Bilirubin (TB) Secondary outcomes included mortality, development of Acute Kidney Injury (AKI) or hypotension and need for supplemental oxygen RESULTS: Sixty patients were included in the analysis Elevation of Aspartate Aminotransferase (AST), Alanine Aminotransferase (ALT) and Alkaline Phosphatase (AP) increased the odds of ICU admission by 5 12 (95% CI: 1 55,16 89;P = 0 007), 4 71 (95% CI: 1 51,14 69;P = 0 01) and 4 12 (95% CI: 1 21,14 06, P = 0 02), respectively Hypoalbuminemia was associated with increased mortality by an odds ratio of 6 79 (CI: 1 27-36 34, P = 0 02) Additionally, there was evidence of liver injury: the change in AST during admission above baseline was significantly higher in patients admitted to the ICU (54 2±15 70 U/L) relative to those who were not (9 2±4 89 U/L;P = 0 01) CONCLUSION: This study found that hypoalbuminemia and abnormalities in hepatobiliary laboratory data are prognostic factors for disease severity in patients admitted to the hospital with Covid-19 Additionally, there may be evidence of liver injury in Covid-19 patients that is more severe in those admitted to the ICU (Table Presented)

N-acetylcysteine (NAC) has been well studied in the treatment of acetaminophen-induced and select non-acetaminophen-induced liver failure. However, its role in the management of sickle cell hepatic crisis resulting in acute liver failure (ALF) is unknown. We describe and discuss the novel and beneficial use of NAC in a 25-year-old man with ALF due to sickle cell hepatic crisis. We further review ALF in sickle cell disease and NAC in the treatment of non-acetaminophen-induced liver failure. Our case highlights the promising role of NAC in sickle cell-related liver injury.

Background & Aims Heavy alcohol consumption is a common cause of acute pancreatitis; however, alcohol abuse does not always result in clinical pancreatitis. As a consequence, the factors responsible for alcohol-induced pancreatitis are not well understood. In experimental animals, it has been difficult to produce pancreatitis with alcohol. Clinically, alcohol use predisposes to hypophosphatemia, and hypophosphatemia has been observed in some patients with acute pancreatitis. Because of abundant protein synthesis, the pancreas has high metabolic demands, and reduced mitochondrial function leads to organelle dysfunction and pancreatitis. We proposed, therefore, that phosphate deficiency might limit adenosine triphosphate synthesis and thereby contribute to alcohol-induced pancreatitis. Methods Mice were fed a low-phosphate diet (LPD) before orogastric administration of ethanol. Direct effects of phosphate and ethanol were evaluated in vitro in isolated mouse pancreatic acini. Results LPD reduced serum phosphate levels. Intragastric administration of ethanol to animals maintained on an LPD caused severe pancreatitis that was ameliorated by phosphate repletion. In pancreatic acinar cells, low-phosphate conditions increased susceptibility to ethanol-induced cellular dysfunction through decreased bioenergetic stores, specifically affecting total cellular adenosine triphosphate and mitochondrial function. Phosphate supplementation prevented ethanol-associated cellular injury. Conclusions Phosphate status plays a critical role in predisposition to and protection from alcohol-induced acinar cell dysfunction and the development of acute alcohol-induced pancreatitis. This finding may explain why pancreatitis develops in only some individuals with heavy alcohol use and suggests a potential novel therapeutic approach to pancreatitis. Finally, an LPD plus ethanol provides a new model for studying alcohol-associated pancreatic injury.

Background and study aims There is a lack of studies on erectile dysfunction (ED) in patients diagnosed with nonalcoholic fatty liver disease (NAFLD). The present study aimed to estimate the prevalence of ED in patients with NAFLD and to determine the independent predictors of ED in these patients. Patients and methods We conducted a prospective, hospital-based study of 192 consecutive male patients with NAFLD. All patients underwent clinical evaluation; abdominal ultrasonography; test for viral hepatitis markers; and estimation of liver chemistry panel, complete blood count, prothrombin time, serum lipids panel, serum testosterone, and fasting serum levels of glucose, insulin, and C-peptide. Results The mean age of the study population was 42.4 ± 7.7 years (79.1% ≥ 40 years). Of the 192 patients with NAFLD, 88 (45.8%) had ED, 28 (14.6%) had metabolic syndrome, 25 (13%) had type-2 diabetes mellitus (DM), and 131 (68.2%) had insulin resistance (IR). The mean level of serum testosterone was 3.17 ± 2.94 ng/mL, while the mean insulin resistance index was 2.9 ± 1.7. Mild ED (38.6%) was the most frequent grade of ED. Age ≥ 40 years (odds ratio [OR] 6.4; 95% confidence interval [CI] 1.7–24.1; p- 0.006), IR (OR 5.9; 95% CI 1.7–20.6; p- 0.005), and low serum testosterone (OR 5.1; 95% CI 1.5–17.1; p- 0.009) were the predictors of ED. Conclusions ED is a common disorder in male patients with NAFLD; both IR and low serum testosterone contribute to its development. Treatment of IR may carry a dual benefit of improving erectile function and decreasing the grade of hepatic steatosis.

To explore the role of cholecalciferol for the prophylaxis against recurrent urinary tract infection (UTI) in patients with benign prostatic hyperplasia (BPH). Our randomized, uncontrolled prospective study included 389 naive BPH patients with moderate/severe symptoms, consecutively. The patients were randomly allocated to two groups; group-A included 193 patients who received tamsulosin, while group-B included another 196 patients who received tamsulosin with cholecalciferol. The study population was followed up for 2 years after the start of the treatment. For all the patients enrolled, clinical evaluation, imaging studies (abdominal and trans-rectal ultrasonography), and laboratory investigations [including urinalysis, urine culture with antibiotic susceptibility testing for positive cultures and estimation of prostate-specific antigen (PSA) level] were provided. The incidence rate of recurrent UTI was 9% among the study population; it was significantly higher among group-A patients compared to those of group-B (13.5% vs. 4.6%, p 0.003, OR 2.7, 95% CI 1.5–4.3). Compared to patients of group-A, those of group-B developed a significantly lower level of PSA at the end of treatment period (0.16 ± 0.03 ng/mL vs. 0.27 ± 0.08 ng/mL, p 0.043, OR 1.9, 95% CI 1.2–6.8). Adjuvant cholecalciferol supplementation may be protective against recurrent UTI among patients with BPH receiving tamsulosin therapy without extra adverse effects.

Background & Aims The NACHT, LRR, and pyrin domain–containing protein 3 (NLRP3) inflammasome induces inflammation in response to organ injury, but little is known about its regulation. Toll-like receptors (TLRs) provide the first signal required for activation of the inflammasome and stimulate aerobic glycolysis to generate lactate. We examined whether lactate and the lactate receptor, G i -protein–coupled receptor 81 (GPR81), regulate TLR induction of signal 1 and limit inflammasome activation and organ injury. Methods Primary mouse macrophages and human monocytes were incubated with TLR4 agonists and lactate and assayed for levels of pro-interleukin (IL)1β, NLRP3, and caspase-1 (CASP1); release of IL1β; and activation of nuclear factor-κB (NF-κB) and caspase-1. Small interfering RNAs were used to reduce levels of GPR81 and arrestin β-2 (ARRB2), and an NF-κB luciferase reporter transgene was transfected in RAW 264.7 cells. Cell lysates were analyzed by immunoprecipitation with an antibody against GPR81. Acute hepatitis was induced in C56BL/6N mice by administration of lipopolysaccharide and D-galactosamine. Acute pancreatitis was induced by administration of lipopolysaccharide and cerulein. Some mice were given intraperitoneal injections of sodium lactate or small interfering RNA against Gpr81. Activation of NF-κB in tissue macrophages was assessed in mice that expressed a reporter transgene. Results In macrophages and monocytes, increasing concentrations of lactate reduced TLR4-mediated induction of Il1B , Nlrp3 , and Casp1 ; activation of NF-κB; release of IL1β; and cleavage of CASP1. GPR81 and ARRB2 physically interacted and were required for these effects. The administration of lactate reduced inflammation and organ injury in mice with immune hepatitis; this reduction required Gpr81 dependence in vivo. Lactate also prevented activation of NF-κB in macrophages of mice, and, when given after injury, reduced the severity of acute pancreatitis and acute liver injury. Conclusions Lactate negatively regulates TLR induction of the NLRP3 inflammasome and production of IL1β, via ARRB2 and GPR81. Lactate could be a promising immunomodulatory therapy for patients with acute organ injury.

The ability of tissue injury to result in inflammation is a well-recognized phenomenon and is central to a number of common liver and pancreatic diseases including alcoholic steatohepatitis and pancreatitis, as well as drug-induced liver injury, non-alcoholic steatohepatitis, and pancreatitis from other causes. The requirements of extracellular damage-associated molecules and a cytosolic machinery labeled the inflammasome have been established in in vitro culture systems and in vivo disease models. This has provided a generic insight into the pathways involved, and the challenge now is to understand the specifics of these mechanisms in relation to the particular insults and organs involved. One reason for the excitement in this field is that a number of therapeutic candidates such a toll-like receptor antagonists and interleukin-1R antagonists are either approved or in clinical trials for other indications.

Question: A 60-yearold obese (body mass index of 50 kg/m2) woman was admitted through the emergency department with a history of severe colicky abdominal pain, abdominal distension, and constipation. She was known to have diverticular disease of sigmoid colon, hypertension, diabetes, and chronic obstructive pulmonary disease. here was no history of any previous abdominal operations. On examination, she was found to have distended abdomen with severe enderness and guarding in the left iliac fossa. Her bowel sounds were increased. She had an elevated white cell count (18,000/mm3) and normal liver function tests. Her plain abdominal film showed large bowel dilatation with cutoff in the sigmoid colon. With the clinical impression of large bowel obstruction with possible acute diverticulitis she underwent an emergency abdominal (Figure A) and pelvic (Figure B) computed tomography (CT). What is the complete diagnosis? Look on page 2279 for the answer and see the GASTROENTEROLOGY web site (www.gastrojournal.org) for more information n submitting your favorite image to Clinical Challenges and Images in GI. Conflicts of interest: The authors disclose no conflicts. © 2011 by the AGA Institute 0016-5085/$36.00 doi:10.1053/j.gastro.2010.11.042

Background/Aim: Both nonalcoholic fatty liver disease (NAFLD) and chronic hepatitis C virus (HCV) infection are common in Egypt, and their coexistence is expected. There is controversy regarding the influence of NAFLD on chronic HCV disease progression. This study evaluates the effect of NAFLD on the severity of chronic hepatitis C (CHC) (necroinflammation and fibrosis) and assesses the relative contribution of insulin resistance syndrome to the occurrence of NAFLD in patients with chronic HCV infection. Patients and Methods: Untreated consecutive adults with chronic HCV infection admitted for liver biopsy were included in this study. Before liver biopsy, a questionnaire for risk factors was completed prospectively, and a blood sample was obtained for laboratory analysis. Results: Our study included 92 male patients. Their mean ± SD age and aspartate aminotransferase (AST) level were 42 ± 7.7 years (range 20-56) and 68 ± 41.7 U/L (range 16-214), respectively. The mean insulin level and insulin resistance index were 15.6 ± 18.3 mIU/mL (range 5.1-137.4) and 5.9 ± 15.2 (range 0.9-136.2), respectively. Fifty four percent of patients had steatosis and 65% had fibrosis. In multivariate analyses, steatosis was associated with insulin resistance and fibrosis was associated with high AST level, age ≥40 years, and steatosis. Conclusions: Steatosis is a histopathologic feature in >50% of patients with chronic HCV infection. Insulin resistance has an important role in the pathogenesis of steatosis, which represents a significant determinant of fibrosis together with high serum AST level and older age.

Activation of the cytosolic inflammasome machinery is responsible for acute and chronic liver inflammation, but little is known about its regulation. The N-methyl-d-aspartate (NMDA) receptor families are heterotetrameric ligand-gated ion channels that are activated by a range of metabolites, including aspartate, glutamate, and polyunsaturated fatty acids. In the brain NMDA receptors are present on neuronal and nonneuronal cells and regulate a diverse range of functions. We tested the role of the NMDA receptor and aspartate in inflammasome regulation in vitro and in models of acute hepatitis and pancreatitis. We demonstrate that the NMDA receptor is present on Kupffer cells, and their activation on primary mouse and human cells limits inflammasome activation by downregulating NOD-like receptor family, pyrin domain containing 3 and procaspase-1. The NMDA receptor pathway is active in vivo, limits injury in acute hepatitis, and can be therapeutically further activated by aspartate providing protection in acute inflammatory liver injury. Downregulation of inflammasome activation by NMDA occurs via a β-arrestin-2 NF-kβ and JNK pathway and not via Ca2+ mobilization. We have identified the NMDA receptor as a regulator of inflammasome activity in vitro and in vivo. This has identified a new area of immune regulation associated by metabolites that may be relevant in a diverse range of conditions, including nonalcoholic steatohepatitis and total parenteral nutrition-induced immune suppression.

Background and study aims Association of ulcerative colitis (UC) with hepatobiliary disorders is well recognised. The most common hepatobiliary complications of inflammatory bowel disease (IBD) are fatty liver infiltration and cholelithiasis. The prevalence of liver dysfunction in IBD remains unclear. The aim of the study is to try to identify the frequency and risk factors of hepatobiliary disorders among patients with UC in Upper Egypt. Patients and methods We prospectively analysed 33 patients with newly diagnosed UC of Tropical Medicine and Gastroenterology Department, Assiut University Hospital. For all participants, the following were conducted: clinical evaluation, abdominal ultrasonography (US) examination and laboratory investigations. Risk factors of hepatobiliary disorders were identified using univariate, then multivariate analysis. Results The frequency of hepatic disorders (fatty liver and elevated liver chemistry) was 75.8% in study patients while the frequency of biliary disorders (gallbladder stones and gallbladder wall thickening) was 54.5%. A higher risk of hepatic disorders was observed with older age (odds ratio (OR) 14, 95% confidence interval (CI) 2–124). A higher risk of biliary disorders was observed with UC severe activity index (OR 27, 95% CI 3–292). Conclusions The frequency of hepatobiliary disorders in patients with UC exceeded what was previously reported. High frequency of hepatic disorders was related to older age, while that of biliary disorders was related to UC activity.