Drug-induced acute pancreatitis in a bodybuilder: a case report.

BACKGROUND: Unregulated use of a variety of drugs and supplements by bodybuilders and athletes is common and can lead to severe adverse complications. Only a small proportion of acute pancreatitis cases are drug induced, and case reports are essential for identifying potential drug-related risks for pancreatitis. Here we present the first case report published of acute pancreatitis linked to recreational use of anabolic-androgenic steroids, subcutaneous growth hormone, and clenbuterol in a previously healthy male after excluding all other causes of pancreatitis. CASE PRESENTATION: A 31-year-old Arab male bodybuilder presented with acute abdominal pain associated with nausea and sharp pain radiating to the back. The patient was not using tobacco or alcohol but was using multiple drugs related to bodybuilding, including anabolic-androgenic steroids, subcutaneous growth hormone, clenbuterol, and multiple vitamin supplements. Laboratory studies revealed a normal white blood cell count, elevated C-reactive protein, minimally elevated aspartate aminotransferase and total bilirubin with normal remaining liver tests, and elevated amylase and lipase. The patient had no hypertriglyceridemia or hypercalcemia, and had had no recent infections, abdominal procedures, trauma, or scorpion exposure. Imaging and laboratory investigations were negative for biliary disease and IgG4 disease. Abdominal computed tomography revealed hepatomegaly and diffuse thickening and edema of the body and tail of the pancreas with peripancreatic fat stranding. An abdominal ultrasound showed slight hepatomegaly with no evidence of cholelithiasis. Genetic testing for hereditary pancreatitis-related mutations was negative. A diagnosis of drug-induced acute pancreatitis was made, and he was treated with aggressive intravenous hydration and pain management. The patient has avoided further use of these drugs and supplements and had no further episodes of pancreatitis during 1 year of follow-up. CONCLUSIONS: This case describes a patient with drug-induced acute pancreatitis after the intake of anabolic-androgenic steroids, subcutaneous growth hormone, and clenbuterol, where all other common causes of acute pancreatitis were excluded. Clinicians should be alert to the possibility of drug-induced acute pancreatitis occurring in bodybuilders and athletes using similar drug combinations.

Optimizing biologic therapy in inflammatory bowel disease: a Delphi consensus in the United Arab Emirates.

BACKGROUND: Inflammatory bowel diseases (IBD) are chronic, relapsing-remitting inflammatory conditions with a substantial negative impact on health-related quality of life and work productivity. Treatment of IBD has been revolutionized by the advent of biologic therapies, initially with anti-TNF agents and more recently with multiple alternatives targets, and yet more under development. OBJECTIVES: Approximatively one third of patients do not respond to biologic therapy and more importantly a significant proportion experiences partial response or loss of response during treatment. The latter are common clinical situations and paradoxically are not addressed in the commercial drug labels and available guidelines. There is therefore a clinical need for physicians to understand when and how eventually to optimize the biologic therapy. DESIGN: This consensus using a Delphi methodology was promoted and supported by the Emirates Society of Gastroenterology and Hepatology to close this gap. DATA SOURCES AND METHODS: Following an extensive systematic review of over 60,000 studies, 81 studies with dose escalation and five addressing drug monitoring were selected and in addition five systematic reviews and three guidelines. RESULTS AND CONCLUSION: after three rounds of voting 18 statements were selected with agreement ranging from of 80% to 100.

First United Arab Emirates consensus on diagnosis and management of inflammatory bowel diseases: A 2020 Delphi consensus.

Ulcerative colitis and Crohn's disease are the main entities of inflammatory bowel disease characterized by chronic remittent inflammation of the gastrointestinal tract. The incidence and prevalence are on the rise worldwide, and the heterogeneity between patients and within individuals over time is striking. The progressive advance in our understanding of the etiopathogenesis coupled with an unprecedented increase in therapeutic options have changed the management towards evidence-based interventions by clinicians with patients. This guideline was stimulated and supported by the Emirates Gastroenterology and Hepatology Society following a systematic review and a Delphi consensus process that provided evidence- and expert opinion-based recommendations. Comprehensive up-to-date guidance is provided regarding diagnosis, evaluation of disease severity, appropriate and timely use of different investigations, choice of appropriate therapy for induction and remission phase according to disease severity, and management of main complications.

Post-sphincterotomy transampullary balloon dilation is a safe and effective technique.

PURPOSE: To evaluate the safety and efficacy of performing ampullary balloon dilation (ABD) following endoscopic sphincterotomy (ES). METHODS: Retrospective review of patients that underwent ABD at Thomas Jefferson University from 2000 to 2007. In all cases, dilation was performed with Hurricane RX hydrostatic balloons (Boston Scientific, Natick MA) or CRE esophageal dilating balloons (Boston Scientific, Natick MA). RESULTS: ABD following ES was performed in 69 patients. The procedure was performed for choledocholithiasis in 58%, abnormal imaging in 26%, and abnormal liver enzymes in 23% of patients. ABD following ES was 86% successful in achieving the intended therapeutic goal of the procedure. Pancreatitis (2.9%) post endoscopic retrograde cholangiopancreatography (ERCP) occurred in two individuals, with one case of hemorrhage (1.5%) and one perforation (1.5%). CONCLUSION: ABD following ES is a safe and effective alternative to ES alone, particularly for the extraction of large common bile duct (CBD) stones.

Endoscopic stenting of esophageal cancer: the clinical impact.

PURPOSE OF REVIEW: To summarize the most relevant articles with regard to endoscopic stenting of esophageal cancer published in 2006. RECENT FINDINGS: In 2006, there were two studies on esophageal stents with experimental designs and adequate size to contribute to an evaluation of esophageal stent technology. A study on an antireflux stent will not measurably change the current use of this device, but emphasizes the need for additional investigation. A study on a self-expanding plastic stent was the largest study to date demonstrating a self-expanding plastic stent to be comparable to self-expanding metal stents. Other published studies in 2006 on esophageal stents include review articles, case reports and small case series that are not addressed in this review. SUMMARY: Self-expanding metal stents remain an important option for the treatment of patients with tracheoesophageal fistulae and esophageal malignancies. Recent innovations are dominated by a shift toward self-expanding esophageal stents that are potentially removable. Such potentially removable stents allow for expanded clinical applications and will be the focus of publications in 2007.

Drug hepatotoxicity.

Drug-induced liver injury is a common but underdiagnosed cause of liver disease with an incidence that is rapidly increasing. The authors address some of the more controversial aspects in relation to drug-induced liver injury: recommendations on the use of anti-tuberculosis therapy in the presence of underlying cirrhosis, the role of periodic liver test monitoring and steroid therapy in relation to drug-induced liver injury, the presence of class effects associated with certain drugs, and the potential use of ursodeoxycholic acid in prolonged cholestasis.

The effect of GI bleeding on Helicobacter pylori diagnostic testing: a prospective study at the time of bleeding and 1 month later.

BACKGROUND: Some case series and cohort studies suggest that acute GI bleeding decreases the sensitivity of Helicobacter pylori diagnostic testing. OBJECTIVE: To assess H pylori biopsy testing in patients with acute upper-GI bleeding and 1 month later. DESIGN: Prospective cohort study using patients as their own controls. SETTING: Urban county hospital. PATIENTS: Sixty-one patients with acute variceal bleeding. INTERVENTIONS: Antral and body endoscopic biopsies at admission and 1 month later. MAIN OUTCOME MEASUREMENTS: CLOtest and histologic examinations were performed and biopsy specimens were coded and mixed for blinded histologic examination for H pylori density and inflammation. RESULTS: CLOtest results changed from H pylori negative at baseline to H pylori positive at 1 month in two patients (3%), from H pylori positive to H pylori negative in 6 patients (10%), and remained the same in 53 (87%). Histologic results changed from H pylori negative at baseline to H pylori positive at 1 month in two patients (3%), from H pylori positive to H pylori negative in 5 patients (8%), and remained the same in 54 (89%). Changes occurred only in patients with low H pylori density. No significant increase in H pylori density or change in inflammatory cell infiltration was seen. CLOtest sensitivity was 8% higher with bleeding vs. 1 month after bleeding (79% vs. 71%; 95% CI of difference was -11% to 27%; i.e., maximal potential decrease in sensitivity with bleeding is 11%). LIMITATIONS: The population is not one for which H pylori testing is recommended, and biopsy test performance was less consistent than expected. CONCLUSIONS: Acute-GI bleeding did not decrease the sensitivity of rapid urease testing, unless the effect lasts more than 1 month. Furthermore, bleeding did not produce falsely negative histologic examinations for H pylori, decrease H pylori density, or alter inflammatory cell infiltration. However, given the lower than expected overall CLOtest sensitivity and frequent use of proton pump inhibitors for GI bleeding, histology may be preferred in this setting.

Marked elevation in serum transaminases: an atypical presentation of choledocholithiasis.

BACKGROUND: Choledocholithiasis causes elevations in levels of alkaline phosphatase out of proportion to aspartate aminotransferase (AST) and alanine aminotransferase (ALT). Isolated marked elevation in AST and ALT levels over 1,000 IU/L has been reported infrequently in patients with choledocholithiasis. METHODS: The charts of 18 patients who presented between 1971 and 2002 with documented choledocholithiasis and AST or ALT levels greater than 1,000 IU/L were retrospectively reviewed. An extensive work-up for coexisting disease processes to account for the abnormal AST and ALT levels was negative. RESULTS: Eighteen patients (16 women, 16 Hispanics, age 38 +/- 3 yr) presented with symptoms of choledocholithiasis and marked transaminase elevation. Peak levels of AST and ALT were 1,062 +/- 129 and 1,119 +/- 90, respectively. Following successful management of gallstone disease, AST and ALT levels fell rapidly to 129 +/- 22 and 268 +/- 61, respectively, within 3-14 days. There was also a concomitant improvement in the levels of bilirubin and alkaline phosphatase. CONCLUSIONS: In the absence of other hepatobiliary or pancreatic disease, choledocholithiasis can result in elevations in AST and/or ALT greater than 1,000 IU/L. These levels fall markedly once the gallstone disease is appropriately managed.

Serum alanine aminotransferase in skeletal muscle diseases.

Although elevation of the levels of serum alanine aminotransferase (ALT) following liver injury is well known, confusion exists concerning skeletal muscle injury as the cause of this rise. We reviewed the records of 16 patients who had muscle necrosis without evidence of liver disease. The patients were divided into three groups: extreme exercise, polymyositis, and seizures. All patients exhibited markedly elevated creatine kinase and lactate dehydrogenase levels consistent with muscle injury. In acute cases, aspartate aminotransferase (AST) and ALT were both elevated, and the AST/ALT ratio was greater than 3, but this ratio approached 1 after a few days because of a faster decline in AST. In conclusion, this difference in half-life accounts for the comparable AST and ALT levels in our cases with chronic muscle injury.

Injury induced neointima formation and its inhibition by retrovirus-mediated transfer of nitride oxide synthase gene in an in-vitro human saphenous vein culture model.

Human saphenous veins were cultured to characterize neointima formation and feasibility of gene transfer to inhibit the intimal proliferative response to injury. Mechanical injury was introduced by abrading the luminal surface of the vein patch with a sterile cotton bud. Both injured and non-injured vein patches were cultured and transduced with retroviral vectors carrying marker or therapeutic genes. After a 14-day culture, the thickness of the intimal layer of non-injured vein patches reached 90+/-28 microm at the edge and 61+/-22 microm at the center (n=29) from the original 22+/-12 microm at harvest (n=6, P=0.02). Mechanical injury to the intimal surface prior to culture resulted in an exaggerated proliferative response. The intimal thickness of injured vein patches increased from 3.4+/-1 microm right after injury to 128+/-23 microm (n=12, P<0.001) at the edge after 14-day culture. Genes were transduced efficiently into a luminal layer of cultured veins using a pseudotyped murine leukemia viral vector. Transduction of gene encoding nitric oxide synthase resulted in reduction of neointima formation to 33+/-7 microm (n=12) at the edge after 14-day culture compared to 90 microm (P<0.01) seen in untransduced non-injured vein patches. Marker gene transduction did not alter intimal proliferative response or its immunohistochemical profile. The data suggest that cultured vein can be used as a model for studying the effects of injury to blood vessels and to evaluate the effects of candidate therapeutic genes.