Colm O'Loughlin

The association of streptococcus bovis bacteremia and gastrointestinal diseases : a retrospective analysis

There is a well-established association between Streptococcus bovis bacteremia (SBB) and colorectal cancer. However, SBB is also frequently associated with chronic liver disease and has been described with other gastrointestinal disorders. The aim of the study was to evaluate the prevalence of gastrointestinal disease in patients with SBB. Retrospective analysis of the microbiology database at Jackson Memorial Medical Center, Miami, Florida, between 1992 and 2002, was performed. Patients’ clinical records were reviewed, with special focus on underlying gastrointestinal disease or other major comorbidities. Thirty-eight patients (83%) were adults and eight (17%) were pediatric patients. Nineteen patients presented with gastrointestinal disorders associated with SBB (41%). Nine adult patients (19%) had end-stage liver disease (five female). Six patients had alcohol-induced liver disease (one with concomitant chronic hepatitis C), with the remaining three cases related to autoimmune hepatitis, primary biliary cirrhosis, and nonalcoholic steatohepatitis. Colonic neoplasms (adenocarcinoma in 3 and adenomatous polyps in 3) were found in 6 of 10 adult patients in whom colonoscopic evaluation was performed. Seven adult patients had acquired immunodeficiency syndrome (AIDS) (18%). Mortality in the patients with AIDS and SBB was high (71%). No significant association with gastrointestinal diseases was found in the pediatric population. Bacteremia due to S. bovis in adults is frequently associated with hepatic dysfunction (1:4), colonic neoplasms (1:6), and AIDS (1:6). This association was valid for our adult population only. SBB is an early clue to the likely presence of these serious underlying conditions and warrants rigorous investigation when recognized.

Collagenous colitis associated with Clostridium difficile: A cause effect?

To the Editor: A widely accepted hypothesis on the etiology of collagenous colitis is that a noxious luminal stimulant leads to an inflammatory reaction that is perpetuated by an immun response to the injury (1). We report a patient with diarrhea who was found to have collagenous colitis and also to be Clostridium difficile toxin positive. His symptoms persisted after treatment of C. difficile. We propose that C. difficile may be a noxious stimulant that could catalyze a chain of events resulting in collagenous colitis. This is the third documented case of an association between C. difficile and collagenous colitis (2, 3). A 73-year-old man presented with a 6-week history of diarrhea. It was of insidious onset, intermittent in course, having 8–10, large-volume, watery bowel movements per day with a nocturnal component. This was associated with increased flatus and with one incidence of fecal incontinence, as well as weight loss of 5 lb over the last 6 months. He had no passage of mucus or blood per rectum, abdominal pain, or tenesmus. He denied recent travel, antibiotic use, or hospitalization in the last year. The patient’s medical history was significant for coronary artery disease, vitiligo, dyslipidemia, gastroespophageal reflux disease, chronic obstructive pulmonary disease, posttraumatic stress disorder, and Alzheimer’s disease. His medications included aspirin, somatostatin, lisinopril, rabeprazol, multivitamin tablets, and amitryptiline. Family history was negative for diarrhea, irritable bowel disease, and cancer. His physical examination and laboratory tests were within normal limits. Stool examinations for ova, parasites and white blood cells were negative. Fecal occult blood tests were negative. A qualitative fecal fat estimation was within normal limits and the fecal osmolal gap was <50 mosm/kg. A stool study for C. difficile toxin using the enzyme immunoassay (EIA) technique was positive. The patient was treated as an outpatient for C. difficile colitis with metronidazole 250 mg, three times a day for one week with very little improvement in his diarrhea. A second course of metronidazole at a dose of 250 mg four times a day for 2 weeks was then initiated and his stool was tested for C. difficile. The follow up C. difficile assay was negative, as were tests for stool ova and parasites, WBCs, and occult blood. A CT of the abdomen and a small bowel follow through were both unremarkable. Colonoscopy was performed and revealed left-sided diverticulosis and normal colonic mucosa to the hepatic flexure. There were no signs of ischemia and/or pseudomembranous colitis. Multiple random biopsies revealed diffuse thickening of the subepithelial collagen layer beneath the basement membrane. There was crypt fission seen in one of the biopsy samples; however, there were no other histopathological changes suggesting inflammatory bowel disease. Double-contrast barium enema was within normal limits. An EGD revealed antritis, and small bowel biopsies revealed normal duodenal mucosa. He was treated with Lomotil, loperamide, and Pepto-Bismol with minimal relief of symptoms. Subsequently he was begun on Asacol 3.6 g/day with clinical improvement. At threemonth follow-up, he was completely free of symptoms and had gained 4 lb. He continues to take Asacol 3.6 g/day. There is strong evidence supporting the contribution of a noxious luminal stimulant to the disease process. Jarnerot et al found that fecal stream diversion via an ostomy induced clinical and histopathologic remission of collagenous colitis (4). Conversely, the disease returned after closure of the ostomy with return of the luminal stream in contact with the colon (4). Recently, bacterial toxins have been implicated as being responsible for collagenous colitis (2, 3, 5, 6). Two separate centers have recently demonstrated the occurrence of collagenous colitis in the presence of C. difficile infection (2, 3). In a retrospective study of six patients diagnosed with collagenous colitis, Makinen et al found that three had had a previous Yersinia enterocolitica infection (6). In another study, an unidentified bacterial toxin found in the stool of a patient with collagenous colitis was shown to have a potent cytotoxic effect on McCoy cells (5). This patient responded favorably to treatment with cholestyramine, a bile-binding resin that can also bind C. difficile toxins. In addition, treatment with cholestyramine significantly decreased stool frequency in 21/27 (78%) of patients with collagenous colitis (7). Patients with collagenous colitis have also been successfully treated with antibiotics, including metronidazole, erythromycin, penicillin G, and sulfhasalazine (5, 8). There are several clues that support the theory of infection as the cause of collagenous colitis. First, there is the sudden onset of symptoms in 43% of patients with collagenous colitis in the Swedish registry (9), which is similar to that seen in an infectious disease. Second, there is the efficacy of antibacterials and a bacterial toxin binding agent, ie, cholestyramine. Third, and the strongest evidence for an association with a luminal irritant, there is the effect of fecal stream diversion on the disease. It is probable that

CASE REPORT: Visceral Varicella Zoster After Bone Marrow Transplantation: An Obscure Cause of an “Acute Abdomen”

Reactivation of latent infection with the varicellazoster virus (VZV) is a common cause of morbidity and mortality after bone marrow transplantation (BMT) (1). The incidence of reactivation ranges from 17% to 52% with the highest rate of recrudescence (70%) occurring within the first six months of transplantation (1–3). In up to 90% of cases reactivation of latent virus is associated with the familiar vesicular skin eruption in a dermatomal distribution; however, in this immunosuppressed group, both cutaneous and visceral dissemination can occur (4). Visceral presentation with VZV infection has been reported in approximately 1% of bone marrow transplant recipients, the majority occurring after allogeneic transplantation. Although relatively uncommon, visceral VZV infection is likely underdiagnosed and is frequently lethal. A 50% mortality from adult respiratory distress syndrome, multiorgan failure, meningoencephalitis, fulminant hepatic failure, and/or severe pancreatitis has been reported (5). Diagnosis is difficult, as the characteristically poorly localized abdominal pain may precede the vesicular eruption by as many as 10 days. This report describes VZV presenting as acute abdomen without cutaneous signs of infection as a late complication of autologous BMT.

Diclofenac Reduces the Incidence of AcutePancreatitis After Endoscopic Retrograde Cholangiopancreatography

Murray et al. conducted a single-center prospective randomized double-blind placebo-controlled study to determine if a single dose of rectally administered diclofenac given after endoscopic retrograde cholangiopancreatography (ERCP) could reduce the incidence of post-ERCP pancreatitis (1). Patients were eligible if they underwent pancreatography, with or without cholangiography, or had pancreatography or cholangiography in the presence of sphincter of Oddi hypertension (SOH). SOH was defined manometrically as a basal pressure >40 mm Hg in the common, biliary, or pancreatic sphincter. Patients were excluded from study participation if they had a contraindication to receiving diclofenac or if they had taken a nonsteroidal anti-inflammatory drug (NSAID) during the preceding week. Five hundred fifty-eight adult patients without acute or chronic pancreatitis were assessed for eligibility between May 1999 and December 2002, and 220 patients were enrolled. In a double-blind randomized fashion with concealed allocation, patients received a suppository containing either diclofenac, 100 mg, or an inert placebo immediately upon entering the recovery area after the procedure. Serum amylase was determined 2 hr after the ERCP as well as the following morning. Patients were interviewed for the presence of abdominal and back pain and examined for abdominal tenderness. Acute pancreatitis was defined as a serum amylase more than four times the upper limit of normal (>800 IU/L) associated with epigastic pain, back pain, and epigastric rebound tenderness. Patients with persistent signs and symptoms of pancreatitis after 48 hr underwent contrast-enhanced computed tomography. The randomization code was broken after 200 patients were enrolled. Analysis of the data at that point suggested a protective effect (P = 0.07). Therefore an additional 20 subjects were enrolled, and data from all 220 patients were reported. The study and the control group contained 110 patients, and the groups were well matched with regard to diagnoses, specific procedure, and risk factors for post-ERCP pancreatitis. One hundred sixteen (diclofenac group, 53; control group, 66) of the 220 patients underwent sphincterotomy. Fifty-three patients, including 26 in the diclofenac group and 27 in the control group, had SOH. Mean serum amylase levels at 2 hr were not significantly different between the groups (diclofenac group, 313 IU/L; control group, 400 IU/L), but at 24 hr there was a significant difference (diclofenac group, 321 IU/L; control group, 507 IU/L; P < 0.01). Of the 220 patients, 24 (10.9%) met the predefined criteria for post-ERCP pancreatitits, 7 of 110 (6.4%) from the diclofenac group and 17 of 110 (15.5%) from the control group (P = 0.049). Fourteen of 116 patients (12.1%) who underwent sphincterotomy developed post-ERCP pancreatitis, of which 2 of 14 had received diclofenac and 12 of 14 had received placebo (P = 0.021). Seven of the 53 patients (13.2%) with SOH developed post-ERCP pancreatitis, 3 in the diclofenac group and 4 in the control group (P = NS), and 17 of the 167 patients (10.2%) without SOH developed post-ERCP pancreatitis, 4 in the diclofenac group and 13 in the control group (P = 0.036). Two of these 24 patients (8%) who developed post-ERCP pancreatitis developed sterile pancreatic necrosis but all patients were discharged from the hospital, after a mean inpatient stay of 3 days in the diclofenac group and 5 days in the control group. No patient who received diclofenac experienced an adverse effect as a result of the medication. The authors concluded that the single dose of rectal diclofenac could reduce the incidence of post-ERCP pancreatitis.

Comparison of polyethylene glycol-electrolyte lavage (PEG-EL) preparation versus standard preparation on small bowel mucosal visualization for wireless capsule endoscopy (WCE)

Comparison of polyethylene glycol-electrolyte lavage (PEG-EL) preparation versus standard preparation on small bowel mucosal visualization for wireless capsule endoscopy (WCE)

Localization of gastric bleeding with wireless capsule endoscopy — the advantages of physiologic endoscopy

Localization of gastric bleeding with wireless capsule endoscopy — the advantages of physiologic endoscopy

43 – Effect of Gender on Pancreatic Disease

This chapter discusses pancreatic lesions that occur more frequently in men or women, evaluates the mechanisms by which they occur, and reviews their clinical course and therapy. Sex steroid hormones (SSH) including estrogens, progestagens, and androgens are responsible for sexual differentiation, and their major target organs are the mammary glands, urogenital tract, bone, cardiovascular and central nervous systems. Epidemiologic, clinical, and biochemical findings have shown the relationship between gender and prevalence of some tumors of the pancreas, the effect of pregnancy on insulin and glucose metabolism, and the identification of SSH receptors in pancreatic tissue. The study of gender-specific pancreatic lesions provides clues regarding their origin, development, tumoral behavior, prognosis, and more specific hormonal therapy. The varying effects of sex steroid hormones (SSH) in development and growth of pancreatic neoplasms may be related to the mechanism affecting carcinogenesis, and may be multifactorial and/or different for each hormone. Clinical trials designed to evaluate the response of cancer of the pancreas to hormonal therapy have been inconclusive.

Independent predictors of cirrhosis in hispanic patients with non alcoholic steatohepatitis (NASH)

Independent predictors of cirrhosis in hispanic patients with non alcoholic steatohepatitis (NASH)

Interobserver variability in the interpretation of wireless capsule endoscopy: interim analysis of 30 cases

A PROSPECTIVE COMPARISON OF ENTEROCLYSIS AND CAPSULE ENDOSCOPY IN THE DIAGNOSIS OF OBSCURE GASTROINTESTINAL BLEEDING Gottumukkala S. Raju, M.D.*, Bincy Abraham, M.D., Melvyn H. Shcreiber, M.D., Guillermo Gomez, M.D., Sharon Boening, R.N., Keith Morris, M.D., Syed Jafri, M.D., Manoop Bhutani, M.D., Gurinder Luthra, M.D., Samir Nath, M.D., Sohaib Faruqi, M.D., Marc Shabot, M.D., Pankaj J. Pasricha, M.D. University of Texas Medical Branch, Galveston, TX.

Extending the sphincterotomy

Brand et al. prospectively studied the outcome of endoscopic sphincterotomy in 29 consecutive patients with biliary-type pain (two or more out of eight criteria), elevated liver enzyme levels (AST, ALP, or γ-glutamyltransferase), and no clear evidence of biliary pathology on transabdominal ultrasound and diagnostic endoscopic retrograde cholangiography. Elevated bilirubin levels (range = 1.3–7.2 mg/dl) were found in 18 patients. The majority of patients (n = 21) had gallbladders in situ. The findings from bile duct exploration after sphincterotomy were recorded, and pain (as measured by a visual analogue scale) and laboratory findings were assessed.The inclusion criteria for endoscopic sphincterotomy were 1) the presence of at least two of any eight characteristics associated with typical biliary-related pain (coliclike, located at the right upper abdomen, radiation to back or right shoulder, pain intensity > 4 on the visual analogue scale [possible range = 0–10], duration of pain > 30 min, postprandial pain, symptoms occurring at night, precise definition of onset and relief of pain), 2) elevated liver enzyme levels (AST, ALP, or γ-glutamyltransferase elevated more than 2-fold) in patients without histories of alcohol abuse or liver disease, and 3) absence of clear pathology on diagnostic endoscopic retrograde cholangiography—that is, no or only mild dilation of the biliary duct system (common bile duct ≤ 12 mm in patients who had undergone cholecystectomies, and ≤ 8 mm in patients with gallbladders in situ) as measured in relation to the diameter of the duodenoscope.Wire-guided sphincterotomy was successful in all patients, whereas uncomplicated pancreatitis occurred in one instance. In 16 patients (55%) there was macroscopic evidence of small stones (n = 2), sludge (n = 12), or both (n = 2) after bile duct exploration with a Dormia basket. In addition, microscopy revealed cholesterol crystals in four patients who had no macroscopic findings. All four patients with elevations of pancreatic enzymes before treatment and four of those eight patients with previous cholecystectomies demonstrated evidence of biliary pathology. The initial median pain intensity was 8 (range = 1–10); 26 patients became pain free within 3 months after endoscopic sphincterotomy. Twenty-six of 28 patients (93%) remained asymptomatic over a median follow-up period of 19 months (range = 12–26); one died of an unrelated malignancy 6 months after therapy.The authors concluded that endoscopic sphincterotomy may be acceptable therapy in patients with clinical presentations suggesting papillary or biliary origins of pain without further diagnostic workup.