The effect of diclofenac on the small intestine studied by wireless endoscopy

Neðst á síðunni er hægt að nálgast greinina í heild sinni með því að smella á hlekkinn View/OpenIntroduction: It is well known that NSAIDs cause erosions and ulcers in the stomach and duodenum but little is known about a possible damage to the small intestine. Direct visualization of the small intestine has not been possible until recently with the introduction of wireless endoscopy. Objectives of study: Primary. To assess the effect of diclofenac on the small intestine using wireless endoscopy and measurement of calprotectin in the stools. Secondary. To assess the possible effect of diclofenac on gastro-intestinal symptoms and on the level of hemoglobin. Methods: Twenty healthy volunteers 21-61 years of age, 10 males and 10 women, received diclofenac 75 mg twice daily for 14 days. Wireless endoscopy was performed before and after diclofenac and also measurements of calprotectin in the stools. The volunteers kept a diary of gastro-intestinal related symptoms during the treatment. In order to eliminate injury and symptoms from the stomach and duodenum, omeprazole 20 mg twice daily was given with the diclofenac. Results: Wireless endoscopy before diclofenac showed no abnormalities in the 20 volunteers. After diclofenac treatment wireless endoscopy showed injuries in 14 volunteers but six had no injury. The number of small intestinal injuries found in each volunteer varied from 2-30. The injuries were equally distributed throughout the small intestine. Two volunteers had an injury in the caecum (ulcer, free blood). Stool calprotectin (normal value <60 mg/L) before diclofenac was 29 mg/L (+/-28) but increased to 148 mg/L (+/-108) (p<0.01) after diclofenac. Fourteen volunteers had gastro-intestinal related symptoms. The mean Hemoglobin concentration decreased from 145.1 to 136.8 g/L (p<0.05) with diclofenac treatment. Conclusions: The administration of diclofenac is associated with injuries in the small intestine similar as have been described in the stomach and duodenum. The symptoms associated with diclofenac in this study could be related to the small intestinal injury.Inngangur: Það er vel þekkt að salílyf valda áverka á slímhúð í maga og skeifugörn en minna er vitað um áhrif þeirra á mjógirni. Ný tækni gerir nú mögulegt að skoða hvaða áhrif salílyf hafa í mjógirni. Lítið holsjárhylki sem sjúklingar kyngja berst með þarmahreyf­ingum eftir mjógirninu og sendir þráðlaust myndir í móttökubúnað sem festur er á kvið viðkomandi. Tilgangur: Að kanna áhrif díklófenacs á mjógirnið metið myndrænt með holsjárhylki og með mælingum á kalprotektíni í hægðum. Ennfremur að kanna áhrif díklófenacs á einkenni frá meltingarfærum og á blóðrauða. Aðferðir: Tuttugu heilbrigðir sjálfboðaliðar 21-61 árs tóku díklófenac 75 mg x 2 á dag í 14 daga. Skoðun með holsjárhylki var gerð fyrir og eftir lyfjatöku og einnig mæling á kalprotektíni í hægðum. Til að hindra áverka á maga var gefið omeprazole 20 mg x 2 á dag. Niðurstöður: Allir sjálfboðaliðar höfðu eðlilegt mjógirni fyrir lyfjatöku. Eftir lyfjatöku komu fram áverkar hjá 14 en sex höfðu engan áverka: Hjá þeim sem höfðu áverka var fjöldi þeirra á bilinu 2 til 30. Tegund áverkanna var frá litlu rofi eða blæðingu í slímhúð yfir í stór sár með fríu blóði. Áverkarnir dreifðust jafnt um mjógirnið og einn sjálfboðaliði hafði stórt sár efst í ristli og annar hafði frítt blóð í ristli. Meðalgildi kalprotectín (normalgildi<60) fyrir lyfjagjöf var 29 mg/L (±28) en 148 mg/L (±108) eftir lyfjagjöf (p< 0,001). Meðalgildi blóðrauða lækkaði úr 145,1 í 136,8 g/L (p<0,05). Tólf sjálfboðaliðar höfðu óþægindi í efri hluta meltingarvegar meðan á lyfjagjöf stóð. Ályktun: Rannsóknin sýnir að gigtarlyfið díklófenac veldur slímhúðaráverkum í mjógirni eins og lýst hefur verið í maga. Óþægindi í kviðarholi sem er vel þekktur fylgikvilli salílyfja getur fullt eins orsakast af mjógirnisáverka

Mechanisms of damage to the gastrointestinal tract from non-steroidal anti-inflammatory drugs

Non-steroidal anti-inflammatory drugs (NSAIDs) can damage the gastrointestinal tract, causing widespread morbidity and mortality. Although mechanisms of damage involve the activities of prostaglandin-endoperoxide synthase 1 (PTGS1 or COX1) and PTGS1 (COX2), other factors are involved. We review mechanisms of gastrointestinal damage induction by NSAIDs, via COX-mediated and COX-independent processes. NSAIDs interact with phospholipids and uncouple mitochondrial oxidative phosphorylation, which initiates biochemical changes that impair function of the gastrointestinal barrier. The resulting increase in intestinal permeability leads to low-grade inflammation. NSAID's inhibition of COX enzymes, along with luminal aggressors, results in erosions and ulcers, with potential complications of bleeding, protein loss, stricture formation, and perforation. We propose a model for NSAID-induced damage to the gastrointestinal tract that includes these complex, interacting, and inter-dependent factors. This model highlights the obstacles for the development of safer NSAIDs. [Abstract copyright: Copyright © 2017 AGA Institute. Published by Elsevier Inc. All rights reserved.

Effect of Pentavac and MMR vaccination on the intestine

Neðst á síðunni er hægt að nálgast greinina í heild sinni með því að smella á hlekkinn View/OpenObjective: The safety of infant vaccination has been questioned in recent years. In particular it has been suggested that the measles, mumps and rubella (MMR) vaccination leads to brain damage manifesting as autism consequent to the development of an "enterocolitis" in the immediate post-vaccination period. Aim: To assess if MMR vaccination is associated with sub-clinical intestinal inflammation which is central to the autistic "enterocolitis" theory. The study was not designed to test directly the association of autism to MMR vaccination. Material and methods: We studied 109/20 infants, before and two and four weeks after immunization with Pentavac and MMR vaccines, for the presence of intestinal inflammation (faecal calprotectin). Results: Neither vaccination was associated with any significant increase in faecal calprotectin concentrations. Conclusions: The failure of the MMR vaccination to cause an intestinal inflammatory response provides evidence against the proposed gut-brain interaction that is central to the autistic "enterocolitis" hypothesis.ilgangur: Að meta hvort MMR-bólusetning (measles, mumps and rubella) valdi þarmabólgu hjá íslenskum börnum. Rannsóknin var ekki hönnuð til að svara spurningunni hvort MMR-bólusetning valdi einhverfu. Aðferðir: Rannsökuð voru 109/20 börn fyrir bólusetningu og tveim, fjórum og 12-18 vikum eftir bólusetningu með Pentavac- og MMR-bóluefnum. Athugað var hvort merki væri um þarmabólgu með því að mæla kalprotectín í hægðasýni. Niðurstöður: Hvorugt bóluefnið var tengt nokkurri marktækri breytingu á þéttni kalprotectíns í hægðum og kom ekkert fram sem benti til þarmabólgu. Ályktun: Þar sem þessi rannsókn hefur sýnt að MMR-bólusetningin tengist ekki þarmabólgu þá mælir það gegn tilgátunni um að MMR tengist einhverfu í gegnum bólgu í þörmum

Contrasting Pattern of Chronic Inflammatory Bowel Disease in Primary and Autoimmune Sclerosing Cholangitis.

To access publisher's full text version of this article click on the hyperlink at the bottom of the pagePrimary sclerosing cholangitis (PSC) and autoimmune sclerosing cholangitis (AISC) are related, but distinct chronic liver diseases. PSC is associated with a high prevalence of ulcerative colitis while the intestinal inflammation associated with AISC is less well characterised.To assess and contrast aspects of intestinal inflammation in patients with AISC and PSC and compare the clinical features with those of patients with ulcerative colitis and Crohn's disease.23 and 22 patients with AISC and PSC, respectively, underwent review of colonoscopy and biopsy findings, capsule enteroscopy and assessment of clinical and inflammatory (faecal calprotectin) disease activity, which was compared with that of patients with ulcerative colitis and Crohn's disease (n = 55 each).Five and 6 patients with AISC and PSC, respectively, had normal colonoscopy and faecal calprotectin levels of 34.4 ± 8.3 and 39.7 ± 8.4 μg/g, respectively (normal 0.05) between patients with intestinal inflammation in AISC (588 ± 549 μg/g), PSC (421 ± 351 μg/g), ulcerative colitis (501 ± 656 μg/g) or Crohn's disease (476 ± 571 μg/g). Capsule enteroscopy showed that 7 of 18 (39%) (p < 0.03) of those with AISC had small bowel mucosal breaks whereas no patient with PSC had these findings.Collectively these findings lend support to the suggestion that the chronic inflammatory bowel disease associated with PSC and in particular AISC may represent a distinct nosologic entity different from classic ulcerative colitis and Crohn's disease

Blood profile holds clues to role of infection in a premonitory state for idiopathic parkinsonism and of gastrointestinal infection in established disease

The two-stage neuroinflammatory process, containment and progression, proposed to underlie neurodegeneration may predicate on systemic inflammation arising from the gastrointestinal tract. Helicobacter infection has been described as one switch in the pathogenic-circuitry of idiopathic parkinsonism (IP): eradication modifies disease progression and marked deterioration accompanies eradication-failure. Moreover, serum Helicobacter-antibody-profile predicts presence, severity and progression of IP. Slow gastrointestinal-transit precedes IP-diagnosis and becomes increasingly-apparent after, predisposing to small-intestinal bacterial-overgrowth (SIBO). Although IP is well-described as a systemic illness with a long prodrome, there has been no comprehensive overview of the blood profile. Here, it is examined in relation to Helicobacter status and lactulose-hydrogen-breath-testing for SIBO

The murky world of the COX-2-selective agents

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