In r.:Ltt 11>n lll the first :1 rea, four i,sue, were cli,cu,sed: def in i rH m of d iscasc• sL•,•eri t y; method, of i nve,t iga unn; rel at 1 ,•e i mp"rt ance pf acid 11ml mot ii 11 y in I he p,ll h,,genesb nf t , ERD; and compl1cnt 11m,. Re.tlarding rhe approach t11 therapy, r; ,ur .1rea, were considered: thernpy with lifl',ry le mL,d i!'icatiun and 1111ual therapy; ma intenance ther:ip\; and med1rn l ven,us surgical thernpy, inc luding tre,llment nf cnmpl1cnt1uns. fa1ch sectl,lll 1,•as 111tnllluceLl 111 1he L'ntire group of pmtic1panls hy prep:1red Laib ,111 background informat ion. Thi, was followed hy ,li,cu. ,,i,111 111 , mall grnup, nf '<'Ven tn 12 particip,mls each. Th e ~1rn1 II group ,css1nns WL're then , ummnrized hy I he sl'ss1, > n Ch,11 rp,•rson, :111d werl' pre,1'111ed h 11• f urthcr di ,c ussinn 111 I he entire g r,1up ,1f 40 p.irtic1p,111t,. The C'hairper,l1n I hen prep.ired a written summary ot the gr,1t1p cli,cw,,wn.Agreemem was re:1chcd 111 mn,1 .irea~ and a , uggested decis1nn tree for 1hc mnnagemem of patients wnh ,;i Rn 11•ns develnpcd: the maJnrit)' ol persim, wit h UFRI) symptoms have mild gn,1r,>e"1ph:1geal reflux d1,e,1se; mnst penple with (i~Rll d,, nnt ,cc ;1 ph ys1c1an, ,md 111l1St ck, wdl o n se lf-admini-,tercd Pver-t he-counter therapy. When the per~nn pre,ems to his/her fom ily physicim1 , the• suggested 111nial lre,11111ent lnr .,\mpwmnu, (,FRI) sh11lild i,:un,1,1 uf li fe,1yle mL,dificauon, m•er-thecnuntertherapy an,l l lz-hlocl..er,. Pr, ,kinetic:, a, initi:1 l 1reat me11t .,h uu Id he used only undcr ,peci,il cund it i1,n,. Prohahly about 1wn persnns in three will improve nn lik,tyle modifkat1on , ,11•er-rhe -cnu111L'r rherapy and H~-hlnckers. If the patient with symptoms l,f l,LRLhloe, nm respond 111 1 h 1, iniri,11 f,>ur weight weeb nf therapy, rhe phy, ician has to , u, pecl the presence ol 1rn,re ,erinus d ise,1sc such ,1, en1s1ve esnphag1us, e,uphag1us wi1 h c, 1111pl 1 cat 1nns, ,ir disease nth,•r th,111 ( ,ERi). Therefore, he fore suming protnn pum11 111hihit,w,. endu,cllp\ b in,licatcd. Di.1gnostic m, ,1il11 y stud ies ( 24 h pH and/or mmilit\' and Bernstein test) arc needed on ly under special condit111m. < 11 Rll 1 ., a c: hn,nic relap, 111g disea,e and frequentl y maintenance therapy is needed, p:irritularly when the p.itienr ha, hnd endosCL1pica lly-proven eru, ive esophagi ti,. Mnin1 enrince therapy , hould he undcrrnken with the least pot ent drug thai prevents relapse. T1, dare, 111 severe disease the hest dma fnr maimenance therapy would favnur the ust' of a prown pump 111h1h1tnr nl'er , rnndard duses of an l lz-h lncker, but h igher do,c,, ,lf H2-blocker therapy m,1y pnwc to lw u,eful in :.ome pat ien1s. Most pat ient, with UER ll (even those with complications) can he managed medically, hut there :ire ,urg1cal indic.11i,1n, Ill he con,idered in individual pati..:nu,. A 'Decision Tree' for rhe suggested management of p,llienb with t 1FIUl wa, devcl,,ped t,, facdira1e t hL• clinical approach to this common clinical ...

The effect of feeding a diet supplemented with lipids and containing 2% cholesterol on the endothelium-dependent relaxation of rabbit aorta to acetylcholine was assessed. The effect of feeding a standard rabbit diet after an initial period of 2% cholesterol feeding was assessed also. Age-matched male, New Zealand white rabbits were fed either a 2% cholesterol diet or a standard rabbit diet. The animals were-anesthetized with pentobarbitone sodium (25 mg/kg) and killed either at the beginning of the study (0 weeks) or at 4, 8, or 10 weeks. The animals in the reversal study were fed the 2% cholesterol diet for 6 weeks and killed after an additional 14 and 32 weeks on standard diet. The extent of atherosclerosis in the aorta was assessed by Sudan Red staining, estimation of tissue cholesterol, and light and electron microscopy. The relaxation response to acetylcholine was measured in rings of the thoracic aorta following precontraction with norepinephrine ( -6.0 log mol/1). The relaxation was significantly impaired in aortas from rabbits fed the 2% cholesteroldiet compared to aortas from animals fed the standard diet. The impairment of relaxation was apparent as early as 4 weeks after the start of the 2% cholesterol diet and remained impaired over the next 6 weeks. No improvement in endothelium-dependent relaxation was seen in rabbits on the reversal diet for 14 and 32 weeks. Thus, endothelium-dependent relaxation is attenuated in animals fed a 2% cholesterol diet, and the loss of relaxation persists for at least 32 weeks after the animals are returned to a standard diet.

The first CanadianHelicobacter pyloriConsensus Conference took place in April 1997. The initial recommendations of the conference were published in early 1998. An update meeting was held in June 1998, and the present paper updates and complements the earlier recommendations. Key changes included the following: the recommendation for testing and treatingH pyloriinfection in patients with known peptic ulcer disease was extended to testing and treating patients with ulcer-like dyspepsia; it was decided that the urea breath test (not serology) should be used for routine diagnosis ofH pyloriinfection unless endoscopy is indicated for another reason; and recommended therapies were a twice daily, seven-day regimen of a proton pump inhibitor (omeprazole 20 mg, lansoprazole 30 mg, pantoprazole 40 mg) or ranitidine bismuth citrate 400 mg, plus clarithromycin 500 mg and amoxicillin 1000 mg, or plus clarithromycin 500 or 250 mg and metronidazole 500 mg. The need was reiterated to have funding for readily accessible, accurate testing forH pyloriinfection with the urea breath test. It was strongly recommended that regional centres be established to monitor the prevalence of antibiotic-resistantH pyloriinfections. The initial consensus document referred to pediatric issues that were not addressed in this update but were the subject of a subsequent CanadianHelicobacterStudy Group meeting, and will be published later in 1999.

Azathioprine is a drug commonly used for the treatment of inflammatory bowel disease, organ transplantation and various autoimmune diseases. Hepatotoxicity is a rare, but important complication of this drug. The cases reported to date can be grouped into three syndromes: hypersensitivity; idiosyncratic cholestatic reaction; and presumed endothelial cell injury with resultant raised portal pressures, venoocclusive disease or peliosis hepatis. The components of azathioprine, 6-mercaptopurine and the imidazole group, may play different roles in the pathogenesis of hepatotoxicity. The strong association with male sex, and perhaps with human leukocyte antigen type, suggests a genetic predisposition of unknown type. Many of the symptoms of hepatotoxicity, such as nausea, abdominal pain and diarrhea, can be nonspecific and can be confused with a flare-up of inflammatory bowel disease. As well, the subtype resulting in portal hypertension can occur without biochemical abnormalities. A 63-year-old man with Crohn's disease who is presented developed the rare idiosyncratic form of azathioprine hepatotoxicity, but also had a severe disabling steroid myopathy, peripheral neuropathy, resultant deep venous thrombosis and pulmonary embolism related to immobility, and a nosocomial pneumonia. His jaundice and liver enzyme levels improved markedly on withdrawal of the drug, returning to almost normal in five weeks. Treating inflammatory bowel disease effectively while trying to limit iatrogenic disease is a continuous struggle. Understanding the risks of treatment is the first important step. There must be a low threshold for obtaining liver function tests, especially in men, and alertness to the need to discontinue the drug or perform a liver biopsy should patients on azathioprine develop liver biochemical abnormalities, unexplained hepatomegaly or signs of portal hypertension.

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