Diverticular Disease: Emerging Evidence in a Common Condition · Munich (Germany), June 17–18, 2005 Diverticular Disease: Emerging Evidence in a Common Condition Congress Short

Munich (Germany), June 17–18, 2005

Diverticular Disease:Emerging Evidencein a Common Condition


148Congress Short Report Falk Symposium

ISBN 3-933186-73-0

Text:Christine VetterMedical JournalistCologne (Germany)

© Photos: I. Gessner

1st edition 2005

Leinenweberstr. 5Postfach 652979041 FreiburgGermany

FALK FOUNDATION e.V.

Publisher

© 2005 Falk Foundation e.V.All rights reserved.

:

Munich (Germany), June 17–18, 2005

Congress Short Report Falk Symposium


148

Introduction

Diverticular disease – a frequent disorder with nowhere to call home

Diverticular disease is by no means rare butactually occurs with a fairly high frequency. Thisfrequency, however, is hardly reflected in thescientific literature and in medical discussions,and diverticula and their health consequencesare only rarely a topic of congresses and sym-posia. There is also a corresponding dearth ofdata on diagnosis and therapy and even thedefinitions of the different forms of the diseaseremain unsettled. Thus the terms diverticulosis,diverticulitis, symptomatic or asymptomaticdiverticular disease are often used imprecisely oreven synonymously. “In surveys, every respon-dent has an answer to the question of whatdiverticula are and how to treat them. Theanswers that one gets, however, are fundamen-tally different,” W. Kruis (Cologne) said inassessing the situation.

More clarity in the area of diverticular diseaseand defining state-of-the-art thinking on thistopic was the objective of the 148th Inter-national Falk Symposium in Munich, which wasattended by more than 450 participants from 31 nations. The symposium was chaired by A. Forbes (Harrow), K.-W. Jauch (Munich), W. Kruis (Cologne) and S.D. Wexner (Weston).

W. Kruis, Cologne (Germany)

K.-W. Jauch, Munich (Germany)

A. Forbes, Harrow (UK)

S.D. Wexner, Weston (USA)

Scientific Organizers

Congress Short Report Falk Symposium 148

3

Page

• Pathogenesis of diverticular disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4

• Clinical picture of diverticular disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9

• Diagnosis of diverticular disease I . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

• Diagnosis of diverticular disease II . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15

• Indications for and controversies regarding imaging methods . . . . . . . . . . . . . . . . . . . . . 16

• Parameters that determine management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17

• Surgery in diverticular disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21

• Conservative treatment of diverticular disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23

• Different aspects of therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30

• Interview with Professor Dr. V. Gross (Amberg) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33

• Moderators, Speakers and Scientific Organizers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35

• Further Congress Short Reports of Falk Symposia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

Session 1

4

Diverticulosis and diverticulitis: The available data areunsatisfactoryThere is a dearth of confirmed data on the diag-nosis and therapy of diverticular disease. This, as speaker after speaker noted, is puzzling giventhe frequency of diverticula in the general pop-ulation. Correspondingly frequent is the entity of diverticular disease, whereby the incidence ofboth diverticulitis and diverticulosis increaseswith advancing age.

Speakers at the symposium were in agreementthat, because of a lack of well-controlled studies,significant uncertainty remains, especially withregard to conservative treatment of diverticulardisease, but also concerning the indications forsurgical management. “The data on diverticulardisease is generally unsatisfactory” – this wasthe most commonly heard remark at the sympo-sium in Munich. Another universal complaintrelated to the fact that this widespread clinicalentity does not receive the medical or scientificattention it deserves.

The pathogenesis of diverticulardisease is still not exactly understoodN.Y. Haboubi (Manchester) suggested, for betterunderstanding of the pathology of diverticulardisease, a classification according to changesthat suggest ulcerative colitis, those that point toCrohn’s disease and finally disease forms charac-terized by herniation of the mucosa as the pre-dominant anatomic feature. Mucosal herniationis seen in up to 90% of patients, while aboutone in ten patients exhibit proliferation of themucosa around the diverticulum. Inflammatoryprocesses are also frequently seen, N.Y. Haboubisaid.

It is probable that several factors operate simul-taneously in the pathogenesis of diverticulardisease. One factor relates to changes in connec-tive tissue and smooth muscle as an effect ofaging. Others include dietary and structuralchanges, as explained by T. Wedel (Lübeck), and also motility disturbances (figure 1).

Pathogenesis of diverticular diseaseChair:W. Kruis, CologneA. Revhaug, Tromsö

N.Y. Haboubi


5

Fig. 1

I Classic pathogenetic concepts (T. Wedel, Lübeck)

Enteric neuropathy and diverticular disease

Classic pathogenetic concepts

Aging ⇒predominant in elderly

Diet ⇒low fiber intake

Connective tissue disorder ⇒elastosis

Smooth muscle disorder ⇒myochosis

Enteric neuropathy ⇒?

Hypersensitivity caused by damageto the enteral nervous systemChanges in the enteral nervous system may alsoplay a role. These may be responsible for anincrease in intraluminal pressure, resulting inincreased motility. Hypersensitivity might alsoexplain the pain sensations (figure 2).

That diverticular disease may actually represent a“neuromuscular derangement” has, according toT. Wedel, been described in the literature, point-ing to reports on the formation of giant gangliaand a general hypertrophy of nerve cells in thesubmucosa (figure 3). Such intestinal neuronaldysplasia is found in about 20% of patients.

Session 1

6

Fig. 2

I Why should enteric nerves be involved? (T. Wedel, Lübeck)

intraluminal pressure motor activity painful sensations


Why should enteric nerves be involved?

… mediated by the enteric nervous system (ENS)

Fig. 3

I Structural alterations of the ENS (T. Wedel, Lübeck)


Structural alterations of the ENS

Intestinal neuronal dysplasia(20% of cases)

• submucous giant ganglia• submucous nerve fiber hypertrophy

⇓Wedel T et al.

Viszeralchirurgie 1999; 34: 307–311

diverticular diseasecontrol


7

High pressure in the sigmoid colontriggers diverticulosisThese neural changes, however, are certainly notthe sole basis of this disease. Diverticular diseaseis best understood as a multifactorial entity, M. Kreis (Munich) said. “There is a widely heldopinion that motility disturbances leading tohigh pressure in the sigmoid colon are the actualcause of this disease,” M. Kreis observed.

M. Kreis

Fig. 4

I Motility studies in subgroups of patients with diverticular disease under basalconditions (M. Kreis, Munich)ADD = asymptomatic diverticular diseaseSUDD = symptomatic uncomplicated diverticular diseaseSCDD = symptomatic complicated diverticular disease

Mo

tilit

y in

dex

(m

ean

/SEM

)

Controls ADD SUDD SCDD

P < 0.001

300

250

200

150

100

50

0

*

*

N = 30 N = 30 N = 30 N = 55

Cortesini C et al. Dis Colon Rectum 1991; 34: 339–342

Studies of motility in healthy controls and inpatients with different types of diverticulardisease appear to confirm this hypothesis. Forexample, while there was no difference betweencontrol persons and patients with asymptomaticdiverticulosis, a significantly increased motilitywas seen in patients with symptomatic, compli-cated diverticular disease. Still more pronouncedwere the motility disturbances in patients withsymptomatic, non-complicated diverticulardisease, both under normal conditions (figure 4)and following ingestion of a meal (figure 5).

Persistence of these motility disturbances over a long period of time together with increasedpressure in the colon appears to play an essentialrole in diverticular disease, M. Kreis said. Itremains unclear whether this triggers the forma-tion of diverticula or whether these represent a secondary phenomenon as a consequence ofstructural changes in the bowel wall.

Session 1

8

Diverticula: There may be a geneticpredispositionIndependent of these factors, according to A. Forbes (Harrow), there is good evidence for agenetic predisposition to diverticular disease,although no specific gene has been implicated

as triggering the development of this disease.The possibility of a significant genetic compo-nent is supported not only by observations that diverticula occur more frequently in somefamilies, but also by studies of twins.

There also appears to be a close association withgenetically caused disorders such as polycystickidney disease, with 83% of patients alsoexhibiting signs of diverticular disease. “This is a significant finding, since normally a prevalenceof only 20–50% would be expected,” A. Forbessaid in Munich.

A. Forbes

Fig. 5

I Motility studies in subgroups of patients with diverticular disease following ameal (gastro-colic response) (M. Kreis, Munich)ADD = asymptomatic diverticular diseaseSUDD = symptomatic uncomplicated diverticular diseaseSCDD = symptomatic complicated diverticular disease

Mo

tilit

y in

dex

(m

ean

/SEM

)

Controls ADD SUDD SCDD

P < 0.001

2000

1500

1000

500

0

*

*

N = 30 N = 30 N = 30 N = 55

Cortesini C et al. Dis Colon Rectum 1991; 34: 339–342

Congress Short Report Falk Symposium 148Session 2

9

Incidence and prevalence are age –dependentBecause the majority of patients remain asymp-tomatic, the exact prevalence of intestinal diver-ticula is difficult to estimate, A. Fingerhut (Poissy)said. It is clear, however, that both incidence andprevalence increase with advancing age. At age40, diverticula are rare and affect only about 5%of persons. Past 65 years, however, a prevalenceabove 65% shows that they are a commonphenomenon, A. Fingerhut said. It is importantto differentiate between diverticulosis, definedas the presence of diverticula with no associateddisease signs or symptoms, and diverticulardisease, in which the diverticula have becomesymptomatic.

The precision of the clinical classification can be further enhanced by differentiating between“symptomatic, non-complicated disease”,“recurrent symptomatic disease” and a “com-plicated disease form” in which bleeding and, in extreme cases, perforation occur.

According to A. Fingerhut, the Hinchey classi-fication of diverticulitis has found wide accept-ance. It assigns patients with this clinical entityto one of four stages. Hinchey I is diverticulitiswith localized abscess; Hinchey II is characterizedby extensive mesenteric abscess; Hinchey III hasprogressed to free perforation; while Hinchey IVrepresents peritonitis after free perforation(figure 6).

Clinical picture of diverticular diseaseChair:M. Anthuber, AugsburgM. Lukas, Prague

A. Fingerhut

Fig. 6

I Hinchey classification (A. Fingerhut, Poissy)

Localizedpericolic abscess(Hinchey stage I)

Large mesentericabscess(Hinchey stage II)

Free perforationcausing fecalperitonitis(Hinchey stage IV)

Free perforation(Hinchey stage III)

Session 2

10

Right-sided and left-sided diverticular disease – two different entities?Diverticular disease may manifest itself in a pre-dominantly left-sided or right-sided pattern oflocalization and it has been suggested thatthese two localizations may actually be evidenceof two different disease entities. For example,

the left-sided form, which often manifests itselfwith pain and is frequently associated withcomplications, such as fistulae and obstructions,less often with bleeding, is most common inEurope.

The situation is somewhat different for right-sided diverticular disease, which, according to R. Cohen (Harrow), is most often described inAsian patients and in which bleeding is the pri-mary symptom. Right-sided diverticular disease isalso more common in younger patients, whichpoints to a genetic predisposition, while the left-sided localization is more common at higherages. This suggests that environmental factorsand especially dietary factors such as a low-fiberdiet may be important in the pathogenesis(figures 7 and 8).

R. Cohen

Fig. 7

I Uncomplicated diverticular disease (R. Cohen, Harrow)

148

11

Differentiating betweencomplicated and non-complicateddiverticulitisIn about 70% of patients, diverticular diseasepresents as diverticulosis, which is asymptomatic,S. Hollerbach (Celle) said. About 10–25% ofpatients, however, go on to develop diverticulitis,which, in 75% of cases, remains non-compli-cated. Patients usually complain of non-specificpain and frequently constipation, and may alsoexperience incontinence or changed bowelhabits.

About 25% of patients with diverticulitisexperience a complicated form of the diseasewith abscess formation, obstructions, fistulationand even perforation (figure 9).

High complication rateAccording to S. Hollerbach, the prognosis inpatients with a first episode of uncomplicateddiverticulitis is good, since they very often do notexperience disease recurrence. It is treated con-servatively and 85% of patients respond withcomplete remission. Long-term, however, about15% of patients will eventually require surgery.

Should diverticulitis recur, the rate of surgeryjumps to 30–40%, associated with a drasticincrease in the rate of complications and ofmortality, which S. Hollerbach put at 1.3–5%.Risk factors for severe disease course includemale sex and obesity. In addition, young patients

Congress Short Report Falk Symposium

Fig. 8

I Diverticular disease – pericolic abscess (R. Cohen, Harrow)

S. Hollerbach

Session 2

12

may be especially at risk for a “virulent” disease course with an increased risk of recurrentdisease flares and complications.

“In patients under 40 with diverticulitis, electivesurgery should be considered,” S. Hollerbachsaid in Munich.

Fig. 9

I Diverticulosis (S. Hollerbach, Celle)

Rose BD, UpToDate in Medicine 1997Young-Fadok TM, Colon and Rectal Surgery 2001Dunn G, Medscape 2004

Asymptomatic

Diverticular BleedingDiverticulosis

Diverticulitis

uncomplicated

complicated

AbscessObstructionPerforation

Fistula

70%

5–10%

10–25% 75%

25%

Congress Short Report Falk Symposium 148Session 3

13

Careful differential diagnosis isessentialA patient presents to your office with symptomssuggestive of diverticular disease. In these cases,according to R. Jones (London), a comprehensiveconsideration of differential diagnoses is crucial.This will include, R. Jones said, the gamut ofdietary intolerances and food poisoning toentities such as irritable bowel syndrome, inflam-matory bowel disease and vascular causes ofsymptoms, such as ischemic colitis. The differen-tial also includes malignancies, but also urinarytract infections.

Laboratory tests are not veryhelpfulLaboratory tests that are reliably diagnostic indiverticular disease are not available, C. Gasché(Vienna) said. Some help is provided by inflam-mation markers, such as C-reactive protein (CRP)and hemoglobin concentration, which, if low,may indicate bleeding complications.

In emergencies, prompt surgicalexploration is requiredTimely recognition of emergencies is crucial.These include fistulae, obstruction and especiallyperforations. “In such cases, exploratory lapa-roscopy must be obtained without delay,” J.M. Müller (Berlin) said (figures 10 and 11).

Diagnosis of diverticular disease IChair:H. Koop, BerlinH. Zirngibl, Wuppertal

R. Jones C. Gasché

Fig. 10

I Diverticulitis: emergency cases (J.M. Müller, Berlin)

uncomplicated

symptomatic firstmanifestation

symptomaticrecurrent Fistulae Perforation Stenosis

free

Peritonitis Abscess

local general

covered

Ileus

complicated

Diverticulitis

Session 3

14

The diagnosis can also be difficult in a patientpresenting with lower gastrointestinal bleeding,J. Schölmerich (Regensburg) said. Althoughdiverticular bleeding resolves spontaneously in80–85% of cases, mortality, the gastroenterol-ogist said, is high at 2–4%.

Diverticulitis is the most common cause of bleed-ing in the lower gastrointestinal tract, followed

by neoplasms and ischemic colitis (figure 12).Prognosis depends on the definitive identifica-tion of the source and localization of the bleed-ing.

J. Schölmerich

Fig. 11

I Acute diverticulitis stage III (J.M. Müller, Berlin)

56 year-old male with 6 weeks obstipation and pelvic pain

The rupture of a localized peridiverticular abscess into the peritoneal cavi-ty did not result in gross peritonitis, presumably because the diverticularneck was obstructed by a fecalith.

Fig. 12

I Lower gastrointestinal bleeding – etiology(J. Schölmerich, Regensburg)

Diverticulosis NeoplasiaIschemic colitis

IBD

Hemor-rhoids

Postpolyp-ectomy

Angio-dysplasia

Unknown Other


15

Session 4

Close parallels to inflammatorybowel diseasesIn the diagnostic work-up of diverticular disease,it is important to think not only about thepossible complications of the disease but alsoabout potential gastrointestinal comorbidity, H.-J. Krammer (Mannheim) said. Patients may be simultaneously suffering from inflammatorybowel disease. These entities may be difficult todifferentiate, because diverticular disease may beassociated with extensive inflammation and mayeven present the picture of “diverticular colitis”.

There are other parallels between inflammatorybowel diseases (IBD) and diverticular disease. Forexample, both entities may present with fairlysimilar patterns of symptoms, dominated bypain, stool irregularities, weight loss and fever. In addition, with both disorders, many patientsrespond well to treatment with mesalazine.

Overlap with irritable bowelsyndromeIn addition, there may be overlap with irritablebowel syndrome and H.-J. Krammer sees closeparallels between these two entities. Patientscomplain of partially comparable symptoms such as constipation, meteorism and flatulence,as well as mucus admixture in the stool andabdominal pains. Because both diverticular disease and irritable bowel syndrome are verycommon, a high comorbidity must be expected, H.-J. Krammer said.

This position was supported whole-heartedly byhis colleague, L.M.A. Akkermans (Utrecht), whoconfirmed the significant overlap between theindividual clinical pictures. This may go so farthat in patients with diverticular disease it mayno longer be possible to determine which symp-toms are due to the diverticula and which arecaused by other structural or functional changes.This differential diagnostic problem must also beconsidered when planning the patient’s futuremanagement.

Diagnosis of diverticular disease IIChair:C. Folwaczny, MunichP. Layer, Hamburg

H.-J. Krammer L.M.A. Akkermans

16

Session 5

Colonoscopy: only after the acutephase has passed?Diverticular disease can also be hard to pin downwith diagnostic imaging methods. Hence, it hasbecome usual, S. Bar-Meir (Tel Hashomer) said,to refer the patient for colonoscopy followingresolution of the acute disease phase. Thereason normally given for not performingcolonoscopy in the acute stage is that there may be an increased risk of bowel perforation.“This worry, however, is not evidence-based,” S. Bar-Meier said.

First experiences with 93 patients, according toS. Bar-Meir, suggest that colonoscopy is possible,even in the acute phase of the disease. Earlycolonoscopy, however, should be limited topatients with recurrent disease phases and tothose in whom computed tomography imagingshows no free air in the vicinity of the diver-ticula. S. Bar-Meir is currently conducting arandomized study comparing the benefits andpotential risks of early colonoscopy compared

with first examination six weeks after resolutionof the acute disease phase.

Include ultrasound in the work-upDiagnostic ultrasound also has a role in thework-up of diverticular disease, S. Schanz(Cologne) said. With a sensitivity and specificityof 97%, the method is, in his opinion, compa-rable to CT and examiners with the appropriateexperience can even reliably detect diverticula in patients with diverticulosis of the left colon.Advantages of ultrasound, according to S. Schanz, are the wide availability of themethod and the fact that the examination isnon-invasive and inexpensive. Beyond the limitsof ultrasound are large and complex fistularsystems, involvement of the distal sigmoid colonin diverticular disease and overlap with othergastrointestinal disorders, especially with IBD or colon carcinoma.

In the opinion of S. Feuerbach (Regensburg), CT remains the most reliable imaging methodfor diagnosing diverticular disease.

Indications for and contro-versies regarding imagingmethodsChair:P. Marteau, ParisS. Post, Mannheim

S. Bar-Meir

S. FeuerbachS. Schanz


17

Session 6

Individual clinical coursedetermines choice of therapyThe management of diverticular disease is deter-mined to a great extent by the patient’s individ-ual disease course. Risk factors for a complicatedclinical course, according to M.Z. Panos (Athens)include low patient age, obesity, male sex and,especially, immunosuppression.

Even in the absence of such risk factors, divertic-ular disease is something that must not be takenlightly. Recurrence rate within one year of the

first disease flare is 2% and this figure rises long-term by 33% per year. In fact, 90% ofpatients with two disease flares can reckon witha recurrence of acute diverticulitis.

Nutrition can trigger diverticulaNutritional behavior plays a contributory role inthe pathogenesis of diverticular disease. Thisstatement is supported, M.Z. Panos said, byobservations that diverticular disease is wide-spread in Western industrial nations, but is

Parameters that determinemanagementChair:C. Hüscher, RomeM. Zeitz, Berlin

M.Z. Panos

Fig. 13

I Prevalence of diverticular disease (M.Z. Panos, Athens)A = autopsy, BE = barium enema / C = colonoscopy

Natural course of diverticular diseaseEpidemiology

Prevalence of diverticular disease

Country Prevalence (%) n Year Reference Method

England 35 109 1967 Manousos A

Scotland 23 12335 1973 Eastwood BE

USA 60 277 1985 Burkitt BE

Thailand 4 289 1980 Vajrabukka BE

China 1 909 1983 Guo-Zong C

Japan 8 12505 1982 Kubo BE

Ghana 4 592 1978 Archmpong BE

Kenia 6 226 1978 Calder BE

Nigeria 0 1420 1987 Jhekwaba AReferences: Manousos O BMJ 1967, Eastwood M Gut 1977, Burkitt DP Lancet 1985, Vajrabukka T Dis Col Rect 1980,Guo-Zong P 1984 Ch Med J, Kubo A 1983 Jap J M, Archmpong EQ 1978 Ann RCSEng, Calder JF 1979 BMJ, JhekwabaFNJRCS Ed

Session 6

18

hardly ever seen in developing countries, wherepeople consume diets high in fiber (figure 13).Also, the fact that younger persons are almostnever affected while the incidence increasesdrastically with age suggests that dietary factorsmay play a decisive role.

Abdominal pains are the mainclinical symptomWhile diverticulosis remains asymptomatic inabout one-third of all cases, the remaining two-thirds develop repeated episodes of pain andbowel irregularities, R.C. Spiller (Nottingham)said (figure 14). The cause for this phenomenon

may be related to increased tension in the bowelwall. The pain may, however, simply be a directconsequence of the inflammatory process.

R.C. Spiller

Fig. 14

I Incidence (R.C. Spiller, Nottingham)

35% of > 50 year old have diverticulosis in UKManousos et al. Br Med J 1967; 3: 762-3

Onset of painful DD at mean age 55 years was 1.8/1000 patient years (6% over next 30 years)

Pop

ula

tio

n (

%)

Diverticulosis

Painfuldiverticulosis

Age (years)

100

50

040 80

Aldoori et al. Am J Clin Nutr 1994; 60: 757-64


19

Do not ignore extraintestinalcomorbidityThe management of diverticular disease dependsnot only in the disease course but also on thequestion of whether there is concomitant ex-traintestinal morbidity, B. Lembcke (Gladbeck)said. For example, obesity contributes significant-ly to surgical risk. In addition, as J.C. Hoffmann(Berlin) noted, other factors must also be consid-ered, such as a potential immunosuppression.

Fig. 15

I Thickened bowel wall (R.C. Spiller, Nottingham)

Circular muscle hypertrophy in acute diverticulitis (AD)and symptomatic complicated diverticular disease (SCDD)

7

6

5

4

3

2

1

1 cm 1 cm 1 cm

Thic

knes

s (m

m)

Control AD CD

Simpson J et al. Eur J Gastroenterol Hepatol 2003; 15: 1005–1010

Control AD SCDD

Kruskal-Wallisp < 0.000

The cause of “post-diverticulitispain” is still unclearAccording to R.C. Spiller, these pains occurepisodically and usually continue for about sevendays. Even after the inflammation resolves, manypatients continue to report abdominal pains anaverage of five days per month. The cause ofthese “post-diverticulitis pains” is unclear, R.C. Spiller said. The thickened bowel wall(figure 15) could be to blame, but the pain mayalso be due to an increased sensitivity to pain,possibly caused by the inflammation.

There are not correlations with patients’ age orsex or with their radiological findings. Mano-metric studies have also found no differences inbowel contractions between healthy controlsand patients with symptomatic, non-complicateddiverticular disease.

B. Lembcke J.C. Hoffmann

Session 6

20

A central issue in the treatment of diverticulardisease, in his opinion, is that to date there is adearth of well-planned controlled studies of thedifferent treatment methods and patients’ out-come. “Most of the literature consists of retro-spective case studies,” J.C. Hoffmann warned.

Therapy recommendations are notevidence-basedThere are very few prospective studies and thereis also no clear, internationally accepted defini-tion or classification of the individual diseasestages. This makes it difficult to assess therespective treatment option in the individual case and it makes the formulation of generallyapplicable recommendations difficult. For

example, J.C. Hoffmann said, it is usually recom-mended to refer the patient for elective surgeryafter the second episode. “The studies do notsupport this recommendation,” he emphasized.

This is of even greater importance since theassociated morbidity of each operation must be considered. This includes not only the directcomplications of surgery but also the risk ofanesthesia as well as potential postoperativecomplications (figure 16).

Fig. 16

I Treatment-related morbidity (J.C. Hoffmann, Berlin)

• Conservative treatment– Antibiotic-associated complications (e.g. pseudomembranous colitis)– General complications: DVT, PE, pneumonia, catheter sepsis, pneu etc.– Recurrence in high-risk groups (e.g. immunosuppression)– Sepsis

• Operative treatment: anesthesia-related– Respiratory failure, pneumonia– General complications: DVT, PE, pneumonia, catheter sepsis, pneu etc.

• Operative treatment: surgery-related– Anastomotic leakage– Uncontrolled sepsis– Bleeding, wound infections, incisional hernia– Fistula– Abscess


21

Session 7

Sigmoid resection after the seconddiverticulitis flareIf the conservative management of diverticulardisease proves unsuccessful, sigmoid resectionmay be considered, N. Senninger (Münster) said,noting that more than 50% of diverticula arelocalized to this bowel segment (figure 17). Atsurgery, complications, such as bleeding, can behandled and surgery in general can help preventthe development of complicated diverticulardisease.

Sigmoid resection essentially removed the “high pressure zone” of the colon. Ideally, N. Senninger explained, the acute situationshould be controlled by conservative methodsand several weeks after resolution sigmoid re-section, if still indicated, should be performed as an elective operation.

Laparoscopic resection is feasibleAccording to A. Fingerhut (Poissy), sigmoidresection, while it can be done as a conventionalopen procedure, is definitely feasible as a laparo-scopic procedure: “The laparoscopic procedure is just as efficient as conventional open surgery.”This is no longer the case, he cautioned, if com-plications, such as fistulae or strictures, havealready occurred, or when there is bleeding,whose source may not be known.

In favor of a laparoscopic approach, said K.-W. Jauch (Munich), is also the fact that theprocedure is usually less stressful for the patient.Laparoscopy is also less expensive, becausepatients’ hospitalizations are shorter. On thispoint, however, there are conflicting data and afinal assessment is probably not possible at thistime. Whether laparoscopy is really gentler and,hence, less stressful is a question that, accordingto V. Schumpelick (Aachen), cannot yet beanswered.

Surgery in diverticular diseaseChair:W.E. Fleig, HalleS.D. Wexner, Weston

N. Senninger K.-W. Jauch

Fig. 17

I Localization of colonic diverticula (N. Senninger, Münster)

Sigmoid 51.3%

Sigmoid + Descending 14.7%

Descending 14.7%

(Jansen und Kaden, 1974)

Session 7

22

Surgical success also depends onthe experience of the surgeonIt is also clear that the success of a procedureand the rate of complications depends to a greatextent on the experience of the surgeon. Laparo-scopic surgery, in addition, has significant limi-tations. According to V. Schumpelick, it is notindicated in the presence of fistulae, perforationor peritonitis. In addition, in an emergency situ-ation, conventional open surgery should gener-ally be selected. Without doubt, however, thelaparoscopic procedure gives better cosmeticresults.

V. Schumpelick


23

Session 8

The therapeutic effects ofroughageThe conservative management of diverticulardisease depends directly on its clinical course.Because of the probable close relationship to alow-fiber diet in the pathogenesis of diverticulardisease, 75% of gastroenterologists surveyedreported recommending a high-fiber diet or thedirect addition of dietary fiber (e.g. with psylli-um) to their patients, J.O. Lindsay (London) said.“In terms of evidence-based data supporting thisrecommendation for therapy with dietary fiber,”he admitted, “there is little.” There are, how-ever, some first controlled studies that do showadvantages, although, to date, only about 250 patients have been included.

Preventive effects are alsoprobableFurthermore, there is also epidemiologicalevidence suggesting that there actually is a closecorrelation between consumption of a diet lowin fiber and the occurrence of diverticulosis. In asurvey of 47,000 American men, the relative risk

was only 0.58 in the group with the highestintake of fiber, suggesting that nutrition may bevery effective in preventing diverticular disease.This leads J.O. Lindsay to postulate that dietaryfiber may be the key to a conservative strategywith both therapeutic and preventive ramifi-cations. The basis for this may be the increase in stool weight secondary to increased fiberintake as well as the fact that colon transit timemay be cut in half, which effectively preventsconstipation.

Finally, J.O. Lindsay cited first studies that sug-gest that dietary fiber may reduce the severity ofcomplaints in patients with diverticular disease.For example, in a study with 40 patients treatedfor six months with increased dietary fiber, asignificant reduction in symptoms was reportedby 60% of patients in the high-fiber group. Thetherapeutic importance of treatment is primarilyin the group of patients with non-complicateddiverticular disease. The more complicated theclinical course, the lower the significance ofnutritional factors (figure 18).

Conservative treatmentof diverticular diseaseChair:R.C. Spiller, NottinghamM. Starlinger, Klagenfurt

J.O. Lindsay

Session 8

24

Antibiotics in symptomatic diseaseformsWhile asymptomatic diverticular disease remainsthe domain of treatment with dietary fiber,antibiotics take center stage in the managementof symptomatic diverticular disease. If there is no evidence of inflammation (figure 19), it is the practice in some countries to treat with rifax-imine, a poorly absorbed antibiotic that is notcurrently licensed in Germany. In this area, too,truly “evidence-based” medicine is not possible.“There simply are no comparison studies be-tween antibiotics or of antibiotic versus place-bo,” G. Latella (L’Aquila) emphasized.

“The choice of antibiotic depends mostly on theclinical scenario,” he added. While he generallydoes not see an indication for antibiotics inasymptomatic patients, the situation is different

in the case of diverticulitis with suspected bac-terial overgrowth. Patients with mild disease canbe treated on an outpatient basis. Broad spec-trum antibiotics, especially the imidazoles andfluoroquinolones, are prescribed and avoidanceof oral food intake is essential.

Patients with severe diverticulitis require inpa-tient hospitalization. Beside absolute avoidanceof oral intake, a combined antibiotic therapy isrequired in most cases. Typically used antibioticsinclude the imidazoles (especially metronidazole)as well as clindamycin, aminoglycosides such as gentamycin and third-generation cephalo-sporins. If patients do not respond to therapy, G. Latella said, an intense work-up for compli-cations must be initiated. The diagnosis must bereconsidered and, where required, referral to asurgeon should follow (figure 20).

Fig. 18

I Summary – NSP in diverticular disease (J.O. Lindsay, London)

Increased stool bulk – insoluble and soluble

Decrease intraluminal pressure

Increase colonic short-chain fatty acids (SCFA)

Prebiotic effect

Evidence for a benefit of NSP


25

Fig. 19

I Symptomatic without inflammation (G. Latella, L’Aquila)

Antibiotic treatment of diverticular disease

Symptomatic without inflammation

Gut microflora in determining symptoms:⇑ fibre fermentation ⇒ constipation, cramps⇑ excessive production of bowel gas ⇒ bloating, pain, discomfort⇑ bacterial overgrowth ⇒ diarrhea

Fig. 20

I Antibiotic therapy of diverticular disease (G. Latella, L’Aquila)

Diverticular Disease

Asymptomatic (80%) Symptomatic (20%)

Without inflammation With inflammation (10–25%) (Diverticulitis)

Perforation Fibrosis

Abdomen Organ

Bleeding Abscess – Peritonitis Fistulae Stenosis

FiberAntibiotics

Antibiotics

Antibiotics

Hospitali-

zation Antibiotics

SurgeryAntibiotics

SurgeryAntibiotics

SurgeryEndoscopy

Surgery

Self-

limiting

Session 8

26

The role of probiotics remainsunclearAccording to A. Gionchetti (Bologna), the role ofprobiotics in the treatment of diverticular diseaseremains unclear. Probiotic activity has been as-cribed to different bacteria, he explained (figure21). To date, however, there is only one studythat reports an improvement in symptoms inpatients with non-complicated diverticulardisease after treatment with E. coli Nissle.

Mesalazine in addition toantibioticsThe data are more convincing with regard tomesalazine, according to V. Gross (Amberg),reporting on the possible therapeutic value ofthis agent as an adjunct to treatment withantibiotics. The rationale for a trial of 5-amino-salicylic acid relates to the broad anti-inflamma-tory activity of this agent, which is already in usefor treatment of inflammatory bowel diseases.

A. Gionchetti

Fig. 21

I Organisms associated with probiotic activity (A. Gionchetti, Bologna)

Non-bacterial organisms:✓ Yeasts (Saccharomyces boulardii)

Other bacterial strains:✓ Enterococci, non-pathogenic E. coli

✓ Lactobacilli✓ Bifidobacteria✓ Streptococci

V. Gross


27

In addition, mesalazine inhibits reactive oxygenmetabolites, with which intestinal bacteria inter-act, thus potentially modifying bacterial activity.The aminosalicylates also inhibit key enzymes inprostaglandin, leukotriene and thromboxanesynthesis as well as of certain pro-inflammatorycytokines (figure 22).

Long-term improvement inabdominal complaintsThe positive effects of these mechanisms ondiverticular disease are shown, V. Gross said, bythe data reports by Trespi et al. in a study of 166 patients with acute, non-complicated diver-ticular disease reporting mild to moderate symp-toms. Patients reported significant improvementin abdominal symptoms during an eight-weekcourse of mesalazine that followed antibiotictherapy. These positive effects even persistedover a follow-up period of four years (figures 23 and 24). Microscopic hemorrhages were also less common in patients treated withmesalazine.

Fig. 22

I Anti-inflammatory activity of 5-ASA (V. Gross, Amberg)

• Prostaglandin synthesis

• Leukotriene synthesis

• Thromboxane synthesis

• PAF synthesis

• Cytokines (IL-1, TNF)

• Reactive oxygen species

• Intestinal bacteria – colonic epithelium

Fig. 23

I Inflammatory recurrences (V. Gross, Amberg)

n

5-ASA

CO

50

40

30

20

10

06 12 18 24 30 36 42 48

Months

Trespi et al.: Further inflammatory recurrences. Kaplan-Meier actuarial estimate

Session 8

28

More patients remain complaint-freeThe advantage of adding mesalazine in patientsreceiving antibiotics has also been shown in astudy by Tursi et al. In this study, 218 patientswith recurrent acute diverticulitis and at leasttwo disease flares during the previous 12 monthsreceived rifaximine, either alone or in combi-nation with mesalazine at a dose of 800 mgthree times a day for seven days each month.The addition of mesalazine resulted in signi-ficantly more patients being complaint-free (figure 25). The difference between the twostrategies in favor of the combined regimenbecame apparent after only three months.

After a year, 86% of patients on the combinedtherapy were complaint-free, compared withonly 49% of those receiving antibiotics alone.According to V. Gross, two further studiesdocument the significant therapeutic effects ofmesalazine in diverticular disease, both in termsof improvement in symptoms and prophylaxis ofrecurrent inflammatory flares.

Fig. 24

I Microhemorrhagic recurrences (V. Gross, Amberg)

n

5-ASA

CO

35

30

25

20

15

10

5

06 12 18 24 30 36 42 48

Months

Trespi et al.: Microhemorrhagic recurrences. Kaplan-Meier actuarial estimate


29

Be careful with analgesics andespecially with NSAIDsBecause diverticular disease is often associatedwith pain, it is justified in the opinion of H. Mönnikes (Berlin) to inquire about the effectsof analgesics and spasmolytics. To date, how-ever, there are no controlled studies addressing

this question. It is important to note that spas-molytics generally weaken muscular contractionand this effect may be responsible for somerelief of pain. Care is important regarding theuse of analgesics, especially NSAIDs, since theseagents increase the risk of gastrointestinal bleed-ing and perforation.

Fig. 25

I 5-ASA plus rifaximine (V. Gross, Amberg)

Sym

pto

m-f

ree

(%)

5-ASA/Rifaximine

Rifaximine

100

80

60

40

20

03 6 9 12

Months

Tursi et al.: 5-ASA + rifaximine vs. rifaximine in patients with recurrent acute diverticulitis

H. Mönnikes

30

Session 9

Surgery: Can you kill two birdswith one stone?Special problems are associated with the surgicaltherapy of diverticular disease when the surgeonis confronted with intra-abdominal comorbidity,such as, for example, gallstones, colonic polyps,or adhesions and scar tissue from earlier opera-tions. Such problems may make sigmoid resec-tion much more difficult. On the other hand, asU. Roblick (Lübeck) asserted, this may be anopportunity to kill two birds with one stone, ifboth a sigmoid resection and cholecystectomy orlysis of adhesions can be done during a singlesurgical session.

Even if the absence of concomitant problems,the operation should only be performed by anexperienced surgeon, since the danger ofpostoperative complications is not negligible, J. Jeekel (Rotterdam) said. Incisional hernias arethe most common complication, occurring in 10–20% of patients.

Independent of the occurrence of postoperativecomplications, there is no guarantee that thepatient will be complaint-free after sigmoidresection, B. Egger (Berne) said. About one infour patients will continue to have complaintsfollowing the procedure, although these areusually mild. Recurrence of diverticulitis, how-ever, is comparatively low at 2%, B. Egger said.

Take advantage of the possibilitiesfor secondary preventionIn any case, every effort should be made to insti-tute secondary preventive measures as prophy-laxis against renewed diverticulitis flares. In theopinion of W.H. Aldoori (Mississauga), this ispossible if patients can be motivated to take a diet high in fiber but low in red meat. “Weknow that the relative risk for developing diver-ticular disease can in general be reduced,” W.H. Aldoori said (figure 26). There is also a very pronounced relationship between physicalactivity and diverticular disease: the more exer-cise, the fewer the disease flares (figure 27).

Different aspects of therapyChair:J. Mössner, LeipzigD. Örtli, Basel

J. Jeekel

W.H. AldooriB. Egger


31

A careful individualized benefit-to-risk analysis is importantBoth in this area and with regard to the opti-mum management of diverticular disease ingeneral many questions remain open and thereis a dearth of controlled studies to validate the

individual measures. Even the recommendationformulated in the European and American guide-lines to refer a patient for sigmoid resection fol-lowing the second disease flare is not evidence-based, D. Meyer (Würzburg) warned in hisreview of the results of the symposium.

In his opinion, one should be careful to avoidgeneralized recommendations and perform acareful benefit-to-risk analysis in each patient.Management options should be discussed withthe patient and selected in relation to the sever-ity of the disease and the respective risks of theplanned procedures.

Fig. 26

I Relative risk of diverticular disease (W.H. Aldoori, Mississauga)

Rel

ativ

e ri

sk

3.5

3

2.5

2

1.5

1

0.5

0Low (< 17) Medium (17–28) High (29+)

Dietary fiber intake (g/day)

High(> 116.6)

Medium (28.6–116.6)

Low (< 28.5)

Red meat intake(g/day)

Relative risk* of diverticular disease by levels of calorie-adjusted dietary fiber and red meat intake

*adjusted for age and total energy

(Aldoori WH, at al. Am J Clin Nutr 1994; 60: 757–764

3.22

3.16

2.60

1.90

1.96 1.79

1.0

2.53

1.73

D. Meyer,

Session 9

32

Fig. 27

VariableCategory P-value

1 2 3 4 5

Total physical 0.9 4.8 11.3 22.6 46.8activity (median of total MET)5

RR1 (95% CI) 1.0 0.89 0.67 0.68 0.57 0.0002(0.67–1.18) (0.49–0.91) (0.50–0.92) (0.41–0.79)

Multivariate RR2 1.0 0.91 0.71 0.74 0.63 0.008(95% CI) (0.68–1.21) (0.52–0.97) (0.54–1.01) (0.45–0.88)

Non-vigorous 0.1 1.4 3.4 7.6 20.8activity (median of total MET)3

RR1 (95% CI) 1.0 1.13 0.78 1.06 0.93 0.41(0.83–1.55) 0.56–1.10) (0.77–1.46) (0.67–1.30)

Multivariate RR2 1.0 1.15 0.79 1.09 0.93 0.65(95% CI) (0.84–1.58) (0.56–1.12) (0.79–1.49) (0.67–1.69)

Vigorous 0 3.5 15.0 41.0activity (median of total MET)4

RR1 (95% CI) 1.0 0.74 0.79 0.53 0.001(0.57–0.97) (0.61–1.03) (0.37–0.75)

Multivariate RR2 1.0 0.78 0.88 0,.60 0.01(95% CI) (0.60–1.02) (0.67–1.15) (0.41–0.87)1 Relative risk (adjusted for age).2 Adjusted for age, energy-adjusted dietary fiber and total fat.3 Includes flight of stairs climbed, walking or hiking outdoors (including walking at golf).4 Includes running (≤ 10 minutes/mile), jogging (≥ 10 minutes/mile), lap swimming, tennis, squash or racquetball,

callisthenics or rowing, bicycling (including stationary machines).5 Total MET (maximal exercise test) = sum of the average time/week spent in each activity x MET-value of each activity.

calorie need/kg bw/hour during activityMET-value = caloric need/kg bw/hour at rest

I Relative risk of diverticular disease by physical activity, non-vigorous, and vigorous activitylevels (W.H. Aldoori, Mississauga)


33

Interview

How important is “broad-spectrum” anti-inflammatorytherapy?Inflammatory processes play a significant role indiverticular disease. The role of anti-inflamma-tory therapy, given this background, and whymesalazine, a mainstay in the management ofinflammatory bowel diseases, can be a goodtherapy option for diverticula are explained by V. Gross (Amberg) in an interview.

Professor Gross, are there parallels andsimilarities between diverticular disease andinflammatory bowel diseases?

Gross: The pathogenesis of diverticulardisease is less well-understood than that ofinflammatory bowel diseases. Evidence frompathology, however, shows that patients withsymptomatic diverticular disease often exhibitmicroscopic inflammation of the mucosa in thevicinity of diverticula. In some cases, there mayeven be extensive inflammation, which is thentermed segmental colitis. Whether this inflam-mation is the actual focus of the diverticulardisease remains unclear. There is also evidencethat the disease may be based on a disorder ofthe enteral nervous system, which may, in turn,be caused by an inflammatory process. As ininflammatory bowel disease, it would appeartherefore to make sense to employ broad anti-inflammatory substances after an acute diseaseflare to prevent the development of recurrentdiverticular disease.

!

?

What are the options for conservativetherapy?

Gross: When discussing the conservativetreatment of diverticular disease, one must dif-ferentiate between the treatment of the acutediverticulitis flare and prophylactic therapy,which is geared primarily at the prevention ofcomplications. With regard to the prophylaxis ofcomplications, patients should always be advisedto take a high-fiber diet in order to prevent highpressure conditions in the bowel. In an acutedisease flare, strict avoidance of oral intake andthe administration of antibiotics are obligatorybecause the cause of acute diverticulitis is alwaysbacterial. Diagnosis is based on physical exami-nation and laboratory studies, as well as onimaging methods, such as ultrasound or, prefer-ably, CT. It is important that the clinical situationimproves under conservative therapy within afew days, with the patient becoming essentiallycomplaint-free within a week’s time. If this doesnot happen, this suggests a complicated diseasecourse with the danger of perforation. In suchcases, the patient must always be referred forsurgical intervention.

!

?

Interview with Professor Dr. V. Gross (Amberg)

V. Gross

Interview

34

One broad anti-inflammatory drug ismesalazine, which is also standard therapy forulcerative colitis. What should one expect fromthis agent in diverticular disease?

Gross: There are only a few studies ofmesalazine in diverticular disease. The principleof such therapy, however, makes sense and isbased on the idea of using the anti-inflammatoryaction of this agent to prevent recurrence of di-verticulitis and the development of symptomaticdiverticular disease. Studies have examined theeffects of mesalazine in the post-acute situationand have shown that patients receiving mesala-zine after resolution of the acute phase hadfewer complaints and less frequently developedrecurrent diverticulitis even over a follow-upperiod of four years. Another study in patientswith acute diverticulitis used mesalazine for oneyear as interval therapy in combination with anantibiotic, in this case the poorly absorbed rifax-imine, which is not currently licensed in Germany.The drugs were taken for one week each month.The group that received mesalazine in addition

!

? to the antibiotic experienced fewer cases ofrecurrent disease. In general, however, the onlyavailable data comes from randomized openstudies, so that a final evaluation of these effectsis not yet possible. I consider the use of mesala-zine to be a therapeutic principle that appears tobe certainly plausible in the treatment of diver-ticular disease and which has already been usedby some colleagues in their own practices withgood results. It would be helpful for the effectsof mesalazine to be verified in a double-blindstudy, especially since the safety and tolerabilityof this medication are very good, as is knownfrom the very extensive experience in patientswith inflammatory bowel diseases.

Professor Gross, thank you very much for thisinterview.


35

Index

Prof. Dr. L.M.A. AkkermansAcademisch Ziekenhuis Utrechtde UithofDept. of Experimental SurgeryG. 04.228Box 85500NL-3508 GA Utrecht The Netherlands

Dr. W.H. AldooriWyeth Consumer Healthcare Inc.Medical Director5975 Whittle RoadMississauga, ON L4Z 3M6Canada

Prof. Dr. M. AnthuberAllgemeinchirurgieKlinikum AugsburgStenglinstr. 2D-86156 AugsburgGermany

Prof. Dr. S. Bar-MeirChaim Sheba Medical CenterDepartment of Gastroenterology2 Sheba RoadIL-52 621 Tel HashomerIsrael

Prof. Dr. R. CohenSt. Mark’s HospitalDepartment of SurgeryLevel 5xWatford RoadHarrow HA1 3UJ, UK

PD Dr. B. EggerInselspitalKlinik für Viszerale undTransplantationschirurgieCH-3010 BernSwitzerland

Prof. Dr. S. FeuerbachRöntgendiagnostikKlinikum der Universität RegensburgD-93042 RegensburgGermany

Prof. Dr. A. FingerhutCentre Hospitalier IntercommunalF-78303 PoissyFrance

Prof. Dr. W.E. FleigInnere Medizin IMartin-Luther-UniversitätHalle-WittenbergErnst-Grube-Str. 40D-06120 HalleGermany

PD Dr. C. FolwacznyMedizinische PoliklinikKlinikum der UniversitätMünchen-InnenstadtNussbaumstr. 20D-80336 MünchenGermany

Dr. A. ForbesSt. Mark’s HospitalDigestive DiseasesResearch CentreWatford RoadHarrow HA1 3UJ, UK

Prof. Dr. C. GaschéUniversitätskliniken WienKlinik für Innere Medizin IVWähringer Gürtel 18–20A-1090 WienAustria

Prof. Dr. P. GionchettiUniversità di BolognaPoliclinico S. OrsolaIstituto di Clinica e GastroenterologiaVia Massarenti 9I-40138 BolognaItaly

Prof. Dr. V. GrossKlinikum St. Marien AmbergInnere Medizin IIMariahilfbergweg 7D-92224 AmbergGermany

Prof. Dr. N.Y. HaboubiTrafford General HospitalSurgical PathologyMoorside Road, DavyhulmeManchester M41 5SL, UK

PD Dr. J.C. HoffmannMedizinische Klinik ICharité UniversitätsmedizinCampus Benjamin Franklin (CBF)Hindenburgdamm 30D-12203 BerlinGermany

PD Dr. S. HollerbachAllgemeines Krankenhaus CelleGastroenterologieSiemensplatz 4D-29223 CelleGermany

Prof. Dr. C. HüscherOspedale San GiovanniDepartment of SurgeryVia dell’Amba Aradam, 9I-00184 RomeItaly

Moderators, Speakers and Scientific Organizers

Index

36

Prof. Dr. K.-W. JauchChirurgieKlinikum der UniversitätMünchen-GroßhadernMarchioninistr. 15D-81377 MünchenGermany

Prof. Dr. J. JeekelErasmus Medical CenterDepartment of SurgeryDr. Molewaterplein 40NL-3015 GD RotterdamThe Netherlands

Prof. Dr. R. JonesUMDS of Guy’s &St. Thomas HospitalsDepartment of General PracticeDivision of Primary Health Care80 Kennington RoadLondon SE11 6SP, UK

Prof. Dr. H. KoopHELIOS Klinikum BerlinKlinikum BuchInnere Medizin IIHobrechtsfelder Chaussee 100D-13125 BerlinGermany

Prof. Dr. H.-J. KrammerII. Med. UniversitätsklinikUniversitätsklinikum MannheimTheodor-Kutzer-Ufer 1–3D-68167 MannheimGermany

PD Dr. M. KreisChirurgieKlinikum der UniversitätMünchen-GroßhadernMarchioninistr. 15D-81377 MünchenGermany

Prof. Dr. W. KruisEvang. Krankenhaus KalkInnere MedizinBuchforststr. 2D-51103 KölnGermany

Dr. G. LatellaUniversita di L’AquilaCattedra di GastroenterologiaVia S. Sisto 22 EI-67100 L’AquilaItaly

Prof. Dr. P. LayerIsraelitisches Krankenhausin HamburgInnere MedizinOrchideenstieg 14D-22297 HamburgGermany

Prof. Dr. B. LembckeSt. Barbara-HospitalInnere MedizinBarbarastr. 1D-45964 GladbeckGermany

Dr. J.O. LindsayThe Royal London HospitalEndoscopy UnitWhitechapelLondon E1 1BB, UK

Dr. M. LukasCharles UniversityFirst Faculty of MedicineV Medical DepartmentU nemocnice 2CZ-128 08 PragueCzech Republic

Prof. Dr. P. MarteauHôpital EuropéenGeorges PompidouService d’Hépato-Gastroentérologie20, rue LeblancF-75908 ParisFrance

PD Dr. D. MeyerChirurgieKlinikum der Universität WürzburgJosef-Schneider-Str. 2D-97080 WürzburgGermany

PD Dr. H. MönnikesHepatologie/GastroenterologieCharité UniversitätsmedizinCampus Virchow-Klinikum (CVK)Augustenburger Platz 1D-13353 BerlinGermany

Prof. Dr. J. MössnerUniversitätsklinikum LeipzigInnere Medizin IIPhilipp-Rosenthal-Str. 27D-04103 LeipzigGermany

Prof. Dr. J.M. MüllerAllgemein- und VisceralchirurgieCharité UniversitätsmedizinCampus Charité MitteSchumannstr. 20–21D-10117 BerlinGermany

Prof. Dr. D. ÖrtliMittlere Strasse 91CH-4012 BaselSwitzerland

Dr. M.Z. PanosEuroclinic9, Athanasiadou StreetGR-11 521 AthensGreece

Prof. Dr. S. PostKlinikum MannheimChirurgieTheodor-Kutzer-Ufer 1–3D-68167 MannheimGermany

Prof. Dr. A. RevhaugUniversity Hospital of TromsøDepartment of SurgeryN-9038 TromsøNorway


37

Dr. Dr. U.J. RoblickUniversitätsklinikum Schleswig-HolsteinCampus LübeckChirurgieRatzeburger Allee 160D-23562 LübeckGermany

Dr. S. SchanzEvang. Krankenhaus KalkInnere MedizinBuchforststr. 2D-51103 KölnGermany

Prof. Dr. J. SchölmerichKlinik für Innere Medizin IKlinikum der Universität RegensburgD-93042 RegensburgGermany

Prof. Dr. V. SchumpelickAllgemeinchirurgieUniversitätsklinikum AachenPauwelsstr. 30D-52074 AachenGermany

Prof. Dr. N. SenningerAllgemeine ChirurgieKlinikum der UniversitätWaldeyerstr. 1D-48149 MünsterGermany

Prof. Dr. R. C. SpillerUniversity HospitalQueen’s Medical CentreDivision of GastroenterologyC Floor, South BlockNottingham NG7 2UH, UK

Prof. Dr. M. StarlingerAllgemeine öffentlicheKrankenanstaltenChirurgische AbteilungSt. Veiter Str. 47A-9026 KlagenfurtAustria

PD Dr. T. WedelAnatomieUniversitätsklinikum Schleswig-HolsteinCampus LübeckRatzeburger Allee 160D-23562 LübeckGermany

S.D. Wexner, M.D.Professor of MedicineCleveland Clinic FloridaDepartment of Colorectal Surgery2950 Cleveland Clinic BoulevardWeston, FL 33331USA

Prof. Dr. M. ZeitzMedizinische Klinik ICharité UniversitätsmedizinCampus Benjamin Franklin (CBF)Hindenburgdamm 30D-12203 BerlinGermany

Prof. Dr. H. ZirngiblHelios Klinikum WuppertalChirurgieHeusnerstr. 40D-42283 WuppertalGermany

38

Further Congress Short Reportsof Falk Symposia

FSK134e“New Findings on Pathogenesis and Progress in Management of Inflammatory Bowel Diseases”Compiled by A.U. Dignass and B. Fessler(2003) 47 pages

FSK142-144e“Autoimmune Liver Diseases”“Pancreatitis: Advances in Pathobiology,Diagnosis and Treatment”“Gastroenterology Yesterday – Today – Tomorrow:A Review and Preview”Compiled by B. Fessler and C. Vetter(2005) 60 pages

These reports are free of charge and can be ordered from Falk Foundation e.V. or the local Falk partner.

Congress Report:The officical congress report of Falk Symposium 148 "Diverticular Disease: Emerging Evidence in aCommon Condition” will be published by Springer, Dordrecht, The Netherlands in the first half of 2006and can be ordered at a reduced price of 3 35,- from Falk Foundation e.V. or the local Falk partner.

ISBN 3-933186-73-0

FSK

148e

1-9

/200

5/3.

000

Kon

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FALK FOUNDATION e.V.Leinenweberstr. 5Postfach 652979041 FreiburgGermany

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Documents

Diverticular Disease: Emerging Evidence in a Common Condition · Munich (Germany), June 17–18, 2005 Diverticular Disease: Emerging Evidence in a Common Condition Congress Short