MODERN APPROACHES IN DIAGNOSTICS AND TREATMENT OF CHRONIC DUODENITIS

UDC: 616.342-002

© Tarasova L.V., Dubov V.V. 2012

Received on 23.10.2012

L.V.TARASOVA, V.V.DUBOV

 

MODERN APPROACHES IN DIAGNOSTICS AND TREATMENT

OF CHRONIC DUODENITIS

 

Republican gastroenterological centre of “Republican clinical hospital”

of HCSD Ministry of Chuvash Republic,

Municipal clinical hospital No.1,

I.N.Ulyanov Chuvash state university, Cheboxary

 

This article describes modern approaches of duodenitis diagnostics, the therapy of duodenitis with Helicobacter pylori.

Key words: Нelicobacter pylori, duodenitis, therapy.

 

Chronic duodenitis is a chronic inflammatory process of mucosa of dodecadactylon, characterised by development in it of structural changes of inflammatory-dystrophic and disregenerator type, leading to atrophy of the glandular apparatus and disturbance of the basic functions of duodenum (first of all, digestive).

Frequency of duodenitis among adult population, according to a number of authors, can reach 20%, and in the structure of diseases of digestive organs can make 30%. Morphological signs of chronic duodenitis meet in 25% gastroenterologic patients ill with dispeptic syndrome, acute duodenitis – in 1.5% of patients.

In 25% of cases there is a primary affect of dodecadactylon (DDC). The secondary duodenitis meets more often and is observed at duodenum peptic ulcer (over 95% of cases), gastritis, pathology of bile passages, liver, pancreas. The secondary duodenitis at pathology of bile passages meets in women more often, and against peptic ulcer prevails in men. In adult population the proportion of women / men, suffering from duodenitis, makes 1:2 and even reaches 1:3.5.

The primary chronic duodenitis meets seldom. Disturbances of alimentary regimen (irregular food, use of acute, acidic nutrition, insufficient chewing of nutrition, strong alcoholic drinks, addicting for strong coffee or tea) make its reasons. Under the influence of irritating nutrition acidity of gastric juice and its damaging action on duodenum mucosa raises.

One of the possible factors, promoting the development of chronic duodenitis, is tobacco smoking. Under the influence of substances, which are in tobacco smoke, gastric juice secretion is stimulated, development of carbonates of pancreatic juice decreases and production of secret DDC having alkaline reaction is oppressed.

The transferred acute duodenitis can be one of the reasons of development of primary chronic duodenitis. There is a certain genetic predisposition to development of primary chronic duodenitis.

The pathogenesis of primary chronic duodenitis is not studied up to the end. Participation of immune mechanisms, disturbances of neurohumoral regulation of function DDC, immediate influence of etiological factors on mucosa DDC is supposed.

The duodenum has close anatomo-physiological interrelations with digestive organs, therefore at diseases of stomach, small intestine, biliar systems, pancreas it can be involved in the process, and chronic duodenitis, in turn, to promote the development of pathological changes in these organs.

One their basic etiological factors of secondary chronic duodenitis is helicobacter infection. Chronic duodenitis develops, as a rule, against chronic helicobacter gastritis and metaplasia of gastric epithelium in DDC. Н. pylori colonizes sites of metaplased gastric epithelium in DDC and causes inflammatory process. The centres of metaplased epithelium are easily damaged by acidic gastric contents, and in metaplasia sites erosions develop. The duodenitis caused by Н. pylori, as a rule, is localised in bulb of DDC.

The secondary chronic duodenitis is observed at chronic gastritis, peptic ulcer of stomach and DDC, chronic pancreatitis, opisthorchosis, lambliasis, food allergy, uremia and series of other diseases and conditions. Besides, immediate influence of the irritating factor on mucosa DDC, in pathogenesis of chronic duodenitis proteolytic action on it of active gastric contents (matters at trophic disturbances, dyskinesias).

The mechanism of development of chronic duodenitis is definitively unknown. The majority of authors consider that at the heart of its development lies disturbance of mutual relation of factors of aggression and protection. Aggressive factors are hyperproduction of hydrochloric acid and pepsinum, trauma of mucosa DDC; protective – optimum condition of cellular neogenesis and circulation of mucosa DDC.

Dudenostasis promotes occurrence and advance of is inflammatory-dystrophic changes in DDC, which more often results from chronic duodenal impassability of functional or organic (arteriomesenteric compression, adherent process, etc.) origin.

At stomach peptic ulcer, the secondary chronic duodenitis develops owing to damaging action of aggressive acid-peptic factor and Н. pylori on mucosa DDC. At chronic pancreatitis, the development of chronic duodenitis is caused by the raised absorption of pancreatic enzymes; depression of secretion of carbonates that promotes acidification of duodenal contents and to action of aggressive factors of gastric juice; the lowered resistance of mucosa DDC; at diseases of lungs and cardiovascular system development of chronic duodenitis is promoted by hypoxia of mucosa DDC. At chronic renal failure development of chronic duodenitis is caused by allocation through mucosa DDC of toxic nitric slags.

In the development of chronic duodenitis at diseases of bile passages an important role is played by intestinal microflora. Especially, big role is played by this factor at depression of secretory function of stomach. It promotes development of disturbance of intestinal microocenosis, thus proximal departments of small intestine, including DDC, occupies bacteriemic microflora unusual to these departments.

Thus, it is possible to separate a number of pathogenetic factors participating in the development of chronic duodenitis:

  • Degree and kind superfluous “acidification” DDC (hypersecretory, biliar, pancreatic, enteral, admixed);

  • Expression of syndrome of disturbance of cavitary digestion and its prevailing kind (chronic biliar insufficiency, exocrinous insufficiency of pancreas admixed);

  • Expression of malabsorbtion syndrome;

  • Expression of disturbance of barrier function;

  • Degree of raised bacillar settling DDC;

  • Degree of hormonal duodenal insufficiency;

  • Expression of motor dysfunction DDC, its prevailing kind (hypomotor, hypermotor, admixed).

The mechanism of development of local duodenites also can be characterised by variety. In most cases, the duodenal papillitis is continuation of dissemination of diffusive inflammation DDC on the big duodenal papilla (BDP). On the other hand, papillitis can be a consequence of available inflammatory process in cholic and pancreatic ducts.

Clinical picture

For acute duodenitis nausea, vomiting, general delicacy, rise in temperature, morbidity are characteristic a pain in epigastric area, at palpation in epigastric area. Acute catarral and erosive-ulcer duodenitis usually come to an end with self-healing in some days, at repeated duodenites transition in the chronic form is possible. Possible complications are as follows: intestinal hemorrhages, punching of a wall of intestine, development of acute pancreatitis. At very rare phlegmonous duodenitis, the general condition of the patient sharply worsens, the strain of muscles of abdominal wall in epigastric area, positive symptom of Shchyotkin-Blumberg, fever is defined.

It is possible to separate some clinical variants of a run of chronic duodenitis: ulcerative-like, gastritis-like, cholecystitis-like, pancreato-like, nervous-vegetative, admixed, latent.

Most often meeting (over 80% of patients) clinical variant of chronic duodenitis is ulcerative-like, corresponding expressed (often erosive) bulbitis, аssociated with Н.pylori, acid-peptic and alimentary factors, or to secondary duodenitis against peptic ulcer DDC. The basic symptom is “the late”, “hungry”, “night”, periodic pain of visceral character, in epigastric area or projection DDC, as a rule, without irradiation, taken out food intake, antacids, antisecretory preparations with localisation in epigastriums and pyloroduodenal zone, accompanying symptoms quite often become perceptible: acidic eructation and bent to constipations.

For gastritis-like variant the early pain in epigastric area, more often functional (from lat. distendo, distensum – to stretch, dilate), visceral character with symptoms of gastric discomfort (severity in epigastriums after food intake, nausea, eructation), intestinal symptoms (meteorism and chronic diarrhoeia), depression of body mass. The given variant corresponds to gastroduodenitis with the expressed atrophy of gastric epithelium, more often associated with Н. pylori, or to secondary duodenitis against atrophic gastritis, peptic ulcer with localisation in stomach, carcinoma of stomach; as well as anomalies of the development DDC causing chronic disturbance of evacuation of nutrition from stomach, gastrostsis and duedenostasis. Acid formation in stomach is usually lowered, up to sneezewort, often expressed duodenogastric reflux is noted.

Cholecysto - and pancreato-like variants are characterised by presence of pain with localisation in right or left hypochondrium, sometimes surrounding character, frequent enough on type biliar colic bound to reception of fat nutrition, which are accompanied by feeling of bitterness in mouth, sometimes nausea, rarer vomiting with bile impurity, diarrhoeia and constipation alternating, meteorism and food disturbance. The semiology is caused by transitional disturbances of outflow of bile and/or pancreatic juice, developed owing to edema and spastic stricture of sphincter or regurgitation of contents of intestine in common bile duct at duodenostasis and atonies of sphincter of Oddi. Thus, the structural pathology is not revealed by accessible methods of inspection. Acid formation in stomach can be lowered, kept or, less often, it is raised, are possible functional, rarer organic, duodenostasis, expressed duodenogastric reflux.

The nervous-vegetative variant often meets in women and is characterised by vegetative astheno-neurotic disturbances, dumping syndrome implications. Symptoms (general delicacy, sweating, palpitation, dyspnea, tremor, liquid stool) appear in some hours after food intake. Disorder of endocrine function DDC (syndrome of duodenal hormonal insufficiency) lies in the basis. The given symptoms can be observed at all clinical variants of duodenitis, but if their expression dominates, their separation in a single variant is possible.

At the admixed variant clinical semiology, characteristic for different variants becomes perceptible.

The latent variant is often observed in older people, for it atrophic changes mucous DDC, which are usually revealed at the endoscopic researches carried out in other occasions, are characteristic.

At the expressed atrophic process, irrespective of pathogenesis of affect DDC, painful syndrome becomes almost constant, expression of other gastric and especially intestinal symptoms (unstable motions, meteorism), vegetative disorders amplifies. Depression of body mass, resistance to carried out therapy (antacids, antisecretory preparations and so forth) becomes perceptible. The symptoms testifying to involving of other organs of the alimentary system, besides, can join.

Diagnostics

Research of the clinical picture is an important stage of diagnostics of any disease. However, it is necessary to remember that clinical symptoms of chronic duodenitis are not specific and not always correlate with endoscopic changes. Besides, in some cases chronic duodenitis proceeds asymptomatically.

The preliminary diagnosis of duodenitis, as a rule, is put in the presence of painful and dyspeptic syndromes similar to those at peptic ulcer DDC, but without radiological and endoscopic signs of ulcer testifying to involving DDC in pathological process. The diagnosis of the isolated duodenitis proves to be true morphological signs of inflammatory infiltration of mucosa of duodenum and absence ulcerative and other affects of organ. As a whole, on analogies to gastritis, duodenitis is morphological concept and its diagnosis should be put only after morphological research. In practice, are usually limited clinico-endoscopic to the data, which do not always coincide with the morphological one.

For the definitive conclusion carrying out of careful laboratory-tool research is necessary for exception of the secondary nature of duodenitis.

Compulsory laboratory-tool researches are as follows:

  1. General analysis of blood, urine, feces.

  2. Biochemical analysis of blood: maintenance of general protein and albuminous fractions, aminotransferases, glucoses, sodium, potassium, sodium chloridums, cholesterol, alpha amylase, urea, creatinine.

  3. Duodenal sounding.

  4. FEGDS with aim biopsy of mucosa of dodecadactylon. Morphological research allows to differentiate forms of duodenitis and to define process stage, expression of atrophy.

  5. Diagnostics of helicobacter infections (mainly by means of non-invasive techniques).

  6. Roentgenoscopy of stomach and dodecadactylon allows:

  • To diagnose deformation DDC, including cicatrical;

  • To distinguish the functional nature of deformation of bulb DDC in patients ill with duodenitis from proof cicatrical deformation at peptic ulcer in the stage of remission of ulcer;

  • To define motor-evacuator characteristics DDC;

  • To estimate the condition of momovement of stomach, ostium of gatekeeper, etc.;

  • To reveal presence of duodenogastral reflux.

  1. Ultrasonic investigation of abdominal cavity organs.

The characteristic signs of chronic duodenitis, revealed at X-ray inspection, are irregular and chaotic peristalsis, periodic spastic reductions DDC (“angry” DDC), sometimes return peristalsis, accelerated passage of barium on loop DDC, increase of calibre of cords. At atrophic duodenitis cords can be considerably reduced. In many patients are observed bulbostasis and increase of volume of bulb, sometimes duodenostasis in connection with sharp rising of a tonus of low-horizontal parts DDC. At erosive duodenitis, the delay of contrast in the form of small maculae on mucosa DDC is possible.

FEGDS concedes to the radiological method in estimation of impellent function of stomach and DDC, but is more informative in estimation of microrelief of mucosa, revealing of focal atrophic changes of mucosa, erosions and flat ulcers. At superficial duodenitis, during endoscopy carrying out irregular puffiness of mucosa in bulb, the top flexure and descending part DDC is revealed; the appreciable spotty hyperemia of mucosa, especially in edema places is natural. In cases of sharply expressed duodenitis, puffiness of duodenal mucosa gets diffusive character. In the most hydropic zones grains acting over the surface in diameter to 1 mm (“semolina”) are found out plural whitish; in sites of spotty hyperemia are frequent and fine-focal hemorrhages. In lumen DDC there are a lot of mucus. At atrophic duodenitis, are endoscopically found out, along with edema and hyperemia, sites of acyanotic mucosa, in which because of essential reduction of its thickness appear through fine vascular furcations. Mucus usually is not present. At erosive duodenitis, plural erosions of different size – from punctulated till the diameter of 0.2-0.5 sm - settle down on the mucosa changed as sharply expressed duodenitis. Their bottom is flat, covered with white scurf, erosions are surrounded with rim hyperemias, easily bleed in the course of endoscopy carrying out. FEGDS is supplemented by the data of morphological research of biopsy materials, allowing to reveal inflammatory changes, sites of gastric metaplasia, dystrophic changes, increase of quantity of goblet cells, and at progressing run – their reduction and the expressed changes of mucosa DDC.

Additional laboratory-tool researches are as follows:

  1. Research of secretory function of stomach by the method of 24-sentry of monitoring рН.

  2. Research of motor function DDC by means of peripheric computer gastroenterography and/or floor manometries.

  3. Fractional chromatic duodenal sounding.

  4. КТ, MRI, ERPHG, МRPHG (under indications, basically for affect exception of gastroduodenal zones diseases of tumoral nature, which has caused secondary duodenitis).

  5. Colonoscopy (irrigoscopy).

  6. Research of fecal elastase 1.

Additional laboratory-tool researches are used for estimation of the condition of organs of the alimentary system at secondary duodenites.

Treatment

The therapy purposes are as follows:

  • Liquidation of clinical, endoscopic and functional implications of recrudescence of chronic duodenitis;

  • Prevention of the development of complications and weighting of the run of disease (development of erosive duodenitis, hemorrhage against reception NPVP, decompensation of duodenostasis, developments of maldigestion and malabsorbtion syndromes, reactive pancreatitis);

  • Prophylaxis of recrudescences.

Traditional conservative therapy of chronic duodenites develops:

  • From general, universal references for all acid-dependent diseases;

  • Private therapeutic actions at special forms of chronic duodenitis, including secondary origin (depends on the concrete etiological form of illness);

  • Therapeutic actions for correction of accompanying functional disorders (digestion, motor-tonic disturbances).

Non-medicamental treatment. At out-patient treatment are necessary adequate rest and sleep, whenever possible influence prevention of stressful factors on the patient. Moderate exercise stresses (walks in the open air, swimming). Refusal of smoking and alcohol use.

In recrudescence, depending on tolerance of foodstuff, first of all, milk and cereal cultures containing gluten, prescribe the eliminative diet, excluding whole milk, products from rye, barley, oats, wheat, a diet in two basic variants. At good tolerance of milk, treatment begins from the diet No.1а, then No.1b, and after remitting of recrudescences of the patient transfer to diets No.1 or No.2 depending on secretory function of stomach, or at accompanying diseases of cholic bubble, bile passages, liver, pancreas - No.5. At intolerance of milk and the expressed recrudescence prescribe diet No.4 or No.4b (to 3-4 days) with the subsequent transfer of the patient to the diet No.4b.

In remission, it is necessary to recommend adequate food with exception of the products badly tolerated by the patient. Spices, radish, onion, garlic, horse-radish, vegetables and fruit containing rasping cellulose are excluded. Meat, smoked products, pickled products, marinades, fried products, strong meat broths, fat, mushrooms, hot spices, aerated drinks, etc. are limited.

At acute catarral and erosive-ulcer duodenitis hunger, confinement to bed are recommended within 1-2 days.

Physiotherapy as an auxiliary method is widely applied in complex treatment at duodenitis recrudescence. For stopping of painful syndrome prescribe thermal procedures (heaters, paraffinic applications, diathermy, etc.), sinusoidal modulated runs or novocainum and platyphyllinum electrophoresis; at functional disorders of nervous system, hydrotherapy is recommended in the form of medical douches, coniferous, oxygen and pearl baths.

Indications to admission. Patients ill with chronic duodenitis basically are treated in out-patient departments. Indications to admission are as follows:

  • expressed symptoms of recrudescence;

  • panduodenitis (periduodenitis);

  • presence or threat of complications (hemorrhage, chronic duodenal impassability);

  • presence of serious comorbidity of stomach, pancreas, hepatoliary systems, etc.;

  • diagnostics hard cases, necessity for differential diagnostics;

  • suspicion on tumoral nature of disease;

  • started cases of disease demanding correction of basic physiological parametres of organism;

  • carrying out of surgical treatment apropos decompensated organic duodenostasis.

Pharmacotherapy

Medicinal therapy of chronic duodenitis is carried out depending on the clinical variant of disease.

In the presence of infection Н. pylori therapy under the schemes regulated by the international Maastricht agreements (Maastricht-4, 2011) and recommendations of the Russian gastroenterological association (2012) is carried out eradicatively.

Standard triad therapy. As the scheme of the first line of treatment the triad scheme of eradicative therapies is accepted:

Inhibitor of proton pomp in standard dose (omeprazole 20 mg, rabeprazole 20 mg, esomeprazole 20 mg, lansoprazole 30 mg, pantoprazole 40 mg) – twice a day.

Clarithromycin 500 mg – twice a day.

Amoxycillin 1000 mg or metronidazole of 500 mg – twice a day.

Duration of therapy is 7 or 10-14 days. Efficiency of standard triad therapy raises at:

Doubling of standard dose of IPP;

Increase of duration of therapy from 7 till 10-14 days;

Addition to therapy of preparation of smuth trikalium dicytrate 240 mg – twice a day;

Addition to standard therapy of probiotic Saccharomyces boulardii (Enterolum);

Detailed instructing of the patient and the control over it for the purpose of maintenance of exact observance of the prescribed regimen of reception of medicines.

Quadrotherapy with a smuth preparation:

  • Inhibitor of proton pomp in standard dose (omeprazole 20 mg, rabeprazole 20 mg, esomeprazole 20 mg, lansoprazole 30 mg, pantoprazole 40 mg) – twice a day.

  • Tetracyclinum of 500 mg – 4 times a day.

  • Metronidazole of 500 mg – 3 times a day.

  • Bismuthum trikalium dicytrate 120 mg – 4 times a day.

Duration of therapy – 10 days. It is applied at intolerance of beta-lactam antibiotics (amoxycillin) as therapy of the first line or as the scheme of therapy of the second line at inefficiency of the standard triad scheme.

One of the basic problems now is development of resistance H. pylori to antibacterial preparations. One of the variants of struggle against resistance – including in schemes of new antibacterial preparations.

The triad scheme with levofloxacin:

  • Inhibitor of proton pomp in standard dose (omeprazole 20 mg, rabeprazole 20 mg, esomeprazole 20 mg, lansoprazole 30 mg, pantoprazole 40 mg) – twice a day.

  • Levofloxacin 500 mg – twice a day.

  • Amoxycillin 1000 mg – twice a day.

Duration of therapy is 10 days. Can be prescribed only by the gastroenterologist after unsuccessful eradication of the first line.

Consecutive therapy is recommended as an alternative variant of the treatment, which administration carries out the gastroenterologist. Within 5 days the patient receives IPP in a standard dose twice a day with amoxycillin 1000 mg twice a day within 5 days, then within 5 days: IPP in standard dose twice a day with clarithromycin 500 mg twice a day and metronidazole (or Tinidazolum) 500 mg twice a day. As a variant of the four-componental scheme addition possibility is discussed to standard triad therapy of metronidazole (or Tinidazolum) 500 mg twice a day.

At ulcerative-like variant, the therapy basis is made of antisecretory preparations: inhibitors of proton pomp (omeprazole, pantoprazole, lansoprazole, rabeprazole, esomeprazole) and Н2-histamine blockers (ranitidine, famotidine).

Patients ill with duodenitis should accept IPP necessarily twice a day (in the morning and in the evening) as only in this case is reached some equal suppression of gastric secretion in day and night hours that is important for night secretion, which is most important for occurrence of night symptoms at patients ill with ulcerative-like variant of duodenitis.

Н2-histamine blockers, as a rule, are used in complex treatment: at “night acid break” against reception IPP, as well as at resistance of the patient to IPP and in therapy “on demand”.

At treatment of duodenitis antacids and alginates are used as additional agents in complex treatment. Besides, antacids can be used for incidental reception “on demand” at painful syndrome, errors in diet. Now, combined nonabsorbable antacids containing in certain parities of compound of aluminium and magnesium (almagelum, maalox), the most corresponding to demands to modern antiacid agents are most often used.

Antacids cannot be prescribed simultaneously with denolom and sucralfat, because of pharmacological incompatility.

Prokinetics (regulators of motor function of gastrointestinal tract). At duodenitis antagonists of dopamine receptors (domperidon and metoclopramidum) and itoprid hydrochloride are applied to restoration of broken gastroduodenal movement, mainly at gastritis-like clinical variant of duodenitis.

The double mechanism of action (antagonism with dopamine D2-receptors and dose-dependent inhibition of activity of acetylcholinesterase) does a choice of preparation itoprid hydrochloride (itomed, ganaton). Itoprid hydrochloride (in the dose of of 50 mg 3 times a day) has specific effect on the top part of gastrointestinal tract, accelerates transit on stomach and improves its evacuation. The preparation renders also antiemetic effect at the expense of interaction with the D2-receptors located in the trigger zone.

Gastroprotective agents: bismuthum preparations (denol), sucralfat (venter, alsucral), misoprostol (sytotek) are applied in complex treatment of gastritis-like and ulcerative-like variants of duodenitis.

At presence duodenogastral reflux, cholecysto-like variant of chronic duodenitis, the secondary duodenitis, which has developed against pathology hepatobiliary systems, use is expedient in complex treatment of preparations of ursodesooxycholic acids (ursosan, ursofalc).

Correction of syndromes accompanying chronic duodenitis of maldigesty and malabsorbtion, functional disorders of biliary tract, exocrinous failures of pancreas is carried out by general rules.

 

REFERENCES

 

  1. Gastroenterology. A national guideline / under ed V.T.Ivashkin T.L.Lapina – M GEOTAR-Media 2008 – 700 p

  2. Grigoryev P.Ya., Yakovenko A.V. Clinical gastroenterology: textbook for students of medical higher schools. – 3 ed., revis. and add. – M.: Medical inform. agency, 2004. – 768 p.

  3. Rational pharmacotherapy of diseases of digestive organs: a guideline for practising doctors / under gen. ed. V.T.Ivashkin. - M.: Litterra, 2007. – 1045 p.

  4. Modern therapy of diseases of digestive organs / under ed. of V.A.Maximov. – M.: Аdamant, 2011. – 712 p.

 

INFORMATION ABOUT AUTHORS:

 

Tarasova Larisa Vladimirovna

Head of the Republican gastroenterological centre of “Republican clinical hospital” of HCSD Ministry of Chuvash Republic, Cand. Sc. (Medicine), associate professor at Hospital therapy No.1 chair with phthisiology course in “I.N.Ulyanov Chuvash state university”, chief gastroenterologist of HCSD Ministry of Chuvash Republic

Dubov Vladimir Vladimirovich

associate professor at faculty therapy chair in “I.N.Ulyanov Chuvash state university”, Deputy head physician for therapy of “Municipal clinical hospital No.1” of HCSD Ministry of Chuvash Republic, chief specialist of public health care organisation in Cheboxary and Novocheboxarsk, HCSD Ministry of Chuvash Republic

 

Correspondence address:

9, Moskovskii pr., Cheboxary, Chuvash Republic, 428015

Tel.: +7(8352) 58-27-26, +7(8352) 44-49-76

E-mail: tlarisagast18@mail.ru, dvv428017@yandex.ru

© All rights reserved. The use of materials without written permission - is prohibited.