Corticosteroid therapy in inflammatory bowel diseases · Treatment with corticosteroids 13 •The...

Corticosteroidtherapy in inflammatory bowel diseases

The informed patient

12th revised edition 2017

U2

Publisher

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


Corticosteroidtherapy in inflammatorybowel diseases

Prof. Dr. Tilo Andus

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Author:Prof. Dr. Tilo AndusKlinik für Allgemeine Innere Medizin, Gastroenterologie, Hepatologie und internistische Onkologie Krankenhaus Bad CannstattKlinikum StuttgartPrießnitzweg 2470374 StuttgartGermany

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Introduction 5

The natural role and regulation of corticosteroids in the body 7

• Anti-inflammatory effects of corticosteroids 12

• The effects of corticosteroids onmetabolism 12

• The effect of corticosteroids onfluid balance 12

Treatment with corticosteroids 13

• The use of synthetic cortico-steroids to improve efficacy and tolerability 13

• Different pharmaceutical forms for the treatment of ulcerative colitis 14

• Topical corticosteroids 15

• Efficacy in inflammatory bowel disease 17

• Ulcerative colitis 18

• Pouchitis 20

• Crohn’s disease 20

• Microscopic colitis (collagenous colitis and lymphocytic colitis) 23

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Contents Page


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Page

• Endemic sprue / celiac disease 24

• Tolerability and side effects 24

• Pregnancy and cortisone therapy 28

• Breastfeeding and cortisone therapy 28

Glossary 29

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Introduction

The discovery of cortisol by E. Kendalland O. Wintersteiner in 1937, and itssynthesis by T. Reichstein in 1938,made it possible for P.S. Hench to usethis substance for the first time in 1948to treat a patient with rheumatoid arthritis.Cortisol belongs to a class of hormonesknown as corticosteroids (often simplycalled “cortisone” in everyday speech).Hormones – this word comes from Greek and means “to set in motion” –are the body’s own messengers. Theyare usually released from special glandsin response to a stimulus and are thencarried in the blood to their destinationsin the body. Hormones then control anumber of metabolic processes in theirtarget organs.The rapid and potent anti-inflammatoryeffect of cortisol quickly established corticosteroids as an effective treatmentin cases of acute and chronic inflamma-tion, and also helped its three discov-erers win the Nobel Prize in 1950.

Even in the early days, it was clear thatthe desired effects of the corticosteroidswere accompanied by unwanted sideeffects. Only gradually were ways foundto avoid these effects as far as possible:by using the drugs in a targeted manner,and by limiting their use.

Introduction

Treatment with corticosteroids was also a significant step forward for patients withinflammatory bowel disease. Even aslate as the 50s, the life-expectancy of these patients was significantly reducedbecause acute flare-ups could only be treated to a very limited extent. For thisreason, many young patients died of theirdisease. The introduction of corticosteroidshas almost restored the life-expectancy of patients with Crohn’s disease and ulce-rative colitis to normal values. The challengetoday is to use corticosteroids in such away that patients also enjoy the highestpossible quality of life as a result of theiruse.

“Cortisone phobia” is a widespread pro-blem, which stems from inadequate know-ledge among the general public and alsoamong some patients with inflammatorybowel disease. This patient advice leafletaims to combat this lack of knowledge byexplaining the most important aspects oftreatment with corticosteroids in a com-prehensible manner.

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Corticosteroids in the body

The natural role and regulation of cortico-ster oids in the body

The endogenous (naturally occurring in the body) hormone cortisol and itsprecursor cortisone are produced in theadrenal cortex.

The adrenal glands, consisting of themedulla and the adrenal cortex, areamong the organs in the body that actas glands (Fig. 1).

Fig. 1: Location of the adrenal glands inrelation to the kidneys

Adrenal glands

Kidneys

Bladder

Ureter

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Cortisol is essential for the body. Theproduction of cortisol in the adrenalglands is stimulated by a controlling hor-mone, the adrenocorticotropic hormone(ACTH) (Fig. 2).ACTH is produced in the pituitary gland(hypophysis), a gland that is only thesize of a cherry stone and which weighsless than 1 g.

The release of ACTH is controlled by a further hormone, the so-called corti-cotrophin releasing hormone (CRH).

Fig. 2: The cortisol control system in thehypothalamus, hypophysis and adrenal cortex

ACTH

Cortisol

+–

–

+

CRH

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CRH is produced in the mid-brain in thecentral nervous system (hypo thalamus).

Within this complex system, cortisolregulates its own release: High concen-trations of cortisol inhibit the release ofcortisol.

This type of control is known as a self-regulating feedback mechanism. Nerv-ous and inflammatory stress factors alsohave an effect on this regulatory loop.

Cortisol is normally produced in a rhythmthat depends upon the time of day.The largest amounts are released in theearly morning, and smaller amounts are released later on (Fig. 3). A second,smaller peak does not occur until theevening. Altogether, the adrenal corticesproduce about 8–25 mg cortisol per day.

Fig. 3: Diurnal (related to the time of day)rhythm of blood cortisol levels

18 20 22 0 2 4 6 8 10 12 14 16 18

25

20

15

10

5

0

Time

Plasma cortisol [µg/100 mL]


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When under severe stress, such as aserious illness, the body requires morecortisol. This is why the adrenal corticeshave the ability to produce up to 200–300 mg per day in such situations.

All corticosteroids, including cortisol, act by “binding” to specific receptors(recognition sites) on cells and thenaltering their metabolism. This is howthey stimulate the breakdown of pro-teins, for instance. Since almost all cellsin the human body have this type ofreceptor, corticosteroids act uponalmost all cells.

These varied effects can be broadlydivided into three groups:

1. the anti-inflammatory effects,which are also important for efficacy inthe treatment of inflammatory bowel disease,

2. the metabolic effects (effects ongeneral metabolism), which are alsoresponsible for the occurrence of sideeffects and

3. the effects on fluid balance (mineralmetabolism).


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Fig. 4: Inhibition of inflammation by corticosteroids

Precursorcells in thebone marrow

Inflammatorycells in theblood stream

MultiplicationSpecialization

Migrationto inflammationsitesActivation

Release ofinflammationfactors

Inflammatory cells, e.g. in the intestines,joints etc.

Co

rtic

ost

ero

ids

–

–

–

+

+


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Anti-inflammatory effects of corticosteroids

The anti-inflammatory effect is due tothe fact that corticosteroids inhibit themultiplication (proliferation) and develop-ment (differentiation) of inflammatorycells in the bone marrow, the migrationof inflammatory cells from the bloodinto the intestines, and the activation ofthese inflammatory cells (Fig. 4). Cortico- steroids also have a direct effect uponall types of inflammatory cells, as wellas on white blood cells (leukocytes).In these cells, corticosteroids inhibit the release of inflammatory hormones,such as cytokines, which stimulateinflammation.

The effects of corticosteroids onmetabolism

The effects on general metabolism areeven more varied. Corticosteroids affectmetabolism in the liver, the muscles, thefatty tissues, the bones and ligaments,and many other organs.

The effect of corticosteroids on fluidbalance

The effect on fluid balance is due to thefact that cortisol bears a certain resem-blance to another hormone – aldos-terone – which affects fluid balance byregulating the excretion of minerals inthe kidneys. Like aldosterone, cortisolincreases the retention of water in thebody.

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Treatment with corticosteroids

Treatment with corticosteroidsNot long after cortisol was first used inthe treatment of inflammatory diseases,attempts were made to increase its effi-cacy, and at the same time reduceunwanted side effects through chemicalmodifications.

The use of synthetic corticosteroidsto improve efficacy and tolerability

The development of corticosteroidssuch as prednisone, prednisolone and 6-methylprednisolone resulted in cortico-steroids with very little or no effects onmineral metabolism, while at the sametime increasing their efficacy as anti-inflammatories.

Prednisolone and prednisone have ananti-inflammatory effect about fourtimes as great as that of endogenouscortisol, and 6-methylprednisolone iseven five times more effective.

Since all anti-inflammatory and metabol-ic effects are mediated by the samereceptors on the cells, it is very difficultto separate the desired effects from theunwanted side effects. In order toachieve progress here, attempts havebeen made to transport the active sub-stance directly to the site of inflamma-tion in order to minimize the systemiceffects and the effects produced by circulation in the blood – and thus alsothe effects on the entire body.

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Different pharmaceutical forms forthe treatment of ulcerative colitis

Initially, pharmaceutical forms for thetreatment of ulcerative colitis were pro-duced that resulted in a high concentra-tion of corticosteroid in particular bowelsegments only, namely in those partswhere the inflammation is located. The development of enemas made itpossible to achieve this goal in part.The use of corticosteroid enemas canachieve relatively high local concentra-tions of corticosteroid in the rectum anddistal sections of the large intestine(Fig. 5).

Nevertheless, some of the corticosteroidapplied in this way is absorbed throughthe intestinal mucosa (the lining of theintestines) causing unwanted sideeffects, albeit to a reduced extent. Corti-costeroid foams are just as effective asenemas, but they are preferred overenemas by most patients because theyare easier to use. In addition, because ofits consistency and volume, mostpatients find foam easier to keep in.In more severe cases of the disease,however, corticosteroids must beadministered in the form of tablets, cap-sules, or even as intravenous injections,in order to achieve an adequate effect.


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Topical corticosteroids

In an effort to preserve the efficacy ofcorticosteroids while further reducingthe side effects of these substances,so-called topical corticosteroids havebeen developed in recent years.The term “topical” means that theeffect is predominantly local, i.e. activeat the site of inflammation. The principleof topical corticosteroids will now beexplained using the example of budeso-nide, which has long been used success-fully in treating asthma and acute flare-

Fig. 5: Location of efficacy of corticosteroidenemas and foam preparations in thelarge intestine


Stomach

Small intestine

Large intestine

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ups of Crohn’s disease with involve-ment of the ileum and/or the ascendingcolon. It has also been approved for oraland rectal treatment of ulcerative colitis.

Budesonide is a very potent cortico-steroid. When administered orally orrectally, it is rapidly absorbed throughthe intestinal mucosa after acting at thesite of the inflammation, and it is thentransported to the liver. Here, in contrast to the corticosteroidsused previously, more than 90% of thebudesonide is broken down during thefirst passage through the liver so thatonly a small proportion gets into thebody. This means that fewer side effectsare to be expected (Fig. 6).

Fig. 6: The uptake and breakdown of budesonide in the body


Oral budesonide

Heart

Stomach

Liver

Large intestineAscending colonSmall intestine

IleumSigmoid colon

Anus (Rectum)

Rectalbudesonide

10% systemicallyactive(activein theentire body)

90% brokendown inthe liver

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In order for oral budesonide to arrive atthe local sites of inflammation in theintestines, it is crucial that it is notabsorbed into the blood stream in theupper segments of the small intestine.Therefore, a special coating must beused to ensure that the active substanceis only released at the sites of inflamma-tion (in the case of Crohn’s disease, thismeans the transition area between thesmall and large intestine in particular,and in the case of ulcerative colitis, thelarge intestine in particular).

However, it should be noted that thesecoatings mean that inflammation in theesophagus, the stomach, and the upperparts of the small intestine, such as theduodenum, cannot be treated in thisway. Furthermore, in cases of severedisease, it may be necessary to use sys-temically active corticosteroids.

Efficacy in inflammatory boweldisease

Generally speaking, corticosteroids are currently the most effective drugsfor the treatment of acute flare-ups ofinflammatory bowel disease (ulcerativecolitis and Crohn’s disease). Long-termtreatment with systemically active corticosteroids should, however, beavoided where possible.


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Ulcerative colitis

Mild to moderately active ulcerative colitis

Treatment with 5-aminosalicylic acid(mesalazine) is adequate for most casesof mild to moderately active ulcerativecolitis. The next line treatment to con-sider is a combination mesalazine thera-py consisting of tablets or granules andenemas/foam preparations. As anotheroption is the administration of 9 mg oforal budesonide-MMX.Where appropriate, a short course ofsystemic corticosteroids (for example40 mg per day of prednisolone), with arapid dosage reduction of 10 mg every 5 days and a halt to corticosteroid treat-ment within 3 weeks, may lead to amore rapid alleviation of the symptoms.Most patients respond rapidly to thistreatment. However, the occurrence ofside effects often somewhat diminishesthe therapeutic advantages of systemiccorticosteroid therapy.

Left-sided ulcerative colitis

In left-sided ulcerative colitis, in whichonly the final 50 cm of the large intes-tine is affected, 5-aminosalicylic acid(mesalazine) enemas or foam prepara-tions are preferred, and – where neces-sary – corticosteroid foam preparationsor enemas, because these achieve thehighest concentrations of active sub-


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stance in the inflamed area. In severecases, it may be necessary to adminis-ter a combination of 5-aminosalicylicacid (mesalazine) and corticosteroid rec-tally, or possibly even a combinationmesalazine therapy composed of ene-mas and oral forms (tablets, granules).

Highly active ulcerative colitis

Highly active ulcerative colitis alwaysrepresents an acute danger to the pa-tient. In these cases, it is often unclearwhether tablets or granules can still beeffective. On the other hand, enemasand foam preparations generally cannotbe retained for a sufficient period oftime owing to the severe diarrhea. Thisis why inpatient treatment and the intra-venous administration of high doses ofcorticosteroids are necessary in suchcases. Depending on the severity of thedisease, additional therapeutic measuresmay be required.

Inactive ulcerative colitis – maintenance of remission

Based on what we currently know aboutcorticosteroids, they should not be usedfor maintenance of remission (remission= freedom from symptoms/absence ofactive disease), because they are noteffective in this regard, and the possibleside effects may be a burden on thepatients. The first-line (i.e. preferred)

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agents in such cases are preparationscontaining 5-aminosalicylic acid(mesalazine). This treatment has beenproven to reduce the risk of colorectalcancer.

In patients who do not toleratemesalazine, E. coli Nissle 1917 may be used.

Pouchitis

When complete surgical removal of the colon is required in patients withulcerative colitis, a small bowel reservoir(pouch) can enable regular bowel move-ments in many cases.

However, in some cases, this pouchmay become chronically inflamed.The standard treatment for this involvesthe administration of the antibioticmetronidazole. Alternatively, budesonidecan be used as an enema or foam if thisis better tolerated.

Crohn’s disease

Mild to moderately active Crohn’sdisease

Today, mild to moderate flare-ups ofacute Crohn’s disease are treated witheither 5-aminosalicylic acid (mesalazine)or corticosteroids. Here, corticosteroidsare more effective than 5-aminosalicylic


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acid preparations. The same applies tothe predominantly topically active corti-costeroid budesonide. In the case ofcorticosteroids, the 6-month treatmentregimen (Tab. 1) for the treatment ofacute Crohn’s disease is increasinglybeing abandoned because the majorityof patients respond much more quicklyto this kind of treatment. Moreover, therate of side effects for systemicallyactive corticosteroids is relatively high.

Nowadays, depending on disease activity, a variable dose reduction is recommended.

The topical corticosteroid budesonide is used as an oral preparation in thetreatment of ileocaecal Crohn’s disease.It is taken in the form of a capsule con-

Tab. 1: Treatment regimen for acute Crohn’sdisease using prednisolone as anexample

Week of treatment Daily doseof prednisolone

1 60 mg2 40 mg3 35 mg4 30 mg5 20 mg6 15 mg7–14 10 mg3–6 months 5–10 mg

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taining granules that are resistant togastric acid.

The granules are also available in asachet containing the daily dose as asingle portion. Budesonide is thenreleased from the granules inside thesmall intestine and the large intestine,and acts directly on the intestinalmucosa. After that, it is rendered in-active in the liver. Due to this mecha-nism of action, it is particularly effectivein treating cases where the final portionof the small intestine (the terminalileum) or the first part of the colon (caecum) is affected. If the rectum isalso affected, additional treatment with enemas or foam preparations will benecessary, or systemically active corticosteroids will need to be used.

Highly active Crohn’s disease

As with ulcerative colitis, such cases arealso serious and require inpatient treat-ment and the administration of a highdose of corticosteroids in the form ofinjections. If necessary, additional thera-peutic measures must also be taken.

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Inactive Crohn’s disease – maintenance of remission(remission = period of absence of symptoms)

Corticosteroids should not be used formaintenance of remission.

Microscopic colitis (collagenous colitis and lymphocytic colitis)

Because cases of microscopic colitis are rare and can only be diagnosed bycareful examination of tissue samplesfrom the colon (normally, they cannot be detected macroscopically in acolonoscopy), it often takes time beforethe diagnosis is made. The conditioncauses chronic watery diarrhea.

Budesonide in the form of capsules orgranules is the first-line treatment forboth forms of microscopic colitis, col-lagenous colitis and lymphocytic colitis,as it is very effective and has few sideeffects.The standard dose is 1 x 9 mg a day or 3 x 3 mg a day. With this treatment,both stool consistency and the frequencyof bowel movements improves in about90% of patients and, in about 80% ofpatients with collagenous colitis, thereis improvement in the collagen depositsthat form in the wall of the colon. Thisis even true in cases in which othertherapies, such as 5-aminosalicylic acid,metronidazole, or prednisolone have


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failed. The budesonide dose can bereduced during the course of treatmentin accordance with the symptoms. However, many patients still requirelong-term treatment.

Endemic sprue / celiac disease

Endemic sprue or celiac disease is achronic inflammatory disorder of thesmall intestine, which is triggered bygluten and gliadin, which are proteinsfound in grains. Patients experiencediarrhea, iron and vitamin deficiencies,weight loss, and growths in the smallintestine.

The standard treatment is a diet that isfree of gluten and gliadin.

Thankfully, cases of endemic sprue orceliac disease that do not respond tothis treatment are rare. When suchtreatment-refractory cases occur,patients are treated with prednisoloneand, more recently, with budesonide, acorticosteroid that is associated with amuch lower rate of side effects.

Tolerability and side effects

Prolonged treatment with systemicallyactive corticosteroids leads to sideeffects that often necessitate a dosereduction or discontinuation of treat-ment. The simultaneous appearance of


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a number of visible side effects of corticosteroids, such as weight gainwith abdominal obesity, moon face, buffalo hump, and stretch marks on theskin (striae), is also known as Cushing’ssyndrome. The possible side effectsof corticosteroids are listed in Table 2.

The long list of possible problems asso-ciated with corticosteroid treatment also


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Tab. 2: Possible side effects of cortico -steroids

Possible side effects of corticosteroids

• Weight gain with abdominal obesity, moonface, buffalo hump

• Striae (stretch marks on the skin), ecchymoses(small hemorrhages in the skin), acne

• Atrophy (shrinkage) of the adrenal cortices• Increase in blood glucose and cholesterollevels

• Increase in blood pressure• Osteoporosis (bone loss) and disorders ofblood flow in the bones (bone necrosis)

• Electrolyte imbalance, e.g. lack of potassium• Cataract and glaucoma• Insomnia, psychosis• Nerve damage• Inflammation of the muscles, muscle wasting• Increased susceptibility to infection (tuberculosis, fungal diseases)

• Growth disorders (in children)

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highlights the importance of the searchfor new corticosteroids with fewer sideeffects.

In the following section, some of thepossible side effects of corticosteroidswill be described in greater detail,together with advice as to what can bedone to combat them.

Osteoporosis is a common and poten-tially severe complication of prolongedtreatment with corticosteroids. Sponta-neous fractures may occur. Cortico-steroids inhibit bone formation and stimulate the breakdown of bone byinhibiting the uptake of calcium in theintestines and stimulating the release of parathyroid hormone (a hormone thatpromotes the breakdown of bone). Calcium and vitamin D supplementsmust be taken in the case of deficiency.There are indications that budesonide ismuch better tolerated than systemiccorticosteroids, including with regard tothe risk of osteoporosis.

Corticosteroid-induced bone necrosis isa severe disorder of the blood supply tothe bone.Fortunately, it is rare. It predominantlyaffects the hip joint and manifests itselfas pain.


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Prolonged treatment with corticosteroidsmay lead to atrophy (shrinkage) of theadrenal glands because the body’s natu-ral cortisol production is suppressed.

It is therefore essential to avoid stop-ping treatment with systemic cortico-steroids abruptly. They must instead betapered down very gradually by reducingthe dose so that the adrenal cortex hassufficient time to regenerate and beginsecreting cortisol again. Severe fatigueand feeling weak are typical symptomsthat may occur if corticosteroids arephased out too quickly.

Other (rare) side effects include cloud-ing of the lens of the eye (cataracts),and an increase in the internal pressureof the eye (glaucoma). In order that adiagnosis can be made at an early stage,regular ophthalmological examinationsshould be performed in patients under-going long-term treatment with corti-costeroids.In some cases, it will be necessary tochange the preparation being used or todiscontinue the treatment.

The suppression of the immune systemcaused by corticosteroids also weakensresistance to infection. Therefore, if thereare palpable masses in the abdomen,the presence of an abscess (collectionof pus) must be ruled out before begin-ning treatment with corticosteroids.


Pregnancy and cortisone therapy

There is no increased risk of miscarriage.If high doses of corticosteroids are usedduring the final phase of pregnancy, thenewborn will need to be carefully exam-ined by a pediatrician. Insufficient treat-ment of inflammatory bowel disease ismore dangerous for both the motherand the baby than cortisone treatmentwith the appropriate dose.

There is not yet enough data available to make a general recommendationregarding the administration of budeso-nide during pregnancy.

Breastfeeding and cortisone therapy

Because cortisone may be excreted inbreast milk, thus entering the infant’sbody, suppression of cortisone produc-tion in the infant is a possibility. Thisshould therefore be carefully monitoredby a pediatrician. Permanent damage isnot expected.


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Glossary

Glossary

5-aminosalicylic acid (5-ASA; mesa-lazine): an active ingredient in many

medicines for the treatment ofinflammatory bowel disease.

Abscess: a collection of pus.

ACTH: adrenocorticotropic hormone; a controlling hormone that stimulatesthe formation and secretion of corti-costeroids. ACTH is produced in thepituitary gland.

Aldosterone: a hormone of the adrenalcortex that affects fluid balance.

Bone necrosis: a severe disorder of theblood supply to the bone, associatedwith destruction of bone tissue.

Budesonide: a locally (topically) acting,potent corticosteroid, which can beadministered in the form of capsules,granules, tablets, foams or enemas.

Cataract: clouding of the lens of theeye caused by a variety of factors(congenital or acquired).

Colon: large intestine.

Collagenous colitis: a type of micro-scopic colitis characterized by thedevelopment of a band of collagenfibers over 10 μm in thickness.

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Glossary

Corticosteroids: a class of hormonesthat are released from the adrenalcortices, e.g. cortisol.

Cortisol: a hormone belonging to the corticosteroid family; regulates manymetabolic processes.

CRH: corticotropin releasing hormone, a controlling hormone that regulatesthe secretion of ACTH. CRH is pro-duced in the hypothalamus.

Crohn’s disease: an inflammatory disease of the digestive tract, namedafter Dr. Burrill B. Crohn, the doctorwho first described the disease.Common in the region of the lowerileum (part of the small intestine) andthe ascending colon.

Cushing’s syndrome: a typical conditionthat is triggered by elevated levels of cortisol in the plasma and whichcan occur if corticosteroids areadministered for a prolonged periodof time or at high doses.

Cytokines: hormones that mediateinflammatory reactions (inflammationmediators).

Differentiation: further development (specialization) of cells.

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Endemic sprue / celiac disease:a chronic inflammatory disorder of the small intestine triggered by intolerance of grain proteins.

Glaucoma: general term for diseases ofthe eye in which the internal pressureof the eye is elevated.

Hormone: a messenger substance produced in the body that regulatesmetabolic processes.

Hypothalamus: the central nervous region of the interbrain.

Ileum: the lowest section of the smallintestine.

Immune system: a complex system that defends the body against foreignsubstances.

Lymphocytic colitis: a type of micro-scopic colitis characterized byincreased numbers of lymphocytes in the tissue samples.

Microscopic colitis: a chronic inflam-matory disorder of the colon, whichcan only be diagnosed by examina-tion of tissue samples obtained from the colon using a microscope(see also collagenous colitis and lymphocytic colitis).

Glossary

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Migration: movement of inflammatorycells from the blood into theintestines.

MMX:Multi Matrix coating; a coatingthat allows targeted release of theactive substance in the large intestine

Osteoporosis: loss of bone tissue due to increased bone loss and/orreduced formation of bone.

Parathyroid hormone: a hormone thatis produced in the adrenal glandswhose effects include increasing therate of bone remodeling.

Pouchitis: inflammation of the pouchafter removal of the colon in the caseof ulcerative colitis.

Proliferation: multiplication of cells.

Psychosis: impairment of the state ofmind causing a fundamentally alteredexperience of reality.

Remission: a state characterized bythe absence of symptoms in thepresence of chronic disease.

Ulcerative colitis: chronic inflammationof the large intestine.

Glossary

Further information for patientswith inflammatory bowel diseases:

– Rectal treatment for inflammatorybowel disease (S97e)29 pages

– Microscopic colitis – Collagenous and lymphocytic colitis (Bu82e)27 pages

– Ulcerative colitis and Crohn’s diseaseAn overview of the diseases and their treatment (S80e)63 pages

– Diet and Nutrition in Crohn’s Disease and Ulcerative ColitisImportant Questions – Real Answers (S84e)62 pages

– Crohn’s disease and its associated disorders(S85e)44 pages

These brochures can be ordered free of chargefrom Falk Foundation e.V. or the local Falk partner.


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