Digestive tract disorders
MUDr. Matěj Hrunka, MUDr. Jakub Pecl, doc. MUDr. Petr Jabandžiev, Ph.D.
Digestive tract disorders
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1. Introduction
The following text is an insight into the world of paediatric gastroenterology. However, the reported
clinical symptoms and diagnoses are not exclusively the domain of paediatrics. Several experts caring
for adult patients will also encounter similar cases, from general practitioners, internists, or surgeons to
pathologists. The issues discussed below are based on precise knowledge from preclinical fields. They
aim to use it for basic differential diagnostic decision-making in a specific clinical scenario.
Diarrhoea is one of the two most common gastrointestinal symptoms, which usually lead
paediatric patients and their parents to visit their doctor. Diarrhoea is the defecation of unformed stool
more than three times a day. It can be acute, lasting for several days, or chronic if it lasts more than
2–4 weeks.
Pathophysiological view of the origin of diarrhoea:
• Osmotic – the result of the accumulation of osmotically active substances in the lumen with
subsequent water retention.
• Secretory – the result of a malfunction of the transport mechanisms of enterocytes.
• Structural damage to the intestinal wall – the result of an absorption failure (usually due to
inflammation), with inflammatory exudation, leucocytes, and plasma cells arising from
ulcerations.
• Hyperfiltration – caused by increased intravascular capillary pressure in the villi or obstruction
of the lymph flow in the mesenteric arteries, which leads to excessive intraluminal loss of
proteins and leucocytes.
• Hypermotility – the result of increased intraluminal transport of solutes and electrolytes,
increased intraluminal secretion and accelerated intestinal transit time.
The second symptom is abdominal pain, which can be acute or chronic. In the case of acute
abdominal pain, it is necessary to look for warning signs of severe disease, the so-called red flags,
which are in particular:
• Vomiting
• General state alteration
• Stool and gas passage failure
• Localisation of pain to one point, strictly localised pain
• Positive signs of peritoneal irritation
• Fever
• Symptoms of pre-shock or shock state (hypotension, tachycardia, etc.)
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These symptoms should lead to a proactive approach resulting in a correct diagnosis as soon as
possible so that optimal therapy can be established. The differential diagnosis of acute abdominal pain
is broad and includes internal and often surgical diagnoses.
On the other hand, there are chronic abdominal pains that occur intermittently or repeatedly over
several weeks or months. A large proportion of paediatric patients with this symptomatology suffer from
so-called functional GI disorders that are not of organic origin. However, in the flood of these patients,
it is necessary to be active in searching for cases with an organic origin requiring more extensive, precise
diagnosis and specific therapy. To correctly select these patients, we use red flags:
• Localised pain (other than around the navel)
• Pain irradiation
• Night-time pain (and generally nocturnal symptomatology, e.g. diarrhoea, vomiting, etc.)
• Weight loss
• Delayed growth and pubertal development
• Bile or blood-stained vomit
• Perianal symptoms (abscesses, fistulas, etc.)
• Jaundice
• General symptoms (fever, arthralgia, rashes, anaemia)
• Positive family history of ulcer disease, coeliac disease, or inflammatory bowel disease (IBD)
The basis of the diagnostic approach to each patient with these symptoms is a detailed analysis of
anamnestic data, including targeted questions about the red flags mentioned above. A precise history
leads paediatricians to select targeted examinations that establish the correct diagnosis. Naturally, an
integral part of this is a careful physical examination. In addition to the usual examination of the
abdomen, we must not forget in its course to examine other parts such as the skin (we look for various
exanthemas such as erythema nodosum, pyoderma gangrenosum, and others), mucous membranes
(we look for aphthous ulcers in particular), joints (signs of arthritis – swelling, pain, redness, etc.), or
the perianal area, including a per rectal examination. An integral part of the physical examination is
an overall assessment of growth and nutrition. The following steps include various laboratory tests,
imaging and sometimes even endoscopic examinations (often requiring general anaesthesia in
children). Indications for these diagnostic methods will be discussed in the following text.
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2. Differential diagnosis of diarrhoea and
abdominal pain (symptoms, diagnostics)
The differential diagnosis of abdominal pain and diarrhoeal diseases is broad. History and clinical
examination are the main clues in deciding the indication for some of the many complementary
examinations. The approach to diagnosis and treatment is individualised for each patient and further
determined by the severity and duration of the problem.
(a) Acute diarrhoea
Acute diarrhoea is one of the most common infectious diseases in minors. In the vast majority
of children, an outpatient examination at a general practitioner's office for children and adolescents with
possible microbiological examination of the stool is sufficient. In typical cases, the diseases are
accompanied by fever (they may not be present in the case of alimentary intoxication, so-called
enterotoxicosis), vomiting (more likely in viral gastroenteritis), and watery diarrhoea, sometimes with
blood or mucus in the stool (predominantly in bacterial enterocolitis). Regarding etiologic agents, they
are mainly viruses (rota-, noro-, adeno- and astroviruses), less often bacteria (campylobacteriosis and
salmonellosis), and rarely parasites (especially Giardia lamblia and Entamoeba histolytica after travel).
In immunosuppressed children, the aetiology can even be mycotic. The incidence of post-antibiotic
colitis caused by Clostridium difficile is increasing, mainly due to aminopenicillin treatment in
predisposed children. Accurate diagnosis of the causative agent of acute diarrhoea in children involves
a microbiological examination of stool (culture, latex agglutination, ELISA, PCR, toxin identification) or
serological tests (Widal test, yersiniosis).
(b) Acute abdominal pain and diarrhoea
Acute abdominal pain and diarrhoea are only symptoms and may be present in several
infectious and non-infectious diseases. In unclear cases or the presence of warning signs, it is
necessary to actively search for the actual origin of the symptoms, which may require early and specific
treatment. For example, vomiting or abdominal pain may be observed in bronchopneumonia,
tonsillopharyngitis, or diabetic ketoacidosis in a child with undiagnosed type 1 diabetes. Diarrhoeal
stools with predominant abdominal pain do not exclude the coexistence of acute appendicitis or ileocecal
intussusception. These situations are relatively rare but require urgent and specific treatment, and their
omission in the differential diagnosis may have fatal consequences.
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(c) Chronic abdominal pain and diarrhoea
Chronic or recurrent abdominal pain and diarrhoea in older children is one of the most common
situations in clinical practice. In the vast majority of cases, it is not the result of a somatic disease (90–
95 %). These patients often require a long-term follow-up, imaging, a series of laboratory tests, or even
an endoscopic examination with multiple biopsies to establish a definitive diagnosis. The differential
diagnosis is broad and requires the collaboration of a paediatric and adolescent general practitioner with
a gastroenterologist and a clinical psychologist.
At the forefront of their collaboration is the need to rule out an organic disease that reported
symptoms could manifest. Complementary examinations are indicated individually based on the course
of the disease, anamnestic data obtained from the patient and parents, and a detailed physical
examination, including a growth assessment (reconstruction of the growth chart over time).
Laboratory methods include the determination of the blood count with a differential leucocyte
count, the erythrocyte sedimentation rate (so-called ESR), serum biochemistry (CRP, urea,
creatinine, bilirubin, aminotransferases, amylase, lipase, glycemia, ionogram, albumin and prealbumin,
iron metabolism, total IgA antibodies and tissue transglutaminase antibodies (tTGA), endomysium
antibodies (EmA), anti-Saccharomyces cerevisiae antibodies (ASCA), and neutrophil cytoplasmatic
antigens antibodies (pANCA) in IgA or IgG classes (in case of selective IgA deficiency)), biochemical,
cytological examination, and urine culture.
A microbiological examination is used to exclude an infectious cause of the symptoms while
including the same tests as in the case of acute problems, plus a parasitological examination of the stool
(usually repeated due to low sensitivity).
Negative stool microbiology results usually lead to stool testing for occult bleeding and
determination of faecal calprotectin (leucocyte cytosolic protein) concentration. These parameters are
not disease-specific, but their negativity indicates the absence of an organic disease underlying the
reported symptoms. Otherwise, the positivity of these parameters strengthens the suspicion of, for
example, inflammatory bowel disease, Meckel's diverticulum and others that require a more detailed
(often invasive) diagnosis.
The primary imaging method is an ultrasound examination of the abdomen. In specific cases,
a native abdominal X-ray (suspicion of intestinal obstruction), CT scan of the abdomen or MR
enterography (to exclude inflammatory involvement of the small intestine) is performed. Endoscopic
examinations (esophagogastroduodenoscopy and colonoscopy) are not among the initial examinations
of chronic abdominal pain and diarrhoea. Since it often requires general anaesthesia in children, it must
be judiciously indicated by a paediatric gastroenterologist based on anamnestic data (especially the
warning signs mentioned earlier) and the above results. Histological findings are crucial for the
diagnosis of eosinophilic gastrointestinal disease (most commonly eosinophilic esophagitis with
infiltration of the oesophageal mucosa by eosinophils) and inflammatory bowel diseases (diffuse
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inflammatory involvement of the mucosa and submucosal tissue in ulcerative colitis, transmural
inflammation with ulcers, fissures, granuloma formation, and vasculitis in Crohn's disease).
A common manifestation of malabsorption is weight loss or failure to thrive. In infants, it is
most commonly encountered in short bowel syndrome (often after necrotising enterocolitis requiring
resection of part of the intestine in premature infants). Allergic enterocolitis is the result of allergy to
cow's milk proteins, especially in infants and toddlers, where the gold standard of diagnosis is the
elimination of cow's milk with the selection of an adequate substitution (formula with extensively
hydrolysed protein or amino acid mixtures) with an oral food challenge. Confirmation of the diagnosis is
the relief of symptoms and their recurrence after the reintroduction of cow's milk proteins into the diet.
Malabsorption in older children (4 years and older) is most often a manifestation of coeliac disease.
Diagnosis of this autoimmune disease involves the determination of tTGA and EmA and in selected
cases histological examination of small bowel biopsies, which is the definitive confirmation of the
diagnosis (increased number of intraepithelial lymphocytes). A wide range of selective intestinal
malabsorption (lactose intolerance, fructose intolerance, isomaltase deficiency, trehalase and others)
is called enzymopathies. These rare disorders (except lactose intolerance, which is not rare) of the
intestinal mucosa require an immunohistochemical examination of an intestinal biopsy for a correct
diagnosis. Clinically, they are mainly characterised by osmotic diarrhoea after ingestion of a specific
food component, with the disorder's resolution after its exclusion from the diet.
Inflammatory bowel involvement in inflammatory bowel disease is accompanied by increased
inflammation parameters (leucocytosis, increase in serum CRP, ferritin or erythrocyte sedimentation
rate), normochromic or sideropenic anaemia, or thrombocytosis. However, physiological laboratory
results do not definitively rule out IBD, so further monitoring should always be recommended in patients
with chronic abdominal pain or diarrhoea. In typical cases, ulcerative colitis manifests in bouts of
diarrhoea with fresh blood and mucus in the stool (imperative defecations), followed by asymptomatic
periods. In most patients with Crohn's disease, the course of the disease is chronic, intermittent with
relapses. However, an aggressive course with the formation of fistulas, abscesses, intestinal
perforations or strictures requiring surgical resection of the affected parts of the intestine is not
uncommon. Some extraintestinal manifestations affect approximately a third of children with IBD and
should be actively sought (examination of joints, perianal area, oral mucosa, etc.). These manifestations
may precede intestinal manifestations by several years. The most common is inflammatory joint
involvement (oligo- or polyarthritis, predominantly affecting the lower limbs but not excluding
spondyloarthritis and sacroiliitis). Mucosal manifestations include aphthous stomatitis and cheilitis,
cutaneous manifestations include erythema nodosum, pyoderma gangrenosum and perianal
involvement, and ocular manifestations include iridocyclitis and uveitis. Hepatobiliary manifestations in
UC are often associated with primary sclerosing cholangitis whereas CD is more commonly associated
with autoimmune hepatitis. Chronic systemic inflammation is a thrombophilic condition; therefore,
thrombotic complications may be one of the first manifestations or complications of active IBD. Other
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consequences of IBD include premature osteoporosis, hypovitaminosis B12, delayed onset of puberty
and growth disorders.
Functional GI disorders result from the individual disposition (so-called visceral hypersensitivity)
in situations of increased psychosocial stress. Currently, they are considered to be psychosomatic
diseases demonstrating the existence of a functional gut-brain axis. This group of disorders includes,
among others, functional dyspepsia and irritable bowel syndrome. In their development, an
important role is played by the child's family, classmates, or environmental overload. The diagnosis is
assessed by anamnestic fulfilment of the so-called Rome criteria, clinical examination (a thriving child
with normal somatic findings), and exclusion of relevant organic diseases (routine laboratory,
ultrasound, and other ancillary examinations). Functional abdominal pain accompanies children from
4 years of age, is usually localised in the epigastrium or around the navel and does not wake the child
from sleep. However, it significantly limits the daily activity of the child and the family, is often
accompanied by polymorphic complaints (headache, limb pain or difficulty falling asleep) and cannot be
trivialised. It is advisable to reassure the parents and the child and follow them up.
3. Therapy
(a) Gastrointestinal infectious diseases
The vast majority of GI infectious diseases do not require specific treatment. Therapy is usually only
symptomatic. It includes ensuring adequate intake of fluids that are lost due to diarrhoea, vomiting, or
fever. If the child is capable of oral intake, special oral rehydration solutions (e.g. according to WHO
or ESPGHAN) should be used. Otherwise, infusion therapy is necessary. It is also advisable to reduce
the fever with antipyretics and ensure adequate re-alimentation. In exceptional cases, targeted therapy
should be considered. It usually involves using antibiotics in certain bacterial intestinal infections,
especially if they are septic (salmonella) or occur in immunosuppressed patients (Campylobacter jejuni
infection). A particular situation is Helicobacter pylori infection, which requires combined therapy with
antibiotics and proton pump inhibitors. Concerning the population of preschool children, there is a
frequent parasitic Enterobius vermicularis infection, which is treated with mebendazole. Other parasitic
diseases are rare in our region apart from the imported ones.
(b) Inflammatory bowel disease
Unfortunately, inflammatory bowel disease (IBD) remains incurable mainly due to its as yet unclear
pathophysiology. Therefore, treating patients with these diagnoses is lifelong, multidisciplinary, and
often very challenging. It usually consists of two basic phases: the induction phase, which aims to
achieve a resting stage of the disease as soon as possible, i.e. remission, and the maintenance phase,
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where the effort is to maintain remission for as long as possible. Concerning the management of IBD,
we use a variety of treatment modalities, ranging from special diets, immunosuppressants, and
biological therapy to surgical procedures. The choice of appropriate treatment modality depends on
the disease's clinical, endoscopic, and histological activity while considering specific risk factors.
Crohn's disease
In patients with Crohn's disease (CD) in the induction phase of treatment, we currently choose a special
therapeutic diet in 70-80 % of cases. There are two options. The older, shorter, but more requiring
patient cooperation (compliance or adherence) is the exclusive enteral nutrition (EEN). In this diet,
the patient is fed only enteral nutrition products (so-called "nutridrinks"). It is not uncommon to be
administered via a nasogastric tube to ensure adequate intake. The diet lasts 6–8 weeks. The EEN
provides the complete caloric intake of the patient. Its great advantage is the absence of side effects
and its efficacy reaching up to 80% remission, comparable to corticosteroids as an alternative to dietary
treatment. Another indisputable advantage is the improvement in the patient's nutritional status. The
disadvantage remains the compliance mentioned above, as eating a monotonous diet for 6–8 weeks is
logically challenging.
Another possibility to induce remission in a patient with CD using a special diet is the so-called
Crohn's disease exclusion diet (CD-ED), consisting of three phases. The first two last six weeks each,
while the last (maintenance) phase is indefinitely long (depending on the patient's tolerance). Again,
part of the patient's energy intake is represented by enteral nutrition products (50% of the energy intake
in the 1st phase, 25% in the 2nd and 3rd phases), and the rest is precisely defined food. It is essential that
this food is fresh and a quality source of macro- and micronutrients. Semi-finished products and other
components of the so-called Western diet (fast food, etc.) are entirely excluded. Even this special diet
has an effect comparable to corticosteroids.
These are appropriate in patients who do not tolerate or refuse dietary treatment. Prednisone
or methylprednisolone is usually administered for 2–3 months. The disadvantage of corticosteroids
remains several side effects (growth retardation, alteration of bone metabolism, risk of steroid diabetes,
steroid acne, etc.); therefore, they cannot be prescribed long-term.
Biological drugs are the last treatment method used to induce remission. They are reserved for
severe forms of CD, such as the perianal form, the fistulating or stenotic disease phenotype, or in case
of severe growth retardation, where remission must be induced as soon as possible. Currently, there
are several biologic drugs with varying efficacy. The most commonly used are drugs with anti-TNF
alpha effect (infliximab and adalimumab).
In most cases, immunosuppressive treatment is required to maintain remission. The most
commonly used is the thiopurine drug azathioprine, which is in tablet form. Concerning this treatment,
it is necessary to think about possible side effects, especially bone marrow suppression, acute
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pancreatitis, or hepatopathy. An alternative to azathioprine is methotrexate, which is used less often
as it has to be administered by subcutaneous injections at the beginning of treatment, which is
particularly difficult for younger children to tolerate. While administering this immunosuppressant, it is
necessary to monitor liver and renal functions closely, as these may be altered. Biologic drugs are also
used in maintenance treatment. They are indicated when the baseline treatment (i.e. diet/corticoids +
azathioprine/methotrexate) fails, or they are continued if they have already been used in the initial
induction phase.
Other treatment modalities include surgical procedures (resection of affected segments,
treatment of perianal manifestations, etc.), anaemia treatment, nutritional support, or antibiotic treatment
of relapses.
Ulcerative colitis
The treatment of paediatric patients with ulcerative colitis (UC) is very similar to the treatment of CD, but
there are some exceptions. One of these is the absence of any therapeutic diet whose efficacy has been
validated by controlled clinical studies and is listed in official guidelines. Therefore, we have to be content
with medical treatment alone. In milder forms of UC, aminosalicylates are often used, especially
mesalamine, and less frequently sulfasalazine. They can be administered systemically, i.e. in tablets
or topically in suppositories or enemas. Aminosalicylates are used not only in the induction phase of
therapy but should be continued in the subsequent maintenance phase. Allegedly, they reduce the risk
of colorectal cancer, a severe complication of UC. Treatment of moderate to severe forms of UC is
usually expanded by corticosteroids. The administration of prednisone or methylprednisolone and the
length of treatment are the same. They can be administered intravenously or orally. If therapy with
corticosteroids fails, biologic drugs are reinstituted. Similar to CD, especially with the anti-TNF alpha
effect.
Subsequent maintenance treatment is virtually identical to CD. Regarding
immunosuppressants, azathioprine is more effective, so we choose it more often. Complementary
therapy is no different from that for Crohn's disease. Perhaps with only one exception, the lower
frequency of surgical interventions, as UC usually requires radical surgery in the form of total or subtotal
colectomy followed by pouch reconstruction.
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Unclassified IBD
Unclassified inflammatory bowel disease (IBD-U) has many features in common with ulcerative colitis.
Therefore, the therapy is based on the treatment principles of this disease.
IBD treatment modalities
Crohn’s disease Ulcerative colitis (IBD-U)
Induction phase Special diet/Corticosteroids Aminosalicylates
Biologic drugs Corticosteroids
Biologic drugs
Maintenance phase Azathioprine/Methotrexate Aminosalicylates
Biologic drugs Azathioprine/(Methotrexate)
Biologic drugs
(c) Malabsorption syndrome
Coeliac disease
The only currently available effective therapy for coeliac disease is a gluten-free diet. Gluten is a protein
complex found in cereals (wheat, barley, and rye). Oats are different. Their proteins are not so
immunologically active, so they are tolerated by up to 95% of coeliac patients. However, secondary
contamination of oats is a common problem in our conditions, so they are generally not recommended
for these patients and, if so, only from reliably uncontaminated preparations and only after disease
remission. Gluten is a significant component of the food industry. It is found in hidden form in several
foodstuffs, so the patient must know the exact composition of each dish. We consider fruit and
vegetables, meat, rice, and legumes or nuts naturally gluten-free. Due to the atrophy of the intestinal
mucosa, a secondary lactase deficiency is often present at the beginning of the disease. Therefore, it is
necessary to recommend a lactose-free diet temporarily.
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(d) Functional GI disorders and others
Irritable bowel syndrome
The therapy of the gastrointestinal tract's functional disorders is very complex and requires a
comprehensive approach. The mental state of the patients plays a crucial role. Therefore, educating
them about the natural history of the disease is as imperative as reassuring them that no danger arises
from their problems. In many cases, cooperation with psychologists is necessary. Empirically, some
patients find various dietary measures helpful. Often a lactose-free diet and a so-called low FODMAP
diet are effective. The latter is a diet restricting fermentable oligosaccharides, poorly absorbed in the
intestine and fermented by intestinal bacteria; this can lead to the typical symptomatology of irritable
bowel syndrome. Sometimes, spasmolytics (e.g. mebeverine, drotaverine, etc.), deflators (e.g.
simethicone), or antidiarrhoeals (e.g. loperamide) are used symptomatically. In some patients, an
appointment with a psychiatrist and the administration of antidepressants are necessary.
Eosinophilic gastrointestinal disease
The treatment of eosinophilic gastrointestinal disease (EGID) is best defined in its most common type,
which is eosinophilic esophagitis (EoE). However, it is very similar to other forms of EGID. The treatment
of eosinophilic esophagitis rests on three pillars: proton pump inhibitors, an elimination diet, and
corticosteroids. The effect of proton pump inhibitors in oesophageal eosinophilia is not completely
clear. However, given the increased presence of eosinophils in oesophageal biopsies in patients with
gastroesophageal reflux disease (GERD), and thus an inevitable overlap between EoE and GERD, they
are an essential part of every patient's therapy.
Since EoE is a manifestation of food allergy, it can be assumed that the disease will cease to
be active once the causative allergen is removed. However, the identification of this allergen remains a
problem. Laboratory and other ancillary examinations are often unfavourable due to the combined
immunopathological reaction (IgE and non-IgE mechanisms). Particularly in younger patients, it is
sometimes difficult to identify which food is causing the problem, so special diets have been formulated
to exclude the most common triggers of this disease from the patient's diet. In our conditions, we prefer
the so-called 6-food or 4-food diet. The 6-food elimination diet removes dairy products, wheat, gluten,
soy, eggs, and fish, while the 4-food elimination diet removes dairy products, eggs, soy, and wheat from
the diet. Subsequently, individual foodstuffs are gradually reintroduced into the diet with histological
control by oesophageal biopsy.
The third treatment modality is corticosteroids, which ensure rapid remission induction. We mainly
choose topical forms, especially budesonide or fluticasone. In severe forms, systemic corticoids can
be administered.
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4. Complications and prognosis of the most common GI
diseases
The most common complication of acute diarrhoea in children is isoosmolar dehydration. Infants and
toddlers are especially at risk. In young children with high fever in acute diarrhoeal diseases, febrile
convulsions are not uncommon. A fearful complication of some intestinal infections is the haemolytic
uremic syndrome, typical of infections caused by Shiga toxin produced by E. coli but also described in
infections caused by certain Shigella or Campylobacter species. A relatively common complication of
intestinal infections is transient parainfectious hepatopathy manifested by increased transaminases
(especially with rotavirus and campylobacteriosis). Salmonellosis or campylobacteriosis, especially in
immunosuppressed children, may be accompanied by extraintestinal complications (sepsis or
meningitis, endocarditis, abscesses, osteomyelitis, etc.). Immune-mediated complications are
relatively rare in children (erythema nodosum after salmonellosis, campylobacteriosis or yersiniosis,
aseptic arthritis, acute Guillain-Barré polyradiculoneuritis after campylobacteriosis). With adequate
rehydration, infectious gastroenteritis in childhood is usually a self-limiting disease with a good
prognosis. The most common complication is post-enteritis syndrome with transient hypolactasia,
which requires the temporary restriction of dietary lactose intake. Complicated cases of acute
gastroenteritis and enterocolitis are more common in children with other underlying diseases (e.g.
primary immunodeficiency, secondary immunosuppression after oncological or autoimmune disease
treatment, psychomotor retardation in cerebral palsy, or cystic fibrosis).
(a) Coeliac disease
Coeliac disease is a lifelong condition often associated with the manifestation of other
autoimmune diseases during life (10–30 times more common than in the general population). The most
frequent are autoimmune thyroiditis (more than 10%) and type 1 diabetes mellitus (4.1%).
Therefore, these complications in patients with coeliac disease should be actively looked for during
regular check-ups. Other disorders associated with coeliac disease include autoimmune hepatitis,
sclerosing cholangitis, primary biliary cirrhosis, systemic lupus erythematosus, Sjögren's syndrome, and
connective tissue diseases, myasthenia gravis, juvenile rheumatoid arthritis, polymyositis, IgA
nephropathy, interstitial pulmonary fibrosis, idiopathic pulmonary hemosiderosis, sarcoidosis, and
microscopic colitis. The predominant symptoms before the diagnosis of coeliac disease may be
metabolic osteopathy and neuropsychiatric manifestations (idiopathic ataxia, behavioural disturbances,
and depression). A severe complication of coeliac disease is a refractory coeliac disease that does
not respond to treatment with an elimination gluten-free diet. Risk factors for its development are
intestinal mucosal atrophy, weight loss, and some of the associated autoimmune diseases mentioned
above. The most severe late complication of coeliac disease is cancer, which affects coeliac patients
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1.3 times more often than the general population. It is predominantly non-Hodgkin's B-lymphoma or
T-lymphoma, which develops as a late complication of coeliac disease in 8–10% of cases. Coeliac
patients also have a higher risk of developing small intestine, oesophagus, and pharynx cancer. The
risk of complications in coeliac patients is inversely proportional to adherence to a gluten-free diet, which
must be lifelong.
(b) Inflammatory bowel disease
Complications of Crohn's disease in children include the formation of abscesses, fistulas with
adhesions, strictures and resulting intestinal obstructions. In ulcerative colitis, a severe complication
is the development of toxic megacolon. This condition is associated with the risk of perforation, sepsis,
electrolyte disturbances and bleeding, requiring immediate surgical intervention. Compared to healthy
children, paediatric patients with IBD have a significantly higher risk of developing a malignant disease,
including small intestine adenocarcinoma and colon cancer. Malnutrition and lack of physical activity in
children with IBD, together with long-term corticosteroid treatment, often contribute to the development
of osteopenia. Chronic malnutrition results in a reduced growth rate and delayed sexual maturation.
The complexity of these complications is a significant stressor, which is why children with IBD are often
associated with anxiety and depressive disorders accompanied by antisocial and addictive behaviour.
IBD is a serious lifelong illness that significantly reduces the quality of life of the affected child and their
parents, and psychological or psychiatric care is an integral part of disease management. Adherence to
treatment and long-term follow-up for early detection of relapses are determining factors in the prognosis
of IBD patients.
(c) Eosinophilic gastrointestinal disease
The risk of a late recognised or inadequately treated eosinophilic disease of the gastrointestinal
tract lies mainly in the transition to the fibrostenosis stage with the development of irreversible
strictures (most often oesophageal strictures). The prevention of this complication is to achieve and
maintain remission of the disease with adequate treatment with the three modalities mentioned above.
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