Mistakes in ... 2021 - 8

ueg education
Mistakes in... 2020
the CDED, is a whole food diet that mimics the
nutritional components of EEN as far as possible,
but offers diverse food and drink options and as
such offers a far more palatable and acceptable
therapy for patients.14
PEN strategies may
be used as a step-down therapy following
completion of EEN and the specific whole food
diets mentioned offer a potential option for
long-term maintenance therapy, especially where
avoidance of immunosuppressant medications is
desired and/or malnutrition is a concern. Further
research on the extended utility of such dietary
therapies is underway.
Bottom line: Unless tailored expertise in the
provision of whole food diets is available, it
is important to achieve maximum efficacy by
emphasising the initial E in EEN!
Mistake 3 Confining EEN to initial
induction therapy for mild-moderate
luminal small-bowel Crohn's disease
Historical practice has limited EEN use to
active small-bowel disease, but it has proven
efficacy regardless of the intestinal site of luminal
involvement. As such, the use of EEN should be
considered for all disease locations. There is also
growing evidence for its use in perianal disease
as an adjunct therapy.4,15
Furthermore, there is
increasing evidence of efficacy for EEN in the
management of exacerbations of Crohn's disease
distinct from its use at diagnosis, with repeat
courses as effective as initial courses.16,17
There is growing support for the use of
perioperative EEN in Crohn's disease; however,
large RCTs are currently lacking.18,19
The pooled,
mainly retrospective, data available indicates that
2-6 weeks of preoperative EEN markedly reduces
postoperative complications versus standard
nutritional care, particularly for those who have
more severe disease.
One of the best illustrations of the benefit of
preoperative EEN is a case-control study of 114
adult Crohn's disease patients with stricturing
or penetrating complications.20
Those who were
given a mean duration of 6 weeks of preoperative
oral EEN therapy had significantly reduced CRP
values and intraoperative times, and a ninefold
reduction in the incidence of postoperative
abscess and/or anastomotic leak. Furthermore,
25% of the EEN group avoided surgery and
were bridged to medical therapy. However, no
statistically significant differences were seen in
readmission or recurrence rates at 12 months in
those who underwent surgery.
A large but unmatched retrospective study
(498 patients; 219 treated with EEN for 4 weeks)
showed a significant reduction of postoperative
complications, rates of stoma creation, and
need for urgent operations for patients given
preoperative EEN.21
Clearly, more robust data
is sought after but it is likely that by improving
26
nutritional status and reducing the inflammatory
burden preoperative EEN improves surgical
outcomes in Crohn's disease patients.
Bottom line: EEN is effective for all disease
locations, in complicated disease, as a
preoperative preparation and can be used for
both induction and subsequent treatment
courses in Crohn's disease.
Mistake 4 Assuming dietary therapies
improve short-term outcomes and patient
well-being only but not other key IBD
targets including markers of remission
and mucosal healing
EEN therapy is associated with benefits over
and above QoL measures and 'hits' many
contemporary Crohn's disease treatment targets.
Marked improvements in biomarkers of disease
activity, including CRP, ESR and albumin, are well
established. More importantly, significant rates of
mucosal healing have been demonstrated with EEN
induction therapy. A prospective paediatric cohort
study from Australia reported an early endoscopic
response in 58% of patients, and 1/3 had complete
transmural healing on small-bowel imaging after
8 weeks of treatment. Similarly designed European
studies have shown that EEN confers superior
mucosal healing rates to steroids when compared
in RCTs.5,6
Concordantly, faecal calprotectin levels
have been shown to decline by approximately 50%
following completion of an EEN course.22
There is growing evidence that EEN
achieves such results through modulation of the
pro-inflammatory state, plus improved epithelial
barrier function and gut dysbiosis, which are
potential key components in the pathogenesis of
IBD.23
Clinical studies show there is a return to a
more 'normal' inflammasome with EEN, based
on microRNA expression indices and down
regulation of inflammatory cytokine signalling,
including from IL-1β, IL-1ra, IL-6, IL-8 and TNF-α.24
It is clear that the microbiome is significantly
altered within days of commencing EEN and how
these changes impact the pro-inflammatory state
are being studied in detail.25
Bottom line: Being aware of the many 'gains'
associated with EEN at both the patient and
mucosal level is essential for the treating team
and for patients and families alike to improve
understanding, uptake, adherence and ultimately
patient outcomes.
Mistake 5 Recommending dietary
restrictions based on limited evidence -
exaggerating the role of food additives
and emulsifiers
Epidemiological and preclinical investigations
have implicated certain food additives, especially
emulsifiers, in the aetiology of IBD. Work in animal
Mistake 6 Assuming diets linked to IBD in
epidemiological studies match up with
those that should be used for dietary
treatment
There is increasing evidence around the
role of diet in the pathogenesis of IBD and the
development of specific exclusion diets as
therapeutic tools. However, there is danger
in prescribing dietary restrictions based on
evidence that is not derived from well-controlled,
interventional, human studies.32,33
models and in vitro suggests food additives may
impair gut health through alterations in the
microbiome, barrier function and gut-based
immune signalling.26,27
Carrageenan, a polysaccharide commonly
used as a food additive, induced an inflammatory
response in experimental models.28,29
also implicated emulsifiers in producing colitis
in mice.30
As such, dietary recommendations and
exclusions have migrated into real-world practice.
However, few convincing studies have established
a causative or exacerbating role for such food
additives in IBD in humans. Rather, recent
in-depth compositional analysis of EEN, in view of
its well-established efficacy in the treatment of IBD,
suggests that such ingredients, at the levels present
in formula, are unlikely to have a significant role at
least as triggers for exacerbation of IBD.31
Food additives implicated in Crohn's disease
aetiology are present in EEN formulas to
varying degrees, and include modified starches
(in 100% of formulas tested), carrageenan (in
22%), carboxymethyl cellulose (in 13%) and
polysorbate 80 (in 5%).31
Others have
Remission rates did not
differ between patients given EEN formulas with
and without those food additives. While such
evidence is clearly not definitive, this research,
along with other work in the area, emphasises the
need for well-conducted in vivo human studies
before wide-ranging dietary interventions are
recommended in clinical practice.
Bottom line: Unnecessary dietary restrictions
negatively impact on a patient's food-related
quality of life. Any restrictions must be based
on validation in IBD patients and not simply on
the translation of epidemiological or laboratorybased
work.
Macronutrients
including fibre, polyunsaturated fatty acids
(PUFAs) and meat protein have been implicated in
IBD, but dietary interventions based around these
elements have not proven successful in mitigating
the disease.34
For instance, a recent systematic review of
23 RCTs involving dietary interventions with
fibre failed to show any significant efficacy in
improving disease outcomes.35
Also, 80% of
formulas investigated in the EEN composition
study contained essentially no fibre.31
Fish
consumption and dietary intake of omega-3 fatty
Mistakes in ... 2021

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