Body Composition in Pediatric Inflammatory Bowel Disease

Abstract

Malnutrition and assessment of body composition is an important topic in inflammatory bowel disease. The pathomechanism of malnutrition is complex and related to anorexia, abnormal digestion, malabsorption, and chronic inflammation. Anthropometric parameters and BMI are not precise to reflect the nutritional status. Meanwhile, recent studies emphasize that low fat-free mass, especially, sarcopenia is associated with a worse prognosis, such as an increased risk for surgery, biological therapy, and disease complications. On the other hand, obesity and increased fat mass are also associated with poor outcomes in patients with inflammatory bowel disease. Furthermore, the dosage of some drugs may need adjustment in the case of obese patients with inflammatory bowel disease.

1. Introduction

Malnutrition has always been the focus of inflammatory bowel disease [IBD] management. Nowadays, it has gained even more attention as we learned more about body composition. Malnutrition and impaired body composition are significantly contributed to unmeasured morbidity in IBD. Altered body composition may influence the course of the illness, response to therapies, outcomes of surgery, and quality of life [QoL].

However, the practice of calculating body mass index [BMI] may fail, since a deficit of lean mass can be masked by fat mass [FM]. Advanced techniques should be used to discover the alteration of body composition. Body composition analysis divides the body into compartments of lean mass and fat mass.

Multiple factors are responsible for the alteration of body composition. Chronic inflammatory activity modifies nutrient utilization, malabsorption, decreased appetite, and physical activity also contribute to the loss of the metabolically active fat-free mass [FFM]. IBD is associated with impaired body composition including reduced bone density and skeletal muscle mass. Furthermore, as obesity becomes widespread, the role of adipose tissue in the inflammatory process has been recognized also in patients with IBD.

Clinical awareness of body composition and appropriate management are a highlight to improve disease outcomes and QoL of patients with IBD.

2. Malnutrition in inflammatory bowel disease

Malnutrition can be defined as “a state resulting from lack of intake or uptake of nutrition that leads to altered body composition (decreased FFM) and body cell mass leading to diminished physical and mental function and impaired clinical outcome from disease” [1]. Malnutrition is related with poor prognosis, impaired body composition, physical and emotional well-being, QoL, and body form. Altered body composition, such as loss of FFM or skeletal muscle mass (SMM), has been demonstrated even in the case of normal BMI.

The IBD itself and its treatment (e.g. systemic corticosteroids) influence the nutritional status and body composition through several mechanisms. First, reduced appetite, nausea, and abdominal pain result in reduced energy and nutrient intake. Micronutrient and vitamin deficiencies along with inflammatory cytokines can impair taste sensation that can contribute to anorexia. Second, diarrhea and malabsorption contribute to the loss of nutrients due to impaired epithelial integrity, bacterial overgrowth, and reduction of absorptive surfaces (intestinal resection, enteric fistulas). Third, inflammatory cytokines (IL-1, TNF- α, IL-6) alter energy metabolism, protein turnover, and increase energy requirements, thus they exert an effect on body composition and trigger signs of cachexia, such as anorexia, and loss of skeletal muscle mass [2]. In addition, patients with chronic gastrointestinal symptoms often start restrictive diets that may increase the risk of malnutrition [3]. Finally, low physical activity due to fatigue and active symptoms can also impact body composition. Regarding the medications, it is well-known, that glucocorticoid therapy is associated with an increase in FM and has catabolic effect on lean mass, meanwhile anti-TNF seems to be effective also in the improvement of FFM. Additionally, anorexigenic side effects of some medications may also complicate the problem of undernutrition in IBD (Figure 1) [4].

Figure 1.

Pathophysiological factors leading to impaired body composition in patients with inflammatory bowel disease.

Body composition includes also fat compartments that can be divided into subcutaneous and visceral fat. Mesenteric adipose tissue belonging to visceral fat has an important role in the regulation of inflammatory processes due to the production of several pro-inflammatory cytokines and mediators. Adipose tissue due to its pro-inflammatory nature and loss of SMM are both associated with poor outcomes in IBD independently from each other. Meanwhile, skeletal muscle releasing anti-inflammatory cytokines (myokines, IL-15) may be protective against poor outcomes [5].

3. Body composition and its measurement

Earlier, BMI was essential in the assessment of nutritional status, however, evidence suggests, that BMI is not precise enough. Although BMI is a useful anthropometric parameter, it is not able to discriminate between excess body fat and increased lean mass [6]. Some studies in IBD patients highlighted that alteration in body parameters, mostly reduced lean mass, despite normal BMI [7].

In everyday practice to evaluate body composition the two-component model is still the most widely used model of body composition (Figure 2). The two-component model differentiates the body into FM (which consists of the visceral and subcutaneous adipose tissue), and FFM, (active metabolizer part of the body). FFM consists of the total body water (including intra- and extracellular water), total body mineral (mainly bone tissue) and protein, and essential lipids (involved in cellular physiology, e.g. phospholipids). Lean body mass (LBM) is frequently used as a synonym for FFM. However, theoretically lean body mass is composed of total body water and mineral, proteins, but not essential lipid components [8]. The weight of essential lipids is negligible, and FFM and LM are applicable to characterize the metabolically active part of the body. A third important compartment is skeletal muscle mass (SMM) included in FFM and LBM, which is also an essential parameter to characterize body composition and sarcopenia in IBD. In contrast to the two-component model, multicomponent models minimize the assumptions, rather they measure each component separately [9]. The three-component model divides body weight into fat-free dry tissue, fat, water. The four-component model separates fat-free dry tissue into protein and mineral [9].

Figure 2.

Two-component model of body composition.

LBM has several functions, and LBM deficits are associated with morbidity via loss of muscle mass and strength, and altered metabolism. In addition, LBM has an important role in the regulation of bone mass, by applying stress to bones, additionally. In contrast, an increase in fat mass is associated with elevated inflammatory markers [10].

3.1 Regulation of body composition compartments

Body composition is influenced by several factors like geography, ethnicity, age, sex. Furthermore, body composition compartments are in interaction with each other throughout hormonal regulation and cell-signaling networks [11]. Pathological conditions can modulate the balance leading to altered body composition.

Adipose tissue takes part in the regulation of metabolism, but is also known to produce pro-inflammatory cytokines. Mesenterial visceral fat (“creeping fat”) has a special role in IBD, especially in CD. Visceral fat releases adipokines (leptin and resistin) and pro-inflammatory cytokines (TNF-α, IFN-γ, IL-6, IL-1). Bacterial lipopolysaccharides induce resistin production, which promotes the secretion of TNF-α and IL-12, activates mononuclear cells, and interact with bone mass, as well. Leptin induces mononuclear and CD4+ T cells and promotes the development of Th1 response.

As mentioned above bone mass is influenced by resistin, which increases the number of osteoclasts, leading to loss of bone mass. Adiponectin also exerts a negative effect on bone mass. In addition, it is well-documented that the bone mass is also affected by chronic inflammation that alters the balance between osteoblasts and osteoclasts via TNF-α, IL-1, and IL-6 [11].

As an important component of FFM, the SMM takes part in the metabolism of glucose and protein metabolism. Furthermore, SMM and physical activity can increase bone mineral density and induce the production of anti-inflammatory cytokines and myokines [12]. In chronic inflammation, the elevated TNF-α and IL-6 induce protein degradation and reduction of myofibrillar proteins via growth hormone resistance in the liver and muscles.

3.2 Assessment of body composition

Anthropometrical parameters such as weight, height, BMI, and body circumferences are essential to assess nutritional status and body composition. However, in clinical practice, impaired body composition often remains unrecognized if only BMI is used. A few studies have demonstrated that BMI is not sensitive to detect a low lean mass, especially since it does not indicate sarcopenia in the case of co-existing obesity (sarcopenic obesity) [4, 13]. The detailed characterization of body composition compartments is only feasible with special techniques. Numerous non-invasive techniques are available to assess body composition for clinical and research purposes. Certainly, all of them have their advantages and disadvantages.

Skinfold thickness measurement is an easy and inexpensive method for assessing fat mass in clinical practice, however, the ratio of subcutaneous and total body fat remains uncertain. Dual-energy x-ray absorptiometry (DEXA) is also a widespread and at the same time reliable tool to estimate lean and fat mass, and bone density. Though, it is expensive and works with radiation exposure [14].

Bioelectrical impedance analysis (BIA) is another non-invasive, safe, easy-to-use method, that can be applied bedside. The theoretical base of BIA is that hydrated tissues conduct electricity and different tissues have different electrical conductivity. The impedance characterizes the resistance level of the tissues. BIA provides data about the weighted sum of extra- and intracellular water. Different empirical equations are applied to calculate FFM [15].

Quantitative CT (qCT) and MRI can be also useful methods to measure body composition, precise quantitative and qualitative information can be achieved about body composition, however, due to high-cost, and the need for expert knowledge, its everyday use may be limited. Furthermore, the high dose of radiation is also a disadvantage of CT.

Other methods like total body potassium (using ⁴⁰K isotope), neutron activation, total body plethysmography, isotope dilution (D₂O dilution or ¹⁸O), and MRI are reliable and extremely precise, however, these methods need special equipment with special knowledge and experience, furthermore, are expensive [9].

4. Body composition of patients with IBD

4.1 Crohn’s disease compared to healthy population

In a systematic review based on 17 studies, the body composition of 631 CD patients was compared to age-and sex-matched controls [4]. The results were heterogeneous due to variable techniques of body composition measurement, variable study sizes, small control groups, and the lack of standardization of patients according to disease duration, localization, therapy (glucocorticoids), diet, and exercise. BMI was reduced in 37% of patients (n = 233), but it was not statistically different from controls in 63% of patients (n = 398). None of the included studies reported any obese or overweight patients based on BMI. A total of 4% of CD patients were underweight (BMI < 20 kg/m²).

In addition to BMI, FFM and FM were also compared in patients and healthy controls in the same systematic review [4]. The FM and FFM were not statistically different from controls in 65 and 66% of patients (n = 394, n = 419, respectively). Meanwhile, the FFM was reduced in 28% of CD subjects compared to controls, and 31% of patients with CD (n = 192) had a statistically significant reduction in FM, and 3% were reported to have increased FM relative to controls (n = 20). It is of note, that patients in remission and in relapse were not separated in these comparisons [4].

4.2 Ulcerative colitis

A systematic review of eight studies suggested that the decrease in BMI, FFM, FM are more frequent in patients with CD than in UC patients [4]. The findings of the study including 295 UC patients were heterogenous. BMI was described not statistically different compared to controls in 68% of UC patients (n = 199). Although 20% of UC patients had reduced BMI (n = 60). In contrast to CD, no patients with UC were reported to be underweight.

In this systematic review, FFM was not reported as statistically different compared to controls in 86% of UC patients (n = 256). FFM was reduced compared with healthy controls in 13% of patients studied (n = 39). In 75% of UC patients (n = 220), FM was not found to be statistically different, only 13% of patients experienced reduced FM (n = 39), and 12% of patients had increased FM compared to controls (n = 36) [4].

4.3 Body composition in children with IBD

Lean tissue deficit is also well-documented in children with IBD, especially in the case of CD. Houtto et al. recently published a systematic review of body composition in children with IBD [3]. They included 1461 patients with CD and a total of 264 patients with UC. Growth, FM and FFM were statistically lower in pediatric CD than reference values or healthy cohorts. The results in children with UC were more variable, some studies reported decreased, others found similar body composition parameters as in controls. It is of note, that in a 24-months follow-up study, Thayu et al. reported the body composition of newly diagnosed IBD patients [16]. By the end of the follow-up, patients achieved remission, though LBM was still reduced in girls compared to controls. Dubner et al. also found that the LBM deficit persisted for 12 months [17].

Besides LBM, FM did not differ significantly in pediatric IBD patients when compared with reference or control values, based on the systematic review of Thangarajah et al. [18]. However, patients were receiving concomitant steroid therapy in most of the studies reporting no difference in FM. There is a lack of long-term follow-up studies investigating FM, Boot et al. showed deficits of FM in all the included CD patients with longer disease duration (mean 2.2 years) [19]. Comparing the body composition of children with CD and UC, some studies did not show any difference in deficits in LBM, meanwhile, FM was lower in CD than UC [18].

4.4 Factors influencing body composition

Though it is known that impaired body composition is related to decreased nutrient intake, nutrient loss, and chronic inflammation, there are some factors that influence the body composition in patients with IBD: (1) sex; (2) disease activity; (3) disease duration; (4) disease localization; (5) medication; (6) smoking [4].

Sex: Body composition of healthy women and men are different. In IBD, body composition is associated with sex according to some studies, though the results are heterogenous. According to the systematic review of Bryant et al., two studies reported lower FFM in both males and females compared to controls [4]. Meanwhile, two other studies found deficits in FFM only in males. In addition, Ulivieri et al. reported that females with UC had decreased FFM compared with controls. Regarding FM, the results were heterogenous, and no trends based on sex could be determined [20].

Disease activity: Body composition is associated with disease activity. According to a recent systematic review, BMI of CD patients was lower in the active disease group compared to patients in remission. Moreover, several studies, though with heterogenous methodology, have proved that patients with active disease have lower lean mass and FM than patients in remission [10]. In a systematic review, Thangarajah et al. demonstrated that lean mass deficit is present in children with active CD and half of the children with active UC [18]. Body fat deficits are associated with undernourishment in active CD, however, in remission body fat recovers. It is of note, that lean mass deficit was still reported in at least half of children with IBD in remission [18].

Disease duration: Persisting chronic inflammation has a role in the modulation of body composition due to altered metabolism, however, the results of studies investigating the association between disease duration and body composition, are inconsistent [4, 18]. In case of children, lean mass and FM seem to recover in IBD after diagnosis, however, deficits in lean mass may persist even when the disease is quiescent [18]. Body composition may be not influenced by the disease duration itself, but by the disease course since diagnosis. Initially, most patients with severe disease activity have impaired body composition, later, due to the treatment most patients reach remission, and parallelly body composition is also restored, though partially. Furthermore, patients with refractory disease or recurring disease activity may have persistent changes in their body composition. The studies analyzing this question included heterogenic patients regarding disease course and treatment, so it is not possible to draw any conclusion.

Disease localization: Patients with small intestinal CD experience malabsorption, protein losing enteropathy that has a greater impact on body composition than a short segment inflammation in ulcerative proctitis. Only a few studies analyzed the relationship between disease extension and body composition. Interestingly, FFM did not differ among ileal, ileocolonic, and colonic CD patients in remission [21]. However, FM was significantly lower in CD patients with ileal and ileocolonic disease. Other studies did not report any association between disease localization and body composition [4].

Medication: There are some medications applied in IBD that are related to changes in body composition. One of the most important is glucocorticoids that cause muscle atrophy and lower bone density. Several studies have demonstrated that glucocorticoids decrease bone mineral density in CD patients. Interestingly, in UC patients Ulivieri et al. found a negative correlation between bone density and steroid treatment only in females [22]. Furthermore, patients receiving corticosteroid therapy had lower FFM compared to those without current steroid treatment [23]. The FM was also associated with glucocorticoid treatment, though FM was increased in females, but not in males. In pediatric CD, exclusive enteral nutrition is recommended for induction instead of corticosteroids. During 6-week exclusive enteral nutrition, FFM improved significantly in children with CD, though fat mass did not change [24]. Furthermore, during anti-TNF therapy lean mass increased both in children and in adults, though FM increased only in adults [25, 26].

Smoking: Though smoking is known to be associated with altered body composition and is an important negative prognostic factor in CD, there is only a few data on smoking and body composition in IBD. Most studies record the smoking status of included patients but did not investigate the effect of smoking on body composition. One study found that smoking was a significant predictor of a reduced BMI, FFM, FM in CD [23].

5. Sarcopenia

The term ‘sarcopenia’ was first applied by Rosenberg to describe the decrease in skeletal muscle mass experienced during aging. According to the recent recommendation of the European Working Group on Sarcopenia in Older People [EWGSOP], sarcopenia can be diagnosed if low lean muscle mass stands together with either low muscle strength or low physical performance [27, 28].

To diagnose sarcopenia according to the current definition, both the mass and the function of the skeletal muscle are to be evaluated. Numerous methods are applied to assess the muscle mass, including BIA, DEXA, CT, and MRI. Functionally, the handgrip strength test with a standard dynamometer or a physical performance test are the gold standard [28].

Recently, the literature demonstrated a correlation between loss of muscle mass in IBD patients with several negative outcomes, such as fatigue, reduced strength, decreased QoL, and increased morbidity [10]. In addition, sarcopenia is considered as a prognostic factor in IBD, like in a variety of other chronic conditions.

The frequency of sarcopenia in IBD varies due to the heterogeneity of the included patient cohorts and the modality used to measure muscle mass. The incidence of sarcopenia was 52% in CD and 37% in UC in a recent systematic review [29]. Notably, in this report, sarcopenia was defined as the reduced muscle mass without functional strength. Data on muscle strength are scarce in IBD patients. Most studies apply hand grip for functional assessments, and they found that IBD patients had lower maximal isometric grip strengths compared to healthy, age,- and sex-matched controls [10]. This was also detected in pediatric CD, but not in UC [30].

Sarcopenia seems to be associated with disease activity via malnutrition and the catabolic effect of inflammation. MRI can be applied to assess sarcopenia. A single cross-sectional MR image at the L3 level for segmentation of skeletal muscle, visceral fat, and subcutaneous adipose tissue areas is used to calculate body composition parameters. The skeletal muscle index [SMI] meaning the ratio of the area of skeletal muscle to the height squared. Labarthe et al. reported that sarcopenia [defined as SMI <38.9 cm²/m² for females and SMI <54.4 cm²/m² in males] was less frequent in patients with inactive CD compared than in patients with active disease [31]. However, 50–60% of patients in remission also suffer from sarcopenia [10].

The distribution of sarcopenia may differ along the body. In a case control study including 23 female UC patients, quadriceps muscle strength was significantly reduced compared with controls and UC patients were significantly slower than controls at the sit-up test. However, the hand grip test did not differ significantly [32]. This finding may indicate assessing muscle functionality with different tests.

To prevent or reduce sarcopenia physical activity with nutritional therapy should be recommended. However, Subramaniam et al. reported an increase in muscle volume and strength at 25 weeks following the commencement of anti-TNF therapy in patients with CD, suggesting that the control of chronic inflammation is also important to overcome sarcopenia [33].

Sarcopenia is certainly an emerging area of interest, given its potential negative effect, and the potential for increased clinical awareness and appropriate management of sarcopenia to improve outcomes and QoL [4].

6. Obesity the impact of obesity in inflammatory bowel disease

Besides the relationship between IBD and undernutrition, there is emerging evidence on the association of obesity with IBD. As obesity rises in the general population, simultaneously the prevalence of obesity is growing in the IBD population. Inflammation is at the core of IBD pathomechanism, and obesity which is a pro-inflammatory status, may also exert an effect on the disease course and severity. It is widely documented that visceral adipose tissue has a role in immunologic dysregulation underlying IBD, known as creeping fat in CD patients. However, data are contradictory regarding the impact of obesity on the frequency of IBD and the disease course [34].

Risk of IBD and obesity First of all, the results of large population-based studies analyzing the association between obesity and IBD are discordant. Based on a recently published pooled analysis of five prospective cohort studies, among 601,009 participants with 10,110,018 person-years of follow-up, 563 incident cases of CD and 1047 incident cases of UC were reported. Obesity was associated with an increased risk of CD compared with normal BMI, meanwhile, no associations were observed between measures of obesity and risk of UC [35].

Frequency of obesity in IBD The rate of obesity in adult CD patients is 8–18% (BMI ≥ 30) in Western countries. Studies in pediatric IBD showed that obesity occurred in 23.6% of CD patients and 30.1% of UC patients [36]. In children with newly diagnosed IBD, the frequency of obesity was 2.28% in CD and 5.48% in UC based on BMI [37].

Obesity and disease activity It is also debated whether obesity influences disease activity and disease course. Some studies suggested that obese CD patients have lower disease activity. CD patients with BMI > 30 kg/m² were more likely to experience an IBD flare-up than patients with normal BMI. The occurrence of structuring and penetrating complications in obese patients with CD is contradictory. Similarly, overweight (BMI > 25 kg/m²) UC patients had more frequency of relapse than patients with normal weight. Additionally, obesity was associated with higher rates of colectomy in UC [4, 34].

Response to therapy Obesity is also related to response to therapy. On one hand, through its role in inflammatory processes, obesity manipulates the pharmacodynamics of medical treatments, on the other hand, the accumulated fat mass may also influence the pharmacokinetics of some drugs. Subtherapeutic levels of metabolites of azathioprine were documented approximately two times more in patients with BMI > 25 kg/m² or BMI > 30 kg/m² than in participants with normal weight [34]. Additionally, a higher BMI has been shown to be associated with the need for dose escalation of adalimumab in CD patients [38]. Furthermore, some studies demonstrated that CD patients on adalimumab or golimumab had higher rates of disease-related hospitalization and operative care compared to infliximab. The explanation for this result is probably the fact that the infliximab dose is adjusted according to weight and intravenously given, whereas adalimumab and golimumab are administered in a fixed dose subcutaneously. Though this was not confirmed in a retrospective study of pediatric IBD patients [34].

Obesity and IBD-related surgeries Higher BMI were also reported to have a negative impact on surgical outcomes in patients with IBD. Intrasurgical complications are mainly related to anatomical difficulties caused by fat tissue [34]. Additionally, obesity may increase the risk of post-surgical morbidity and mortality. According to a recently published meta-analysis, obese patients had longer operative times, higher intra-operative blood loss, longer length of stay, higher wound infection rates, conversion to laparotomy, and higher total postoperative complication rates [39, 40]. Furthermore, post-surgical complications in a nationwide study of hospitalized IBD patients reported that there was no variation in cardiovascular complications, perforations, venous thromboembolism, or death when comparing obese with nonobese patients [34].

Regardless of all controversies, the impact of obesity on the progression of IBDs to further consequences is undeniable [34].

7. Burden of altered body composition

Quality of life: Body composition may affect the quality of life in patients with IBD. As it is known that obese patients have lower QoL compared to healthy populations, and patients with sarcopenia may have lower QoL due to their limited daily activities. Only one study examined this question in adults and did not find any relationship, between altered body composition and QoL, these data are similar to the findings of studies in children [4, 25, 30].

Response to treatment: Body composition can influence treatment response via different mechanisms, such as pharmacokinetics. There are some data on decreased lean mass and response to anti-TNF treatment. Lower skeletal muscle mass was associated with primary non-response to anti-TNF in CD patients [41]. Furthermore, in a retrospective study, CD patients with lower SMM experienced shorter median time to anti-TNF failure defined as treatment escalation, post-induction hospitalization, surgery, and new perianal fistula. In addition, Csontos et al. demonstrated an inverse correlation between FFM index and adalimumab trough levels [42]. Interestingly, not only SMM but also FM is associated with the response to anti-TNF treatment. Lim et al. investigated the correlation between body composition measured by CT/MRI scans and trough levels of anti-TNF treatment in a cross-sectional study. They reported higher rate of secondary loss of response to adalimumab in patients with increased total adipose area and an inverse association infliximab trough level and between visceral fat area [43]. Several studies showed that patients on anti-TNF treatment experienced catch-up growth [3]. Data on the impact of body composition on response to new biologicals and small molecules are scarce. However, one study reported that obesity did not influence the efficacy and safety of tofacitinib in UC patients [44].

Prognosis and complications: Changes in body composition has been documented to be associated with complicated CD, increased post-operative complications, and decreased efficacy of medical therapy [10].

8. Recommendation for practice

The association between impaired body composition in IBD such as sarcopenia and increased adiposity and poor clinical outcomes highlights the importance of routine nutritional screening in the care of IBD patients to optimize IBD outcomes. Once realizing impaired body composition, the next challenge is the modulation of body composition through controlling disease activity, nutritional therapy, and physical activity. Excessive FM should also be addressed, and particularly warrants avoidance of steroid therapy.

Since inflammatory cytokines exert a negative effect on appetite and on SMM, one of the first steps to alter lean mass is to control disease activity and achieve remission. It has been demonstrated in a study that during infliximab therapy skeletal muscle mass and muscle strength increased [33].

Nutritional therapy also has a pivotal role in the supportive therapy of IBD patients. In CD patients, concomitant enteral nutrition has been reported to be more effective than infliximab alone. Patients treated with partial enteral nutrition was shown that patients receiving enteral nutrition were less likely to lose response to infliximab compared to controls [45]. Additionally, Gerasimidis et al. found that lean mass improved after the completion of exclusive enteral nutrition [46].

Physical activity with resistance exercise was shown to prevent and even reverse the progression of sarcopenia [47]. Exercise may also contribute to the reduction of the severity of CD and accompanying anorexia while modifying the release of adipokines and ghrelin [12]. Studies on patients with inactive or mildly active CD reported that moderate exercise (walk, yoga) leads to improvement in the quality of life and stress levels [48].

In addition, sarcopenic obesity occurs in some patients, which should be also targeted during the management of IBD patients. Due to the variability of altered body composition experienced in IBD, patients need personalized nutritional intervention.

9. Conclusion

In summary, available data, although heterogeneous, shows that the body composition of patients with IBD may be impaired to a variable extent in comparison with either healthy controls or reference values. However, impaired body composition may not be detected via routine measurement of anthropometrical parameters. The finding of several studies suggests that the prognosis of IBD patients is associated with the alteration of fat and lean mass. The modulation of body composition with nutritional intervention and physical activity can contribute to improve IBD outcomes, including reducing rates of hospitalization, treatment failure, need for surgical intervention and decreasing the incidence of postoperative complications, additionally, it can improve QoL and mental health in IBD patients.