Impact of Inflammatory Bowel Disease on Skeletal Muscle Health

M S et al | DOI: 10.65188/nurexus.1031

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Journal of MedVerse Research & Practice

ISSN: 3107-4278

Impact of Inflammatory Bowel Disease on Skeletal Muscle Health

Dr. Srimathi M

, Dr. Sugumaran V

Postgraduate, Associate Professor

Department of Gastroenterology and Hepatology, Tirunelveli Medical College,

Email: srimathimohan56@gmail.com

Submission Date: 28.06.2025

Accepted Date: 25.07.2025

Published Date: 31.07.2025

DOI: 10.65188/nurexus.1031

article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits

unrestricted use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.

Abstract

Background: Inflammatory Bowel Diseases (IBD), encompassing Ulcerative Colitis (UC) and Crohn’s Disease

(CD), are associated with systemic inflammation that can adversely impact nutritional status and muscle health. This

study aimed to assess muscle mass, strength, and nutritional indicators in IBD patients and evaluate their correlation

with disease activity.

Methods: A cross-sectional study was conducted among 100 IBD patients (50 UC and 50 CD). Anthropometric

measurements, Subjective Global Assessment (SGA), Mid-Arm Muscle Circumference (MAMC), and Handgrip

Strength (HGS) were used to assess nutritional and muscle status. Laboratory parameters, including serum albumin,

CRP, ESR, and haemoglobin, were also recorded. Correlations between disease activity (Mayo score for UC, CDAI

for CD) and muscle/nutritional indices were analysed.

Results: Malnutrition (SGA B+C) was observed in 58% of participants, more prevalent in CD (64%) than UC (52%).

Low BMI (<18.5 kg/m²) was noted in 29% overall. Serum albumin <35 g/L was seen in 36%, with a higher

frequency in CD (42%). Mean HGS was significantly lower in women (17.4 ± 4.8 kg) than men (28.1 ± 6.3 kg); 26%

of participants had HGS below cutoff. Significant negative correlations were found between disease activity and BMI

(r = –0.38, p = 0.001), serum albumin (r = –0.42, p < 0.001), MAMC (r = –0.29, p = 0.004), and HGS (r = –0.46, p <

0.001).

Conclusion: Malnutrition and impaired muscle function are highly prevalent in IBD, particularly in CD. Muscle

strength and nutritional indicators correlate inversely with disease activity, highlighting the importance of routine

assessment of muscle health in IBD management.

Keywords: Inflammatory Bowel Disease, Ulcerative Colitis, Crohn’s Disease, Malnutrition, Sarcopenia, Muscle

Strength, Nutritional Status

Introduction

Inflammatory Bowel Diseases (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), are

long-standing inflammatory conditions of the gastrointestinal tract that exhibit periodic relapses and

remissions. These disorders not only affect the gut but also have systemic implications, with emerging

attention on their extraintestinal manifestations such as impaired muscle health [1].

Sarcopenia, defined as the gradual loss of skeletal muscle mass and function, has been identified in up to

60% of individuals with IBD [2]. This decline in muscle health leads to increased fatigue, diminished

physical function, and worsened clinical outcomes, such as extended hospital stays, postoperative

complications, and higher mortality rates [3,4]. In contrast to age-related sarcopenia, muscle deterioration

in IBD is usually a consequence of secondary factors, including chronic systemic inflammation, inadequate

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nutrient absorption, prolonged corticosteroid use, and physical inactivity [5,6]. A key contributor to muscle

wasting in IBD is persistent inflammation. Elevated levels of cytokines - such as tumour necrosis factor-

alpha (TNF-α) and interleukin-6 (IL-6) - inhibit muscle protein synthesis while activating proteolytic

systems like the ubiquitin–proteasome and autophagy–lysosome pathways, which promote muscle

degradation [7,8]. Additionally, the ongoing gastrointestinal symptoms, coupled with increased resting

energy expenditure and anorexia, create a caloric deficit that further accelerates muscle loss [9].

Malnutrition is another prevalent complication in IBD, often coexisting with muscle dysfunction.

Inadequate intake of proteins and essential micronutrients - such as vitamin D, iron, and magnesium-

impairs muscle regeneration and mitochondrial efficiency [10,11]. Furthermore, medications frequently

used in IBD management, such as corticosteroids and biologics, may contribute to muscle atrophy by

altering hormonal balance and mitochondrial pathways [12].

Recent advancements have enabled the use of imaging modalities like computed tomography (CT) and

magnetic resonance imaging (MRI) to assess muscle mass objectively, particularly at the L3 vertebral level

- a validated site for estimating whole-body muscle mass [13]. Alongside imaging, functional tools such as

handgrip strength and gait speed have gained recognition for their ability to evaluate early signs of

sarcopenia and functional decline [14]. Despite the growing evidence of its clinical relevance, muscle

health remains under-assessed in the routine management of IBD. Current guidelines seldom include

structured muscle evaluations. Early recognition of sarcopenia and its association with malnutrition and

disease activity is essential for developing comprehensive strategies-such as personalized nutrition plans,

resistance exercise, and anti-inflammatory treatments preserve muscle integrity and improve long-term

outcomes [15].

Materials & Methods

A prospective observational study was conducted in the Department of Gastroenterology and Hepatology,

Tirunelveli Medical College, over a period of 12 months. A total of 100 patients were enrolled - 50 with

Ulcerative Colitis (UC) and 50 with Crohn’s Disease (CD), either in active disease or remission at

enrolment. Adults over 18 years diagnosed with Ulcerative Colitis (UC) or Crohn’s Disease (CD),

confirmed through clinical, biochemical, endoscopic, and histopathological findings, were included.

Patients with comorbidities affecting muscle mass (e.g., chronic kidney/liver disease, heart failure, COPD,

malignancy, neuromuscular disorders, diabetes) were excluded. Written informed consent was obtained

from all participants.

Assessments were conducted at baseline, 6 weeks, and 12 weeks. Disease activity was measured using the

Mayo Score for UC (remission ≤2, severe >10, response ≥3-point reduction) and CDAI for CD (remission

<150, mild 150–220, moderate 220–450, severe >450). Nutritional assessment included BMI, SGA (A:

well-nourished; B: moderate malnutrition; C: severe malnutrition), and serum albumin. Undernutrition was

defined as BMI <18.5 kg/m², SGA B/C, or albumin <35 g/L. Body composition was assessed using mid-

arm circumference, triceps skinfold thickness, and mid-arm muscle circumference (MAMC). Muscle

strength was evaluated using handgrip strength (HGS) via a Smedley dynamometer, with low strength

defined as <26 kg for men and <18 kg for women. Data collected included demographics, disease severity,

lab parameters, endoscopic findings, and nutritional and muscle health indicators. No biological specimens

were collected.

The present study was approved by the Institutional Ethics Committee of Tirunelveli Medical College (Ref

No: TMC/IEC/2024/27358). A detailed Participant Information Sheet was provided to all participants, and

written informed consent was obtained prior to their inclusion in the study.

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Statistical Analysis: Data were analysed using SPSS v26.0. Continuous variables were presented as mean

± SD or median (IQR), and categorical data as frequencies and percentages. Categorical comparisons: Chi-

square or Fisher’s exact test. Continuous data: Student’s t-test or Mann–Whitney U test. Longitudinal data:

Repeated Measures ANOVA or Friedman test. Correlation: Pearson’s or Spearman’s coefficients.

Significance set at p < 0.05

Results

Table 1: Baseline Demographic and Clinical Characteristics (n = 100)

Characteristic

Total (n = 100)

UC (n = 50)

CD (n = 50)

p-value

Age (years), mean ± SD

36.7 ± 12.5

38.1 ± 11.2

35.3 ± 13.7

0.241

Male, n (%)

58 (58%)

30 (60%)

28 (56%)

0.683

Duration of illness (yrs)

3.4 ± 2.1

3.2 ± 1.9

3.6 ± 2.3

0.427

Smokers, n (%)

22 (22%)

8 (16%)

14 (28%)

0.134

The mean age was 36.7 ± 12.5 years, with no significant difference between UC and CD groups (p =

0.241). Males comprised 58% of the total, similarly distributed across both groups (p = 0.683). The average

disease duration was 3.4 years, comparable between UC and CD (p = 0.427). Smoking was more common

in CD (28%) than UC (16%), though not statistically significant (p = 0.134).

Figure 1: Disease Activity Scores

At baseline, 40% of UC patients and 36% of CD patients were in clinical remission. Mild disease was seen

in 20% (UC) and 24% (CD), moderate in 24% (UC) and 28% (CD), and severe activity in 16% (UC) and

12% (CD). The mean Mayo score for UC was 5.6 ± 2.3, while the mean CDAI for CD was 235.7 ± 78.4,

indicating moderate disease activity in both groups.

Table 2: Nutritional Status (SGA, BMI, Albumin)

Nutritional Indicator

Total (n = 100)

UC (n = 50)

CD (n = 50)

p-value

SGA A (Well-nourished)

42 (42%)

24 (48%)

18 (36%)

0.203

SGA B (Mild–Moderate malnutrition)

38 (38%)

18 (36%)

20 (40%)

0.692

SGA C (Severe malnutrition)

20 (20%)

8 (16%)

12 (24%)

0.315

BMI <18.5 kg/m²

29 (29%)

12 (24%)

17 (34%)

0.237

Serum albumin <35 g/L

36 (36%)

15 (30%)

21 (42%)

0.181

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Overall, 42% of patients were well-nourished (SGA A), while 38% had mild to moderate malnutrition

(SGA B), and 20% showed severe malnutrition (SGA C). UC patients had a slightly higher proportion of

well-nourished individuals (48%) compared to CD (36%), though not statistically significant. A BMI <18.5

kg/m² was more frequent in CD (34%) than UC (24%). Similarly, hypoalbuminemia (serum albumin <35

g/L) was observed in 42% of CD patients versus 30% of UC patients. However, none of these differences

reached statistical significance.

Table 3: Anthropometric Measurements

Parameter

Total (mean ± SD)

UC (mean ± SD)

CD (mean ± SD)

p-value

Height (cm)

165.3 ± 8.5

164.7 ± 7.9

165.9 ± 9.1

0.521

Weight (kg)

58.2 ± 11.2

59.6 ± 10.4

56.8 ± 12.0

0.248

MAC (cm)

26.4 ± 3.2

26.7 ± 3.0

26.1 ± 3.4

0.354

TSF (mm)

9.8 ± 2.5

10.2 ± 2.3

9.4 ± 2.7

0.118

MAMC (cm)

20.3 ± 2.7

20.6 ± 2.4

20.0 ± 2.9

0.321

The mean height and weight were similar across both groups, with UC patients averaging 164.7 cm and

59.6 kg, and CD patients 165.9 cm and 56.8 kg (p > 0.05). Mid-arm circumference (MAC), triceps skinfold

thickness (TSF), and mid-arm muscle circumference (MAMC) were also comparable, with slightly higher

values in UC patients, but none of the differences were statistically significant. These findings suggest

overall comparable anthropometric measurements between UC and CD groups.

Table 4: Handgrip Strength (HGS) Measurements

Sex

Mean HGS (kg) ± SD

HGS Below Cutoff, n (%)

Men

28.1 ± 6.3

12 (20.7%)

Women

17.4 ± 4.8

14 (33.3%)

Total

100

23.5 ± 7.1

26 (26%)

The overall mean handgrip strength (HGS) among participants was 23.5 ± 7.1 kg, with 26% of individuals

falling below the gender-specific cutoff values. Men had a significantly higher mean HGS (28.1 ± 6.3 kg)

compared to women (17.4 ± 4.8 kg). However, a greater proportion of women (33.3%) had reduced HGS

compared to men (20.7%), indicating a higher prevalence of muscle weakness among female patients.

Table 5: Laboratory Parameters

Parameter

UC (mean ± SD)

CD (mean ± SD)

p-value

Hemoglobin (g/dL)

11.8 ± 1.4

11.2 ± 1.7

0.048*

CRP (mg/L)

10.3 ± 7.1

13.7 ± 9.4

0.027*

ESR (mm/hr)

28.6 ± 13.5

33.2 ± 14.8

0.091

Serum Albumin (g/L)

37.2 ± 4.3

35.5 ± 5.1

0.049*

Crohn’s disease (CD) patients exhibited significantly lower hemoglobin levels (11.2 ± 1.7 g/dL) compared

to ulcerative colitis (UC) patients (11.8 ± 1.4 g/dL, p = 0.048), indicating a greater burden of anemia in CD.

Inflammatory markers were also more elevated in CD, with CRP significantly higher (13.7 ± 9.4 mg/L vs.

10.3 ± 7.1 mg/L, p = 0.027), while ESR showed a non-significant trend towards elevation. Serum albumin

was notably lower in CD patients (35.5 ± 5.1 g/L) than in UC (37.2 ± 4.3 g/L, p = 0.049), reflecting poorer

nutritional and inflammatory status.

Table 6: Correlation of Disease Activity with Muscle Mass and Strength (n = 100)

Variable

Disease Activity Score

r (Pearson/Spearman)

p-value

BMI

Mayo/CDAI

–0.38

0.001**

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Serum Albumin

Mayo/CDAI

–0.42

<0.001**

MAMC

Mayo/CDAI

–0.29

0.004**

HGS

Mayo/CDAI

–0.46

<0.001**

Disease activity (Mayo/CDAI) showed significant negative correlations with BMI (r = –0.38, p = 0.001),

serum albumin (r = –0.42, p < 0.001), MAMC (r = –0.29, p = 0.004), and handgrip strength (r = –0.46, p <

0.001). These findings highlight that higher disease activity in IBD is associated with poorer nutritional

status and reduced muscle mass and strength.

Discussion

Our study assessed muscle health and nutritional indicators in patients with ulcerative colitis (UC) and

Crohn’s disease (CD). Findings showed a significant proportion of IBD patients had impaired muscle mass,

decreased handgrip strength (HGS), and indicators of malnutrition, with more pronounced derangements

among CD patients. In our cohort, reduced HGS was observed in 26% of patients, with a higher prevalence

in females. This aligns with Schneider et al., who documented diminished muscle strength in 27% of IBD

patients, especially in women and those with active disease (16). Bryant et al. also emphasized that muscle

dysfunction can manifest even before noticeable muscle mass loss, highlighting the utility of functional

tools like HGS in early detection (17). Although differences in anthropometric indicators like MAMC and

BMI were not statistically significant between UC and CD, CD patients tended to have lower values. This

is consistent with existing literature indicating that CD is more often associated with nutritional deficiencies

and sarcopenia, primarily due to its small bowel involvement and frequent relapses (18).

Serum albumin was significantly lower in CD patients (35.5 ± 5.1 g/L) compared to UC (37.2 ± 4.3 g/L),

reflecting systemic inflammation and reduced protein intake. Valentini et al. reported similar findings,

noting that hypoalbuminemia in CD correlated with both inflammation and nutritional impairment (19).

Gender-specific trends were evident in HGS values, with female patients exhibiting significantly lower

mean HGS and a higher proportion below the cutoff. Boparai et al. observed a comparable gender disparity

in their study and suggested that body composition differences and hormonal influences could explain these

findings (20). We identified significant negative correlations between disease activity and BMI, MAMC,

serum albumin, and HGS, indicating that increased disease severity is associated with poorer nutritional

and muscle health. Subramaniam et al. similarly demonstrated a direct link between inflammatory burden

and catabolic muscle loss in IBD patients (21). Severe malnutrition (SGA C) was found in 20% of our

participants. This is within the range reported in other studies, which suggest that 15–25% of IBD patients

experience severe nutritional compromise, particularly during active disease phases (22). Moreover,

underweight status (BMI <18.5 kg/m²) was seen in 29% of patients, closely aligning with the findings of

O’Sullivan et al., who stressed that nutritional risk often remains underdiagnosed in IBD patients during

routine care (23).

Conclusion

This study shows that patients with IBD, especially Crohn’s disease, often have poor nutritional status and

reduced muscle strength. Higher disease activity was linked to lower BMI, MAMC, serum albumin, and

handgrip strength. Simple tools like SGA and HGS can help identify at-risk patients early and guide timely

interventions.

Conflict of Interest: Nil

Reference

1. Abraham C, Cho JH. Inflammatory bowel disease. N Engl J Med. 2009 Nov 19;361(21):2066-78.

2. Fiorindi C, Caprioli F, Furfaro F, et al. Extraintestinal manifestations and other complications in

M S et al | DOI: 10.65188/nurexus.1031

Page 6

inflammatory bowel disease. J Clin Med. 2022;11(2):350.

3. Ryan E, McNicholas D, Creavin B, et al. Sarcopenia and inflammatory bowel disease: a systematic review.

Inflamm Bowel Dis. 2019 Sep 17;25(1):67–73.

4. Zhang T, Cao L, Cao T, et al. Prevalence of sarcopenia and its impact on postoperative outcome in patients

with inflammatory bowel disease. Gastroenterol Res Pract. 2020; 2020:4987343.

5. Adams DW, Gurwara S, Silver HJ, et al. Sarcopenia is common in patients with inflammatory bowel disease

and is associated with adverse outcomes. Dig Dis Sci. 2022;67(4):1470–9.

6. Holt DQ, Moore GT. Inflammation, nutrition and enteric microbiota in the pathogenesis of sarcopenia in

inflammatory bowel disease. Nutrients. 2020;12(9):2603.

7. D’Haens G, Panaccione R, Higgins PDR, et al. The London position statement of the World Congress of

Gastroenterology on biological therapy for IBD: corticosteroids in IBD. Am J Gastroenterol.

2011;106(4):590–7.

8. Tominaga K, Sugaya T, Oshima T, et al. TNF-α induces skeletal muscle atrophy in a mouse model of

Crohn’s disease. J Gastroenterol. 2020;55(7):703–15.

9. Dalle S, Rossmeislova L, Koppo K. The role of inflammation in age-related sarcopenia. Front Physiol.

2017;8:1045.

10. Nguyen DL, Ma G, Nguyen ET. Review: Impact of inflammatory bowel disease on nutrition status. Nutr

Clin Pract. 2019;34(3):340–50.

11. Benjamin JL, Mckernan DP, Hedin CRH, et al. Vitamin D and inflammatory bowel disease: mechanisms,

therapy, and prevention. Curr Opin Gastroenterol. 2020;36(3):192–9.

12. Opstelten JL, de Vries JHM, Wools A, et al. Diet and inflammatory bowel disease: review of patient-targeted

recommendations. Clin Nutr. 2019;38(6):2435–45.

13. Cushing KC, Ly L, Godat LN, et al. Corticosteroids and sarcopenia: a retrospective cohort study in

inflammatory bowel disease. JPEN J Parenter Enteral Nutr. 2021;45(3):531–7.

14. Mourtzakis M, Prado CM, Lieffers JR, et al. A practical and precise approach to quantification of body

composition in cancer patients using computed tomography images. Curr Opin Clin Nutr Metab Care.

2008;11(5):735–42.

15. Karmiris K, Koutroubakis IE, Kouroumalis EA. The role of muscle performance and physical function

assessment in patients with IBD. World J Gastroenterol. 2015;21(43):12204–10.

16. Schneider SM, Al-Jaouni R, Filippi J, Wiroth JB, Zeanandin G, Arab K, et al. Muscle strength loss in

patients with Crohn’s disease: A functional approach beyond the assessment of body composition. Clin Nutr.

2008;27(6):868–74.

17. Bryant RV, Ooi S, Schultz CG, Goess C, Grafton R, Hughes J, et al. Low muscle mass and sarcopenia:

Common and predictive of osteopenia in inflammatory bowel disease. J Crohns Colitis. 2015;9(9):640–6.

18. Nguyen DL, DeChicco D, Nguyen ET, Bechtold ML. Sarcopenia in inflammatory bowel disease: A review

of current knowledge and practical clinical considerations. World J Gastroenterol. 2017;23(23):3881–91.

19. Valentini L, Schaper L, Buning C, Hengstermann S, Koernicke T, Tillinger W, et al. Malnutrition and

impaired muscle strength in patients with Crohn’s disease: Relationship to disease activity and duration.

Nutrition. 2008;24(7-8):694–702.

20. Boparai RS, Malik P, Gupta D, Kaur K. Gender differences in muscle strength and nutritional status among

inflammatory bowel disease patients in India. Eur J Clin Nutr. 2018;72(10):1365–9.

21. Subramaniam K, Fallon K, McKay R, Shadbolt B, Falk GL. Influence of disease activity and body

composition on muscle strength in inflammatory bowel disease patients. Gut Liver. 2013;7(2):173–80.

22. Lomer MCE, Thompson RPH, Powell N, Lindsay JO. A multi-centre UK study assessing nutritional status in

adult patients with inflammatory bowel disease. Br J Nutr. 2009;101(7):1031–40.

23. O’Sullivan M, O’Morain C. Malnutrition in inflammatory bowel disease: A neglected but treatable

complication. Clin Gastroenterol Hepatol. 2006;4(5):698–703.