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Review
Anorectal benign disease
 Pharmacotherapy for fecal incontinence: potential treatment with a traditional Japanese medicine Kampo
Kotaro Maeda1orcid, Toshinobu Sasaki2orcid, Tomohisa Hattori3orcid
Annals of Coloproctology 2025;41(5):369-378.
DOI: https://doi.org/10.3393/ac.2025.00283.0040
Published online: October 23, 2025

1Department of Surgery, Medical Corporation Himawariseishinkai Ome Imai Hospital, Tokyo, Japan

2Division of Research and Development, Department of International Pharmaceutical Planning, Tsumura & Co., Tokyo, Japan

3Faculty of Pharmaceutical Sciences, Aomori University, Aomori, Japan

Correspondence to: Kotaro Maeda, MD, PhD Department of Surgery, Medical Corporation Himawariseishinkai Ome Imai Hospital, 1-2609-2 Imai Ome, Tokyo 198-0023, Japan Email: kmaeda@fujita-hu.ac.jp
• Received: March 13, 2025   • Revised: May 28, 2025   • Accepted: May 28, 2025

© 2025 The Korean Society of Coloproctology

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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  • Fecal incontinence (FI) significantly impairs patient quality of life and creates substantial distress not only for affected individuals but also for nurses and caregivers. The prevalence of FI among older adults is estimated at up to 20%, although the sensitive nature of the condition often prevents active reporting by patients. This article reviews risk factors and pharmacotherapies for FI, emphasizing the therapeutic potential of Daikenchuto (DKT). The etiology of FI is multifactorial and lacks a singular definition. Currently, no prescription drugs specifically approved for FI are available, leaving treatment options limited. Nonetheless, major clinical guidelines have identified several viable pharmacological approaches. Strongly recommended treatments include the antidiarrheal agent loperamide and stool bulking or solidifying agents, such as dietary fiber and polycarbophil. Other therapeutic options include ramosetron, a 5-HT3 receptor antagonist; amitriptyline, a tricyclic antidepressant; and sodium valproate and diazepam, which are GABAergic neuromodulators. Recently, research has explored the efficacy and mechanism of action of DKT, a traditional Japanese medicine Kampo. Historically used for abdominal symptoms like bloating and known for promoting intestinal motility, emerging evidence suggests DKT may also effectively manage FI.
  • Keywords: Fecal incontinence; Drug therapy; Daikenchuto; Kampo medicine; Anal sphincter
Fecal incontinence (FI) is a condition characterized by involuntary stool leakage from the anus, resulting in a loss of bowel control. Multiple definitions exist, with the Rome IV criteria—an internationally recognized standard—defining FI as the "recurrent uncontrolled passage of fecal material in an individual with a developmental age of at least 4 years" [1]. In contrast, the Clinical Practice Guidelines for Fecal Incontinence, 2nd ed, published by the Japanese Society of Coloproctology (JSCP) in 2024, defines FI as "symptoms of fecal leakage from the anus unconsciously or against the patient’s intention" [2]. Despite differences in definitions, FI essentially represents a loss of control over defecation, and its treatment aims to restore bowel control to improve patient well-being.
Given its nature, FI causes considerable social and psychological stress, affecting not only patients experiencing severe leakage almost daily but also those with milder symptoms. Despite the significant psychological and economic burdens associated with FI, many patients neither seek nor receive adequate treatment. Feelings of embarrassment, along with resignation attributed to aging, often contribute to the underreporting and undertreatment of FI [3]. As the population in high-income nations continues to age, the prevalence of pelvic floor dysfunction, including FI, is rising [4]. Physicians and healthcare providers play critical roles in guiding patients toward effective treatments by assessing their living conditions (home or care facility), care requirements, and medical histories—including previous surgeries or structural alterations in the rectal and anal regions. The primary goal of treatment is to improve patient quality of life (QOL) by reducing distress from incontinence and alleviating the associated burden on nurses and caregivers.
This review primarily used PubMed as the main database, supplemented with searches on Google Scholar. Studies published between 1980 and 2025 were included, with database searches conducted using combinations of terms such as FI, epidemiology, etiology, pharmacotherapy, pharmacology, and Daikenchuto (DKT). Reference lists from relevant articles, reviews, and commentaries were also examined to identify additional articles not captured by initial searches.
FI is classified into 3 types based on its pathogenesis: passive, urge, and mixed [2]. Passive FI involves involuntary, passive stool leakage, typically caused by impaired internal anal sphincter (IAS) contraction and other factors, including reduced rectal sensation [5]. Urge FI occurs when patients sense the need to defecate but cannot retain stool, leading to leakage. It results from external anal sphincter injury or dysfunction, pudendal nerve damage, or diminished rectal distensibility and retention capacity. Mixed FI displays symptoms characteristic of both passive and urge FI. Although few studies have quantified each FI type's prevalence, one prospective US study classified patients as 5% passive FI, 35% urge FI, and 6% mixed FI, with 55% unspecified [6]. In contrast, a survey conducted in Japan found that 49% of patients had passive FI, 16% had urge FI, and 35% had mixed FI [7].
The etiology of FI is diverse, involving dysfunction of the anal sphincter (idiopathic, traumatic, or neurogenic), impaired sensory perception, rectal reservoir dysfunction, chronic diarrhea, and abnormal stool consistency. Additional contributing factors include congenital diseases, childbirth trauma, surgical interventions, colorectal disorders, medical injuries, and neurological conditions affecting the central, spinal, or peripheral nervous systems [5].
Childbirth-related anal sphincter defects constitute a significant cause of FI. Ultrasonographic assessments within 2 months postpartum indicate an anal sphincter defect incidence rate of approximately 27% to 35% in primiparous women [8]. Such trauma impairs anorectal function and increases the risk of developing FI, with incidence rates rising further in subsequent years post-delivery [9]. Stretching or damage to the pelvic floor nerves during childbirth is also considered a contributory factor [10].
Anorectal disorders, such as hemorrhoids, mucosal and anal fissures, rectal prolapses, and fistulas, represent significant risk factors for FI [11]. Surgical treatments for these conditions, particularly internal anal sphincterotomy or fistulotomy, carry notable risks of postoperative soiling (35%–45%) [12]. Low anterior resection of the rectum is another significant risk factor. Postoperative FI following low anterior resection results primarily from the loss of rectal reservoir function and reduced neorectal capacity, collectively known as low anterior resection syndrome (LARS) [11].
Pelvic floor radiotherapy also correlates with FI occurrence. Post-radiotherapy complications, including radiation-induced proctosigmoiditis, small bowel injury, fistula formation, diminished rectal capacity, impaired sphincter function, and reduced rectal mucosal sensitivity, may contribute to FI development [11–13]. Additionally, diabetes mellitus significantly increases the risk of FI (odds ratio of 2.74 compared to nondiabetic controls), suggesting diabetic neuropathy affects the defecation reflex [14]. Certain medications and dietary factors further influence FI development. Antibiotics, laxatives, alcohol, coffee, and similar stimulants soften stool and induce diarrhea, exacerbating FI [15]. Microscopic colitis, a chronic inflammatory condition of the colon that is challenging to detect visually, has also been identified as an underlying cause of FI [16].
Conservative FI management involves initial therapies such as dietary modifications and bowel habit training, and specialized interventions like pelvic floor muscle training, biofeedback, transanal bowel cleansing, and pharmacotherapy. Currently, no prescription medications are specifically approved for FI by regulatory authorities. However, major clinical guidelines have identified several pharmacological treatment options. The American College of Gastroenterology (ACG) guidelines strongly recommend loperamide, clonidine, and other antidiarrheal agents, although the evidence supporting these recommendations is considered low [17]. Loperamide is similarly recommended by Rome IV [1], the European Society for Coloproctology (ESCP) [18], National Institute for Health and Care Excellence (NICE) [19], and JSCP guidelines [2]. Both ESCP and JSCP guidelines also recommend bulking agents despite a low level of supporting evidence. Additionally, the JSCP guidelines list DKT, a traditional Japanese medicine Kampo, as a "proposed drug," despite limited evidence and a weak recommendation. Therefore, this review provides an overview of the effects of several pharmacotherapies for FI, including DKT.
Loperamide hydrochloride binds to opioid receptors in the intestines, reducing peristalsis. It also modulates water and electrolyte secretion and absorption within the intestinal tract, increasing stool formation and solidifying the stool [20], thereby reducing defecation frequency.
Several randomized controlled trials (RCTs) have demonstrated loperamide’s efficacy. Palmer et al. [21] compared loperamide with codeine and diphenoxylate in 30 patients experiencing diarrhea, 19 of whom had FI. They found that loperamide significantly reduced defecation frequency, improved stool consistency, and decreased FI episodes. Compared to centrally acting opioids like codeine and diphenoxylate, loperamide generally has fewer central side effects such as nausea, vomiting, drowsiness, dizziness, depression, and blurred vision. Sze and Hobbs [22], in an open-label study involving 69 women with FI, investigated the combined effect of loperamide and methylcellulose. Although some participants developed constipation, women treated with this combination showed significantly higher cure rates than those receiving expectant management alone (46% vs. 0%, P<0.01). Fox et al. [23], in a double-blind, placebo-controlled crossover study involving 10 obese participants experiencing FI due to increased bowel lipids from orlistat (a lipase inhibitor), demonstrated that loperamide, compared to placebo, significantly alleviated incontinence symptoms (P<0.05) and increased anal resting pressure (P<0.01). Markland et al. [24] compared loperamide with psyllium and reported significant reductions in FI episodes and improvements in symptom severity and QOL in both groups, with no significant intergroup differences. However, constipation occurred more frequently in the loperamide group (29%) compared to the psyllium group (10%).
Loperamide reduces intestinal motility, solidifies stool consistency, and enhances anal resting and squeeze pressures in patients with FI, particularly those with decreased anal sphincter contractility [25]. These therapeutic effects may involve acetylcholine release modulation and prostaglandin synthesis inhibition.
Although multiple RCTs have reported the efficacy of this drug, the level of evidence remains variable, as some studies were open label or involved a small number of patients, and efficacy was demonstrated only in a before-and-after comparison [22–24]. Regarding safety, loperamide overdose can cause central nervous system depression, particularly in children, and paralytic ileus. In patients with active inflammatory bowel disease, loperamide should be cautiously administered due to risks such as toxic megacolon [26].
Fiber-based stool bulking agents are useful conservative treatments for FI symptoms [27]. Natural fiber, which refers to botanical components not easily degraded by digestive enzymes, is effective because it is transported to the intestinal tract without digestion or absorption.
There are 2 types of natural fiber: soluble and insoluble. Psyllium is a representative soluble fiber. When mixed with water, psyllium forms a gel-like matrix that slows digestion, regulates blood glucose and cholesterol, and modulates nutrient absorption due to its viscosity [28]. Although clinical studies specifically evaluating dietary fiber in FI treatment are limited, experience-based evidence supports fiber supplementation as a first-line treatment for mild FI symptoms [29]. Studies involving healthy participants and hospitalized patients have demonstrated reductions in soft stool frequency with increased dietary fiber intake. Furthermore, fiber supplementation in enteral feeding formulations has been associated with decreased stool frequency [28, 30]. Bliss et al. [27] conducted an open-label study involving 39 patients who received daily dietary fiber for 1 month, resulting in a 50% reduction in FI episodes. Similarly, a single-blind, randomized, placebo-controlled study involving 189 patients with FI reported significantly reduced FI frequency in the psyllium-treated group [31].
Calcium polycarbophil, a synthetic fiber, is a hydrophilic macromolecular polymer resistant to gastrointestinal digestion. In the acidic gastric environment, calcium ions dissociate, releasing polycarbophils. These polymers absorb more than 70 times their original weight under neutral intestinal conditions, effectively increasing stool volume [32]. Saito et al. [33] demonstrated calcium polycarbophil’s efficacy in improving fecal characteristics and decreasing defecation frequency and stool water content in sennoside-induced diarrhea. Animal models of constipation have shown that calcium polycarbophil increases defecation frequency and stool weight without inducing diarrhea, indicating potential utility for FI management [34]. Abe et al. [35], in a clinical case-control study involving 72 FI patients, found that calcium polycarbophil treatment improved FI scores from 11 to 5. They reported adverse drug reactions (ADRs), including constipation, hard stools, and abdominal bloating, were reported in 14% of the patients in that study. Although no RCTs have evaluated calcium polycarbophil’s efficacy specifically for FI, it remains a commonly utilized treatment option in Japan [7]. In Japan, calcium polycarbophil is an ethical-use prescription drug, whereas in other countries, it is distributed as an over-the-counter medication.
Ramosetron, a 5-hydroxytryptamine receptor subtype 3 (5-HT3) receptor antagonist, may be utilized to manage urge FI in patients with diarrhea-predominant irritable bowel syndrome (IBS). By blocking 5-HT3 receptors in the intestine, this medication reduces diarrhea through inhibition of stress-induced colonic transport acceleration. Additionally, it reportedly alleviates abdominal pain and visceral hypersensitivity by inhibiting 5-HT3 receptors located on afferent nerve endings [36]. Although no RCTs have specifically assessed ramosetron for FI, several studies have demonstrated its beneficial effects on bowel urgency in IBS patients. Matsueda et al. [37] compared ramosetron (5 µg/day for 12 weeks) with placebo in 539 Japanese patients with diarrhea-predominant IBS, showing decreased bowel movement frequency and improved stool consistency with ramosetron. Similarly, Fukudo et al. [38], in an RCT involving 576 female patients with diarrhea-predominant IBS, reported stool solidification and improved QOL with a daily dose of 2.5 µg ramosetron. Furthermore, in an RCT for patients with severe LARS, treatment with ramosetron (5 µg/day for 4 weeks) reduced severe LARS scores from 88% to 58% [39, 40]. While these studies did not specifically target FI, the results indicate potential efficacy of ramosetron for urge FI.
Frequent adverse events associated with ramosetron include abdominal distension, constipation, and hard stools; these are typical side effects associated with 5-HT3 receptor antagonists [41].
Amitriptyline, a tricyclic antidepressant, has been empirically utilized to relieve symptoms of idiopathic FI and IBS. In an open-label study, Santoro et al. [42] compared FI symptoms in 18 idiopathic FI patients treated with amitriptyline (20 mg/day for 4 weeks) against 24 untreated healthy individuals. Significant improvement in the Cleveland Clinic Florida Incontinence Score (CCFIS) was observed in 89% of treated patients [43], with median scores improving from 16 before treatment to 3 after treatment. Furthermore, 72% of patients achieved complete system remission, maintaining control even after 6 months. Amitriptyline also reduced defecation frequency, rectal pressure, and improved anal pressure (P<0.001). Its therapeutic effects are attributed to the suppression of rectal activity through anticholinergic, antimuscarinic, and serotonergic pathways, along with improved anal sphincter contractility during rectal contractions. Future RCTs are required to rigorously evaluate amitriptyline’s efficacy for FI. Commonly reported ADRs include dry mouth, drowsiness, somnolence, sedation, and fatigue, reflecting typical parasympathetic effects of tricyclic antidepressants [44].
Clonidine, an α2-adrenergic agonist, suppresses gastrointestinal motor activity by inhibiting acetylcholine release through presynaptic mechanisms at enteric plexus and neuromuscular junctions. This medication reportedly decreases colonic tone, enhances colonic compliance, reduces colonic sensation, and diminishes rectal compliance and sensitivity in healthy individuals. It has also shown symptomatic improvements in diarrhea-dominant IBS patients. Bharucha et al. [45] conducted an open-label, uncontrolled study and reported that clonidine alleviated urge FI symptoms in 12 women, with symptomatic improvement correlating to increased rectal compliance and reduced rectal sensation. However, further RCTs are necessary to validate these findings. The major ADRs of clonidine are dry mouth and sedation [46].
Kusunoki et al. [47] observed that sodium valproate, an antiepileptic drug, effectively decreased daily stool frequency, soiling incidents, and perianal skin irritation while increasing resting anal pressure. These effects suggest that sodium valproate’s action involves γ-aminobutyric acid (GABA) receptors in the IAS, potentially improving incontinence symptoms [48]. The most frequent side effects include transient gastrointestinal disturbances, such as anorexia, nausea, and vomiting, reported in approximately 16% of patients [49].
Similarly, Maeda et al. [50] reported that diazepam—a hypnotic, sedative, anxiolytic, anticonvulsant, and muscle relaxant—effectively managed FI symptoms in patients with LARS. Although the exact mechanism is unknown, diazepam likely influences the nervous system through direct stimulation of GABA receptors in the brain [51], indicating a potential GABA receptor-mediated action similar to sodium valproate. Common ADRs associated with diazepam include central nervous system and respiratory depression, dependence, benzodiazepine withdrawal syndrome, sedation, fatigue, and confusion [52].
DKT is a traditional Japanese medicine (Kampo), derived from a classical Chinese medical text but further developed independently in Japan. It comprises a mixture of 3 botanical ingredients: processed ginger, Japanese pepper, and Asian ginseng [53]. Since 1986, DKT has been widely used in Japan as an ethical-use drug for gastrointestinal symptoms.
Double-blind RCTs have reported the efficacy of DKT for postoperative ileus [54, 55]. Additionally, an RCT in healthy individuals demonstrated that DKT significantly increased small intestinal motility (P<0.04) and showed a tendency to enhance ascending colon motility (P<0.07) [56]. Preclinical studies have also shown that DKT ameliorates gastrointestinal dysfunction in rat models of ileus [57, 58].
Fig. 1 presents the 3-dimensional high-performance liquid chromatography analysis of DKT. The principal ingredients, hydroxy-α-sanshool (HAS) and hydroxy-β-sanshool (HBS), induce intestinal contractions in animal models, such as mice and guinea pigs [59, 60]. Additionally, HAS stimulates peristalsis in isolated intestinal tissues [61].
Although not officially approved by the Japanese Ministry of Health, Labor and Welfare specifically for treating FI, DKT is used in specialized medical institutions and has been proposed as a potential therapeutic agent in the 2024 edition of the JSCP guidelines for FI management [2]. No RCT has directly evaluated the efficacy of DKT for FI, but several observational studies have investigated its use. In a retrospective study involving 157 patients with FI (mean age, 74 years) who experienced defecation disorders, such as difficult or incomplete defecation, DKT significantly improved the CCFIS, a gold-standard measure of FI severity, from 10.4 to 8.4 (P<0.001). Examining individual CCFIS components, the scores for "solid," "liquid," and "pads use" improved significantly from 1.5 to 0.9 (P<0.001), 2.5 to 1.7 (P<0.001), and 2.7 to 2.4 (P=0.018), respectively (Table 1) [62]. Moreover, DKT administration appeared to normalize stool consistency, as assessed by the Bristol Stool Scale [63].
A prospective study involving patients over 70 years of age with FI accompanied by abdominal pain and bloating also showed significant improvements in CCFIS, from 12.1 to 7.7, following 4 weeks of DKT treatment (15 g/day) (Table 2) [64]. Significant improvements were also observed in the individual components, including “solid,” “liquid,” “pads use,” and “lifestyle alteration.” Furthermore, the Fecal Incontinence Quality of Life scale, which is a QOL assessment index characteristic of FI [65], also improved significantly in the study [64]. In addition, retrospective and prospective studies have reported that DKT administration increased anorectal resting pressure by approximately 20%.
Several hypotheses regarding DKT’s mechanism of action have been proposed, illustrated schematically in Fig. 2. DKT promotes intestinal motility through the activation of transient receptor potential ankyrin 1 (TRPA1) [60] and transient receptor potential vanilloid 1 (TRPV1) receptors in the intestine [66]. Moreover, DKT increases blood flow in the small intestine and colon in rats [67, 68], with adrenomedullin release via TRPA1 activation playing a key role [69].
Regarding FI specifically, DKT has been demonstrated to directly induce contraction of the IAS in canine models [70]. Another study identified HBS, a Japanese pepper component, as potentially mediating this effect [71]. Hasebe et al. [72] found that several weeks of DKT administration in mice led to increased populations of intestinal microbiota such as Clostridium and Lactococcus. These bacteria play roles in regulating intestinal inflammation and maintaining intestinal barrier integrity [73, 74], potentially contributing to the beneficial effects of DKT on stool consistency observed in FI patients, as shown by Abe et al. [62].
Furthermore, Iturrino et al. [75] observed that DKT tends to decrease rectal sensory thresholds in patients with functional constipation. This effect could potentially support normal defecation in patients with FI characterized by stool impaction due to diminished rectal sensation.
No placebo-controlled RCTs have yet assessed DKT specifically for FI. Published placebo-controlled RCTs have investigated the effects of DKT on colonic motility in healthy subjects and postoperative ileus after hepatectomy and gastrectomy. These studies suggest DKT's influence on bowel function, but not directly on FI, highlighting the need for placebo-controlled RCTs to confirm its intrinsic effectiveness for FI.
A study conducted in Japan found the incidence of ADRs with DKT to be 2.0%, with gastrointestinal disorders being the most common [76]. Due to its pharmacological effect of enhancing intestinal motility, careful physician monitoring is recommended, particularly in patients whose FI is associated with diarrhea, as DKT may exacerbate symptoms in such cases.
The etiology of FI is complex and multifactorial, with no single causative factor identified. Regarding pharmacotherapy, antidiarrheal agents such as loperamide and stool bulking agents are frequently employed as conservative treatments, demonstrating some efficacy. Recently, observational studies have reported beneficial effects of DKT, a traditional Japanese medicine Kampo, in improving FI symptoms. Clinical studies suggest DKT’s mechanisms may involve the direct contraction of IAS (smooth muscle tissue) and enhancement of rectal sensory function. Given these properties, DKT could be particularly beneficial in older patients who exhibit decreased rectal sensation and low resting anal pressure. Nonetheless, placebo-controlled RCTs are necessary to definitively confirm DKT’s intrinsic efficacy for managing FI.

Conflict of interest

Kotaro Maeda is the co-editor-in-chief of this journal, but was not involved in the peer reviewer selection, evaluation, or decision process of this article. Kotaro Maeda and Tomohisa Hattori received honoraria for consultation from Tsumura & Co., and Toshinobu Sasaki is an employee of Tsumura & Co. No other potential conflict of interest relevant to this article was reported.

Funding

None.

Author contributions

Conceptualization: KM; Data curation: all authors; Formal analysis: all authors; Visualization: all authors; Writing–original draft: KM, TS; Writing–review & editing: all authors. All authors read and approved the final manuscript.

Fig. 1.
Three-dimensional high-performance liquid chromatography of Daikenchuto ingredients, showing chemical structures of its main ingredients. Image provided by Tsumura & Co. (data are from the representative lot; not all ingredients of Daikenchuto are indicated).
ac-2025-00283-0040f1.jpg
Fig. 2.
Schematic of the mechanism of Daikenchuto (DKT). TRPA1, transient receptor potential ankyrin 1; TRPV1, transient receptor potential vanilloid 1; 5-HT, 5-hydroxytryptamine (serotonin); Ach, acetylcholine; NK1, neurokinin 1.
ac-2025-00283-0040f2.jpg
Table 1.
Changes in the CCFIS before and after treatment (n=149)
Component CCFIS P-value
Baseline After 1 mo
Solid 1.5±1.5 0.9±1.4 <0.001
Liquid 2.5±1.4 1.7±1.6 <0.001
Gas 2.3±1.7 2.3±1.7 0.854
Pads use 2.7±1.6 2.4±1.8 0.018
Lifestyle alteration 1.4±1.8 1.2±1.7 0.275
Total CCFIS 10.4±4.5 8.4±5.4 <0.001

Values are presented as mean±standard deviation. Statistical testing was performed using the Wilcoxon rank sum test.

CCFIS, Cleveland Clinic Florida Incontinence Score.

Modified from Abe et al. [62], available under the Creative Common license.

Table 2.
Time course of fecal incontinence severity in CCFIS after treatment
Component CCFIS P-valuea
0 wk (A) After 2 wk (B) After 4 wk (C) A vs. B A vs. C
Solid 2.0±1.3 1.0±1.2 1.2±1.3 0.001** 0.001**
Liquid 2.3±1.4 1.1±1.4 1.0±1.4 0.004** 0.005**
Gas 1.9±1.7 1.4±1.6 1.4±1.6 0.118 0.324
Pads use 3.8±0.7 3.3±1.3 3.0±1.6 0.125 0.031*
Lifestyle alteration 2.1±1.7 1.5±1.7 1.2±1.7 0.125 0.016*
Total CCFIS 12.1±5.1 8.2±4.9 7.7±5.3 <0.001*** 0.002**

Values are presented as mean±standard deviation. CCFIS was evaluated before and 2 and 4 weeks after Daikenchuto administration.

CCFIS, Cleveland Clinic Florida Incontinence Score.

aAnalyzed by the Wilcoxon signed rank test.

*P<0.05; **P<0.01; ***P<0.001.

Modified from Shimazutsu et al. [64], available under the Creative Common license.

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        Pharmacotherapy for fecal incontinence: potential treatment with a traditional Japanese medicine Kampo
        Ann Coloproctol. 2025;41(5):369-378.   Published online October 23, 2025
        DOI: https://doi.org/10.3393/ac.2025.00283.0040
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      Pharmacotherapy for fecal incontinence: potential treatment with a traditional Japanese medicine Kampo
      Image Image
      Fig. 1. Three-dimensional high-performance liquid chromatography of Daikenchuto ingredients, showing chemical structures of its main ingredients. Image provided by Tsumura & Co. (data are from the representative lot; not all ingredients of Daikenchuto are indicated).
      Fig. 2. Schematic of the mechanism of Daikenchuto (DKT). TRPA1, transient receptor potential ankyrin 1; TRPV1, transient receptor potential vanilloid 1; 5-HT, 5-hydroxytryptamine (serotonin); Ach, acetylcholine; NK1, neurokinin 1.

      Fig. 1.

      Fig. 2.

      Pharmacotherapy for fecal incontinence: potential treatment with a traditional Japanese medicine Kampo
      Component CCFIS P-value
      Baseline After 1 mo
      Solid 1.5±1.5 0.9±1.4 <0.001
      Liquid 2.5±1.4 1.7±1.6 <0.001
      Gas 2.3±1.7 2.3±1.7 0.854
      Pads use 2.7±1.6 2.4±1.8 0.018
      Lifestyle alteration 1.4±1.8 1.2±1.7 0.275
      Total CCFIS 10.4±4.5 8.4±5.4 <0.001
      Component CCFIS P-valuea
      0 wk (A) After 2 wk (B) After 4 wk (C) A vs. B A vs. C
      Solid 2.0±1.3 1.0±1.2 1.2±1.3 0.001** 0.001**
      Liquid 2.3±1.4 1.1±1.4 1.0±1.4 0.004** 0.005**
      Gas 1.9±1.7 1.4±1.6 1.4±1.6 0.118 0.324
      Pads use 3.8±0.7 3.3±1.3 3.0±1.6 0.125 0.031*
      Lifestyle alteration 2.1±1.7 1.5±1.7 1.2±1.7 0.125 0.016*
      Total CCFIS 12.1±5.1 8.2±4.9 7.7±5.3 <0.001*** 0.002**
      Table 1. Changes in the CCFIS before and after treatment (n=149)

      Values are presented as mean±standard deviation. Statistical testing was performed using the Wilcoxon rank sum test.

      CCFIS, Cleveland Clinic Florida Incontinence Score.

      Modified from Abe et al. [62], available under the Creative Common license.

      Table 2. Time course of fecal incontinence severity in CCFIS after treatment

      Values are presented as mean±standard deviation. CCFIS was evaluated before and 2 and 4 weeks after Daikenchuto administration.

      CCFIS, Cleveland Clinic Florida Incontinence Score.

      aAnalyzed by the Wilcoxon signed rank test.

      *P<0.05; **P<0.01; ***P<0.001.

      Modified from Shimazutsu et al. [64], available under the Creative Common license.

      Table 1.

      Table 2.

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