- Case Report
- Open Access
Cholestyramine treatment in two dogs with presumptive bile acid diarrhoea: a case report
Canine Medicine and Genetics volume 8, Article number: 1 (2021)
In people, bile acid diarrhoea is a prevalent complication of Crohn’s disease and diarrhoea-associated irritable bowel syndrome. Affected patients typically respond to bile acid sequestrants, such as cholestyramine, but human gastroenterologists often fail to recognize bile acid diarrhoea. Consequently, bile acid diarrhoea is regarded as an underrecognized and undertreated condition in human medicine. Due to lack of diagnostic tools, clinical response to bile acid sequestrants is often used to confirm a diagnosis of bile acid diarrhoea in people.
Several recent studies have shown that bile acid dysmetabolism also occurs in dogs with chronic enteropathies. It has further been shown that dogs with chronic enteropathies have significantly decreased expression of a bile acid transport protein in the ileum compared to healthy dogs, which correlates with faecal bile acid dysmetabolism. Consequently, in spite of the lack of reports in the literature, bile acid diarrhoea is likely to exist in dogs as well.
Two dogs, an 8-year old Rottweiler and a 4.5-year old Siberian Husky were evaluated for chronic watery diarrhoea. Neither dog responded to dietary trials, probiotics, cyclosporine, faecal microbial transplantations or metronidazole. One of the dogs responded to high daily doses of corticosteroids, which were however associated with unacceptable side effects. The other dog was refractory to all standard treatment protocols, including cyclosporine and corticosteroids. Since none of the dogs responded satisfactorily to standard treatment or modulation of the intestinal microbiome, a suspicion of possible bile acid diarrhoea was raised. Treatment with cholestyramine, a bile acid sequestrant was initiated and resulted in marked improvement of faecal consistency, frequency of defecation and activity level in both dogs.
This report presents two dogs with presumed bile acid diarrhoea that were successfully treated with cholestyramine. Therefore, bile acid diarrhoea should be considered as a possible diagnosis in dogs with treatment-refractory chronic diarrhoea.
Plain English summary
Bile acids are produced by the liver and excreted in the small intestine where they are required for proper digestion of fat. They get absorbed in the last segment of the small intestine. In people with Crohn’s disease or irritable bowel syndrome associated with diarrhoea, absorption mechanisms fail, and excessive amounts of bile acids reach the large intestine where they can cause what is known as bile acid diarrhoea (BAD). Cholestyramine, a drug that binds bile acids, is used for treatment of BAD in people. Recent research has shown that dogs with chronic small intestinal inflammation may also have difficulty absorbing bile acids and end up with excessive concentrations in the large intestine. We describe two dogs with chronic diarrhoea that responded well to cholestyramine treatment when all other treatments had failed. We believe that BAD should be considered as a diagnosis in dogs with chronic small intestinal inflammation and diarrhoea that are refractory to standard treatment, and that cholestyramine treatment may be useful in these situations.
Primary bile acids (BAs) are synthesized in the liver and secreted into the small intestine, where they participate in fat absorption. Approximately 95% of BAs are reabsorbed in the ileum and undergo enterohepatic circulation . This process is mediated by the apical sodium-dependent BA transporter (ASBT). Unabsorbed BAs are transformed by 7α-dehydroxylating colonic bacteria (e.g., Clostridium hiranonis in dogs) to secondary BAs . In people, various chronic gastrointestinal disorders are associated with increased amounts of BAs in the colon. This stimulates electrolyte and water secretion and increases mucosal permeability and colonic motility . Bile acid dysmetabolism and BA diarrhoea (BAD) have been reported in 40% of patients with Crohn’s disease and 32% of patients with diarrhoea-predominant irritable bowel syndrome (IBS-D) . Patients with BAD typically respond to BA sequestrants (e.g., cholestyramine). However, despite a high prevalence, BAD is considered an underdiagnosed and undertreated condition in gastroenterology .
Bile acid dysmetabolism has recently been reported in several studies in dogs with chronic enteropathy (CE) [6,7,8,9]. Furthermore, decreased expression of the ASBT in the ileum of dogs with CE has been documented . However, the authors could not find any published reports describing the clinical course and treatment of BAD in dogs. Therefore, the aim of this report was to describe the clinical presentation and response to cholestyramine treatment in two dogs with chronic refractory diarrhoea.
An 8-year old neutered male Rottweiler with a body weight (BW) of 52 kg and a body condition score (BCS) of 5/9 was presented for a severe flare-up of watery diarrhoea and anorexia. The dog was already under treatment as an outpatient for previously diagnosed CE at a referral animal hospital, and was now admitted for fluid therapy and supportive care at the same animal hospital. On admission, the dog was on maintenance treatment with budesonide (3 mg on 2 days out of 3, Entocort; Tillotts Pharma GmbH, Rheinfelden, Germany) and a single protein source diet. The dog had been clinically stable with normal faeces for 2.5 years. Diarrhoea appeared once when budesonide had been tapered to 3 mg every other day, but was absent on a maintenance dose of 3 mg budesonide 2 days out of 3. Biopsies from the gastrointestinal tract had been collected endoscopically 4 years previously and showed mild to moderate lymphocytic-plasmacytic inflammation. Laboratory and imaging data at the time of admission to the animal hospital are shown in Tables 1 and 2.
Prednisolone (Prednisolon; Pfizer, Sollentuna, Sweden) at a dose of 10 mg q 24 h was added to the maintenance dose of budesonide for 3 weeks, which brought the diarrhoea temporarily into remission but led to calcinosis cutis, prompting cessation of prednisolone treatment and tapering of budesonide to 3 mg q 48 h. This was associated with recurrence of diarrhoea. The dog continued to have diarrhoea as well as excessive flatulence and halitosis during the following 12 months. Numerous treatment protocols, including additional immunosuppressive treatments such as cyclosporine and mycophenolate mofetil, metronidazole and dietary changes were tried at different times during this period (Table 3). A faecal microbiota transplantation was given once as a rectal enema at a dose of 5 g of frozen donor stool per kg body weight as described by Chaitman and co-workers . The stool was thawed and blended with 0.9% saline on the day of administration. The donor dog was clinically healthy, free of intestinal parasites, bacterial pathogens and extended beta-lactamase resistant E.coli.
The dog was refractory to all treatments and had liquid diarrhoea 4–5 times daily, including once at night, and a canine inflammatory bowel disease activity (CIBDAI) index of 7 (consistent with moderate IBD) . The poor response to medical and dietary intervention raised the suspicion of BAD. Cholestyramine (Kolestyramin Alternova; Orifarm Generics, Odense, Denmark) treatment was started with 2 g q 24 h for a week. The owners immediately noticed that the faeces became much firmer during 12 h after cholestyramine administration, but watery diarrhoea reappeared later during the day. The dose was increased to 2 g q 12 h, which further improved the quality of the faeces, reduced the frequency of defecation to 2–3 times daily, and markedly reduced flatulence. After increasing the dose to 3 g q 12 h, the diarrhoea stopped, CIBDAI had decreased to 2 (clinically insignificant disease) and faecal scores had improved from 5/5 (liquid diarrhoea) to 3/5 (formed but soft faeces) . Dose reduction to 2 g cholestyramine q 12 h led to return of unformed feces within 36 h. The cholestyramine dose was again successfully increased to 3 g q 12 h. At the time of writing, diarrhoea had not recurred for 11 months, excessive flatulence had disappeared, and vomiting had ceased. Furthermore, the BCS had increased to 7/9 and the dog owner described the dog as more playful than during the past several years.
A 4.5-year old male neutered Siberian Husky with a BW of 34 kg and a BCS of 6.5/9 was referred for FMT. The dog had a life-long history of partially food-responsive chronic diarrhoea that had been somewhat stable as long as the dog only ate a hydrolyzed soy protein diet (Purina HA) with a probiotic supplement (Purina Fortiflora). Even when keeping a strict diet and using the probiotic supplement, flare-ups of diarrhoea and hyporexia occurred every week and lasted for 1–3 days. Several other diets had been tried previously, all resulting in diarrhoea (Table 3). The condition had deteriorated during the last 4 months to persistent diarrhoea, lethargy, marked hyporexia and 15% loss of BW. The dog defecated up to 7 times daily with a faecal score of 3–5/5 and had a CIBDAI score of 13 (severe IBD) . For financial reasons, endoscopy had never been performed. Co-morbidities included zinc-responsive dermatosis and chronic blepharitis. Treatment with elemental zinc improved the skin condition partially. Neither cyclosporine treatment for 3.5 months, nor prednisolone improved the gastrointestinal signs. Metronidazole had been prescribed several times, without improvement of faecal quality. Laboratory and imaging data at the time of referral are shown in Tables 1 and 2. On physical examination, the dog was quiet with marked blepharitis, periorbital dermatitis and moderate facial crusting of the mucocutaneous junctions. The abdomen was moderately tense and painful on palpation. Liquid faeces were detected upon rectal palpation. FMT was given as a rectal enema, using the same donor and protocol as previously described, which initially was associated with a remarkable improvement regarding faecal quality, appetite, activity level and periorbital dermatitis . However, ten days later, the dog appeared to have abdominal pain and diarrhoea returned, followed by pica, hyporexia and lethargy. Four days later, the dog came back for a second FMT. The same donor and protocol were used for the procedure, but no improvement of the gastrointestinal signs was noted. Budesonide treatment, 3 mg q 24 h, was initiated but led to more severe diarrhoea and was stopped after a few days. Loperamide was then prescribed without any improvement. A third FMT was performed 14 days later, without clinical improvement. At this time, cholestyramine at 2 g q 24 h was prescribed. Faecal quality and activity level improved during the first 12 h after each cholestyramine dose, but deteriorated during the following 12 h until the next dose. The cholestyramine dose was increased to 2 g q 12 h, which led to resolution of diarrhoea, decreased frequency of defecation, improved appetite and a more active and playful behaviour. Five months later at follow-up, twice daily cholestyramine treatment was still effective against diarrhoea, hyporexia and lethargy, and the CIBDAI score had decreased to 3 (clinically insignificant disease). Although occasional flare-ups of hyporexia and diarrhoea still occurred, these episodes were much shorter and occurred less frequently than before. Furthermore, the flare-ups of zinc-responsive dermatosis and chronic blepharitis occurred significantly less frequently than before.
This report describes successful treatment of chronic refractory diarrhoea with a BA sequestrant in two dogs. Recent studies have reported faecal BA dysmetabolism and decreased expression of ASBT in the ileum of dogs with CE [6,7,8,9]. Dogs with CE had significantly lower amount of total secondary BAs, and increased percentage of primary BAs compared to healthy dogs [7,8,9]. Similar BA dysmetabolism has been shown in people with inflammatory bowel disease too . In another recent study, the serum concentration of 7α-hydroxy-4- cholesten-3-one (C4), a serum biomarkers of hepatic BA synthesis, was compared between healthy dogs and dogs with chronic diarrhoea . Three of 17 dogs with chronic diarrhoea had serum C4 concentrations significantly above the calculated upper limit of the reference interval. These dogs were all partly or fully refractory to conventional therapy. Based on these previous studies it is likely that bile acid diarrhoea is a disease entity in dogs too, but reports on the clinical course and treatment of BAD in dogs are lacking.
It is estimated that 5–27% of dogs with CE have non-responsive enteropathy (NRE), if studies including only dogs with protein-losing enteropathy are excluded [15,16,17,18,19,20,21,22,23]. If dogs with food responsive enteropathy were excluded, the odds ratio (OR) of becoming refractory to treatment was significantly higher in steroid-responsive dogs compared to food-responsive dogs . Potentially, some dogs with NRE may have BAD.
Bile acid diarrhoea is prevalent in humans with Crohn’s disease and IBS-D. Recent recommendations state that BAD should be considered early in patients with chronic diarrhoea . Still, BAD remains an underrecognized and undertreated condition [5, 24]. There are several pathogenetic mechanisms described that lead to BAD in humans with gastrointestinal disorders, the most common of which is malabsorption of BAs in patients with ileal disease, and dysbiosis, which is associated with a decreased ability to convert primary BAs to secondary BAs. Clostridium hiranonis is a bacterial species that plays a prominent role in converting primary BAs to secondary BAs . Decreased abundance of C. hiranonis has been reported in dogs with CE [9, 25]. However, one of the dogs in this report had a normal dysbiosis index and faecal C. hiranonis abundance, leaving malabsorption the most likely reason for BAD.
Treatment with glucocorticoids in rodent models and healthy human volunteers is associated with increased expression of ASBT, which likely increases BA reabsorptive capacity in the ileum [26, 27]. This positive effect on BA transport might have affected one of the case dogs as well, since diarrhoea ceased with higher doses of corticosteroids. However, this may also have been due to the anti-inflammatory and immune-suppressive properties of corticosteroids.
Cholestyramine is a sequestrant with a high affinity for BAs. When binding to BAs, an insoluble complex is formed that is excreted in the feces. Cholestyramine is recommended for use in dogs at an oral dose of 0.5–2.0 g/dog q 12 h for reduction of idiopathic hypercholesterolaemia . Furthermore, cholestyramine has successfully been used to treat cyanobacterial toxicosis in a dog at a dose of 172 mg/kg for 17 days . Several drugs and toxins must be bound to BAs to undergo enterohepatic circulation. Therefore, the irreversible binding of BAs to cholestyramine inhibits systemic toxin absorption and increases faecal excretion. In healthy laboratory Beagle dogs, the elimination rate of the non-steroidal anti-inflammatory drug (NSAID) tenoxicam was drastically accelerated when multiple doses of oral cholestyramine were given following tenoxicam injection, in contrast to both placebo and charcoal administration . In Plumb’s Veterinary Drugs, cholestyramine is recommended to treat cyanotoxin exposure, NSAID toxicosis and vincristine overdose .
One recent study reported that a cholestyramine dose of 0.7 g/kg q 24 h administered for 14 days to 12 healthy Beagle dogs appeared to be clinically safe . No side effects or weight loss were noted. The faecal dry matter content increased with cholestyramine treatment, but the number of bowel movements did not increase and faecal scores were still in the normal range. Macro- nutrient apparent total tract digestibility decreased after cholestyramine treatment, but remained in the normal range. It should be noted that the dose used in these studies was 7 times higher than the doses used in this case report (0.058 g/kg q 12 h and 0.059 g/kg q 12 h, respectively). However, the long term consequences of cholestyramine treatment in dogs need to be studied.
In people, first-line treatment of BAD is cholestyramine, but gastrointestinal side effects, such as constipation, bloating, nausea, flatulence, abdominal pain and worsening diarrhoea are common . This could affect compliance and make it difficult to titrate dosages to clinical effect. Side effects were less prominent and compliance was better when using newer and more expensive BA sequestrants such as colesevelam or colestipol. Besides gastrointestinal side effects, an over 3-fold increase in alanine aminotransferase (ALT) was noted in 11/67 healthy volunteers . This increase was considered benign, and was not documented in any of the case dogs at follow-up visits. A few cases of vitamin K malabsorption and spontaneous bleeding have been reported in people treated long term with cholestyramine [34,35,36,37]. No negative effect on vitamin K absorption was noted in healthy laboratory Beagle dogs treated with dicumarol and Vitamin K when cholestyramine was given at a dose of 200 mg/kg q 24 h . When the cholestyramine dose was increased to 1.0 g/kg, vitamin K absorption was somewhat delayed, but normalized within 24 h. A massive dose of 3.0 g/kg q 24 h of cholestyramine was associated with decreased absorption of vitamin K if the vitamin and cholestyramine was given at the same time, but not if cholestyramine was given 17 h prior to vitamin K.
In people, 3 categories of tests are available to confirm the diagnosis of BAD . The SeHCAT test measures loss of fecal BAs and is considered the gold standard test, but is only available in very few laboratories worldwide . Alternately, serum levels of of bile acid synthesis, including 7α-hydroxy-4-cholesten-3-one (C4) or the ileal regulatory hormone, fibroblast growth factor 19 (FGF19), can be measured by high-performance liquid chromatography (HPLC). These tests have good specificity and negative predictive value for BA malabsorption in patients with IBS-D or functional diarrhoea, but a lower sensitivity for other types of BA malabsorption. The C4 test is regarded as a good screening test to rule out BA malabsorption, but both C4 and FGF 19 have diurnal variation, which can cause false positive results [3, 40]. Measurement of faecal BAs can be performed using HPLC, but requires a 48 h stool collection period, which is not popular among patients . These diagnostic tests are not widely available. Hence, clinical response to cholestyramine is often used to diagnose BAD in people . This approach can be problematic, as a failed empiric trial with cholestyramine, often due to side effects, does not exclude BAD as a diagnosis . However, the lack of tests to diagnose BAD should not exclude patients with chronic diarrhoea from empiric treatment.
In dogs, analysis of faecal BAs has been described, but a reference interval from a larger population of healthy dogs is lacking [6,7,8,9]. Until tools to diagnose BAD in veterinary medicine are validated and available, we hypothesize that, as in people, empirical treatment with BA sequestrants can be tried in dogs with chronic refractory diarrhoea. This treatment saved the two case dogs from euthanasia.
This case report describes successful treatment of two dogs with chronic, long-lasting refractory diarrhoea with cholestyramine. Clinical response to cholestyramine is often used to diagnose BAD in people. Based on response to treatment of the two dogs in this study, we presume that the dogs in this report had BAD. Cholestyramine might serve as an alternative treatment option for dogs with intractable diarrhoea that do not respond to standard treatment protocols.
Availability of data and materials
Data sharing is not applicable to this article as no datasets were generated or analysed during the current study, but details from the clinical records are available from the corresponding author on reasonable request.
Apical sodium-dependent bile acid transporter
Bile acid diarrhoea
Body condition score
Canine inflammatory bowel disease activity index
Fibroblast growth factor 19
Faecal microbiota transplantation
High-performance liquid chromatography
Inflammatory bowel disease
Diarrhoea predominant irritable bowel syndrome
Non-steroidal anti-inflammatory drug
- q hrs:
75selenium homotaurocholic acid test
Hofmann AF. The syndrome of ileal disease and the broken enterohepatic circulation: cholerheic enteropathy. Gastroenterology. 1967;52(4):752–7.
Kitahara M, Takamine F, Imamura T, Benno Y. Clostridium hiranonis sp. nov., a human intestinal bacterium with bile acid 7alpha-dehydroxylating activity. Int J Syst Evol Microbiol. 2001;51(Pt 1):39–44.
Camilleri M. Bile acid diarrhea: prevalence, pathogenesis, and therapy. Gut Liver. 2015;9(3):332–9.
Walters JR, Pattni SS. Managing bile acid diarrhoea. Ther Adv Gastroenterol. 2010;3(6):349–57.
Khalid U, Lalji A, Stafferton R, Andreyev J. Bile acid malabsoption: a forgotten diagnosis? Clin Med (Lond). 2010;10(2):124–6.
Honneffer JB, Guard BC, Steiner JM, Suchodolski JS. Untargeted metabolomics reveals disruption within bile acid, cholesterol, and tryptophan metabolic pathways in dogs with idiopathic inflammatory bowel disease. (Abstract). Gastroenterology. 2015;148(4):S715.
Giaretta PR, Rech RR, Guard BC, Blake AB, Blick AK, Steiner JM, et al. Comparison of intestinal expression of the apical sodium-dependent bile acid transporter between dogs with and without chronic inflammatory enteropathy. J Vet Intern Med. 2018;32(6):1918–26.
Blake AB, Guard BC, Honneffer JB, Lidbury JA, Steiner JM, Suchodolski JS. Altered microbiota, fecal lactate, and fecal bile acids in dogs with gastrointestinal disease. PLoS One. 2019:14(10). https://doi.org/10.1371/journal.pone.0224454.
Guard BC, Honneffer JB, Jergens AE, Jonika MM, Toresson L, Lawrence YA, et al. Longitudinal assessment of microbial dysbiosis, fecal unconjugated bile acid concentrations, and disease activity in dogs with steroid-responsive chronic inflammatory enteropathy. J Vet Intern Med. 2019;33(3):1295–305.
Chaitman J, Ziese AL, Pilla R, Minamoto Y, Blake AB, Guard BC, et al. Fecal microbial and metabolic profiles in dogs with acute diarrhea receiving either fecal microbiota transplantation or Oral metronidazole. Front Vet Sci. 2020;7:192. https://doi.org/10.3389/fvets.2020.00192.
Jergens AE. Clinical assessment of disease activity for canine inflammatory bowel disease. J Am Anim Hosp Assoc. 2004;40(6):437–45.
The WALTHAM™ Faeces Scoring System Available at: https://www.waltham.com/sites/g/files/jydpyr1046/files/2020-05/waltham-scoring.pdf. Accessed 12 Oct 2020.
Duboc H, Rajca S, Rainteau D, Benarous D, Maubert MA, Quervain E, et al. Connecting dysbiosis, bile-acid dysmetabolism and gut inflammation in inflammatory bowel diseases. Gut. 2013;62(4):531–9.
Kent AC, Cross G, Taylor DR, Sherwood RA, Watson PJ. Measurement of serum 7alpha-hydroxy-4-cholesten-3-one as a marker of bile acid malabsorption in dogs with chronic diarrhoea: a pilot study. Vet Rec Open. 2016;3(1):e000163 eCollection 2016.
Craven M, Simpson JW, Ridyard AE, Chandler ML. Canine inflammatory bowel disease: retrospective analysis of diagnosis and outcome in 80 cases (1995-2002). J Small Anim Pract. 2004;45(7):336.
Allenspach K, Wieland B, Grone A, Gaschen F. Chronic enteropathies in dogs: evaluation of risk factors for negative outcome. J Vet Intern Med. 2007;21(4):700–8.
Luckschander N, Hall JA, Gaschen F, Forster U, Wenzlow N, Hermann P, et al. Activation of nuclear factor-kappaB in dogs with chronic enteropathies. Vet Immunol Immunopathol. 2010;133(2–4):228–36.
Heilmann RM, Jergens AE, Ackermann MR, Barr JW, Suchodolski JS, Steiner JM. Serum calprotectin concentrations in dogs with idiopathic inflammatory bowel disease. Am J Vet Res. 2012;73(12):1900–7.
Pietra M, Fracassi F, Diana A, Gazzotti T, Bettini G, Peli A, et al. Plasma concentrations and therapeutic effects of budesonide in dogs with inflammatory bowel disease. Am J Vet Res. 2013;74(1):78–83.
Heilmann RM, Otoni CC, Jergens AE, Grutzner N, Suchodolski JS, Steiner JM. Systemic levels of the anti-inflammatory decoy receptor soluble RAGE (receptor for advanced glycation end products) are decreased in dogs with inflammatory bowel disease. Vet Immunol Immunopathol. 2014;161(3–4):184–92.
Heilmann RM, Volkmann M, Otoni CC, Grutzner N, Kohn B, Jergens AE, et al. Fecal S100A12 concentration predicts a lack of response to treatment in dogs affected with chronic enteropathy. Vet J. 2016;215:96–100.
Heilmann RM, Berghoff N, Mansell J, Grutzner N, Parnell NK, Gurtner C, et al. Association of fecal calprotectin concentrations with disease severity, response to treatment, and other biomarkers in dogs with chronic inflammatory enteropathies. J Vet Intern Med. 2018;32(2):679–92.
Otoni CC, Heilmann RM, Garcia-Sancho M, Sainz A, Ackermann MR, Suchodolski JS, et al. Serologic and fecal markers to predict response to induction therapy in dogs with idiopathic inflammatory bowel disease. J Vet Intern Med. 2018;32(3):999–1008.
Mottacki N, Simren M, Bajor A. Review article: bile acid diarrhoea - pathogenesis, diagnosis and management. Aliment Pharmacol Ther. 2016;43(8):884–98.
AlShawaqfeh MK, Wajid B, Minamoto Y, Markel M, Lidbury JA, Steiner JM, et al. A dysbiosis index to assess microbial changes in fecal samples of dogs with chronic inflammatory enteropathy. FEMS Microbiol Ecol. 2017;93(11):10. https://doi.org/10.1093/femsec/x136.
Nowicki MJ, Shneider BL, Paul JM, Heubi JE. Glucocorticoids upregulate taurocholate transport by ileal brush-border membrane. Am J Phys. 1997;273(1 Pt 1):G197–203.
Jung D, Fantin AC, Scheurer U, Fried M, Kullak-Ublick GA. Human ileal bile acid transporter gene ASBT (SLC10A2) is transactivated by the glucocorticoid receptor. Gut. 2004;53(1):78–84.
Ramsey I, editor. BSAVA Small Animal Formulary. 7th ed. Quedgeley, Gloucester: British Small Animal Veterinary Association; 2011. p. 82–3.
Rankin KA, Alroy KA, Kudela RM, Oates SC, Murray MJ, Miller MA. Treatment of cyanobacterial (microcystin) toxicosis using oral cholestyramine: case report of a dog from Montana. Toxins. 2013;5(6):1051–63.
Guentert TW, Schmitt M, Defoin R. Acceleration of the elimination of tenoxicam by cholestyramine in the dog. J Pharmacol Exp Ther. 1986;238(1):295–301.
Plumb’s Veterinary Drugs. Available at: http://www.plumbsveterinarydrugs.com.libproxy.helsinki.fi/#!/monograph/LIZ2iyvCBC. Accessed 12 Oct 2020.
Alexander C, Guard BC, Suchodolski JS, Swanson KS. Cholestyramine decreases apparent total tract macronutrient digestibility and alters fecal characteristics and metabolites of healthy adult dogs. J Anim Sci. 2019;97(3):1020–6.
Singhal R, Harrill AH, Menguy-Vacheron F, Jayyosi Z, Benzerdjeb H, Watkins PB. Benign elevations in serum aminotransferases and biomarkers of hepatotoxicity in healthy volunteers treated with cholestyramine. BMC Pharmacol Toxicol. 2014;15:42.
Gross L, Brotman M. Hypoprothrombinemia and hemorrhage associated with cholestyramine therapy. Ann Intern Med. 1970;72(1):95–6.
Acuna R, Gonzalez CM. Hypoprothrombinemia and bleeding associated to treatment with cholestyramine (author's transl). Rev Med Chil. 1977;105(1):27–8.
Shojania AM, Grewar D. Hypoprothrombinemic hemorrhage due to cholestyramine therapy. CMAJ. 1986;134(6):609–10.
Vroonhof K, van Rijn HJ, van Hattum J. Vitamin K deficiency and bleeding after long-term use of cholestyramine. Neth J Med. 2003;61(1):19–21.
Robinson HJ, Kelley KL, Lehman EG. Effect of Cholestyramine, a bile acid binding polymer, on vitamin K1 absorption in dogs. Proc Soc Exp Biol Med. 1964;115:112–5.
Vijayvargiya P, Camilleri M. Current practice in the diagnosis of bile acid diarrhea. Gastroenterology. 2019;156(5):1233–8.
Schiller LR. Good news about BAD. Clin Gastroenterol Hepatol. 2020;18(1):45–7.
We would like to thank the dog owners for excellent cooperation.
LT is partly supported by the Swedish Veterinary Care Foundation. The sponsors had no involvement in study design, collection of samples, analysis of the data, or interpretation of data, in the writing process, or in the decision to submit the article for publication.
Ethics approval and consent to participate
Consent for publication
The owners of both dogs agreed to publication.
JMS and JSS work for the Gastrointestinal Laboratory at Texas A&M University that performs measurement of the dysbiosis index on a fee for service basis. LT has no financial or personal relationships that could inappropriately influence or bias the content of the paper.
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
The original version of this article was revised: “The unit mg/kg should be g/kg in the Discussion section.”
About this article
Cite this article
Toresson, L., Steiner, J.M. & Suchodolski, J.S. Cholestyramine treatment in two dogs with presumptive bile acid diarrhoea: a case report. Canine Genet Epidemiol 8, 1 (2021). https://doi.org/10.1186/s40575-021-00099-x
- Bile acids