Standing up for the veterinary profession
08 Aug 2024
18 Mar 2016 | Dr Elise Robertson
Inflammatory bowel disease (IBD) has been a major topic of discussion and research in feline gastroenterology for at least 20 years. At times IBD has been stated to be the most common cause of chronic gastrointestinal signs in our feline patients.
Inflammatory bowel disease (IBD) has been a major topic of discussion and research in feline gastroenterology for at least 20 years. At times IBD has been stated to be the most common cause of chronic gastrointestinal signs in our feline patients; however, one of the problems with talking about IBD is that it has had different definitions applied both clinically, diagnostically and histopatholgically, and no clear consensus as to exactly what constitutes IBD has been established.
In some cases, IBD has been referred to in the context of a histopatholigical diagnosis by finding inflammation in intestinal biopsies, while in other cases IBD has been defined as ‘idiopathic’ intestinal inflammation in which histopathology by itself is inadequate for diagnosis. By taking a One Health approach, I’ve started to question the simplicity of the words ‘lymphoplasmacytic IBD’ written on my laboratory reports and have often wondered if our patients instead experience IBS with or without true IBD?
Irritable bowel syndrome (IBS) is a chronic functional disorder that is commonly diagnosed in human gastroenterology. The prevalence of IBS in humans is approximately 7–10% worldwide and is associated with a significant reduction in quality of life. Patients with IBS will often experience abdominal pain and altered bowel habit, with either predominantly diarrhoea (IBS-D), constipation (IBS-C), or both (IBS-M).
In 1978 AP Manning created the first set of formal criteria, called the ‘Manning Criteria’, in an attempt to allow IBS to be positively diagnosed rather than being a diagnosis of exclusion. More recently, the Rome III Classification was established for the functional gastrointestinal disorders (FGID).
Current theories on IBS pathophysiology include: gut motility, inflammation, intestinal bacteria, diet, and psychosocial factors without the use of immunosuppressant medications such as corticosteroids. Interestingly, research has indicated that 40-60% of IBS patients also exhibit symptoms of interstitial cystitis, whilst up to 52% of IC patients also have symptoms consistent with IBS. For patients who struggle with both conditions, the connection is often baffling until you consider the role of the nerves.
Pain is a major problem in IBS. This is thought, in part, to be due to disturbances affecting normal enteric movement/motility. This may be due to visceral hypersensitivity which can be influenced by several factors such as stretching/distension and stress. Like IC, alterations in the brain-gut axis are thought to be a major factor in IBS pathophysiology.
Because the exact aetiology remains unknown, the management of IBS has mainly focused on amelioration of symptoms including increasing fibre intake to regulate defaecation, control of spasm with hyoscine and peppermint oil, antidepressants, including tricyclic antidepressants and selective serotonin reuptake inhibitors, 5-hydroxytryptamine-3 (5-HT3) receptor antagonists, 5-HT4 agonists, diet (low FODMAP) antibiotics, and probiotics. Despite numerous studies, there are still no universally accepted definitive treatment recommendations.
Approximately 10–20% of dogs and cats presented with gastrointestinal signs, including diarrhoea, constipation, pain, bloating, lethargy, and inappetence, had no pathologic lesions identified on extensive investigation, including endoscopy and full thickness biopsies. With these cases we might use the ‘diagnosis’ of lymphoplasmacytic IBD on the laboratory report to give us permission to prescribe corticosteroids to manage the condition, but how do we know if (a) the lymphoplasmacytic IBD is actually pathogenic, and (b) the cause of the pet’s condition?
Despite our attempts to standardise our histopatholoigical interpretations, are we confident that these changes are truly IBD? Or are these changes a ‘normal variation of normal’ due to direct exposure to enteric antigen over the years? We’ve not routinely obtained intestinal biopsies from healthy/asymptomatic patients to compare our findings to those samples from clinical/symptomatic patients and can thus only presume the changes directly correlate with clinical presentation? Do our patients have both IBD with symptoms of IBS? Or what if our patient’s clinical presentation is in fact due to IBS and not IBD? Would this knowledge change how we manage these cases?
To add even more confusion, we now know humans who suffer from interstitial cystitis are prone to IBS as well due to aberrations in their hypothalamic-pituitary -adrenal and autonomic axes of the stress response system. Do cats also experience the same? In particular ‘highly strung’ species such as the oriental lines, which could explain why they experience gastric retention and pyloric outflow ‘stenosis’?
It’s entirely possible that these animals may have motility dysfunction, with or without IBD. Unfortunately, at present, extensive investigations are still required to completely rule out neoplasia. Small cell lymphoma in particular can show signs similar to those of IBD at clinical presentation.
The main reason to extrapolate human criterion to our cats is in an attempt to make informed choices about long term management that could ultimately affect quality of life, positively and negatively. Many patients may improve by the use of pro-motility agents, low carbohydrate diets, and reducing environmental stressors without the use of immunosuppressive agents. This seems true for humans who suffer from both FIC and IBS.
At present, IBS is an under-recognised syndrome in cats. Given our poor ability to detect mild to moderate pain in this species, many cats may be living, undetected, with varying degrees of IBS and not IBD.
Join Elise on our clinical problem-solving CPD course Feline GIT disease - there's more than meets the IBD in Manchester on 5 May 2016.
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