In this second part of the article Dr. Weiner illuminates how IBS (Irritable Bowel Syndrome) is now appreciated for containing an inflammatory component and can be part of IBD (Inflammatory Bowel Disease). He explains the relationship between IBS and IBD to offer a deeper understanding of these conditions.
This original article was published on January 11, 2016 at ndnr.com. It is the fourth part of our new in depth series of posts exploring IBS, IBD, and SIBO, all still very relevant in 2019.
The previous posts in the series were about Treating IBD. Look forward to additional articles in this series on the differences between IBS, IBD, and SIBO, Use of Elemental Diets in IBS and IBD, and additional videos and summary articles including posts related to Chinese Medicine and Acupuncture as treatments for IBS, IBD, and SIBO.
Gary Weiner, ND, LAc
THE VALUE OF DICHOTOMY – DISCERNING IBS VS IBD
Even if IBS and IBD exist on a continuum, there is value in maintaining a division between them. Both IBS and IBD include altered and irregular bowel habits, diarrhea, constipation, and abdominal pain. The pain and discomfort of both IBS and IBD can present as cramping, aching, or bloating, though I do associate frank distension as more of an IBS symptom than an IBD one. Both IBS and IBD display bowel urgency and frequency, or constipation, and both can feature “ineffectual” stooling or mucus (though I see mucus more in IBD). When these common symptoms are presenting, it may be difficult to know what you are observing along the IBS-IBD continuum. This difficulty is compounded by IBD medications that can control inflammation (or not), thus masking the picture, but also irritate the bowel.
What is unique to IBD is often the degree or virulence of the presenting urgency and frequency of bowel movements during acute exacerbation. When extreme, a patient might complain of as many as 10-20 movements in a day. The hematochezia seen in IBD is generally not part of IBS, unless there are active hemorrhoids. And weight loss, fever, and the host of extraintestinal manifestations of either CD or UC – including joint pain, anorectal lesions, mouth ulcers, as well as various skin, eye, and associated hepatobiliary diseases – do not appear with IBS. Nor does the fistulization of CD appear in IBS. Nocturnal bowel symptoms (mainly pain and urgency) are not typical IBS symptoms, but are very common in IBD and are representative of activity on the IBD side of the spectrum.
IBS, while not having a known mechanism leading to particular extraintestinal manifestations, does, however, have a high correlation with headaches, rheumatologic, and genitourinary symptoms such as night frequency and urgency, dyspareunia, sexual dysfunction, and sleep-related disturbances. In fact, epidemiological studies show comorbidities in IBS patients for a lot of what have been considered the “functional” disorders: fibromyalgia syndrome, chronic back pain, chronic pelvic pain, chronic headache, and temporomandibular joint (TMJ) dysfunction, which exist in approximately half of all patients with IBS.18 These should not be confused with the extraintestinal manifestations that are often exacerbated with IBD flaring.
CD causes growth retardation in children, which would not be seen in IBS. The nutritional deficits, weight loss, and failure to thrive, that are seen in acute IBD, are not manifestations of IBS. Nor does IBS feature the strictures and bowel obstruction seen in CD, though both can feature constipation. The inflammation of IBD can cause dysmotility, and also SIBO, which then produces symptoms. Methanogen overgrowth is highly correlated with constipation, and the appearance of constipation in IBD may be reflective of SIBO; however, constipation can also occur due to stricture, obstruction, or acute IBD inflammation. Indeed, the constipation of IBS and IBD are difficult to differentiate without the help of laboratory assessment.
In mild-to-moderate IBD with effective allopathic management, consider that symptomatology may be related more or less to IBS rather than IBD – or to other functional considerations, such as side effects of GI or other medications, or other allergic, psycho-emotional, and neuroendocrine factors. Do not make assumptions that all exacerbations of bowel symptoms are produced by the IBD. Look for the red flags before drawing the conclusion that your IBD patient’s current exacerbation of confusing symptoms that overlap with IBS are actually manifestations on the IBD side of the continuum. Examples include weight loss, nocturnal symptoms, blood mixed with the stools, intense pain, symptoms of intestinal obstructions, and extraintestinal manifestations connected to IBD.
TOOLS FOR THE TEASING
Teasing out IBS from IBD is no easy feat. The patient’s symptoms guide you in conjunction with what is expected given the patient’s medical history. Know the staging of the patient’s IBD, including the medical diagnosis, location, and severity of the disease. This is discerned from medical records or through coordination with a gastroenterologist. If the IBD is stable, it may be that current symptoms are explained through the IBS end of the continuum. Or, it may be that IBS and IBD symptomatology are coexisting. If there is no recent staging, you may have to initiate the process of coordinating care so that information can be obtained. Use history to tease out the common symptoms from the patient, and identify manifestations that point toward one end of the continuum or the other. Then use laboratory evaluation to help you make clinical decisions and construct a treatment plan:
Fecal calprotectin (FC) is a calcium-binding heterodimer that is abundant in the cytoplasm of neutrophils. Inflammation causes neutrophil activation, which results in FC release proportionate to the degree of inflammation.19 This test is the clinician’s best friend during critical periods between gold-standard surveillance procedures, such as colonoscopy, as a highly sensitive way of differentiating IBS and IBD. To distinguish between IBS (“non-organic disease”) and IBD (“organic disease”), the FC cut-off of 50 µg/g returned a sensitivity and specificity of 88% and 78%, respectively, for IBD.19 FC displayed up to an 87% negative predictive value to exclude IBD, and cut-offs less than 250 µg/g had a 90% sensitivity to determine remission of IBD. A negative FC can suggest IBD in remission, thus ruling out active IBD, and sparing most people with IBS from requiring invasive investigations such as colonoscopy.20 When treating IBD patients, whether they are on medications or a naturopathic treatment plan, or both, the FC will indicate whether the IBD is active, with a high degree of reliability, correlating significantly with endoscopic disease activity.21 I use this test frequently to tease out whether I am looking at the IBS within the IBD, rather than the IBD alone. A negative FC does not mean the patient is cured of IBD, rather that it is likely quiescent and you are looking at the presenting symptoms at the IBS end of the IBS-IBD continuum, to be treated accordingly. If the FC is elevated, with symptoms consistent with IBD, you may regard this as flaring IBD and treat accordingly. If you have a patient on prednisone and the FC remains elevated, you are often looking at prednisone resistance, which will further guide your interventions and advice regarding care. Implementing naturopathic therapies while following the patient’s FC allows you to track the degree of mucosal healing that is likely occurring. However, IBS symptoms may still present concomitantly that need to be addressed.
Stool lactoferrin (SL) is an iron-binding protein covering many mucosal surfaces. SL increases significantly with infiltration of neutrophils in the intestinal tract. The sensitivity of SL in IBD approaches 80% when compared with IBS, which is similar to FC and better than C-reactive protein (64%).22 Similar to FC, SL provides a valid method for discriminating between inflammatory and non-inflammatory bowel disease.23
Anti-CdtB and anti-vinculin antibodies is a serum test that can further tease out the IBS within the IBD, providing insight into etiology. Cytolethal distending toxin B (CdtB), produced by bacteria that cause acute gastroenteritis, cross-reacts with the cytoskeleton protein, vinculin, to produce an IBS-like phenotype. These biomarkers tend to be elevated in IBS-D, compared to non-IBS subjects, hence might be helpful in distinguishing IBS-D from IBD in the workup of chronic diarrhea24 or in identifying a predisposition to IBS (in your IBD patient). I have used this test to confirm that I am looking at IBS phenomena when treating IBD patients.
C-reactive protein (CRP) is considered an important protein in acute inflammation. Secreted by hepatocytes, CRP maintains a low level of circulation in healthy individuals (<1 mg/L), but sharply increases (even reaching up to 350-400 mg/L) when there is acute inflammation induced by IL-6, TNFα, and IL-1β. With a short half-life of 19 hours, CRP increases rapidly with acute inflammation, and also sharply decreases.25 However, while CD is associated with a strong CRP response, UC has a very modest or even absent response, which is important to know when you use it to discern what you are observing in a case.25 Consider CRP a useful biomarker to follow when it is elevated in acute phases of CD (not UC) to track success or failure of therapies. While less sensitive then FC and SL, it is nonetheless easy to obtain a serum sample, and results are often available in 24 hours to help confirm that you are looking at predominantly CD symptoms (if there is difficulty distinguishing them from IBS).
Erythrocyte sedimentation rate (ESR) indicates sedimentation speed of red blood cells in plasma, which reflects degree of inflammation. Conditions such as anemia, polycythemia, and thalassemia also affect ESR,26 which must be factored in, as many IBD patients are anemic due to blood loss, poor nutrient absorption, or malnutrition. Compared with CRP, ESR will peak much less rapidly and may also take several days to decrease, even if the clinical condition of the patient or the inflammation is ameliorated.27
Complete blood count (CBC) can be helpful to confirm acute IBD. You will often see an increase in WBCs, anemia patterns that may include decreases in RBCs, hemoglobin, and hematocrit, and an increase in total platelets,28 also a decrease in mean platelet volume (MPV)29 and an increase in red cell distribution width (RDW).30 These markers can help you understand the role of IBD in the symptoms you are observing. IBS will not produce this pattern in the CBC (although comorbid factors could still be producing them).
Comprehensive metabolic panel (CMP) can help you tease out IBD and IBS manifestations within IBD, as acute IBD can include hypoalbuminemia (albumin <3.5 g/dL), hypokalemia (potassium <3.5 mEq/L), and hypomagnesemia (magnesium <1.5 mg/dL). You may also see an elevated alkaline phosphatase. This pattern is not seen at the IBS end of the spectrum unless there are coincidental comorbid factors.31
Stool studies are used to exclude other causes of symptoms, and may include fecal leukocytes, ova and parasite studies, and culture for bacterial pathogens, including C difficile. It is important to distinguish pathogens, potential pathogens, or manifestations of dysbiosis in stool, from positive breath tests representing SIBO.
Hydrogen and methane breath testing functions as a simple, non-invasive method for teasing out the role that IBS may be playing in IBD. The test detects hydrogen (H2) and methane (CH4) gases produced by bacterial fermentation of unabsorbed intestinal carbohydrate excreted in the breath. Results are then used to diagnose carbohydrate malabsorption, SIBO, and to measure the orocecal transit time. Malabsorption of carbohydrates is a key trigger of IBS-type symptoms, such as diarrhea and/or constipation, bloating, excess flatulence, headaches, and lack of energy.32 Results can then help determine the direction of treatment, selection of the most prudent antimicrobial therapies, and further provide insight into the symptoms of dysmotility being observed in IBD.
This is the first part of a multipart article. The remaining parts will be published soon. Full reference list available at the original source.
Dr. Gary Weiner, ND. L.Ac. is the medical director of Pearl Natural Health in Portland, Oregon, where he has developed an alternative and complementary care program for inflammatory bowel disease. He graduated from NCNM in 1997 and completed a 1-year residency in family medicine. He has served as adjunct faculty and clinical supervisor at NCNM, and is on the medical advisory board of the Northwest Crohn’s and Colitis Foundation of America. He is a sought after speaker and lecturer on IBD, IBS and SIBO, speaking to both naturopathic and conventional medical doctors. Dr Weiner lives with his wife and daughter.